A 20-year-old woman with insignificant medical history was referred to our emergency department from another hospital for vomiting, fever, and impaired consciousness with a tentative diagnosis of bacterial meningitis. She had taken an over-the-counter antihistamine for pollinosis. Her vital signs on arrival were as follows: blood pressure 175/84 mmHg, heart rate 134 b.p.m., respiratory rate 28 breaths/min with an oxygen saturation of 96% on room air, and body temperature 38.0°C. Her Glasgow Coma Scale was 11 (E4V1M6), and we could not detect any significant neurological signs such as weakness of her limbs. Her pupils were bilaterally dilated to 5 mm. No nuchal rigidity or other meningeal signs were observed. Laboratory tests revealed glutamic oxaloacetic transaminase 30 IU/L, glutamic pyruvic transaminase 14 IU/L, C-reactive protein 0.43 mg/dL, white cell count 17,180/μL, (band cells 6.4%, segmented cells 89.4%, lymphocytes 2.2%, and monocytes 1.8%), and PCT over 10 ng/mL. Urine test, chest X-ray, computed tomography of the head, and cerebrospinal fluid test showed normal findings. We initially suspected systemic bacterial infection because of her fever and impaired consciousness, which is why we tested PCT. Although the cerebrospinal fluid test was normal, we cannot completely rule out bacterial infection due to the PCT elevation; therefore, we started treatment with empiric antimicrobials. Gradually, her level of consciousness improved; she confessed that she had taken 100 tablets of an ephedrine extract (Lipodrene, Hi-Tech Pharmaceuticals. Inc., Norcross, GA, USA), which contains caffeine (10 g), theophylline (amount unknown), yohimbine (amount unknown), and ephedrine (2.5 g), intending to commit suicide. We speculated that her low Glasgow Coma Scale on arrival was due to selective mutism because she had suicidal ideation and mood disorders. Her general condition stabilized, and blood tests showed no aggravation. Blood and cerebrospinal fluid culture results were negative on day 4. The PCT level decreased to 0.32 ng/mL on day 5, and she was discharged from hospital on the same day.
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 [].