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EN107405
|
Exam: CK7
|
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: synaptophysin
|
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: CD56
|
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: SCAN
|
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: fever
|
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: WBC
|
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: aminotransferase
|
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: ALT
|
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: LDH
|
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: phosphatase
|
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: Entamoeba
|
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: echinococcus
|
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: leismania
|
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: brucella
|
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: amikacin
|
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: cefepime
|
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: ciprofloxacin
|
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: gentamycin
|
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: meropenem
|
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: chromogranin
|
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: Synaptophysin
|
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: CD10
|
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: Ki-67
|
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: pressure
|
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: HIV
|
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: HCV
|
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: HB
|
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: Platelets
|
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: INR
|
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: AFP
|
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: Her2neu
|
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: ER
|
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: PR
|
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.
|
EN100655
|
Exam: polypnea
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: hemoglobin
|
9.5 g/dl.
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: MCV
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: Albumin
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: Creatinine
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: echocardiography
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: ultrasound
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: hyper-calciuria
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: OHD
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: immunofixation
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: T-score
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: hypocalcemia
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: proteinuria
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: calcium
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: iPTH
|
not available
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: fever
|
39°C.
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN100655
|
Exam: CRP
|
Result:
0) dalla data 2019-WXX:
dopo -15 eventi: 75 mm/h. [\MULTI_ANSWER]
in contemporanea: 2.43mg. [\MULTI_ANSWER]
dopo 1 eventi: 3 mg/L.
| 8 |
Patient information: a 9-month-old boy presented to the emergency room with a 3-day history of refusal to bear weight on the right lower extremity and febrile peaks of up to 38.5°C for 24 hours. His parents had noted an ankle trauma in the previous week. The primary care physician had initially suspected a talus fracture. His right ankle was immobilized by a plaster splint and his parents were instructed to apply ice. However, the child continued to experience ankle pain and fever. He was returned to the emergency room after two days. His symptoms were aggravated. The ankle was noted to be slightly edematous, but warm to the touch, and diffusely tender to palpation. His temperature was 39°C. Diagnostic assessment: the hemoglobin was 9.5 g/dl, the white blood cell count was 18800/mm 3, and the C-reactive protein (CRP) was 75 mm/h. Serum laboratory studies, including CBC count and inflammatory markers, were all elevated. An X-ray of the ankle showed a posterior-medial lytic lesion of the talus and soft tissue swelling around the ankle joint. However, the computed tomography (CT) scan findings revealed a talus fracture. A magnetic resonance imaging (MRI) was not done as it was not available. Given the clinical findings a talar osteomyelitis with septic arthritis of the ankle was suspected despite the result of the CT scan. The bone scintigraphy demonstrated a septic arthritis and the presence of bone marrow edema in the talus without being able to reach a precise diagnosis of osteomyelitis. Therapeutic intervention: the patient was urgently taken to the operating room. During the operation, the ankle joint was explored through an anterior approach. There were some false membranes, a thin turbid fluid and a pertuit at the junction bone cartilage of the talus. The talar cartilage was regular and normal-looking. The pertuit, allowing access to a cavity, was cleaned and the yellow organized fibrinous pus was drained. The biopsy specimens for the histopathological examination and culture were taken at that site. Curettage and irrigation were performed, and the joint was closed over suction drains. An empirical antibiotic treatment IV (cephalosporin + gentamycine) was initiated. Follow-up and outcomes: febrile peaks persisted during the first three days. The blood culture and the specimen of the joint isolated Staphylococcus aureus Meti-R. The anatomopathological analysis of the ankle specimen showed histological features of an abscess and hyperplastic synovial cells. So, the IV antibiotic treatment was substituted by teicoplanin with a better clinical and biological progression. Drainage was maintained for twelve days (until normalization of CRP) and intravenous antibiotics for 3 weeks. In the third week, the peripheral leukocytes count was 8600/mL, and the CRP decreased to 2.43mg. The patient's antibiotic was then substituted by oral pristinamycin for three weeks. In the fourth week, the ESR and CRP were 7 mm/hr and 3 mg/L, respectively. At that time, the patient did not complain of any pain or limitation of the range of motion of the ankle. The cast was removed six weeks after surgery. At six months, radiographies showed that the lesion healed completely. The parents were very satisfied. Their child acquired walking at the age of 14 months. In the last follow-up visit at 18 months postoperatively, the patient had no pain or limitation in walking and running.
|
EN103220
|
Exam: fever
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: polypnea
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: hemoglobin
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: MCV
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: Albumin
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: Creatinine
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: echocardiography
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: ultrasound
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: hyper-calciuria
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: OHD
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: immunofixation
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: T-score
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: hypocalcemia
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: proteinuria
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: calcium
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: iPTH
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN103220
|
Exam: CRP
|
not available
| 8 |
Here we report a case of aggressive metastatic cholangiocarcinoma (MCC) in 72-year-old man, sequentially treated with two targeted chemotherapies. Initially disease quickly progressed during best clinical practice care (gemcitabine in combination with cisplatin or capecitabine), which was accompanied by significant decrease of life quality. Monotherapy with TKI sorafenib was prescribed to the patient, which resulted in stabilization of tumor growth and elimination of pain. The choice of the inhibitor was made based on high-throughput screening of gene expression in the patient's tumor biopsy, utilized by Oncobox platform to build a personalized rating of potentially effective target therapies. However, time to progression after start of sorafenib administration did not exceed 6 months and the regimen was changed to monotherapy with Pazopanib, another TKI predicted to be effective for this patient according to the same molecular test. It resulted in disease progression according to RECIST with simultaneous elimination of sorafenib side effects such as rash and hand-foot syndrome. After 2 years from the diagnosis of MCC the patient was alive and physically active, which is substantially longer than median survival for standard therapy.
|
EN100017
|
Exam: haemoglobin
|
10.9 g/dl.
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
|
EN100017
|
Exam: creatinine
|
Result:
0) dalla data 2012-08-12:
dopo -1 eventi: 1.0 mg/dl. [\MULTI_ANSWER]
dopo -1 eventi: normal.
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
|
EN100017
|
Exam: sodium
|
Result:
0) dalla data 2012-08-12:
dopo -1 eventi: 137 mmol/L. [\MULTI_ANSWER]
dopo -1 eventi: normal.
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
|
EN100017
|
Exam: potassium
|
Result:
0) dalla data 2012-08-12:
dopo -1 eventi: 3.7 mmol/L. [\MULTI_ANSWER]
dopo -1 eventi: normal.
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
|
EN100017
|
Exam: proteinurea
|
Result:
0) dalla data 2012-08-12:
in contemporanea: three pluses. [\MULTI_ANSWER]
in contemporanea: two pluses.
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
|
EN100017
|
Exam: FDP
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
|
EN100017
|
Exam: ALP
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
|
EN100017
|
Exam: INR
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
|
EN100017
|
Exam: fibrinogen
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
|
EN100017
|
Exam: pressure
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
|
EN100017
|
Exam: temperature
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
|
EN100017
|
Exam: metacarpophalangeal
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
|
EN100017
|
Exam: interphalagienne
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
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EN100017
|
Exam: interphalageal
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
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EN100017
|
Exam: gonadotropin
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
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EN100017
|
Exam: fetoprotein
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
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EN100017
|
Exam: were-pulse
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
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EN100017
|
Exam: BP
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
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EN100017
|
Exam: Sp02
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
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EN100017
|
Exam: SARS-CoV-2
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
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EN100017
|
Exam: CRP
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
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EN100017
|
Exam: LDH
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
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EN100017
|
Exam: weight
|
not available
| 9 |
A 14-year old boy with no significant past medical history presented to a small district hospital in southern Sierra Leone with a 4 day history of facial puffiness, peripheral pitting oedema, abdominal pains, and reduced urine output. On examination he was afebrile, BP150/110, heart rate 70. He had significant periorbital and facial oedema, pitting oedema from the feet to the knees, a distended abdomen, ascites, and tender hepatomegaly. Lab results showed haemoglobin 10.9 g/dl, packed cell volume 35%, and positive malaria parasites. Urea (14 mg/dl), creatinine (1.0 mg/dl), sodium (137 mmol/L), and potassium (3.7 mmol/L) were normal. Urinalysis, using a urine dipstick, revealed three pluses of proteinurea, which equates to ≥3g urinary protein per day. Lab facilities for the measurement of serum albumin were not available. The diagnosis of nephrotic syndrome was made and the patient was started on a course of prednisolone 60mg/day, Enalapril 2.5mg daily, anti-malarial treatment, and empirical broad spectrum IV antibiotics to cover bacterial infections, in addition to a salt-restricted diet. On day 3 of admission he showed a clinical response to treatment, as the facial oedema, ascites, and BP had reduced. Urinalysis showed two pluses of proteinurea (0.5-1.0 gram per day per day). The child complained of a moderate headache, but had no fever, meningism, or focal neurological signs. He was started on oral paracetamol. The next morning (day 4 of admission) his symptoms evolved: his headache became severe, he had pain behind both eyes, and he was vomiting. Examination showed a right VI nerve palsy, diplopia, and tinnitus in the right ear, with some hearing loss. He later became drowsy and had a generalised seizure. Diagnosis and commencement of treatment was delayed due to the absence of CT/MRI brain imaging facilities in the local district. In the context of the child's nephrotic status and focal neurological signs, we had a high suspicion of cerebral venous thrombosis, and made a presumptive diagnosis. The child was started on high dose subcutaneous unfractionated heparin daily. This decision was made cautiously, but it was felt that the advantages surpassed the risks. He also received dexamethasone, high flow oxygen, and elevation of the head to 45 degrees, in order to treat features of raised intracranial pressure. On day 6 of admission his headache had improved and his focal neurological signs began to resolve. He still had a partial right VI nerve palsy and a convergent squint. His oedema resolved completely by day 10 of treatment, and he was discharged on day 18. He continued prednisolone 60mg daily for a total of 6 weeks, followed by a reduced dose of 40mg on alternate days for 6 weeks. At 12 weeks follow-up, his urinalysis showed a trace proteinurea but he remained in remission.
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EN100156
|
Exam: haemoglobin
|
not available
| 9 |
A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
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EN100156
|
Exam: creatinine
|
not available
| 9 |
A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
|
EN100156
|
Exam: sodium
|
not available
| 9 |
A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
|
EN100156
|
Exam: potassium
|
not available
| 9 |
A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
|
EN100156
|
Exam: proteinurea
|
not available
| 9 |
A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
|
EN100156
|
Exam: FDP
|
not available
| 9 |
A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
|
EN100156
|
Exam: ALP
|
not available
| 9 |
A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
|
EN100156
|
Exam: INR
|
not available
| 9 |
A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
|
EN100156
|
Exam: fibrinogen
|
not available
| 9 |
A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
|
EN100156
|
Exam: pressure
|
not available
| 9 |
A 38-year-old man presented with a seven month history of progressively worsening bilateral knees pain with associated swelling. The pain was present when the patient was at rest, and worsened when the legs was bearing weight, thus restricting his walking to short distances. His knees had become increasingly swollen. He was otherwise fit and well. His medical history was unremarkable and he was only taking a paracetamol, codeine and anti-inflammatory drugs for the pain.
Upon examination, the patient was seen to have visibly swollen popliteal fossa and marked quadriceps wasting of his right lower limb. On palpation, the masses was hard, mobile, well defined, and measured 0.5 - 04 cm. The swelling was non-tender and there were no associated skin changes. He could fully extend his knee, but flexion was restricted to only 110 degrees. There was a McMurray test proved equivocal and no ligamentous instability. An examination of the patient’s hip revealed no abnormality.
A plain radiograph of the patient’s knees revealed multiple calcific densities within the soft tissues surrounding it on the right one. Although some of these appeared to lie within the capsule, the majority appeared to be outside of it, and a solitary image on the left knee. These appearances were thought to be consistent with idiopathic tumoral calcinosis. However, to further scrutinize these calcifications, a magnetic resonance imaging (MRI) scan was recommended. It showed an extensive thickening of the patient’s synovium, multiple intraarticular calcific and ossific loose bodies, and large calcified bursal extensions. These findings were thought to be consistent with very extensive bilateral synovial chondromatosis. The patient’s blood tests were normal: C-reactive protein 5 mg/l and the phosphate calcium balance without errors.
A two-stage procedure was planned following the findings of the MRI scan. The first stage was arthroscopy, which was able to note Grade IV osteoarthritis alongside florid synovial chondromatosis in the lateral compartment of the right knee. There were multiple loose bodies within this compartment and nodules were fixed to the synovium. On the left one, we found an isolated synovial metaplasia in the subvastus quadriceps-sparing. A synovectomy with debridement and excision of these bodies was thus performed.
The second stage involved an open exploration of the patient’s popliteal fossa. Multiple calcified masses were found, all enclosed in bursal sacs. They were lateral to the semimembranosus at the level of the oblique popliteal ligament. All the masses were excised. A histological review confirmed our diagnosis of synovial chondromatosis. The sections showed nests of chondrocytes with focal ossification and focally attenuated synovium overlying the nodules. After the operation, the patient underwent functional rehabilitation sessions focusing on quadriceps strengthening, with a daily exercise regime to supplement this. He recovered well and ten weeks after the operation, has regained his right knee’s full range of movement with flexion increased to 130 degrees, which is equal to that of his left knee.
|
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