Background: Portal vein thrombosis (PVT) refers to venous thrombosis that develops within the extrahepatic portal venous system and can extend to the branches of the intrahepatic portal vein or up to splenic veins and superior mesenteric. A few cases have been reported about portal vein thrombosis in non-cirrhotic patient. Asymptomatic or non-specific symptom of portal vein thrombosis may lead to misdiagnosed or delay the diagnosis until the complications develop. We report a case of Portal vein thrombosis in type one diabetes associated with acute pyelonephritis. Case report: 18 years old female with type one diabetes on insulin pump present with epigastric abdominal pain for three days associated with nausea and vomiting of three days duration. On examination; conscious alert oriented young female looks in pain, vital sign were stable temperature 37oC, heart rate 89 beat per minute, blood pressure 103/72 mmHg, respiratory rate 20 per minute, oxygen saturation 100% and random blood sugar (RBS) 179 mg/dl. Abdominal examination revealed soft and lax abdomen with tenderness in the epigastric area and right renal angle. No sign of rigidity or rebound tenderness. Bowel sound was present. No sign of ascites, splenomegaly or hepatomegaly. Investigations showed; WBC: 10.2, neutrophil 65%, urine analysis WBCs 30-50 per high field microscopy, RBC 5-10, PH 7, negative nitrate and culture did not show any growth. ESR was 48 and CRP was 4.2. Thrombophilic screen was done and all within normal. Computed tomography (CT) reveled reduced enhancement of right kidney likely indicating acute pyelonephritis and portal vein edema with complete occlusion of left branch of portal vein. Local factors and prothrombotic disorders were ruled out. The patient was managed with ciprofloxacin, enoxaparin and warfarin. The patient was symptomatic free and discharge home with a therapeutic range INR. Conclusion: Portal vein thrombosis is uncommon condition in absence of liver diseases. Few case report liking between sepsis and portal vein thrombosis. Sepsis can create a predisposed environment for hypercoagulability.

Background: Adipsic diabetes insipidus (ADI) is a rare disorder triggered by injury to the hypothalamus impairing thirst osmoreceptors and the antidiuretic hormone syntheses leading to absence of thirst. We are reporting a rare case of ADI Post astrocytoma resection who presented with a severe hypernatremia postoperatively. Clinical Case: A 16-year-old female known to have hypothalamic pilocystic astrocytoma post incomplete resection in 2014. She presented in 2018 with one week history of sudden onset heachache, progressively worsen overtime, worst in the morning, there were no relieving factors. On examination she was conscious alert oriented GCS 15/15, Vital signs were normal, fundus exam within normal, pupil equal bilateral reactive to light, there was no focal neurological deficit. Systemic examination was unremarkable. Radiological imaging revealed interval size progression of previously seen suprasella region with extension into the floor of the third ventricle. Investigations: Renal profile & pituitary hormonal profile were normal. She underwent second stage resection. Postoperatively, she developed asymptomatic hypernatremia with inability to sense thirst. On examination: Conscious, alert, BP:100/65, no postural drop, Pulse:95, Fluid balance negative 1L. Systemic examination was unremarkable. Laboratory investigations: Creat 0.77mg/dl (0.6–1), Na 173mEq/dl(136–145), K 3.3mEq/dl(3.5–5.1), Cl 134mEq/dl(98–107), Serum osmolality 363mOs/kg(285 -295), Urine osmolality 468mOs/kg(300 -1600), Urine Na 29mEq/L(20- 110) & Urine volume 1900. Diagnosis of ADI was made where she was treated with desmopressin. Her response was good with reduction in Na level of around 7- 9 mEq/L/Day. She was maintained on twice daily vasopressin, instructed to maintain her fluid intake 1–1.5 L/day and good urine output. Conclusions: Astrocytoma rarely linked with development of central diabetes insipidus and even fewer with adipsia. The absence of polydipsia and polyuria can be misleading. Long-term therapy should consider the benefits of vasopressin and fluid therapy against the risk of brain edema/herniation. Body weight and electrolytes monitoring essential & should be maintained a long with strict fluid intake.