AUTONOMIC DYSFUNCTION AFTER HEAD TRAUMA. C. Eze 1 , J. Wiese 1 ; 1 Tulane University, New Orleans, LA (Tracking ID #77084) LEARNING OBJECTIVES: 1. Identify the subtle presentation of autonomic dysfunction in the elderly. 2. Recognize the association between autonomic dysfunction and spinal cord lesions. CASE INFORMATION: An 81-year-old man presented with acute confusion following six months of progressive lower extremity weakness. He had fallen two weeks prior resulting in a periorbital hematoma. A CT had been obtained on two prior ER visits to exclude a sub-dural hematoma, and was negative on both occasions. His initial blood pressure was 122/60 mmHg with a pulse of 84. Fifteen minutes later his blood pressure dropped to 64/42 with a pulse of 134. Intravenous fluids resulted in a blood pressure of 175/104 mmHg with fifteen minutes. Ten minutes later his blood pressure again declined to 55/39 mmHg He was placed on an epinephrine drip with an immediate and sustained response of his blood pressure to 169/101 mmHg. His examination was notable for flat neck veins, no S3, and normal lung sounds. His reflexes were absent in both lower extremities without a Babinski's response; his upper extremity reflexes were 1+. His laboratory values, including cortisol, were normal. The EKG revealed atrial fibrillation. There was no subdural hematoma on repeat head CT. Owing to the suspicion of autonomic insufficiency, cervical-spine X-ray was obtained, revealing compression fractures involving the C4 to C7 vertebrae. He was admitted to the ICU and neurosurgery was consulted. IMPLICATIONS/DISCUSSION: Wide hemodynamics variations should prompt consideration of autonomic dysfunction, that should in turn prompt suspicion for an occult spinal cord lesion. This is especially true in elderly patients who may not be able to verbalize cervical pain. Hypertention and bradycardia may result from spinal cord reflexes unopposed by central regulatory mechanisms. Support of vascular tone with vasopressors is critical to resuscitation. This case emphasizes the importance of a careful cervical spine evaluation in all falls involving the elderly. LEARNING OBJECTIVES: To recognize that high dose simvastatin monotherapy, although having an excellent safety profile, can cause significant rhabdomyolysis, acute renal failure and hepatitis in the right patient population. To recognize that the addition of a potent or weak cytochrome P450 inhibitor is not needed for the significant adverse effects of simvastatin to occur. CASE INFORMATION: A 62 y.o. woman developed increasing myalgias, malaise, shortness of breath and dyspnea on exertion over 1 week and left lower extremity swelling. Medications included simvastatin 80mg daily with normal baseline transaminase levels and diltiazem for the past year. CXR revealed mild bilateral pulmonary edema and an ultrasound of the left lower extremity revealed no deep vein thrombosis. Exam revealed in ill appearing female in moderate distress secondary to myalgias, mild rhonchi bilaterally, normal heart tones and bilateral lower extremity dependent edema (Lt>Rt). Laboratory studies: alkaline phosphatase 177, AST 1511, ALT 224, LDH 1396; creatinine 5.6 (baseline 1.4±1.7); BUN 92; potassium 5.6; phosphate 6.5; calcium 8.8; creatinine phosphokinase >20,000; troponin <0.05; CKMB 171; TSH wnl; uric acid 8.0. Urinalysis revealed a large amount of blood with only 4±10 red blood cells. Simvastatin was discontinued. Aggressive treatment with sodium bicarbonate, intravenous hydration and hemodialysis was begun. Over a sixty-plus day hospital course, the patient's renal failure resolved (baseline creatinine now 2.2±2.4) and transaminases normalized. The patient was eventually discharged to home to continue physical rehabilitation with no permanent requirement for hemodialysis. IMPLICATIONS/DISCUSSION: Simvastatin's long term safety profile is excellent. Simvastatin induced rhabdomyolysis is reported with low incidence (0.6% in one study involving 80mg of simvastatin) and it is seldom associated with acute renal failure or hepatitis. Myopathy and rhabdomyolysis increases with dose and with concomitant use or addition of potent cytochrome P450 3A4 (CYP450) inhibitors, i.e. fibrates, cyclosporine, azathiaprine. A baseline severe renal insufficiency (creatinine clearance by the Cockroft-Gault method, 17cc/ min) and a urinary tract infection treated with a fluoroquinolone 2 days prior, combined to increase the risk of this patient developing rhabdomyolysis. Published reports of simvastatin induced myopathy involve the addition of potent or weak CYP450 inhibitors. Our patient had been stable on high dose simvastatin and diltiazem (a weak CYP450 inhibitor) for over 1 year prior to presentation and did correlate with the addition of known CYP450 inhibitors. Additionally unique, this is the first reported case involving the combined toxicities of rhabdomyolysis, acute renal failure and hepatitis with high dose simvastatin monotherapy. 2) Recognize the dangers of rapid correction of hyponatremia. CASE INFORMATION: A 56 year-old man with a history of alcohol abuse was admitted to an outside hospital with altered mental status. On exam, the patient was disoriented, but neurological exam was otherwise nonfocal. Computerized tomography (CT) of the head was unremarkable. Laboratory results revealed hyponatremia with sodium of 104 mmol/L. The patient was given hypertonic saline, and the sodium was corrected to 123 within the first 24 hours. The patient was then transferred to our facility for continuation of his care. Physical examination on arrival revealed multiple focal neurological findings including bilateral eye deviation to the left, neck deviation to the left, absent gag reflex, and poor motor coordination with spastic movement of all extremities. The patient's speech was severely dysarthric and unintelligible. Magnetic resonance imaging (MRI) of the brain showed enhancement of the motor cortex of both cerebral hemispheres and enhancement of the frontal eye fields on the left with sparing of the adjacent sensory cortex. In consideration of the MRI findings, neurology consultation was sought. The patient's severe dysarthria, dysphagia, ataxia, and optic apraxia were attributed to extrapontine (as opposed to central pontine) myelinolysis from rapid correction of the patient's hyponatremia. IMPLICATIONS/DISCUSSION: Severe symptomatic hyponatremia should be treated with hypertonic saline, but with a correction in plasma sodium of not more than 1±2 mmol/liter/ hour and a maximum increase of 8 mmol/liter during the first 24 hours. Our patient's sodium was corrected from 104 to 123, with an increment of 19 within 24 hours. Rapid correction may result in osmotic demyelination or central pontine myelinolysis, which is characterized by flaccid paralysis, dysarthria, and dysphagia. Isolated extrapontine myelinolysis is extremely rare, with only two cases reported in the literature. The neurologic deficits depend on the anatomical location of osmotic demyelination. Treatment is supportive, and recovery is slow within weeks to months. Gradual correction of hyponatremia is important because aggressive correction can cause not only central pontine myelinolysis but also the unusual manifestation of extrapontine myelinolysis. LEARNING OBJECTIVES: 1) Construct a differential diagnosis of chronic ataxia. 2) Review the etiology, presentation, and prognosis of paraneoplastic cerebellar degeneration. CASE INFORMATION: A 55-year-old male ex-smoker with no significant past medical history presented to clinic with paresthesias of the right upper and lower extremities, followed by gradual onset of ataxia, diplopia, and dysarthria over a period of five months. The patient also reported weight loss and a chronic dry cough. The patient had no history of toxic exposures or family history of inherited ataxias. Physical exam revealed optical dysmetria, truncal ataxia, finger-to-nose dysmetria, and dysdiadochokinesis. The patient's speech was severely dysarthric, and sensation was decreased on the right upper and lower extremities. Magnetic resonance imaging (MRI) of the brain was normal. HIV and RPR serologies were negative, and TSH was within normal limits. Lumbar puncture revealed paraneoplastic antibodies, including anti-Hu, anti-P/Q type calcium channel, and anti-acetycholine receptor. Computerized tomography (CT) of the thorax demonstrated a 2 cm left hilar mass. Bronchoscopy and endobronchial biopsy were negative, but subsequent thoracotomy and biopsy revealed small cell lung carcinoma (SCLC). IMPLICATIONS/DISCUSSION: The differential diagnosis of chronic ataxia includes primary and metastatic neoplasms, paraneoplastic syndromes, progressive multifocal leukoencephalopathy, multiple sclerosis, hypothyroidism, tabes dorsalis, inherited ataxia syndromes, vitamin E deficiency, toxic exposures, and stable gliosis due to stroke or demyelination plaque. In approximately 80% of cases with paraneoplastic cerebellar degeneration, the underlying tumor is SCLC. Fifty-one percent of patients with cerebellar degeneration and SCLC have detectable anti-Hu antibodies. Other antibodies found in paraneoplastic cerebellar degeneration include anti-P/Q calcium channel, anti-Yo, anti-Ma1, anti-Tr, and anti-CV2, but their exact sensitivities and specificities are not yet known. Therapy is supportive, and symptoms usually do not improve with immunosuppression or treatment of the tumor. In conclusion, paraneoplastic cerebellar degeneration with paraneoplastic antibodies should be considered in all patients with chronic ataxia without other predisposing etiologies. LEARNING OBJECTIVES: 1. Discuss the presentation of primary bacterial peritonitis. 2. Recognize group A beta-hemolytic Streptococcus as a rare but serious cause of primary peritonitis. CASE INFORMATION: A 52 year old woman presented to the Emergency Room with a four day history of fevers, chills, and profuse watery diarrhea with associated crampy lower abdominal pain. She denied any nausea, vomiting, cough, dysuria, or headaches. She denied any recent travel or sick contacts, but noted that the symptoms began hours after having eaten at a Chinese restaurant. Her past medical history was remarkable for a prior appendectomy, she was on no medications, and her family history was significant only for colon cancer in her mother. Her exam revealed a temperature of 38.7 C, a blood pressure of 72/40, and a pulse of 112, with abdominal tenderness and guarding in both lower quadrants. Labs showed a white cell count of 5.7 (with a bandemia of 52), a potassium of 2.4, a bicarbonate of 15, a Blood Urea Nitrogen of 52, and a creatinine of 3.7. Liver function tests, amylase, lipase, and urinalysis were all normal. Fecal leukocytes were absent and her abdominal film showed only a few air-fluid levels. It was the impression of all clinicians involved that the patient's presentation was most consistent with acute infectious diarrhea and profound dehydration complicated by renal failure and electrolyte derangement. Following aggressive hydration with IV crystalloids, the patient's blood pressure improved to 120/80 and her heart rate slowed to 88. After blood, urine, and stool cultures were taken, she was started on IV ciprofloxacin for empiric treatment of her presumed acute infectious diarrhea. She continued to have diarrhea over her hospital course, but her abdominal pain and temperature curve lessened, and she appeared to be improving clinically. All cultures (including c. difficle and giardia screens) had returned negative. On hospital day four, her fever and abdominal pain worsened and her abdomen became distended, rigid, and equisitely tender. An abdominal CT showed diffuse thickening of her colon with ascites and dilated loops of small bowel. An emergent exploratory laparotomy was performed and several liters of cloudy yellow ascites were drained. A nectrotic mesenteric lymph node filled with pus was resected and her abdomen was irrigated with several liters of saline. Gram stains of both the pus from the lymph node and the ascitic fluid revealed gram positive cocci in chains, and she was promptly started on IV clindamycin. Cultures of the ascites and pus grew group A betahemolytic Streptococci, and she was continued on the clindamycin. She continued to improve over her hospitalization and made a full and healthy recovery. IMPLICATIONS/DISCUSSION: Primary bacterial peritonitis occurs as a result of bacterial infection of the peritoneal cavity and is distinguished from secondary peritonitis by the absence of any underlying cause or demonstrable abdominal source. The onset is often rapid and insidious, and is marked by the appearance of fever, nausea, abdominal pain, and diarrhea. The patient typically has abdominal rigidity and rebound with features of systemic inflammation (tachycardia, hypotension, tachypnea, etc.) which may progress to frank shock. Streptococcus pyogenes, or group A Streptococcus, is a very common human pathogen, with up to 15% of asymptomatic individuals carrying the bacterium (typically in the upper respiratory tract). However, primary bacterial peritonitis due to Streptococcus pyogenes is exceptionally uncommon with very few adult case reports documented in the literature. It may be slightly more common in women, with asymptomatic colonization of the genital tract acting as a portal of entry. The diagnosis is often made only at laparotomy and despite the profound morbiditiy associated with the disease, rapid initiation of the appropriate antibiotics usually results in a successful cure.