Foster Kennedy syndrome secondary to a giant prolactinoma with a remarkable response to cabergoline.

Summary: Pituitary adenomas are intracranial neoplasms, usually demonstrating a benign phenotype. We present the case of 21-year-old male with an 18-month history of reduced visual function (acuity and field) in the left eye. Based on neuroimaging and endocrine profile, a giant prolactinoma causing hypogonadotropic hypogonadism was diagnosed and cabergoline was commenced. After a month of treatment, the tumour size reduced, and visual function improved to normal; however, he developed Foster Kennedy syndrome with a swollen right optic disc. After almost 1 year of follow-up, he regained full visual functioning. Two years since his diagnosis, his prolactin remains normal with no adverse effects or further visual complications. Learning points: Foster Kennedy syndrome is a rare entity but can be a feature of pituitary adenomas. Visual deterioration secondary to a compressive optic neuropathy can be reversible, provided that diagnosis and treatment are prompt. This case highlights the importance of frequent monitoring of visual function during follow-up of these lesions, particularly when there are deficits at diagnosis.

Mortality of Patients with Cushing's Disease.

Cushing's disease is a rare condition of cortisol excess attributed to a pituitary adenoma with an annual incidence of 1.2-2.4 cases per million population. It is associated with several co-morbidities leading to increased mortality predominantly due to cardiovascular disease. Despite the advances in its diagnosis and management, survival can be compromised even after apparent successful treatment. Minimizing the duration and extent of exposure to hypercortisolaemia by early diagnosis and rapid, effective therapeutic interventions, as well as close monitoring and aggressive control of cardiovascular risk factors are vital for improving outcomes of the patients.

Beyond thrombocytopaenia, haemorrhage and shock: the expanded dengue syndrome.

Dengue infection classically presents with fever, thrombocytopaenia, and varying degrees of plasma leakage, giving rise to shock. However, a myriad of other manifestations, involving the cardiovascular system, the nervous system, the liver, the kidneys, the gut and the haematological system have been reported in dengue. This review summarizes these varied presentations.

Dengue fever with diffuse cerebral hemorrhages, subdural hematoma and cranial diabetes insipidus.

BACKGROUND: Neurological manifestations in dengue fever occur in <1 % of the patients and known to be due to multisystem dysfunction secondary to vascular leakage. Occurrence of wide spread cerebral haemorrhages with subdural hematoma during the leakage phase without profound thrombocytopenia and occurrence of cranial diabetes insipidus are extremely rare and had not been reported in published literature earlier, thus we report the first case. CASE PRESENTATION: A 24 year old previously healthy lady was admitted on third day of fever with thrombocytopenia. Critical phase started on fifth day with evidence of pleural effusion and moderate ascites. Thirty one hours into critical phase she developed headache, altered level of consciousness, limb rigidity and respiratory depression without definite seizures. Non-contrast CT brain done at tertiary care level revealed diffuse intracranial haemorrhages and sub arachnoid haemorrhages in right frontal, parietal, occipital lobes and brainstem, cerebral oedema with an acute subdural hematoma in right temporo- parietal region. Her platelet count was 40,000 at this time with signs of vascular leakage. She was intubated and ventilated with supportive care. Later on she developed features of cranial diabetes insipidus and it responded to intranasal desmopressin therapy. In spite of above measures signs of brainstem herniation developed and she succumbed to the illness on day 8. Dengue was confirmed serologically. CONCLUSIONS: Exact pathophysiological mechanism of diffuse cerebral haemorrhages without profound thrombocytopenia is not well understood. Increased awareness and high degree of clinical suspicion is needed among clinicians for timely diagnosis of this extremely rare complication of dengue fever. We postulate that immunological mechanisms may play a role in pathogenesis. However further comprehensive research and studies are needed to understand the pathophysiological mechanisms leading to this complication.