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EN100022
|
Exam: temperature
|
39° C.
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: pressure
|
70/40 mmHg.
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: HB
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: WBC
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: lymphocytes
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: Monocytes
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: Eosinophils
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: Platelets
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: HBsAg
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: HBeAg
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: VDRL
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: AFP
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: HIV
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: HCV
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: protein
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: albumin
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
|
EN100022
|
Exam: infection
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
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EN100022
|
Exam: actin
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not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
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EN100022
|
Exam: SMA
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not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
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EN100022
|
Exam: desmin
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not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
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EN100022
|
Exam: cytokeratin
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not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
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EN100022
|
Exam: CD34
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not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
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EN100022
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Exam: catenin
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not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
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EN100022
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Exam: Ki67
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not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
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EN100022
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Exam: polypneic
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not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
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EN100022
|
Exam: saturation
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not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
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EN100022
|
Exam: glucose
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not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
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EN100022
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Exam: HMB
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not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
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EN100022
|
Exam: Melan-A
|
not available
| 0 |
A 60 year-old man presented to an outside institution for septic shock with hematesis. He had a medical history of diabetes mellitus, hypertension and he was amputated right leg (trans-femoral amputation) for diabetic arteriopathy six months before admission complicated by venous thrombosis. Home medications included daily pioglitazone, atenolol, furosemide and anticoagulant with poor compliance. Initial examination revealed a patient in state of septic shock, respiratory rate 28 cycles per min, his pulse was regular with an apical rate of 120 beats/min, temperature 39° C, blood pressure 70/40 mmHg, he had necrotic and suppurative amputation stump with peripheral pulse abolished. Patient was given immediately oxygen, fluids, antibiotics, and drugs to increase blood pressure. Six hours later, the patient presented a single episode of hematemesis. There was no associated melena or abdominal pain. He had no history of alcohol use, liver disease, varices, peptic ulcer disease, abdominal aortic surgery, nonsteroidal anti inflammatory drug use, gastroparesis, or previous GI bleeding. Physical examination was unremarkable. Pertinent laboratory studies included a hemoglobin level of 10 g/dL, platelet count was normal, blood urea of 1,2 g/l (0,18-0,45 g/L), and a creatinine level of 68 mg/L (7-13 mg/L). After hemodynamic stabilization, an oesophageo-gastro-duodenoscopy was performed which showed: The upper third of the esophagus was circumferentially congestive, but the middle and lower third showed circumferential black pigmentation: the mucosa was black and covered by an exudate of the same color associated with diffuse bleeding. Gastric mucosa was strictly normal in direct vision and in retrovision, the bulb and duodenum were normal. Biopsie specimens were showed necrotic debris, mucosal submucosal necrosis with a local inflammatory response. The treatment of this condition was based continuous high dose omeprazole (8 mg / h) after bolus of 80mg and total parenteral nutrition. The patient experienced no further hematemesis or melena. Due to the severity of the necrosis, and with deterioration of his condition and persistent sepsis he died later in the same day.
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EN100265
|
Exam: temperature
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
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EN100265
|
Exam: pressure
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
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EN100265
|
Exam: HB
|
10.3g/dl.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: WBC
|
10200 cells/dl.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: lymphocytes
|
26.1%.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: Monocytes
|
10.1%.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: Eosinophils
|
2.7%.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: Platelets
|
350000/ul.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: HBsAg
|
positive.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: HBeAg
|
negative.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: VDRL
|
positive.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: AFP
|
>50000KU/L.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: HIV
|
negative.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: HCV
|
negative.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: protein
|
Result:
0) dalla data EN10026510419:
dopo 3 eventi: low. [\MULTI_ANSWER]
dopo 3 eventi: 44g/L. [\MULTI_ANSWER]
dopo 5 eventi: >50000KU/L.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: albumin
|
Result:
0) dalla data EN10026510419:
dopo 3 eventi: low. [\MULTI_ANSWER]
dopo 3 eventi: 29g/L.
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: infection
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: actin
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: SMA
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: desmin
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: cytokeratin
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: CD34
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: catenin
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
|
EN100265
|
Exam: Ki67
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
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EN100265
|
Exam: polypneic
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
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EN100265
|
Exam: saturation
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
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EN100265
|
Exam: glucose
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
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EN100265
|
Exam: HMB
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
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EN100265
|
Exam: Melan-A
|
not available
| 0 |
A 36 year old female farmer gravida 5 para 4 at 27 weeks gestation presented to our facility. Her main complaint was a 3 month history of epigastric abdominal pain, which was gradual in onset, dull and persistent. Pain had gradually worsened over the months with no known relieving or aggravating factors but with intermittent radiation to the chest. There was a history of significant weight loss but no associated early satiety, jaundice, fever, itch or spontaneous bleeding. No history of blood transfusion and patient was on her routine hematinic from the antenatal clinic (ANC). She is not a known diabetic, Hypertensive and has no known chronic illness. Patient did not know her Hepatitis status. Denied to taking any alcohol or smoking. There were no cardiorespiratory nor urogenital symptoms. She did not store grains at home and had no known contact with chemicals or ionizing radiation.
Clinical signs on examination included wasting, mild pallor, a tinge of jaundice but well hydrated, afebrile and no palpable lymphnodes. She had palmer erythema but no clubbing and parotid enlargement. Respiratory, cardiovascular and neurological examinations were unremarkable. Abdomen was grossly distended with distorted contour in the upper half and visibly distended anterior abdominal wall veins draining away from the umbilicus. Liver was enlarged 12cm below the costal margin with a span of 17cm. The liver was hard, nodular with irregular edge, mild tendernes and had a bruit on auscultation. The spleen was not palpable but with demonstrable mild ascites and bipedal eodema up to the mid shin. Symphysio fundal height was 26 cm, with longitudinal lie and breech presentation. Fetal heart rate was 134 bpm and regular. Rectal and vaginal examination were unremarkable. Initial diagnosis of hepatocellular Carcinoma in pregnancy was made. Laboratory assesment revealed HB-10.3g/dl, WBC 10200 cells/dl; Neutrophils 59.3%, lymphocytes 26.1%, Monocytes 10.1% and Eosinophils 2.7%. Platelets 350000/ul. Normal bilirubin but GGT and AST were raised (4 times upper limit). Total protein and albumin were low, 44g/L and 29g/L respectively with INR-1.3.HBsAg was positive, HBeAg negative with HBV DNA level of 126869 IU/ml \(Viral load). VDRL positive but TPHA not done. Alphafeto protein (AFP) >50000KU/L. She tested negative to HIV and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lessions. The liver measured 17.2cm and there was mild ascites. Pelvic scan revealed a 27 week, 3 day old fetus, with active fetal movements. A revised diagnosis of hepatocellular carcinoma on a cirrhotic liver with decompensation in pregnancy was made. She was managed with analgesia, furosemide, spironolactone and lamivudine added for prevention of mother to child trasmission of the hepatitis B infection. The plan was to allow pregnancy to continue to at least 32 completed weeks to improve the chance of neonatal survival. However because of the progressive unbearable abdominal pain, pregnancy was terminated at 30 weeks 3days by successful induction of labour. The outcome was a fresh stillbirth weight 1.2kg. Pain was markedly reduced post delivery and was discharged home after 5 days. She was booked for a follow up visit at the gastrointestinal clinic. She was seen at the clinic at 2 weeks and four weeks post discharge but was lost to follow up afterwards.
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EN100427
|
Exam: temperature
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
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EN100427
|
Exam: pressure
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: HB
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: WBC
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
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EN100427
|
Exam: lymphocytes
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
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EN100427
|
Exam: Monocytes
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
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EN100427
|
Exam: Eosinophils
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
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EN100427
|
Exam: Platelets
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
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EN100427
|
Exam: HBsAg
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: HBeAg
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: VDRL
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: AFP
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: HIV
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: HCV
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: protein
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: albumin
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: infection
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: actin
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: SMA
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: desmin
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: cytokeratin
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: CD34
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: catenin
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: Ki67
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: polypneic
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: saturation
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: glucose
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: HMB
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100427
|
Exam: Melan-A
|
not available
| 0 |
A 61-year-old woman, gravida 3 para 3, presented with an increased size of ovarian cyst. Her history revealed a diagnosis of left ovarian cyst 3cm in diameter 3 years previously. Her serum cancer antigen (CA) 125 and CA 19-9 levels were within the normal ranges, and she was followed up at 6-month intervals at a private hospital. The ovarian cyst size had not changed in size and structure on biannual transvaginal ultrasound (TVS). However, she was referred to our institution in July 2016 with progression of ovarian cyst to 6cm on a pelvic ultrasonogram 2 weeks ago. The patient underwent menopause at age 48 years, with an uneventful past menstrual cycle. She had no medical history except the benign thyroid nodule, no relevant surgical history and had not received hormonal therapy. Routine blood chemistry and serum tumor marker analysis showed that the levels of carcinoembryonic antigen, CA 19-9, CA 125, and human epididymis protein 4 were all within the normal ranges. Uterine cervical cytology at the time of admission was normal. TVS showed a left ovarian unilocular cyst, size 6cm × 5cm × 4cm, with diffuse low-level internal echoes, thin walled, smooth margined, no septa and no papillary projections. The uterus size was 6cm × 4cm × 3cm, and a 1cm uterine myoma was found in the fundus. Pelvic contrast-enhanced computed tomography (ECT) images revealed a unilocular cystic lesion measuring 6 cm at its widest dimension, without enhancing solid intramural nodules and no evidence of lymphadenopathy or ascites. CT scan indicated benign ovarian cystic tumors.
The patient underwent laparoendoscopic single-site (LESS) surgery. On laparoscopic inspection, the cyst was found to be located in the ampullary and fimbrial regions of the left fallopian tube. The left fallopian tube was grossly unremarkable and the left ovary was atrophied. The left ovary and tube were completely separate from the cyst and the cyst was surrounded by a translucent wall with serous cystic components, but solid components were not seen inside. Clinical diagnosis was suggestive of left paratubal cyst. The patient underwent hysterectomy and BSO. Although tumor markers were normal and there was no presence of papillary projections, the progression in size in the postmenopausal woman indicated a possible malignancy. Frozen sections were prepared from surgery specimens and confirmed a benign cyst. After surgery, the pelvic cavity was explored and no specific findings were found in the abdominal cavity.
Histopathological examination of the paratubal cyst revealed the presence of polypoid lesions on the internal surface of the cyst. The tumor cells showed nuclear atypism and stratification, which are histological characteristics of borderline tumor. A final diagnosis of paratubal borderline serous tumor was confirmed. The patient was discharged from the hospital on postoperative day 3. CT images were retrospectively evaluated, focusing on the left ovary, fallopian tube, and paratubal cyst after surgery. Multiplanar reconstruction CT imaging revealed linear fat planes between the left ovary and the cyst, indicating that the left ovary, fallopian tube and paratubal cyst were separate structures, similar to those seen during surgery. The tumor was not completely staged, and a comprehensive surgical staging operation was recommended; however, the patient refused adjuvant surgical treatment and opted for close follow-up. Pelvic ECT, TVS and tumor markers were checked every three months. The patient remains asymptomatic and follow-up at 24 months showed no evidence of recurrence or metastasis.
|
EN100705
|
Exam: temperature
|
not available
| 0 |
We report the case of a male patient, 79 years old, diabetic for 10 years on metformin, hypertensive for 5 years on amilodipine; occasional alcoholic weaned 4 years ago. He was initially admitted for mental confusion with sudden onset dysarthria dating back 48 hours before. Initial assessment found Glasgow score (GCS) of 12/15 (eye opening at 5, verbal response at 2, motor response at 5), symmetrical and reactive pupils, without feeling-motor deficit, normal osteotendinous reflexes, slightly polypneic at 24 cycles/min, pulsed oxygen saturation (SpO 2) at 97% in ambient air, he was tachycardic at 115 bpm and hypertensive at 160/95 mmHg, his capillary blood glucose at 2.24 g/L, and glycosuria on the urine dipstick test without ketonuria. The patient was apyretic. Arterial gas testing showed normal corrected anion gap metabolic acidosis, with hypokalaemia at 3 mmol/L and normal lactatemia at 0.43 mmol/L. Diagnosis of diabetes decompensation was made despite absence of ketone bodies on urine dipstick test. After conditioning, the patient was put on a hydration regimen with hypokalaemia correction and insulin therapy, and then referred to intensive care for additional management in face of non-improvement in his neurological condition. A brain scan was performed objectifying multiple parietal ischemic foci, chest scanner showed a thickening of the septal and foci of bronchial dilation without sign of pneumopathy linked to COVID-19 infection; abdominal ultrasound did not show any abnormalities. An electrocardiogram was performed showing no electrical signs of hypokalaemia or repolarization disturbances, transthoracic echocardiography was normal, as was ultrasound of supraortic trunks. Laboratory workup showed an elevated C-reactive protein (CRP) of 45.5 with negative procalcitonin (0.04 ng/ml), white blood cells at 12,500 (PNN at 9280 and normal lymphocytes at 2140), no thrombocytopenia, normal ferritinemia, fibrinogen levels elevated to 5.37 and negative D-dimers. Natremia, magnesemia, corrected serum calcium, phosphoremia and thyroid assessment was normal. SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) by nasopharyngeal swab was negative, COVID-19 serology (IgM and IgG) was also negative. Faced with concept of ischemic lesions on a brain scan, anticoagulation at a prophylactic dose, antiplatelet aggregation with aspirin and statins were initiated as well as an antibiotic therapy at a meningeal dose with ceftriaxone pending results of the lumbar puncture which subsequently showed a clear liquid with a high proteinorachia at 0.58g/l (normal between 0.15 and 0.45), a normal glycorachia/blood sugar ratio at 0.58 (normal at 0.5); with a culture showing less than 3 elements, sterile after 24 hours. Cerebral Magnetic resonance angiography performed on day 2 of admission showed signs in favor of vascular leukopathy, with some calcifications in basal ganglia and cortical atrophy. Electroencephalogram showed signs of epilepsy, which prompted us to retain the diagnosis of nonketotic hyperglycemia-related epileptic seizures. Anticonvulsant treatment was started with sodium valproate. The Patient worsened neurologically despite correction of his metabolic acidosis, he was intubated on day 3 of his admission (day 5 of symptoms onset). A cerebral computerized tomography (CT) scan was performed without showing any progressive lesions. Faced with installation of lymphopenia (HIV serologies 1 and 2 negative) with increased CRP, a multiplex RT-PCR in protected distal bronchial sample as well as in Cerebrospinal fluid (CSF) were performed, the first was positive to SARS-CoV-2. Reverse transcription polymerase chain reaction of SARS-CoV-2 in CSF was positive but with a cycle threshold (CT) of 38.6. The diagnosis of SARS-CoV-2 encephalopathy was retained. The patient is still in intensive care.
|
EN100705
|
Exam: pressure
|
not available
| 0 |
We report the case of a male patient, 79 years old, diabetic for 10 years on metformin, hypertensive for 5 years on amilodipine; occasional alcoholic weaned 4 years ago. He was initially admitted for mental confusion with sudden onset dysarthria dating back 48 hours before. Initial assessment found Glasgow score (GCS) of 12/15 (eye opening at 5, verbal response at 2, motor response at 5), symmetrical and reactive pupils, without feeling-motor deficit, normal osteotendinous reflexes, slightly polypneic at 24 cycles/min, pulsed oxygen saturation (SpO 2) at 97% in ambient air, he was tachycardic at 115 bpm and hypertensive at 160/95 mmHg, his capillary blood glucose at 2.24 g/L, and glycosuria on the urine dipstick test without ketonuria. The patient was apyretic. Arterial gas testing showed normal corrected anion gap metabolic acidosis, with hypokalaemia at 3 mmol/L and normal lactatemia at 0.43 mmol/L. Diagnosis of diabetes decompensation was made despite absence of ketone bodies on urine dipstick test. After conditioning, the patient was put on a hydration regimen with hypokalaemia correction and insulin therapy, and then referred to intensive care for additional management in face of non-improvement in his neurological condition. A brain scan was performed objectifying multiple parietal ischemic foci, chest scanner showed a thickening of the septal and foci of bronchial dilation without sign of pneumopathy linked to COVID-19 infection; abdominal ultrasound did not show any abnormalities. An electrocardiogram was performed showing no electrical signs of hypokalaemia or repolarization disturbances, transthoracic echocardiography was normal, as was ultrasound of supraortic trunks. Laboratory workup showed an elevated C-reactive protein (CRP) of 45.5 with negative procalcitonin (0.04 ng/ml), white blood cells at 12,500 (PNN at 9280 and normal lymphocytes at 2140), no thrombocytopenia, normal ferritinemia, fibrinogen levels elevated to 5.37 and negative D-dimers. Natremia, magnesemia, corrected serum calcium, phosphoremia and thyroid assessment was normal. SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) by nasopharyngeal swab was negative, COVID-19 serology (IgM and IgG) was also negative. Faced with concept of ischemic lesions on a brain scan, anticoagulation at a prophylactic dose, antiplatelet aggregation with aspirin and statins were initiated as well as an antibiotic therapy at a meningeal dose with ceftriaxone pending results of the lumbar puncture which subsequently showed a clear liquid with a high proteinorachia at 0.58g/l (normal between 0.15 and 0.45), a normal glycorachia/blood sugar ratio at 0.58 (normal at 0.5); with a culture showing less than 3 elements, sterile after 24 hours. Cerebral Magnetic resonance angiography performed on day 2 of admission showed signs in favor of vascular leukopathy, with some calcifications in basal ganglia and cortical atrophy. Electroencephalogram showed signs of epilepsy, which prompted us to retain the diagnosis of nonketotic hyperglycemia-related epileptic seizures. Anticonvulsant treatment was started with sodium valproate. The Patient worsened neurologically despite correction of his metabolic acidosis, he was intubated on day 3 of his admission (day 5 of symptoms onset). A cerebral computerized tomography (CT) scan was performed without showing any progressive lesions. Faced with installation of lymphopenia (HIV serologies 1 and 2 negative) with increased CRP, a multiplex RT-PCR in protected distal bronchial sample as well as in Cerebrospinal fluid (CSF) were performed, the first was positive to SARS-CoV-2. Reverse transcription polymerase chain reaction of SARS-CoV-2 in CSF was positive but with a cycle threshold (CT) of 38.6. The diagnosis of SARS-CoV-2 encephalopathy was retained. The patient is still in intensive care.
|
EN100705
|
Exam: HB
|
not available
| 0 |
We report the case of a male patient, 79 years old, diabetic for 10 years on metformin, hypertensive for 5 years on amilodipine; occasional alcoholic weaned 4 years ago. He was initially admitted for mental confusion with sudden onset dysarthria dating back 48 hours before. Initial assessment found Glasgow score (GCS) of 12/15 (eye opening at 5, verbal response at 2, motor response at 5), symmetrical and reactive pupils, without feeling-motor deficit, normal osteotendinous reflexes, slightly polypneic at 24 cycles/min, pulsed oxygen saturation (SpO 2) at 97% in ambient air, he was tachycardic at 115 bpm and hypertensive at 160/95 mmHg, his capillary blood glucose at 2.24 g/L, and glycosuria on the urine dipstick test without ketonuria. The patient was apyretic. Arterial gas testing showed normal corrected anion gap metabolic acidosis, with hypokalaemia at 3 mmol/L and normal lactatemia at 0.43 mmol/L. Diagnosis of diabetes decompensation was made despite absence of ketone bodies on urine dipstick test. After conditioning, the patient was put on a hydration regimen with hypokalaemia correction and insulin therapy, and then referred to intensive care for additional management in face of non-improvement in his neurological condition. A brain scan was performed objectifying multiple parietal ischemic foci, chest scanner showed a thickening of the septal and foci of bronchial dilation without sign of pneumopathy linked to COVID-19 infection; abdominal ultrasound did not show any abnormalities. An electrocardiogram was performed showing no electrical signs of hypokalaemia or repolarization disturbances, transthoracic echocardiography was normal, as was ultrasound of supraortic trunks. Laboratory workup showed an elevated C-reactive protein (CRP) of 45.5 with negative procalcitonin (0.04 ng/ml), white blood cells at 12,500 (PNN at 9280 and normal lymphocytes at 2140), no thrombocytopenia, normal ferritinemia, fibrinogen levels elevated to 5.37 and negative D-dimers. Natremia, magnesemia, corrected serum calcium, phosphoremia and thyroid assessment was normal. SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) by nasopharyngeal swab was negative, COVID-19 serology (IgM and IgG) was also negative. Faced with concept of ischemic lesions on a brain scan, anticoagulation at a prophylactic dose, antiplatelet aggregation with aspirin and statins were initiated as well as an antibiotic therapy at a meningeal dose with ceftriaxone pending results of the lumbar puncture which subsequently showed a clear liquid with a high proteinorachia at 0.58g/l (normal between 0.15 and 0.45), a normal glycorachia/blood sugar ratio at 0.58 (normal at 0.5); with a culture showing less than 3 elements, sterile after 24 hours. Cerebral Magnetic resonance angiography performed on day 2 of admission showed signs in favor of vascular leukopathy, with some calcifications in basal ganglia and cortical atrophy. Electroencephalogram showed signs of epilepsy, which prompted us to retain the diagnosis of nonketotic hyperglycemia-related epileptic seizures. Anticonvulsant treatment was started with sodium valproate. The Patient worsened neurologically despite correction of his metabolic acidosis, he was intubated on day 3 of his admission (day 5 of symptoms onset). A cerebral computerized tomography (CT) scan was performed without showing any progressive lesions. Faced with installation of lymphopenia (HIV serologies 1 and 2 negative) with increased CRP, a multiplex RT-PCR in protected distal bronchial sample as well as in Cerebrospinal fluid (CSF) were performed, the first was positive to SARS-CoV-2. Reverse transcription polymerase chain reaction of SARS-CoV-2 in CSF was positive but with a cycle threshold (CT) of 38.6. The diagnosis of SARS-CoV-2 encephalopathy was retained. The patient is still in intensive care.
|
EN100705
|
Exam: WBC
|
not available
| 0 |
We report the case of a male patient, 79 years old, diabetic for 10 years on metformin, hypertensive for 5 years on amilodipine; occasional alcoholic weaned 4 years ago. He was initially admitted for mental confusion with sudden onset dysarthria dating back 48 hours before. Initial assessment found Glasgow score (GCS) of 12/15 (eye opening at 5, verbal response at 2, motor response at 5), symmetrical and reactive pupils, without feeling-motor deficit, normal osteotendinous reflexes, slightly polypneic at 24 cycles/min, pulsed oxygen saturation (SpO 2) at 97% in ambient air, he was tachycardic at 115 bpm and hypertensive at 160/95 mmHg, his capillary blood glucose at 2.24 g/L, and glycosuria on the urine dipstick test without ketonuria. The patient was apyretic. Arterial gas testing showed normal corrected anion gap metabolic acidosis, with hypokalaemia at 3 mmol/L and normal lactatemia at 0.43 mmol/L. Diagnosis of diabetes decompensation was made despite absence of ketone bodies on urine dipstick test. After conditioning, the patient was put on a hydration regimen with hypokalaemia correction and insulin therapy, and then referred to intensive care for additional management in face of non-improvement in his neurological condition. A brain scan was performed objectifying multiple parietal ischemic foci, chest scanner showed a thickening of the septal and foci of bronchial dilation without sign of pneumopathy linked to COVID-19 infection; abdominal ultrasound did not show any abnormalities. An electrocardiogram was performed showing no electrical signs of hypokalaemia or repolarization disturbances, transthoracic echocardiography was normal, as was ultrasound of supraortic trunks. Laboratory workup showed an elevated C-reactive protein (CRP) of 45.5 with negative procalcitonin (0.04 ng/ml), white blood cells at 12,500 (PNN at 9280 and normal lymphocytes at 2140), no thrombocytopenia, normal ferritinemia, fibrinogen levels elevated to 5.37 and negative D-dimers. Natremia, magnesemia, corrected serum calcium, phosphoremia and thyroid assessment was normal. SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) by nasopharyngeal swab was negative, COVID-19 serology (IgM and IgG) was also negative. Faced with concept of ischemic lesions on a brain scan, anticoagulation at a prophylactic dose, antiplatelet aggregation with aspirin and statins were initiated as well as an antibiotic therapy at a meningeal dose with ceftriaxone pending results of the lumbar puncture which subsequently showed a clear liquid with a high proteinorachia at 0.58g/l (normal between 0.15 and 0.45), a normal glycorachia/blood sugar ratio at 0.58 (normal at 0.5); with a culture showing less than 3 elements, sterile after 24 hours. Cerebral Magnetic resonance angiography performed on day 2 of admission showed signs in favor of vascular leukopathy, with some calcifications in basal ganglia and cortical atrophy. Electroencephalogram showed signs of epilepsy, which prompted us to retain the diagnosis of nonketotic hyperglycemia-related epileptic seizures. Anticonvulsant treatment was started with sodium valproate. The Patient worsened neurologically despite correction of his metabolic acidosis, he was intubated on day 3 of his admission (day 5 of symptoms onset). A cerebral computerized tomography (CT) scan was performed without showing any progressive lesions. Faced with installation of lymphopenia (HIV serologies 1 and 2 negative) with increased CRP, a multiplex RT-PCR in protected distal bronchial sample as well as in Cerebrospinal fluid (CSF) were performed, the first was positive to SARS-CoV-2. Reverse transcription polymerase chain reaction of SARS-CoV-2 in CSF was positive but with a cycle threshold (CT) of 38.6. The diagnosis of SARS-CoV-2 encephalopathy was retained. The patient is still in intensive care.
|
EN100705
|
Exam: lymphocytes
|
2140.
| 0 |
We report the case of a male patient, 79 years old, diabetic for 10 years on metformin, hypertensive for 5 years on amilodipine; occasional alcoholic weaned 4 years ago. He was initially admitted for mental confusion with sudden onset dysarthria dating back 48 hours before. Initial assessment found Glasgow score (GCS) of 12/15 (eye opening at 5, verbal response at 2, motor response at 5), symmetrical and reactive pupils, without feeling-motor deficit, normal osteotendinous reflexes, slightly polypneic at 24 cycles/min, pulsed oxygen saturation (SpO 2) at 97% in ambient air, he was tachycardic at 115 bpm and hypertensive at 160/95 mmHg, his capillary blood glucose at 2.24 g/L, and glycosuria on the urine dipstick test without ketonuria. The patient was apyretic. Arterial gas testing showed normal corrected anion gap metabolic acidosis, with hypokalaemia at 3 mmol/L and normal lactatemia at 0.43 mmol/L. Diagnosis of diabetes decompensation was made despite absence of ketone bodies on urine dipstick test. After conditioning, the patient was put on a hydration regimen with hypokalaemia correction and insulin therapy, and then referred to intensive care for additional management in face of non-improvement in his neurological condition. A brain scan was performed objectifying multiple parietal ischemic foci, chest scanner showed a thickening of the septal and foci of bronchial dilation without sign of pneumopathy linked to COVID-19 infection; abdominal ultrasound did not show any abnormalities. An electrocardiogram was performed showing no electrical signs of hypokalaemia or repolarization disturbances, transthoracic echocardiography was normal, as was ultrasound of supraortic trunks. Laboratory workup showed an elevated C-reactive protein (CRP) of 45.5 with negative procalcitonin (0.04 ng/ml), white blood cells at 12,500 (PNN at 9280 and normal lymphocytes at 2140), no thrombocytopenia, normal ferritinemia, fibrinogen levels elevated to 5.37 and negative D-dimers. Natremia, magnesemia, corrected serum calcium, phosphoremia and thyroid assessment was normal. SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) by nasopharyngeal swab was negative, COVID-19 serology (IgM and IgG) was also negative. Faced with concept of ischemic lesions on a brain scan, anticoagulation at a prophylactic dose, antiplatelet aggregation with aspirin and statins were initiated as well as an antibiotic therapy at a meningeal dose with ceftriaxone pending results of the lumbar puncture which subsequently showed a clear liquid with a high proteinorachia at 0.58g/l (normal between 0.15 and 0.45), a normal glycorachia/blood sugar ratio at 0.58 (normal at 0.5); with a culture showing less than 3 elements, sterile after 24 hours. Cerebral Magnetic resonance angiography performed on day 2 of admission showed signs in favor of vascular leukopathy, with some calcifications in basal ganglia and cortical atrophy. Electroencephalogram showed signs of epilepsy, which prompted us to retain the diagnosis of nonketotic hyperglycemia-related epileptic seizures. Anticonvulsant treatment was started with sodium valproate. The Patient worsened neurologically despite correction of his metabolic acidosis, he was intubated on day 3 of his admission (day 5 of symptoms onset). A cerebral computerized tomography (CT) scan was performed without showing any progressive lesions. Faced with installation of lymphopenia (HIV serologies 1 and 2 negative) with increased CRP, a multiplex RT-PCR in protected distal bronchial sample as well as in Cerebrospinal fluid (CSF) were performed, the first was positive to SARS-CoV-2. Reverse transcription polymerase chain reaction of SARS-CoV-2 in CSF was positive but with a cycle threshold (CT) of 38.6. The diagnosis of SARS-CoV-2 encephalopathy was retained. The patient is still in intensive care.
|
EN100705
|
Exam: Monocytes
|
not available
| 0 |
We report the case of a male patient, 79 years old, diabetic for 10 years on metformin, hypertensive for 5 years on amilodipine; occasional alcoholic weaned 4 years ago. He was initially admitted for mental confusion with sudden onset dysarthria dating back 48 hours before. Initial assessment found Glasgow score (GCS) of 12/15 (eye opening at 5, verbal response at 2, motor response at 5), symmetrical and reactive pupils, without feeling-motor deficit, normal osteotendinous reflexes, slightly polypneic at 24 cycles/min, pulsed oxygen saturation (SpO 2) at 97% in ambient air, he was tachycardic at 115 bpm and hypertensive at 160/95 mmHg, his capillary blood glucose at 2.24 g/L, and glycosuria on the urine dipstick test without ketonuria. The patient was apyretic. Arterial gas testing showed normal corrected anion gap metabolic acidosis, with hypokalaemia at 3 mmol/L and normal lactatemia at 0.43 mmol/L. Diagnosis of diabetes decompensation was made despite absence of ketone bodies on urine dipstick test. After conditioning, the patient was put on a hydration regimen with hypokalaemia correction and insulin therapy, and then referred to intensive care for additional management in face of non-improvement in his neurological condition. A brain scan was performed objectifying multiple parietal ischemic foci, chest scanner showed a thickening of the septal and foci of bronchial dilation without sign of pneumopathy linked to COVID-19 infection; abdominal ultrasound did not show any abnormalities. An electrocardiogram was performed showing no electrical signs of hypokalaemia or repolarization disturbances, transthoracic echocardiography was normal, as was ultrasound of supraortic trunks. Laboratory workup showed an elevated C-reactive protein (CRP) of 45.5 with negative procalcitonin (0.04 ng/ml), white blood cells at 12,500 (PNN at 9280 and normal lymphocytes at 2140), no thrombocytopenia, normal ferritinemia, fibrinogen levels elevated to 5.37 and negative D-dimers. Natremia, magnesemia, corrected serum calcium, phosphoremia and thyroid assessment was normal. SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) by nasopharyngeal swab was negative, COVID-19 serology (IgM and IgG) was also negative. Faced with concept of ischemic lesions on a brain scan, anticoagulation at a prophylactic dose, antiplatelet aggregation with aspirin and statins were initiated as well as an antibiotic therapy at a meningeal dose with ceftriaxone pending results of the lumbar puncture which subsequently showed a clear liquid with a high proteinorachia at 0.58g/l (normal between 0.15 and 0.45), a normal glycorachia/blood sugar ratio at 0.58 (normal at 0.5); with a culture showing less than 3 elements, sterile after 24 hours. Cerebral Magnetic resonance angiography performed on day 2 of admission showed signs in favor of vascular leukopathy, with some calcifications in basal ganglia and cortical atrophy. Electroencephalogram showed signs of epilepsy, which prompted us to retain the diagnosis of nonketotic hyperglycemia-related epileptic seizures. Anticonvulsant treatment was started with sodium valproate. The Patient worsened neurologically despite correction of his metabolic acidosis, he was intubated on day 3 of his admission (day 5 of symptoms onset). A cerebral computerized tomography (CT) scan was performed without showing any progressive lesions. Faced with installation of lymphopenia (HIV serologies 1 and 2 negative) with increased CRP, a multiplex RT-PCR in protected distal bronchial sample as well as in Cerebrospinal fluid (CSF) were performed, the first was positive to SARS-CoV-2. Reverse transcription polymerase chain reaction of SARS-CoV-2 in CSF was positive but with a cycle threshold (CT) of 38.6. The diagnosis of SARS-CoV-2 encephalopathy was retained. The patient is still in intensive care.
|
EN100705
|
Exam: Eosinophils
|
not available
| 0 |
We report the case of a male patient, 79 years old, diabetic for 10 years on metformin, hypertensive for 5 years on amilodipine; occasional alcoholic weaned 4 years ago. He was initially admitted for mental confusion with sudden onset dysarthria dating back 48 hours before. Initial assessment found Glasgow score (GCS) of 12/15 (eye opening at 5, verbal response at 2, motor response at 5), symmetrical and reactive pupils, without feeling-motor deficit, normal osteotendinous reflexes, slightly polypneic at 24 cycles/min, pulsed oxygen saturation (SpO 2) at 97% in ambient air, he was tachycardic at 115 bpm and hypertensive at 160/95 mmHg, his capillary blood glucose at 2.24 g/L, and glycosuria on the urine dipstick test without ketonuria. The patient was apyretic. Arterial gas testing showed normal corrected anion gap metabolic acidosis, with hypokalaemia at 3 mmol/L and normal lactatemia at 0.43 mmol/L. Diagnosis of diabetes decompensation was made despite absence of ketone bodies on urine dipstick test. After conditioning, the patient was put on a hydration regimen with hypokalaemia correction and insulin therapy, and then referred to intensive care for additional management in face of non-improvement in his neurological condition. A brain scan was performed objectifying multiple parietal ischemic foci, chest scanner showed a thickening of the septal and foci of bronchial dilation without sign of pneumopathy linked to COVID-19 infection; abdominal ultrasound did not show any abnormalities. An electrocardiogram was performed showing no electrical signs of hypokalaemia or repolarization disturbances, transthoracic echocardiography was normal, as was ultrasound of supraortic trunks. Laboratory workup showed an elevated C-reactive protein (CRP) of 45.5 with negative procalcitonin (0.04 ng/ml), white blood cells at 12,500 (PNN at 9280 and normal lymphocytes at 2140), no thrombocytopenia, normal ferritinemia, fibrinogen levels elevated to 5.37 and negative D-dimers. Natremia, magnesemia, corrected serum calcium, phosphoremia and thyroid assessment was normal. SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) by nasopharyngeal swab was negative, COVID-19 serology (IgM and IgG) was also negative. Faced with concept of ischemic lesions on a brain scan, anticoagulation at a prophylactic dose, antiplatelet aggregation with aspirin and statins were initiated as well as an antibiotic therapy at a meningeal dose with ceftriaxone pending results of the lumbar puncture which subsequently showed a clear liquid with a high proteinorachia at 0.58g/l (normal between 0.15 and 0.45), a normal glycorachia/blood sugar ratio at 0.58 (normal at 0.5); with a culture showing less than 3 elements, sterile after 24 hours. Cerebral Magnetic resonance angiography performed on day 2 of admission showed signs in favor of vascular leukopathy, with some calcifications in basal ganglia and cortical atrophy. Electroencephalogram showed signs of epilepsy, which prompted us to retain the diagnosis of nonketotic hyperglycemia-related epileptic seizures. Anticonvulsant treatment was started with sodium valproate. The Patient worsened neurologically despite correction of his metabolic acidosis, he was intubated on day 3 of his admission (day 5 of symptoms onset). A cerebral computerized tomography (CT) scan was performed without showing any progressive lesions. Faced with installation of lymphopenia (HIV serologies 1 and 2 negative) with increased CRP, a multiplex RT-PCR in protected distal bronchial sample as well as in Cerebrospinal fluid (CSF) were performed, the first was positive to SARS-CoV-2. Reverse transcription polymerase chain reaction of SARS-CoV-2 in CSF was positive but with a cycle threshold (CT) of 38.6. The diagnosis of SARS-CoV-2 encephalopathy was retained. The patient is still in intensive care.
|
EN100705
|
Exam: Platelets
|
not available
| 0 |
We report the case of a male patient, 79 years old, diabetic for 10 years on metformin, hypertensive for 5 years on amilodipine; occasional alcoholic weaned 4 years ago. He was initially admitted for mental confusion with sudden onset dysarthria dating back 48 hours before. Initial assessment found Glasgow score (GCS) of 12/15 (eye opening at 5, verbal response at 2, motor response at 5), symmetrical and reactive pupils, without feeling-motor deficit, normal osteotendinous reflexes, slightly polypneic at 24 cycles/min, pulsed oxygen saturation (SpO 2) at 97% in ambient air, he was tachycardic at 115 bpm and hypertensive at 160/95 mmHg, his capillary blood glucose at 2.24 g/L, and glycosuria on the urine dipstick test without ketonuria. The patient was apyretic. Arterial gas testing showed normal corrected anion gap metabolic acidosis, with hypokalaemia at 3 mmol/L and normal lactatemia at 0.43 mmol/L. Diagnosis of diabetes decompensation was made despite absence of ketone bodies on urine dipstick test. After conditioning, the patient was put on a hydration regimen with hypokalaemia correction and insulin therapy, and then referred to intensive care for additional management in face of non-improvement in his neurological condition. A brain scan was performed objectifying multiple parietal ischemic foci, chest scanner showed a thickening of the septal and foci of bronchial dilation without sign of pneumopathy linked to COVID-19 infection; abdominal ultrasound did not show any abnormalities. An electrocardiogram was performed showing no electrical signs of hypokalaemia or repolarization disturbances, transthoracic echocardiography was normal, as was ultrasound of supraortic trunks. Laboratory workup showed an elevated C-reactive protein (CRP) of 45.5 with negative procalcitonin (0.04 ng/ml), white blood cells at 12,500 (PNN at 9280 and normal lymphocytes at 2140), no thrombocytopenia, normal ferritinemia, fibrinogen levels elevated to 5.37 and negative D-dimers. Natremia, magnesemia, corrected serum calcium, phosphoremia and thyroid assessment was normal. SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) by nasopharyngeal swab was negative, COVID-19 serology (IgM and IgG) was also negative. Faced with concept of ischemic lesions on a brain scan, anticoagulation at a prophylactic dose, antiplatelet aggregation with aspirin and statins were initiated as well as an antibiotic therapy at a meningeal dose with ceftriaxone pending results of the lumbar puncture which subsequently showed a clear liquid with a high proteinorachia at 0.58g/l (normal between 0.15 and 0.45), a normal glycorachia/blood sugar ratio at 0.58 (normal at 0.5); with a culture showing less than 3 elements, sterile after 24 hours. Cerebral Magnetic resonance angiography performed on day 2 of admission showed signs in favor of vascular leukopathy, with some calcifications in basal ganglia and cortical atrophy. Electroencephalogram showed signs of epilepsy, which prompted us to retain the diagnosis of nonketotic hyperglycemia-related epileptic seizures. Anticonvulsant treatment was started with sodium valproate. The Patient worsened neurologically despite correction of his metabolic acidosis, he was intubated on day 3 of his admission (day 5 of symptoms onset). A cerebral computerized tomography (CT) scan was performed without showing any progressive lesions. Faced with installation of lymphopenia (HIV serologies 1 and 2 negative) with increased CRP, a multiplex RT-PCR in protected distal bronchial sample as well as in Cerebrospinal fluid (CSF) were performed, the first was positive to SARS-CoV-2. Reverse transcription polymerase chain reaction of SARS-CoV-2 in CSF was positive but with a cycle threshold (CT) of 38.6. The diagnosis of SARS-CoV-2 encephalopathy was retained. The patient is still in intensive care.
|
EN100705
|
Exam: HBsAg
|
not available
| 0 |
We report the case of a male patient, 79 years old, diabetic for 10 years on metformin, hypertensive for 5 years on amilodipine; occasional alcoholic weaned 4 years ago. He was initially admitted for mental confusion with sudden onset dysarthria dating back 48 hours before. Initial assessment found Glasgow score (GCS) of 12/15 (eye opening at 5, verbal response at 2, motor response at 5), symmetrical and reactive pupils, without feeling-motor deficit, normal osteotendinous reflexes, slightly polypneic at 24 cycles/min, pulsed oxygen saturation (SpO 2) at 97% in ambient air, he was tachycardic at 115 bpm and hypertensive at 160/95 mmHg, his capillary blood glucose at 2.24 g/L, and glycosuria on the urine dipstick test without ketonuria. The patient was apyretic. Arterial gas testing showed normal corrected anion gap metabolic acidosis, with hypokalaemia at 3 mmol/L and normal lactatemia at 0.43 mmol/L. Diagnosis of diabetes decompensation was made despite absence of ketone bodies on urine dipstick test. After conditioning, the patient was put on a hydration regimen with hypokalaemia correction and insulin therapy, and then referred to intensive care for additional management in face of non-improvement in his neurological condition. A brain scan was performed objectifying multiple parietal ischemic foci, chest scanner showed a thickening of the septal and foci of bronchial dilation without sign of pneumopathy linked to COVID-19 infection; abdominal ultrasound did not show any abnormalities. An electrocardiogram was performed showing no electrical signs of hypokalaemia or repolarization disturbances, transthoracic echocardiography was normal, as was ultrasound of supraortic trunks. Laboratory workup showed an elevated C-reactive protein (CRP) of 45.5 with negative procalcitonin (0.04 ng/ml), white blood cells at 12,500 (PNN at 9280 and normal lymphocytes at 2140), no thrombocytopenia, normal ferritinemia, fibrinogen levels elevated to 5.37 and negative D-dimers. Natremia, magnesemia, corrected serum calcium, phosphoremia and thyroid assessment was normal. SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) by nasopharyngeal swab was negative, COVID-19 serology (IgM and IgG) was also negative. Faced with concept of ischemic lesions on a brain scan, anticoagulation at a prophylactic dose, antiplatelet aggregation with aspirin and statins were initiated as well as an antibiotic therapy at a meningeal dose with ceftriaxone pending results of the lumbar puncture which subsequently showed a clear liquid with a high proteinorachia at 0.58g/l (normal between 0.15 and 0.45), a normal glycorachia/blood sugar ratio at 0.58 (normal at 0.5); with a culture showing less than 3 elements, sterile after 24 hours. Cerebral Magnetic resonance angiography performed on day 2 of admission showed signs in favor of vascular leukopathy, with some calcifications in basal ganglia and cortical atrophy. Electroencephalogram showed signs of epilepsy, which prompted us to retain the diagnosis of nonketotic hyperglycemia-related epileptic seizures. Anticonvulsant treatment was started with sodium valproate. The Patient worsened neurologically despite correction of his metabolic acidosis, he was intubated on day 3 of his admission (day 5 of symptoms onset). A cerebral computerized tomography (CT) scan was performed without showing any progressive lesions. Faced with installation of lymphopenia (HIV serologies 1 and 2 negative) with increased CRP, a multiplex RT-PCR in protected distal bronchial sample as well as in Cerebrospinal fluid (CSF) were performed, the first was positive to SARS-CoV-2. Reverse transcription polymerase chain reaction of SARS-CoV-2 in CSF was positive but with a cycle threshold (CT) of 38.6. The diagnosis of SARS-CoV-2 encephalopathy was retained. The patient is still in intensive care.
|
EN100705
|
Exam: HBeAg
|
not available
| 0 |
We report the case of a male patient, 79 years old, diabetic for 10 years on metformin, hypertensive for 5 years on amilodipine; occasional alcoholic weaned 4 years ago. He was initially admitted for mental confusion with sudden onset dysarthria dating back 48 hours before. Initial assessment found Glasgow score (GCS) of 12/15 (eye opening at 5, verbal response at 2, motor response at 5), symmetrical and reactive pupils, without feeling-motor deficit, normal osteotendinous reflexes, slightly polypneic at 24 cycles/min, pulsed oxygen saturation (SpO 2) at 97% in ambient air, he was tachycardic at 115 bpm and hypertensive at 160/95 mmHg, his capillary blood glucose at 2.24 g/L, and glycosuria on the urine dipstick test without ketonuria. The patient was apyretic. Arterial gas testing showed normal corrected anion gap metabolic acidosis, with hypokalaemia at 3 mmol/L and normal lactatemia at 0.43 mmol/L. Diagnosis of diabetes decompensation was made despite absence of ketone bodies on urine dipstick test. After conditioning, the patient was put on a hydration regimen with hypokalaemia correction and insulin therapy, and then referred to intensive care for additional management in face of non-improvement in his neurological condition. A brain scan was performed objectifying multiple parietal ischemic foci, chest scanner showed a thickening of the septal and foci of bronchial dilation without sign of pneumopathy linked to COVID-19 infection; abdominal ultrasound did not show any abnormalities. An electrocardiogram was performed showing no electrical signs of hypokalaemia or repolarization disturbances, transthoracic echocardiography was normal, as was ultrasound of supraortic trunks. Laboratory workup showed an elevated C-reactive protein (CRP) of 45.5 with negative procalcitonin (0.04 ng/ml), white blood cells at 12,500 (PNN at 9280 and normal lymphocytes at 2140), no thrombocytopenia, normal ferritinemia, fibrinogen levels elevated to 5.37 and negative D-dimers. Natremia, magnesemia, corrected serum calcium, phosphoremia and thyroid assessment was normal. SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) by nasopharyngeal swab was negative, COVID-19 serology (IgM and IgG) was also negative. Faced with concept of ischemic lesions on a brain scan, anticoagulation at a prophylactic dose, antiplatelet aggregation with aspirin and statins were initiated as well as an antibiotic therapy at a meningeal dose with ceftriaxone pending results of the lumbar puncture which subsequently showed a clear liquid with a high proteinorachia at 0.58g/l (normal between 0.15 and 0.45), a normal glycorachia/blood sugar ratio at 0.58 (normal at 0.5); with a culture showing less than 3 elements, sterile after 24 hours. Cerebral Magnetic resonance angiography performed on day 2 of admission showed signs in favor of vascular leukopathy, with some calcifications in basal ganglia and cortical atrophy. Electroencephalogram showed signs of epilepsy, which prompted us to retain the diagnosis of nonketotic hyperglycemia-related epileptic seizures. Anticonvulsant treatment was started with sodium valproate. The Patient worsened neurologically despite correction of his metabolic acidosis, he was intubated on day 3 of his admission (day 5 of symptoms onset). A cerebral computerized tomography (CT) scan was performed without showing any progressive lesions. Faced with installation of lymphopenia (HIV serologies 1 and 2 negative) with increased CRP, a multiplex RT-PCR in protected distal bronchial sample as well as in Cerebrospinal fluid (CSF) were performed, the first was positive to SARS-CoV-2. Reverse transcription polymerase chain reaction of SARS-CoV-2 in CSF was positive but with a cycle threshold (CT) of 38.6. The diagnosis of SARS-CoV-2 encephalopathy was retained. The patient is still in intensive care.
|
EN100705
|
Exam: VDRL
|
not available
| 0 |
We report the case of a male patient, 79 years old, diabetic for 10 years on metformin, hypertensive for 5 years on amilodipine; occasional alcoholic weaned 4 years ago. He was initially admitted for mental confusion with sudden onset dysarthria dating back 48 hours before. Initial assessment found Glasgow score (GCS) of 12/15 (eye opening at 5, verbal response at 2, motor response at 5), symmetrical and reactive pupils, without feeling-motor deficit, normal osteotendinous reflexes, slightly polypneic at 24 cycles/min, pulsed oxygen saturation (SpO 2) at 97% in ambient air, he was tachycardic at 115 bpm and hypertensive at 160/95 mmHg, his capillary blood glucose at 2.24 g/L, and glycosuria on the urine dipstick test without ketonuria. The patient was apyretic. Arterial gas testing showed normal corrected anion gap metabolic acidosis, with hypokalaemia at 3 mmol/L and normal lactatemia at 0.43 mmol/L. Diagnosis of diabetes decompensation was made despite absence of ketone bodies on urine dipstick test. After conditioning, the patient was put on a hydration regimen with hypokalaemia correction and insulin therapy, and then referred to intensive care for additional management in face of non-improvement in his neurological condition. A brain scan was performed objectifying multiple parietal ischemic foci, chest scanner showed a thickening of the septal and foci of bronchial dilation without sign of pneumopathy linked to COVID-19 infection; abdominal ultrasound did not show any abnormalities. An electrocardiogram was performed showing no electrical signs of hypokalaemia or repolarization disturbances, transthoracic echocardiography was normal, as was ultrasound of supraortic trunks. Laboratory workup showed an elevated C-reactive protein (CRP) of 45.5 with negative procalcitonin (0.04 ng/ml), white blood cells at 12,500 (PNN at 9280 and normal lymphocytes at 2140), no thrombocytopenia, normal ferritinemia, fibrinogen levels elevated to 5.37 and negative D-dimers. Natremia, magnesemia, corrected serum calcium, phosphoremia and thyroid assessment was normal. SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) by nasopharyngeal swab was negative, COVID-19 serology (IgM and IgG) was also negative. Faced with concept of ischemic lesions on a brain scan, anticoagulation at a prophylactic dose, antiplatelet aggregation with aspirin and statins were initiated as well as an antibiotic therapy at a meningeal dose with ceftriaxone pending results of the lumbar puncture which subsequently showed a clear liquid with a high proteinorachia at 0.58g/l (normal between 0.15 and 0.45), a normal glycorachia/blood sugar ratio at 0.58 (normal at 0.5); with a culture showing less than 3 elements, sterile after 24 hours. Cerebral Magnetic resonance angiography performed on day 2 of admission showed signs in favor of vascular leukopathy, with some calcifications in basal ganglia and cortical atrophy. Electroencephalogram showed signs of epilepsy, which prompted us to retain the diagnosis of nonketotic hyperglycemia-related epileptic seizures. Anticonvulsant treatment was started with sodium valproate. The Patient worsened neurologically despite correction of his metabolic acidosis, he was intubated on day 3 of his admission (day 5 of symptoms onset). A cerebral computerized tomography (CT) scan was performed without showing any progressive lesions. Faced with installation of lymphopenia (HIV serologies 1 and 2 negative) with increased CRP, a multiplex RT-PCR in protected distal bronchial sample as well as in Cerebrospinal fluid (CSF) were performed, the first was positive to SARS-CoV-2. Reverse transcription polymerase chain reaction of SARS-CoV-2 in CSF was positive but with a cycle threshold (CT) of 38.6. The diagnosis of SARS-CoV-2 encephalopathy was retained. The patient is still in intensive care.
|
EN100705
|
Exam: AFP
|
not available
| 0 |
We report the case of a male patient, 79 years old, diabetic for 10 years on metformin, hypertensive for 5 years on amilodipine; occasional alcoholic weaned 4 years ago. He was initially admitted for mental confusion with sudden onset dysarthria dating back 48 hours before. Initial assessment found Glasgow score (GCS) of 12/15 (eye opening at 5, verbal response at 2, motor response at 5), symmetrical and reactive pupils, without feeling-motor deficit, normal osteotendinous reflexes, slightly polypneic at 24 cycles/min, pulsed oxygen saturation (SpO 2) at 97% in ambient air, he was tachycardic at 115 bpm and hypertensive at 160/95 mmHg, his capillary blood glucose at 2.24 g/L, and glycosuria on the urine dipstick test without ketonuria. The patient was apyretic. Arterial gas testing showed normal corrected anion gap metabolic acidosis, with hypokalaemia at 3 mmol/L and normal lactatemia at 0.43 mmol/L. Diagnosis of diabetes decompensation was made despite absence of ketone bodies on urine dipstick test. After conditioning, the patient was put on a hydration regimen with hypokalaemia correction and insulin therapy, and then referred to intensive care for additional management in face of non-improvement in his neurological condition. A brain scan was performed objectifying multiple parietal ischemic foci, chest scanner showed a thickening of the septal and foci of bronchial dilation without sign of pneumopathy linked to COVID-19 infection; abdominal ultrasound did not show any abnormalities. An electrocardiogram was performed showing no electrical signs of hypokalaemia or repolarization disturbances, transthoracic echocardiography was normal, as was ultrasound of supraortic trunks. Laboratory workup showed an elevated C-reactive protein (CRP) of 45.5 with negative procalcitonin (0.04 ng/ml), white blood cells at 12,500 (PNN at 9280 and normal lymphocytes at 2140), no thrombocytopenia, normal ferritinemia, fibrinogen levels elevated to 5.37 and negative D-dimers. Natremia, magnesemia, corrected serum calcium, phosphoremia and thyroid assessment was normal. SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) by nasopharyngeal swab was negative, COVID-19 serology (IgM and IgG) was also negative. Faced with concept of ischemic lesions on a brain scan, anticoagulation at a prophylactic dose, antiplatelet aggregation with aspirin and statins were initiated as well as an antibiotic therapy at a meningeal dose with ceftriaxone pending results of the lumbar puncture which subsequently showed a clear liquid with a high proteinorachia at 0.58g/l (normal between 0.15 and 0.45), a normal glycorachia/blood sugar ratio at 0.58 (normal at 0.5); with a culture showing less than 3 elements, sterile after 24 hours. Cerebral Magnetic resonance angiography performed on day 2 of admission showed signs in favor of vascular leukopathy, with some calcifications in basal ganglia and cortical atrophy. Electroencephalogram showed signs of epilepsy, which prompted us to retain the diagnosis of nonketotic hyperglycemia-related epileptic seizures. Anticonvulsant treatment was started with sodium valproate. The Patient worsened neurologically despite correction of his metabolic acidosis, he was intubated on day 3 of his admission (day 5 of symptoms onset). A cerebral computerized tomography (CT) scan was performed without showing any progressive lesions. Faced with installation of lymphopenia (HIV serologies 1 and 2 negative) with increased CRP, a multiplex RT-PCR in protected distal bronchial sample as well as in Cerebrospinal fluid (CSF) were performed, the first was positive to SARS-CoV-2. Reverse transcription polymerase chain reaction of SARS-CoV-2 in CSF was positive but with a cycle threshold (CT) of 38.6. The diagnosis of SARS-CoV-2 encephalopathy was retained. The patient is still in intensive care.
|
EN100705
|
Exam: HIV
|
not available
| 0 |
We report the case of a male patient, 79 years old, diabetic for 10 years on metformin, hypertensive for 5 years on amilodipine; occasional alcoholic weaned 4 years ago. He was initially admitted for mental confusion with sudden onset dysarthria dating back 48 hours before. Initial assessment found Glasgow score (GCS) of 12/15 (eye opening at 5, verbal response at 2, motor response at 5), symmetrical and reactive pupils, without feeling-motor deficit, normal osteotendinous reflexes, slightly polypneic at 24 cycles/min, pulsed oxygen saturation (SpO 2) at 97% in ambient air, he was tachycardic at 115 bpm and hypertensive at 160/95 mmHg, his capillary blood glucose at 2.24 g/L, and glycosuria on the urine dipstick test without ketonuria. The patient was apyretic. Arterial gas testing showed normal corrected anion gap metabolic acidosis, with hypokalaemia at 3 mmol/L and normal lactatemia at 0.43 mmol/L. Diagnosis of diabetes decompensation was made despite absence of ketone bodies on urine dipstick test. After conditioning, the patient was put on a hydration regimen with hypokalaemia correction and insulin therapy, and then referred to intensive care for additional management in face of non-improvement in his neurological condition. A brain scan was performed objectifying multiple parietal ischemic foci, chest scanner showed a thickening of the septal and foci of bronchial dilation without sign of pneumopathy linked to COVID-19 infection; abdominal ultrasound did not show any abnormalities. An electrocardiogram was performed showing no electrical signs of hypokalaemia or repolarization disturbances, transthoracic echocardiography was normal, as was ultrasound of supraortic trunks. Laboratory workup showed an elevated C-reactive protein (CRP) of 45.5 with negative procalcitonin (0.04 ng/ml), white blood cells at 12,500 (PNN at 9280 and normal lymphocytes at 2140), no thrombocytopenia, normal ferritinemia, fibrinogen levels elevated to 5.37 and negative D-dimers. Natremia, magnesemia, corrected serum calcium, phosphoremia and thyroid assessment was normal. SARS-CoV-2 reverse transcription polymerase chain reaction (RT-PCR) by nasopharyngeal swab was negative, COVID-19 serology (IgM and IgG) was also negative. Faced with concept of ischemic lesions on a brain scan, anticoagulation at a prophylactic dose, antiplatelet aggregation with aspirin and statins were initiated as well as an antibiotic therapy at a meningeal dose with ceftriaxone pending results of the lumbar puncture which subsequently showed a clear liquid with a high proteinorachia at 0.58g/l (normal between 0.15 and 0.45), a normal glycorachia/blood sugar ratio at 0.58 (normal at 0.5); with a culture showing less than 3 elements, sterile after 24 hours. Cerebral Magnetic resonance angiography performed on day 2 of admission showed signs in favor of vascular leukopathy, with some calcifications in basal ganglia and cortical atrophy. Electroencephalogram showed signs of epilepsy, which prompted us to retain the diagnosis of nonketotic hyperglycemia-related epileptic seizures. Anticonvulsant treatment was started with sodium valproate. The Patient worsened neurologically despite correction of his metabolic acidosis, he was intubated on day 3 of his admission (day 5 of symptoms onset). A cerebral computerized tomography (CT) scan was performed without showing any progressive lesions. Faced with installation of lymphopenia (HIV serologies 1 and 2 negative) with increased CRP, a multiplex RT-PCR in protected distal bronchial sample as well as in Cerebrospinal fluid (CSF) were performed, the first was positive to SARS-CoV-2. Reverse transcription polymerase chain reaction of SARS-CoV-2 in CSF was positive but with a cycle threshold (CT) of 38.6. The diagnosis of SARS-CoV-2 encephalopathy was retained. The patient is still in intensive care.
|
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