CASE INFORMATION: The patient is a 42 year-old male who ingested 90 500 mg tablets of valproic acid following an argument with his wife. The exact time of ingestion was unclear, but was felt to be 6 to 8 hours prior to presentation. The patient's wife assumed that he was sleeping, but when found to be unresponsive again several hours later, he was brought to the emergency department. On physical examination, the patient was unresponsive, hypotensive, and without hyperreflexia or clonus on neurological examination. Laboratory values revealed normal liver function tests, hypocalcemia, valproate level of 1157 (ref 50±150 ug/ml), and an ammonia level of 270 (ref 9±33 umol/L). The patient's electrocardiogram was notable for QT prolongation. CT scan of the head and lumbar puncture were unremarkable. Intravenous fluids were administered and dopamine was initiated for blood pressure support. The patient's respiratory status declined, he was unable to protect his airway and therefore intubated. Carnitine was administered for the hyperammonemia on a daily basis. The valproic acid and ammonia levels declined over the next 48 hours and his mental status improved. He was extubated after approximately 72 hours. The patient did well and was transferred to psychiatry. IMPLICATIONS/DISCUSSION: Hyperammonemia results when valproic acid is metabolized to propionic acid, which inhibits carbamyl phosphate synthetase, the first enzyme involved in the urea cycle. Valproic acid also binds to carnitine, a molecule important in the metabolism of long-chain fatty acids and ketoacid analogues of various amino acids, thereby depleting serum concentrations of carnitine. Valproic acid also causes increased renal production of ammonia by reducing the synthesis of glutamine. Administration of exogenous carnitine is thought to decrease ammonia levels by binding to valproic acid, and also by relieving the inhibition of carbamyl phosphate synthetase and thus urea synthesis. Management of valproic acid intoxication is largely supportive. Patients who present early may benefit from gastric lavage and a single dose of activated charcoal; however, multiple-dose activated charcoal does not increase the elimination of valproic acid. Other interventions may involve blood pressure support with intravenous fluids and vasopressors, correction of electrolyte abnormalities, and correction of acid/base disorders (commonly an anion gap metabolic acidosis). Mechanical ventilation may be necessary in patients who require airway protection. In the majority of cases, this management strategy results in favorable outcomes. Hemodialysis and charcoal hemoperfusion are additional treatment options. Typically, extracorporeal removal is employed in patients with renal abnormalities, hypotension refractory to all supportive measures, severe metabolic abnormalities, active seizure, or those who are persistently comatose. However there are no controlled trials that demonstrate an improvement in outcome with these measures. year old female initially presented to her primary physician 5 years ago with a blood pressure of 159/98. Repeat readings were similar and she was started on hydralazine 25 mg. There was a modest effect from hydralazine, but control was never acheived. Four months later hydralazine was changed to losartan 50 mg. No significant lowering was obtained. Losartan was increased one month later to 100mg and two months later hydrochlorothiazide 25 mg was added. Her blood pressure stabalized to 140/90 for 6 months. Then a gradual increase in her blood pressure was noticed, so diltiazem was added. Her physical exam and lab values were unremarkable. Due to failure of multiple antihypertensive medications,a magnetic resonance arteriogram of the renal artery was conducted which revealed renal artery stenosis. An angiogram was conducted showing segments of stenosis and dilatation of the right renal artery, consistent with the diagnosis of fibromuscular dysplasia. Renal artery angioplasty was performed, and follow up blood pressure normalized on two medications. IMPLICATIONS/DISCUSSION: This is an elderly female with hypertension refractory to medications. A secondary cause was sought out with an imaging study, which showed a unilateral fibromuscular dysplasia of the right renal artery. It is unusual for a women in this age group to present with this type of secondary hypertension. Patients with fibromuscular dysplasia respond well to angioplasty. LEARNING OBJECTIVES: 1. The reader should be able to list three common causes for hypophosphatemia. 2. The reader should be able to explain why phosphate repletion is typically not be necessary for hypophosphatemia from respiratory alkalosis. CASE INFORMATION: Hyperventilation can precipitate life-threatening alkalosis and severe hypophosphatemia that does not require phosphate repletion. A 36 yo female who was status post cadaveric tracheal transplant and multiple stent placements presented with suspected stent re-stenosis, complaining of dyspnea, increased work of breathing, and inability to clear secretions. Her respiratory rate was 30±34 with normal oxygenation. Emergent bronchoscopy revealed only minimally occlusive concretions, however peri-procedure labs revealed an arterial blood pH of 7.71 and a phosphate of 0.6 mg/dL. The patient reported weakness and paresthesias in all four extremities plus arthralgias in her hands. The patient was started on a NaPO4 infusion @ 0.6 mmol/kg over 6 hrs. She was given supportive care and reassurance for her hyperventilation. After only three hours, the PO4 was 3.3 mg/dL and the infusion was stopped. Repeat ABG showed a pH of 7.49, with improvement in pCO2 from 14 to 27 mmHg. The patient's symptoms resolved. IMPLICATIONS/DISCUSSION: Severe hypophosphatemia, defined as a serum PO4 <1.5 mg/dL, has been reported in 0.22±2.15% of adult hospital admissions. It occurs more commonly in alcoholics and malnourished patients and has a variety of causes, including respiratory alkalosis. In respiratory alkalosis, carbon dioxide readily diffuses from the intracellular space resulting in higher intracellular pH. This activates glycolysis and the formation of phosphatecontaining compounds. Phosphate is used from the circulating inorganic phosphate pool, depleting extracellular stores. This process induces relative hypophosphatemia. This contrasts with metabolic alkalosis where excess extracellular bicarbonate is only poorly diffusible and does not significantly raise intracellular pH. Severe hypophosphatemia can be a lifethreatening disturbance but may not represent total body phosphate depletion or require supplementation. An understanding of the basic physiology guides therapy. 67 year old male initially seen in the emergency room five days before admission for right lower extremity redness, pain and swelling. He was given pain medication and sent home. He returned the following day and two days later with persistent symptoms and was given appropriate oral antibiotics for presumed cellulitis. An ultrasound showed no thrombosis. After his fourth ER visit he was admitted for intravenous antibiotics. Additionally, over the past three months he had noted bilateral lower extremity pain with walking over one block. Work up to date included normal resting and exercise ankle/brachial indices a CT scan of the lumbar spine, which showed disc bulges at L3-4 and L4-5 with mild spinal stenosis. When we met him, he complained of severe pain despite oral narcotics and also endorsed difficulty with his gait over the past week. On physical exam, temperature was 98.60 and the right lower extremity had diffuse anterior erythema without distinct borders. There were no breaks in the skin but onychomycosis was present on bilateral toes. There was 2+ edema on the right and none on the left. Dorsalis pedis pulse was noted only by doppler on the right, but was intact on the left. Neurologic exam revealed significant difficulty with dorsiflexion of the right foot which was presumed to be secondary to pain or possibly related to his known spinal stenosis. Labs revealed a normal white blood cell count, elevated C-reactive protein, small blood in the urine with 0±5 red cells and a creatinine slightly above his baseline. Plain radiographs were normal. Broad spectrum intravenous antibiotics, elevation and pain control were initiated at admission. After two days, the redness and swelling improved but a foot drop and pain persisted. Neurology felt his foot drop could be consistent with his known disc disease but also suggested surgical evaluation. Anterior compartment syndrome was subsequently diagnosed based on a direct compartment pressure reading of 45 mmHg. Because of the delay in diagnosis, the fact that pulses were present and that there was no tissue necrosis or abscess seen on subsequent scanning, the decision was made not to operate. The patient's pain and swelling gradually resolved over weeks but he was left with a permanent foot drop. IMPLICATIONS/DISCUSSION: Compartment syndrome is a surgical emergency that must be detected early to avoid potential serious sequelae. Causes are many and include closed trauma (most commonly), vascular injury and reperfusion, burns, prolonged surgery or traction, overexertion/exercise, and infection. It occurs most commonly in the arm or leg but can be seen in the foot, abdomen, retroperitoneum and mediastinum. Recognition depends on clinical suspicion and can be remembered as the five P's: pain (severe and out of proportion to injury); pulselessness, paralysis (excluding concomitant nerve injury); paresthesia and pallor. Laboratory may show myoglobin in the urine or elevated creatine kinase. Imaging studies may help rule out other causes but direct measurement of compartment pressures are needed for diagnosis. Also well described is the syndrome of chronic compartment syndrome, which is typically thought of as an overuse injury in runners but remains as an interesting possible explanation for this patient's claudication history. LEARNING OBJECTIVES: Early recognition and treatment of Alcohol Withdrawal Syndrome (AWS) may reduce perioperative morbidity and mortality. Intravenous Ethanol (IVE) is still used for the peri-operative management AWS. This case illustrates the importance of 1) identifying patients who require AWS treatment and using evidence-based treatments early to prevent AWS peri-operative complications, 2) exploring the use of alcohol to treat perioperative AWS, and 3) discussing optimum treatments of AWS with patients and family prior to surgery. CASE INFORMATION: T.O. is a 65 year-old man with history of hypertension, congestive heart failure and peripheral vascular disease with bilateral thigh claudication admitted for aortobifemoral bypass. Initial documentation of alcohol use consisted of an admission nursing note stating that the patient drank alcohol. After an uncomplicated surgery, he was successfully extubated and on post-operative day (POD) 2 was transferred to a general surgical bed. On POD 3, he became increasingly agitated and combative. AWS was suspected and Lorazepam 1±2 mg PRN was ordered. Over the next three days he did not improve and was returned to the SICU for re-intubation for airway protection and IV benzodiazapine treatment. After being informed of his clinical condition, the patient's son requested his father receive alcohol to prevent delirium tremens since his father had not consented to``detoxification''. A 10% ethanol drip was begun to 100 cc/h on POD 8 and on POD 9 he was successfully extubated. Although he became more alert and interactive, attempts to wean his IVE caused increased agitation. On POD 11 he was transferred to a general surgical bed, his IVE was discontinued, and he was ordered 12 ounces beer PRN. On POD 12, he continued to be confrontational and was discharged to home. IMPLICATIONS/DISCUSSION: AWS is a complex constellation of signs and symptoms related to autonomic hyperactivity in alcohol dependent patients whose alcohol intake is decreased or discontinued. Severe AWS includes life-threatening delirium tremens that may be exacerbated by the stress of surgery. Pre-or peri-operative detoxification from alcohol may also increase surgical morbidity. Symptom triggered, appropriate dosing of benzodiazapines are effective first line treatment for AWS. However, intravenous and oral alcohol use continues to be used in the perioperative period. Although multiple case reports exist detailing the use of IVE or oral alcohol to prevent withdrawal symptoms, no clinical trials exist to demonstrate its efficacy in management of peri-operative AWS. The use of IVE in the perioperative period is complicated by electrolyte disturbances, pancreatic complications, and difficulty in objectively measuring treatment efficacy. Use of oral alcohol may also reinforce unhealthy outpatient alcohol drinking behavior. Insufficient evidence-based studies exists to guide clinicians regarding the optimum management of peri-operative AWS and until such time, alcohol treatments will continue to be used.