A 24-year-old woman was admitted to the emergency department after ingesting ∼8000 mg (153.8 mg/kg) of acetaminophen in 12 h. She arrived at the emergency room after closely spaced ingestion of 4 tablets every 3 h for a total of 16 tablets from 08:00 to 22:00. On admission, the patient was mentally alert, although she suffered from epigastric pain, nausea, and vomiting. Vital signs upon arrival at our emergency department were as follows: blood pressure, 110/80 mm Hg; pulse rate, 66 times/min; respiratory rate, 20 times/min; and body temperature, 37.0°C. The patient reported direct tenderness around the epigastric area. However, she did not show signs of rebound tenderness or costovertebral angle tenderness.\nN-acetylcysteine was administrated for 20 h, ∼13 h after the first intake of acetaminophen by the patient. C-reactive protein (CRP), glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and white blood cell (WBC) counts were normal. However, PCT was measured at 31.89 ng/mL at ∼60 h after the first intake of acetaminophen by the patient. Acetaminophen drug level was <5.0 μg/mL at ∼27 h after the first intake of acetaminophen. All laboratory results are summarized in Table . An ultrasound did not reveal any abnormal hepatic parenchymal echogenicity or bile duct dilatation. There were no indications suggesting the probability of infection such as rigor or fever. The patient was discharged from the hospital without complications four days after she was first admitted to the emergency department.
A 60-year-old gentleman with a three-year history of Parkinson's disease was admitted with severe rigidity, fever and altered sensorium following repeated bouts of vomiting. There was no associated abdominal pain, headache or diarrhea. He was on thrice-daily schedule of one tablet of L-Dopa+carbidopa (100 mg + 25 mg), since the last eight months. Prior to the initiation of dopa, he was on amantadine 100 mg twice daily. The Parkinsonian symptoms were reasonably controlled on dopa. He had good compliance and was taking dopa regularly.\nOn admission, the patient had a temperature of 101.5°F and was dehydrated and stuporous. He was akinetic rigid, with severe axial and appendicular rigidity and had pronounced and disproportionate retrocollis [Figures , ]. Serum sodium was 109 meq/L. There was leucocytosis (15,000 /mm3) and the creatine phosphokinase (CPK) level was elevated (1500 U/L). Non-contrast CT brain was normal, as were the Cerebrospinal fluid (CSF) study, thyroid function test and the rest of the metabolic parameters. No obvious focus of sepsis was detected. Serum osmolality was 265 mOsm/Kg and urine spot sodium concentration was 10 meq/L.\nA diagnosis of hypovolemic hyponatremia and malignant syndrome precipitated by hyponatremia was made. Adequate hydration using intravenous fluids and external cooling by tepid sponging was done. Serum sodium was slowly corrected at a rate of 8 meq/L per 24 hours, initially with hypertonic saline (3%) and subsequently with isotonic saline (0.9%). Bromocriptine 2.5 mg thrice daily was added. Dopa was continued in thrice daily schedule. Serum sodium was corrected to 124 meq/L, in forty eight hours. Gradually, sensorium normalized. By the fifth day, serum sodium level normalised and subsequently the patient was mobilized. Over a period of two weeks, retrocollis reverted completely and rigidity decreased. In two weeks, he reverted to the pre morbid state [].