WHAT IS THE MEANING OF TRISMUS? H.A. Batal 1 , R.H. Harris 1 ; 1 Denver Health Medical Center, Denver, CO (Tracking ID #74878) LEARNING OBJECTIVES: 1) Identify the differential for trismus. 2) Recognize the acute presentation of tetanus. CASE INFORMATION: A 20 yo previously healthy Mexican native presented with 4 days of left cheek spasm associated with pain. He denied any trauma, abrasions or lacerations, thought that he had received his vaccines as a child, and denied any systemic symptoms such as fever or myalgias. He also denied sore throat or dental pain and did not have a personal or family history of neurologic problems, including tics. He had bitten his tongue a number of times due to his left cheek spasm and was finding it difficult to eat solid food, although his intake of liquids was adequate. On examination he had normal vital signs and did not appear to be in any distress. He spoke through slightly clenched lips, but was handling his secretions without difficulty. He had no apparent spasms or tics involving other muscle groups. His neurologic exam was normal, although he refused to protrude his tongue, as he was afraid that he would bite it. His exam showed poor dentition but no localizing dental infection and no evidence of pharyngeal abscess. Submandibular and parotid glands were non-tender. He was noted to have spasm of his left masseter muscle, and broke a tongue blade when an attempt was made to keep his mouth open for examination. He was only able to open his jaw approximately 2 cm. Laboratory examination showed a normal CBC, calcium, and electrolytes. A dental consultant was unable to find any underlying odontogenic etiology for the patient's trismus. Dental radiographs and head MRI were unrevealing. Because the diagnosis of acute tetanus was entertained, the patient was admitted for 48 hours of observation during which time his symptoms did not change. He was discharged with a diagnosis of trismus of unknown etiology and therapy with tegretol at 200 mg bid was initiated. IMPLICATIONS/DISCUSSION: Trimus is defined as spasm of the masticatory muscles, with difficulty in mouth opening, and is a characteristic early symptom of tetanus commonly referred to as lockjaw. The differential diagnosis of trismus is limited and besides acute tetanus includes odontogenic infections, peritonsilar abscess, strychnine poisoning, and drug-induced dystonic reaction. In addition, trismus can be confused with the jaw claudication seen in temporal arteritis as well as the pain of trigeminal neuralgia. Widsom tooth (3rd molar) infections are the most common odontogenic cause of trismus and notably can present without evidence facial swelling. Acute tetanus is important to recognize because it can progress to death as a result of respiratory failure, but the prognosis can be favorable if supportive treatment is initiated promptly. Predictors of inadequate immunity are older age, birth outside the US, low educational status, and poverty. LEARNING OBJECTIVES: To recognize the presentation and therapy of thyrotoxic periodic paralysis. CASE INFORMATION: A 26 yo Latino male was brought to the ER complaining of 12 hours of progressive upper and lower extremity weakness to the point that he could no longer get out of bed. The symptoms began with leg cramps shortly after a family picnic. He had no complaints of abnormal sensation, difficulty breathing or swallowing. He denied recent illness or vaccinations, or ingestion of canned food. He also denied past medical problems, medications, or illicit drug use. His mother and sister had hypothyroidism. The examination showed an alert, well developed male with a mildly enlarged thyroid, but no tremor or lid lag. Strength in the upper extremities was 3/5, and 2/5 in the lower extremities. Deep tendon reflexes were 1 plus bilaterally, and the cranial nerve exam was normal. Labs were remarkable for Na 142, K 1.8, Cl 111, CO2 20. A TSH was drawn. The EKG showed SR with flattened T waves and prominent U waves. After a total of 120 meq of combined IV and PO KCL, the serum K was 5.1 and the patient's symptoms and EKG findings had completely resolved. The following day, the TSH and FT4 returned at <0.03 and 2.48 respectively, consistent with hyperthyroidism. The patient was diagnosed with thyrotoxic periodic paralysis. Propranolol was initiated and a thyroid scan scheduled as an outpatient. Despite compliance with medications, the patient returned to the ER with a recurrence of symptoms after a large Christmas dinner. The iodine uptake scan showed a mildly enlarged gland with homogeneously increased uptake: 20 % (5±17%) at 4h, and 48 % (8±30%) at 24 hours, consistent with Graves disease. Therefore, the patient was treated with radioactive iodine ablation. Four months into followup, the patient was doing well, but had become hypothyroid. IMPLICATIONS/DISCUSSION: Thyrotoxic periodic paralysis is a well described disease in up to 2 percent of all Asian men afflicted with hyperthyroidism. However, it is being increasingly recognized in patients of other racial backgrounds including Native Americans, Latinos and rarely Caucasians or those of African descent. This disorder is caused by overactivity of the Na-K-ATPase channel in the presence of increased thyroid hormone, which shifts potassium intracellularly. The inital treatment involves modest potassium supplementation and non-selective beta blockers. The more common familial periodic paralysis is related to the Na-Ca channel, and presents in a similar fashion, frequently after a carbohydrate rich meal or exercise. It is important for clinicians to understand that thyrotoxicosis of any etiology is an underlying cause of hypokalemic periodic paralysis because treatment of the thyroid disorder will also prevent further paralytic episodes.