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EN100497
|
Exam: globulin
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: nitrogen
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: cholesterol
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: Echocardiogram
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: hemoglobin
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: amylase
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: lipase
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: cytokeratin
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: CK7
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: synaptophysin
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: CD56
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: SCAN
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: fever
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: WBC
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: aminotransferase
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: ALT
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: LDH
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: phosphatase
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: Entamoeba
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: echinococcus
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: leismania
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: brucella
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: amikacin
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: cefepime
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: ciprofloxacin
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: gentamycin
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: meropenem
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: chromogranin
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: Synaptophysin
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: CD10
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: Ki-67
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: pressure
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: HIV
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: HCV
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: HB
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: Platelets
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: INR
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: AFP
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: Her2neu
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: ER
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100497
|
Exam: PR
|
not available
| 7 |
A 26 years old nulliparous woman presented to our observation for severe right-sided epistaxis, non self-limiting. She had few episodes in the previous two weeks of epistaxis, even 3-4 per day, usually stopping spontaneously. She reported a negative ENT consultation except for mild hyperemia of nasal mucosa. The pregnancy was unremarkable, considered at low risk, at 39.6 weeks of gestation. Her familiar and personal history was negative for blood coagulopathies and hypertension. We tried to stop severe epistaxis with nasal packing and intravenous tranexamic acid. On the basis of the failure of our procedures an otolaryngologist performed an endoscopy identifying bleeding enlarged vessels. Nasal packing with hemostatic sponge was successful, the pregnant woman was admitted to ob&gyn department. Her hemoglobin levels dropped down to 6 mg/dl and she needed 4 red cell packs. The day after her right nostril despite the tampons started bleeding again. She was referred to otolaryngologist who packed again the nose, bilaterally and used hemostatic glue. After 2 more days she started bleeding again, her nose was again packed with glue and tampons and further 2 red cell packs were given. The obstetric scan revealed biometry at 40 th centile, the Bishop score was 5, so we decided to induce labour after obtaining her informed written consent. The labour induction was performed with intravaginal prostaglandins (10 mg dinoprostone). After 18 hours the labour seemed to proceed well with cervical dilatation of 6 cm, level of head 0, but the cardiotocography (CTG) trace revealed anomalies that after 1 hour induced the shift versus cesarean section. No epistaxis happened during labour nor during cesarean section. Two days after nasal tampons were removed, the patient was discharged the day after. One month later the woman reported general good health and no epistaxis episodes, nor mild nor massive.
|
EN100593
|
Exam: radiogram
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: electrocardiogram
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: phosphokinase
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
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EN100593
|
Exam: troponin
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
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EN100593
|
Exam: lymphopenia
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: nitrogen
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: cholesterol
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: Echocardiogram
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: hemoglobin
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: amylase
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: lipase
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: cytokeratin
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: CK7
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: synaptophysin
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
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EN100593
|
Exam: CD56
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
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EN100593
|
Exam: SCAN
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
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EN100593
|
Exam: WBC
|
37500 cells/dL.
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: aminotransferase
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: ALT
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: LDH
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: phosphatase
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: Entamoeba
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: echinococcus
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: leismania
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: brucella
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: amikacin
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: cefepime
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: ciprofloxacin
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: gentamycin
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: meropenem
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: chromogranin
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: Synaptophysin
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: CD10
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: Ki-67
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: pressure
|
100/70 mmHg.
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: fever
|
4times upper limit.
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: globulin
|
positive.
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: HIV
|
negative.
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: HCV
|
negative.
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: HB
|
8.4g/dL.
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: Platelets
|
436000/ul.
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: INR
|
2.57.
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: AFP
|
Result:
0) dalla data EN1005936864:
dopo 3 eventi: higher. [\MULTI_ANSWER]
dopo 3 eventi: 2232 ng/mL.
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: Her2neu
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: ER
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
|
EN100593
|
Exam: PR
|
not available
| 7 |
A 27-year-old pregnant woman presented to our facility at 35 weeks' gestation with a 3-months history of right upper abdominal pain associated with generalized itch, tea colored urine, mastic -colored stool, and significant weight loss. No headache, blurred vision or spontaneous bleeding were mentioned. She was not a known diabetic or hypertensive and has no history of blood transfusion. Clinical signs on examination included mild pallor and cholestatic jaundice. Her blood pressure was 100/70 mmHg with a pulse rate of 98 beats/min, respiratory rate about 16/min and oral temperature of 37°C. Respiratory, cardiovascular and neurological examinations were unremarkable. The abdomen was grossly distended with visible collateral veins. Liver was enlarged, hard, nodular with a painful irregular edge. The spleen was not palpable. There was bipedal edema up to the mid shin. Fetal heart rate was 140 bpm and regular. Laboratory examination showed leukocytosis, anemia and normal platelet counts. Aspartate aminotransferase (AST) were raised (4times upper limit), total protein and albumin were low, 43g/L and 25g/L respectively, INR 1.20 and glycaemia 0.70g/L. Her alphafeto-protein (AFP) was higher (2232 ng/mL). HBsAg was positive. She tested negative to human immunodeficiency viruses (HIV) and HCV. Abdominal ultrasound showed a heterogeneous coarse liver with multiple hypoechoic lesions. Pelvic scan revealed a normal fetus with a gestational age of about 35 weeks. The diagnosis of hepatocellular carcinoma on a decompensated cirrhosis was made. She was managed with analgesia, spironolactone and tenofovir added for prevention of mother-to-child transmission of the hepatitis B infection. The plan was to have the mother's health improved to securely induce the labour. Unfortunately, at day two of hospitalization, the patient experienced progressive loss of conscious along with epistaxis and multi-organ failure. Laboratory assessment revealed HB-8.4g/dL, WBC 37500 cells/dL, Platelets 436000/ul, INR-2.57 and recurrent hypoglycemia. Cesarean section was urgently performed and the outcome was a healthy newborn weighted 2.9kg but the mother died soon after.
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EN107405
|
Exam: radiogram
|
not available
| 7 |
A 37-year-old Arabian woman presented with 12 months of progressive Cushing's syndrome-like symptoms. Biochemical evaluation confirmed adrenocorticotropic hormone -dependent Cushing's syndrome. However, the anatomical site of her excess adrenocorticotropic hormone secretion was not clearly delineated by further investigations. Magnetic resonance imaging of our patient's pituitary gland failed to demonstrate the presence of an adenoma. Spiral computed tomography of her chest only revealed the presence of a non-specific 7 mm lesion in her left inferobasal lung segment. Functional imaging, including a positron emission tomography scan using 18-fluorodeoxyglucose and gallium-68-DOTA-D-Phe1-Tyr3-octreotide, also failed to show increased metabolic activity in the lung lesion or in her pituitary gland. Our patient was commenced on medical treatment with ketoconazole and metyrapone to control the clinical features associated with her excess cortisol secretion. Despite initial normalization of her urinary free cortisol excretion rate, levels began to rise eight months after commencement of medical treatment. Repeated imaging of her pituitary gland, chest and pelvis again failed to clearly localize a source of her excess adrenocorticotropic hormone secretion. The bronchial nodule was stable in size on serial imaging and repeatedly reported as having a nonspecific appearance of a small granuloma or lymph node. We re-explored the treatment options and endorsed our patient's favored choice of resection of the bronchial nodule, especially given that her symptoms of cortisol excess were difficult to control and refractory. Subsequently, our patient had the bronchial nodule resected. The histological appearance of the lesion was consistent with that of a carcinoid tumor and immunohistochemical analysis revealed that the tumor stained strongly positive for adrenocorticotropic hormone. Furthermore, removal of the lung lesion resulted in a normalization of our patient's 24-hour urinary free cortisol excretion rate and resolution of her symptoms and signs of hypercortisolemia.
|
EN107405
|
Exam: electrocardiogram
|
not available
| 7 |
A 37-year-old Arabian woman presented with 12 months of progressive Cushing's syndrome-like symptoms. Biochemical evaluation confirmed adrenocorticotropic hormone -dependent Cushing's syndrome. However, the anatomical site of her excess adrenocorticotropic hormone secretion was not clearly delineated by further investigations. Magnetic resonance imaging of our patient's pituitary gland failed to demonstrate the presence of an adenoma. Spiral computed tomography of her chest only revealed the presence of a non-specific 7 mm lesion in her left inferobasal lung segment. Functional imaging, including a positron emission tomography scan using 18-fluorodeoxyglucose and gallium-68-DOTA-D-Phe1-Tyr3-octreotide, also failed to show increased metabolic activity in the lung lesion or in her pituitary gland. Our patient was commenced on medical treatment with ketoconazole and metyrapone to control the clinical features associated with her excess cortisol secretion. Despite initial normalization of her urinary free cortisol excretion rate, levels began to rise eight months after commencement of medical treatment. Repeated imaging of her pituitary gland, chest and pelvis again failed to clearly localize a source of her excess adrenocorticotropic hormone secretion. The bronchial nodule was stable in size on serial imaging and repeatedly reported as having a nonspecific appearance of a small granuloma or lymph node. We re-explored the treatment options and endorsed our patient's favored choice of resection of the bronchial nodule, especially given that her symptoms of cortisol excess were difficult to control and refractory. Subsequently, our patient had the bronchial nodule resected. The histological appearance of the lesion was consistent with that of a carcinoid tumor and immunohistochemical analysis revealed that the tumor stained strongly positive for adrenocorticotropic hormone. Furthermore, removal of the lung lesion resulted in a normalization of our patient's 24-hour urinary free cortisol excretion rate and resolution of her symptoms and signs of hypercortisolemia.
|
EN107405
|
Exam: phosphokinase
|
not available
| 7 |
A 37-year-old Arabian woman presented with 12 months of progressive Cushing's syndrome-like symptoms. Biochemical evaluation confirmed adrenocorticotropic hormone -dependent Cushing's syndrome. However, the anatomical site of her excess adrenocorticotropic hormone secretion was not clearly delineated by further investigations. Magnetic resonance imaging of our patient's pituitary gland failed to demonstrate the presence of an adenoma. Spiral computed tomography of her chest only revealed the presence of a non-specific 7 mm lesion in her left inferobasal lung segment. Functional imaging, including a positron emission tomography scan using 18-fluorodeoxyglucose and gallium-68-DOTA-D-Phe1-Tyr3-octreotide, also failed to show increased metabolic activity in the lung lesion or in her pituitary gland. Our patient was commenced on medical treatment with ketoconazole and metyrapone to control the clinical features associated with her excess cortisol secretion. Despite initial normalization of her urinary free cortisol excretion rate, levels began to rise eight months after commencement of medical treatment. Repeated imaging of her pituitary gland, chest and pelvis again failed to clearly localize a source of her excess adrenocorticotropic hormone secretion. The bronchial nodule was stable in size on serial imaging and repeatedly reported as having a nonspecific appearance of a small granuloma or lymph node. We re-explored the treatment options and endorsed our patient's favored choice of resection of the bronchial nodule, especially given that her symptoms of cortisol excess were difficult to control and refractory. Subsequently, our patient had the bronchial nodule resected. The histological appearance of the lesion was consistent with that of a carcinoid tumor and immunohistochemical analysis revealed that the tumor stained strongly positive for adrenocorticotropic hormone. Furthermore, removal of the lung lesion resulted in a normalization of our patient's 24-hour urinary free cortisol excretion rate and resolution of her symptoms and signs of hypercortisolemia.
|
EN107405
|
Exam: troponin
|
not available
| 7 |
A 37-year-old Arabian woman presented with 12 months of progressive Cushing's syndrome-like symptoms. Biochemical evaluation confirmed adrenocorticotropic hormone -dependent Cushing's syndrome. However, the anatomical site of her excess adrenocorticotropic hormone secretion was not clearly delineated by further investigations. Magnetic resonance imaging of our patient's pituitary gland failed to demonstrate the presence of an adenoma. Spiral computed tomography of her chest only revealed the presence of a non-specific 7 mm lesion in her left inferobasal lung segment. Functional imaging, including a positron emission tomography scan using 18-fluorodeoxyglucose and gallium-68-DOTA-D-Phe1-Tyr3-octreotide, also failed to show increased metabolic activity in the lung lesion or in her pituitary gland. Our patient was commenced on medical treatment with ketoconazole and metyrapone to control the clinical features associated with her excess cortisol secretion. Despite initial normalization of her urinary free cortisol excretion rate, levels began to rise eight months after commencement of medical treatment. Repeated imaging of her pituitary gland, chest and pelvis again failed to clearly localize a source of her excess adrenocorticotropic hormone secretion. The bronchial nodule was stable in size on serial imaging and repeatedly reported as having a nonspecific appearance of a small granuloma or lymph node. We re-explored the treatment options and endorsed our patient's favored choice of resection of the bronchial nodule, especially given that her symptoms of cortisol excess were difficult to control and refractory. Subsequently, our patient had the bronchial nodule resected. The histological appearance of the lesion was consistent with that of a carcinoid tumor and immunohistochemical analysis revealed that the tumor stained strongly positive for adrenocorticotropic hormone. Furthermore, removal of the lung lesion resulted in a normalization of our patient's 24-hour urinary free cortisol excretion rate and resolution of her symptoms and signs of hypercortisolemia.
|
EN107405
|
Exam: lymphopenia
|
not available
| 7 |
A 37-year-old Arabian woman presented with 12 months of progressive Cushing's syndrome-like symptoms. Biochemical evaluation confirmed adrenocorticotropic hormone -dependent Cushing's syndrome. However, the anatomical site of her excess adrenocorticotropic hormone secretion was not clearly delineated by further investigations. Magnetic resonance imaging of our patient's pituitary gland failed to demonstrate the presence of an adenoma. Spiral computed tomography of her chest only revealed the presence of a non-specific 7 mm lesion in her left inferobasal lung segment. Functional imaging, including a positron emission tomography scan using 18-fluorodeoxyglucose and gallium-68-DOTA-D-Phe1-Tyr3-octreotide, also failed to show increased metabolic activity in the lung lesion or in her pituitary gland. Our patient was commenced on medical treatment with ketoconazole and metyrapone to control the clinical features associated with her excess cortisol secretion. Despite initial normalization of her urinary free cortisol excretion rate, levels began to rise eight months after commencement of medical treatment. Repeated imaging of her pituitary gland, chest and pelvis again failed to clearly localize a source of her excess adrenocorticotropic hormone secretion. The bronchial nodule was stable in size on serial imaging and repeatedly reported as having a nonspecific appearance of a small granuloma or lymph node. We re-explored the treatment options and endorsed our patient's favored choice of resection of the bronchial nodule, especially given that her symptoms of cortisol excess were difficult to control and refractory. Subsequently, our patient had the bronchial nodule resected. The histological appearance of the lesion was consistent with that of a carcinoid tumor and immunohistochemical analysis revealed that the tumor stained strongly positive for adrenocorticotropic hormone. Furthermore, removal of the lung lesion resulted in a normalization of our patient's 24-hour urinary free cortisol excretion rate and resolution of her symptoms and signs of hypercortisolemia.
|
EN107405
|
Exam: globulin
|
not available
| 7 |
A 37-year-old Arabian woman presented with 12 months of progressive Cushing's syndrome-like symptoms. Biochemical evaluation confirmed adrenocorticotropic hormone -dependent Cushing's syndrome. However, the anatomical site of her excess adrenocorticotropic hormone secretion was not clearly delineated by further investigations. Magnetic resonance imaging of our patient's pituitary gland failed to demonstrate the presence of an adenoma. Spiral computed tomography of her chest only revealed the presence of a non-specific 7 mm lesion in her left inferobasal lung segment. Functional imaging, including a positron emission tomography scan using 18-fluorodeoxyglucose and gallium-68-DOTA-D-Phe1-Tyr3-octreotide, also failed to show increased metabolic activity in the lung lesion or in her pituitary gland. Our patient was commenced on medical treatment with ketoconazole and metyrapone to control the clinical features associated with her excess cortisol secretion. Despite initial normalization of her urinary free cortisol excretion rate, levels began to rise eight months after commencement of medical treatment. Repeated imaging of her pituitary gland, chest and pelvis again failed to clearly localize a source of her excess adrenocorticotropic hormone secretion. The bronchial nodule was stable in size on serial imaging and repeatedly reported as having a nonspecific appearance of a small granuloma or lymph node. We re-explored the treatment options and endorsed our patient's favored choice of resection of the bronchial nodule, especially given that her symptoms of cortisol excess were difficult to control and refractory. Subsequently, our patient had the bronchial nodule resected. The histological appearance of the lesion was consistent with that of a carcinoid tumor and immunohistochemical analysis revealed that the tumor stained strongly positive for adrenocorticotropic hormone. Furthermore, removal of the lung lesion resulted in a normalization of our patient's 24-hour urinary free cortisol excretion rate and resolution of her symptoms and signs of hypercortisolemia.
|
EN107405
|
Exam: nitrogen
|
not available
| 7 |
A 37-year-old Arabian woman presented with 12 months of progressive Cushing's syndrome-like symptoms. Biochemical evaluation confirmed adrenocorticotropic hormone -dependent Cushing's syndrome. However, the anatomical site of her excess adrenocorticotropic hormone secretion was not clearly delineated by further investigations. Magnetic resonance imaging of our patient's pituitary gland failed to demonstrate the presence of an adenoma. Spiral computed tomography of her chest only revealed the presence of a non-specific 7 mm lesion in her left inferobasal lung segment. Functional imaging, including a positron emission tomography scan using 18-fluorodeoxyglucose and gallium-68-DOTA-D-Phe1-Tyr3-octreotide, also failed to show increased metabolic activity in the lung lesion or in her pituitary gland. Our patient was commenced on medical treatment with ketoconazole and metyrapone to control the clinical features associated with her excess cortisol secretion. Despite initial normalization of her urinary free cortisol excretion rate, levels began to rise eight months after commencement of medical treatment. Repeated imaging of her pituitary gland, chest and pelvis again failed to clearly localize a source of her excess adrenocorticotropic hormone secretion. The bronchial nodule was stable in size on serial imaging and repeatedly reported as having a nonspecific appearance of a small granuloma or lymph node. We re-explored the treatment options and endorsed our patient's favored choice of resection of the bronchial nodule, especially given that her symptoms of cortisol excess were difficult to control and refractory. Subsequently, our patient had the bronchial nodule resected. The histological appearance of the lesion was consistent with that of a carcinoid tumor and immunohistochemical analysis revealed that the tumor stained strongly positive for adrenocorticotropic hormone. Furthermore, removal of the lung lesion resulted in a normalization of our patient's 24-hour urinary free cortisol excretion rate and resolution of her symptoms and signs of hypercortisolemia.
|
EN107405
|
Exam: cholesterol
|
not available
| 7 |
A 37-year-old Arabian woman presented with 12 months of progressive Cushing's syndrome-like symptoms. Biochemical evaluation confirmed adrenocorticotropic hormone -dependent Cushing's syndrome. However, the anatomical site of her excess adrenocorticotropic hormone secretion was not clearly delineated by further investigations. Magnetic resonance imaging of our patient's pituitary gland failed to demonstrate the presence of an adenoma. Spiral computed tomography of her chest only revealed the presence of a non-specific 7 mm lesion in her left inferobasal lung segment. Functional imaging, including a positron emission tomography scan using 18-fluorodeoxyglucose and gallium-68-DOTA-D-Phe1-Tyr3-octreotide, also failed to show increased metabolic activity in the lung lesion or in her pituitary gland. Our patient was commenced on medical treatment with ketoconazole and metyrapone to control the clinical features associated with her excess cortisol secretion. Despite initial normalization of her urinary free cortisol excretion rate, levels began to rise eight months after commencement of medical treatment. Repeated imaging of her pituitary gland, chest and pelvis again failed to clearly localize a source of her excess adrenocorticotropic hormone secretion. The bronchial nodule was stable in size on serial imaging and repeatedly reported as having a nonspecific appearance of a small granuloma or lymph node. We re-explored the treatment options and endorsed our patient's favored choice of resection of the bronchial nodule, especially given that her symptoms of cortisol excess were difficult to control and refractory. Subsequently, our patient had the bronchial nodule resected. The histological appearance of the lesion was consistent with that of a carcinoid tumor and immunohistochemical analysis revealed that the tumor stained strongly positive for adrenocorticotropic hormone. Furthermore, removal of the lung lesion resulted in a normalization of our patient's 24-hour urinary free cortisol excretion rate and resolution of her symptoms and signs of hypercortisolemia.
|
EN107405
|
Exam: Echocardiogram
|
not available
| 7 |
A 37-year-old Arabian woman presented with 12 months of progressive Cushing's syndrome-like symptoms. Biochemical evaluation confirmed adrenocorticotropic hormone -dependent Cushing's syndrome. However, the anatomical site of her excess adrenocorticotropic hormone secretion was not clearly delineated by further investigations. Magnetic resonance imaging of our patient's pituitary gland failed to demonstrate the presence of an adenoma. Spiral computed tomography of her chest only revealed the presence of a non-specific 7 mm lesion in her left inferobasal lung segment. Functional imaging, including a positron emission tomography scan using 18-fluorodeoxyglucose and gallium-68-DOTA-D-Phe1-Tyr3-octreotide, also failed to show increased metabolic activity in the lung lesion or in her pituitary gland. Our patient was commenced on medical treatment with ketoconazole and metyrapone to control the clinical features associated with her excess cortisol secretion. Despite initial normalization of her urinary free cortisol excretion rate, levels began to rise eight months after commencement of medical treatment. Repeated imaging of her pituitary gland, chest and pelvis again failed to clearly localize a source of her excess adrenocorticotropic hormone secretion. The bronchial nodule was stable in size on serial imaging and repeatedly reported as having a nonspecific appearance of a small granuloma or lymph node. We re-explored the treatment options and endorsed our patient's favored choice of resection of the bronchial nodule, especially given that her symptoms of cortisol excess were difficult to control and refractory. Subsequently, our patient had the bronchial nodule resected. The histological appearance of the lesion was consistent with that of a carcinoid tumor and immunohistochemical analysis revealed that the tumor stained strongly positive for adrenocorticotropic hormone. Furthermore, removal of the lung lesion resulted in a normalization of our patient's 24-hour urinary free cortisol excretion rate and resolution of her symptoms and signs of hypercortisolemia.
|
EN107405
|
Exam: hemoglobin
|
not available
| 7 |
A 37-year-old Arabian woman presented with 12 months of progressive Cushing's syndrome-like symptoms. Biochemical evaluation confirmed adrenocorticotropic hormone -dependent Cushing's syndrome. However, the anatomical site of her excess adrenocorticotropic hormone secretion was not clearly delineated by further investigations. Magnetic resonance imaging of our patient's pituitary gland failed to demonstrate the presence of an adenoma. Spiral computed tomography of her chest only revealed the presence of a non-specific 7 mm lesion in her left inferobasal lung segment. Functional imaging, including a positron emission tomography scan using 18-fluorodeoxyglucose and gallium-68-DOTA-D-Phe1-Tyr3-octreotide, also failed to show increased metabolic activity in the lung lesion or in her pituitary gland. Our patient was commenced on medical treatment with ketoconazole and metyrapone to control the clinical features associated with her excess cortisol secretion. Despite initial normalization of her urinary free cortisol excretion rate, levels began to rise eight months after commencement of medical treatment. Repeated imaging of her pituitary gland, chest and pelvis again failed to clearly localize a source of her excess adrenocorticotropic hormone secretion. The bronchial nodule was stable in size on serial imaging and repeatedly reported as having a nonspecific appearance of a small granuloma or lymph node. We re-explored the treatment options and endorsed our patient's favored choice of resection of the bronchial nodule, especially given that her symptoms of cortisol excess were difficult to control and refractory. Subsequently, our patient had the bronchial nodule resected. The histological appearance of the lesion was consistent with that of a carcinoid tumor and immunohistochemical analysis revealed that the tumor stained strongly positive for adrenocorticotropic hormone. Furthermore, removal of the lung lesion resulted in a normalization of our patient's 24-hour urinary free cortisol excretion rate and resolution of her symptoms and signs of hypercortisolemia.
|
EN107405
|
Exam: amylase
|
not available
| 7 |
A 37-year-old Arabian woman presented with 12 months of progressive Cushing's syndrome-like symptoms. Biochemical evaluation confirmed adrenocorticotropic hormone -dependent Cushing's syndrome. However, the anatomical site of her excess adrenocorticotropic hormone secretion was not clearly delineated by further investigations. Magnetic resonance imaging of our patient's pituitary gland failed to demonstrate the presence of an adenoma. Spiral computed tomography of her chest only revealed the presence of a non-specific 7 mm lesion in her left inferobasal lung segment. Functional imaging, including a positron emission tomography scan using 18-fluorodeoxyglucose and gallium-68-DOTA-D-Phe1-Tyr3-octreotide, also failed to show increased metabolic activity in the lung lesion or in her pituitary gland. Our patient was commenced on medical treatment with ketoconazole and metyrapone to control the clinical features associated with her excess cortisol secretion. Despite initial normalization of her urinary free cortisol excretion rate, levels began to rise eight months after commencement of medical treatment. Repeated imaging of her pituitary gland, chest and pelvis again failed to clearly localize a source of her excess adrenocorticotropic hormone secretion. The bronchial nodule was stable in size on serial imaging and repeatedly reported as having a nonspecific appearance of a small granuloma or lymph node. We re-explored the treatment options and endorsed our patient's favored choice of resection of the bronchial nodule, especially given that her symptoms of cortisol excess were difficult to control and refractory. Subsequently, our patient had the bronchial nodule resected. The histological appearance of the lesion was consistent with that of a carcinoid tumor and immunohistochemical analysis revealed that the tumor stained strongly positive for adrenocorticotropic hormone. Furthermore, removal of the lung lesion resulted in a normalization of our patient's 24-hour urinary free cortisol excretion rate and resolution of her symptoms and signs of hypercortisolemia.
|
EN107405
|
Exam: lipase
|
not available
| 7 |
A 37-year-old Arabian woman presented with 12 months of progressive Cushing's syndrome-like symptoms. Biochemical evaluation confirmed adrenocorticotropic hormone -dependent Cushing's syndrome. However, the anatomical site of her excess adrenocorticotropic hormone secretion was not clearly delineated by further investigations. Magnetic resonance imaging of our patient's pituitary gland failed to demonstrate the presence of an adenoma. Spiral computed tomography of her chest only revealed the presence of a non-specific 7 mm lesion in her left inferobasal lung segment. Functional imaging, including a positron emission tomography scan using 18-fluorodeoxyglucose and gallium-68-DOTA-D-Phe1-Tyr3-octreotide, also failed to show increased metabolic activity in the lung lesion or in her pituitary gland. Our patient was commenced on medical treatment with ketoconazole and metyrapone to control the clinical features associated with her excess cortisol secretion. Despite initial normalization of her urinary free cortisol excretion rate, levels began to rise eight months after commencement of medical treatment. Repeated imaging of her pituitary gland, chest and pelvis again failed to clearly localize a source of her excess adrenocorticotropic hormone secretion. The bronchial nodule was stable in size on serial imaging and repeatedly reported as having a nonspecific appearance of a small granuloma or lymph node. We re-explored the treatment options and endorsed our patient's favored choice of resection of the bronchial nodule, especially given that her symptoms of cortisol excess were difficult to control and refractory. Subsequently, our patient had the bronchial nodule resected. The histological appearance of the lesion was consistent with that of a carcinoid tumor and immunohistochemical analysis revealed that the tumor stained strongly positive for adrenocorticotropic hormone. Furthermore, removal of the lung lesion resulted in a normalization of our patient's 24-hour urinary free cortisol excretion rate and resolution of her symptoms and signs of hypercortisolemia.
|
EN107405
|
Exam: cytokeratin
|
not available
| 7 |
A 37-year-old Arabian woman presented with 12 months of progressive Cushing's syndrome-like symptoms. Biochemical evaluation confirmed adrenocorticotropic hormone -dependent Cushing's syndrome. However, the anatomical site of her excess adrenocorticotropic hormone secretion was not clearly delineated by further investigations. Magnetic resonance imaging of our patient's pituitary gland failed to demonstrate the presence of an adenoma. Spiral computed tomography of her chest only revealed the presence of a non-specific 7 mm lesion in her left inferobasal lung segment. Functional imaging, including a positron emission tomography scan using 18-fluorodeoxyglucose and gallium-68-DOTA-D-Phe1-Tyr3-octreotide, also failed to show increased metabolic activity in the lung lesion or in her pituitary gland. Our patient was commenced on medical treatment with ketoconazole and metyrapone to control the clinical features associated with her excess cortisol secretion. Despite initial normalization of her urinary free cortisol excretion rate, levels began to rise eight months after commencement of medical treatment. Repeated imaging of her pituitary gland, chest and pelvis again failed to clearly localize a source of her excess adrenocorticotropic hormone secretion. The bronchial nodule was stable in size on serial imaging and repeatedly reported as having a nonspecific appearance of a small granuloma or lymph node. We re-explored the treatment options and endorsed our patient's favored choice of resection of the bronchial nodule, especially given that her symptoms of cortisol excess were difficult to control and refractory. Subsequently, our patient had the bronchial nodule resected. The histological appearance of the lesion was consistent with that of a carcinoid tumor and immunohistochemical analysis revealed that the tumor stained strongly positive for adrenocorticotropic hormone. Furthermore, removal of the lung lesion resulted in a normalization of our patient's 24-hour urinary free cortisol excretion rate and resolution of her symptoms and signs of hypercortisolemia.
|
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