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 [].
A 51-year-old man was admitted to emergency department at 8 h after ingesting 23,600 mg of acetaminophen (279.6 mg/kg). This patient was also mentally alert on admission. He explained that he felt generally weak without any discomfort. Vital signs on arrival in the emergency department were as follows: blood pressure, 100/60 mm Hg; pulse rate, 84 times/min; respiratory rate, 20 times/min; and body temperature, 36.0°C. A physical examination of the patient did not reveal anything unusual or anything out of the ordinary. N-acetylcysteine was also administered for 20 h ∼8 h after the first intake of acetaminophen by the patient. CRP, GOT, GPT, and WBC count were also normal.\nBy the second day of admission, GOT and GPT increased to 2508 and 1473 IU/L, respectively. Approximately at 56 h after first intake of acetaminophen, PCT level was elevated to 45.66 ng/mL. Acetaminophen drug level was 116.9 μg/mL. On the third day of admission, GOT and GPT decreased to 1382 and 1370 IU/L, respectively. Laboratory findings are summarized in Table . An ultrasound revealed a mild degree of fatty liver with hepatomegaly without bile duct dilatation. This patient did not show any signs associated with infection such as rigor or fever during his entire stay at the hospital. On the sixth day of admission, GOT and GPT was 53 and 357 IU/L, respectively. The patient was discharged since he did not show any unusual symptoms in addition to the daily decrease of his liver enzyme levels. He revisited to the out-patient department of gastroenterology the next day for a follow-up examination. There were no unusual symptoms. His liver enzyme returned to normal levels (GOT at 32 IU/L and GPT at 31 IU/L). The results of the laboratory tests performed in the out-patient department of gastroenterology are also summarized in Table .\nInformed consent was obtained for the current case report. Approval (IRB no. 2019-03-010) from the Institutional Review Board of Kangdong Sacred Heart Hospital, Hallym University School of Medicine, Seoul, Republic of Korea, was obtained.