OH NO, NOT``NPO''. UNCOVERING OCCULT DIABETES INSIPIDUS. S. Mcelhattan 1 , R. Granieri 1 ; 1 University of Pittsburgh, Pittsburgh, PA LEARNING OBJECTIVES: 1. To recognize that occult diabetes insipidus can be unmasked when a patient is no longer able to maintain adequate free water intake. 2. To recognize diagnosis and discuss pathophysiology of lithium-induced diabetes insipidus. CASE INFORMATION: An 81 year-old male was admitted with aspiration pneumonia and dehydration two weeks after head and neck surgery. Postoperatively, he was maintained on nasogastric tube feedings but otherwise kept NPO. His past medical history was notable for bipolar disorder requiring lithium for 20 years. On physical, he was lethargic and orthostatic with dry mucous membranes. His sodium was 157 and creatinine was 2.6. The free-water deficit was calculated, and appropriate IVF therapy was initiated. However, despite increasing IVF administration and free-water boluses, hypernatremia and polyuria persisted. Urine osmolality was 171 and serum osmolality was 324. A water restriction test was not performed as the clinical occurrence of nephrogenic diabetes insipidus was suspected. The patient was given larger and more frequent free-water boluses with improvement. DISCUSSION: Nephrogenic diabetes insipidus (DI) is resistance to endogenous ADH at the level of the kidney. Up to 20 percent of patients on chronic lithium therapy develop nephrogenic DI. Patients generally adjust their lifestyle and maintain normal fluid balance to keep up with the polyuria. Although the etiology is not totally understood, it is thought that lithium enters the renal collecting tubule cells via a sodium channel and inhibits adenylate cyclase. Lithium may also reduce the density of ADH receptors or downregulate the expression of aquaporin-2 molecules. The diagnosis is substantiated by a water restriction test. As water is restricted, urine and plasma osmolality are measured hourly. If a steady urine osmolality is measured for three successive hours or if the plasma osmolality reaches 300 and the urine osmolality remains below normal, exogenous ADH is given. If urine osmolality increases, central DI is diagnosed but if the urine osmolality does not change, a diagnosis of nephrogenic DI is made. In our patient, it may have remained clinically silent for many years if he had not been NPO. It is essential that all patients on lithium who are made NPO be monitored for the development of hypernatremia and fluid imbalance. Abdominal pain is one of the most common ambulatory patient complaints. Its etiologies can be numerous, leaving the meticulous physician to pursue leads by the history, physical examination and laboratory or imaging tests. We present an unusual cause of abdominal pain that presented in the outpatient setting. CASE: A previously healthy 58 yearold male presented to the office with a two-day history of``heartburn.'' His abdominal pain worsened post-prandially and he noted early satiety, but denied nausea, vomiting, melena, or hematochezia. Alka-Seltzer and aspirin provided no relief. He denied usage of tobacco or illicit drugs, and reported occasional alcohol use, though none over the preceding days. His exam was significant only for mid-epigastric tenderness, without rebound or guarding. His rectal exam revealed brown colored stool, negative for occult blood. Laboratory data was significant only for a mildly elevated ALT. He was treated empirically with cimetidine for possible dyspepsia, gastritis, or peptic ulcer disease. Two days later, the patient was emergently seen for worsening abdominal pain. His exam was unchanged and laboratory data continued to be unremarkable. An urgent abdominal ultrasound surprisingly revealed acute portal, superior mesenteric, and splenic vein thromboses and an enlarged prostate. He was admitted for treatment and diagnostic work-up, which failed to reveal an underlying etiology for the thromboses. DISCUSSION: Portal vein thrombosis (PVT) is a rare condition associated with inherited hypercoagulable states, underlying myeloproliferative disorders, neoplasms, infections, and other inflammatory processes. It remains idiopathic in 8% to 15% of cases. Abdominal pain is commonly reported when thrombosis also involves the superior mesenteric vessels and produces bowel ischemia, though not present in our patient. The treatment has traditionally focused on complications, most commonly acute gastrointestinal bleeding. The role of anticoagulation therapy remains controversial, but appears to be indicated in patients with acute thrombotic events without intestinal ischemia, as was the case with our patient. While rare, PVT remains an important cause of abdominal pain. A high index of clinical suspicion is necessary for successful diagnosis.