The 21-year-old male was found unconscious by his parents at home. The attending ambulance crew measured severe hypoglycaemia. After the serum glucose level was normalised by iv. glucose infusion the patient was transferred to the Accident and Emergency Department with oxygen supplementation via a face mask. Regarding his medical history he was fit and well, not on any regular medication.\nOn the first assessment he was tachypnoeic (30/min) and had a SpO2 of 98%, sinus tachycardia (135/min), and a blood pressure of 96/67 mmHg. His neurological examination showed a Glasgow Coma Scale of 9 with no meningeal signs, dilated, equal pupils reacting for light, bulbs fixed to the left, and right sided hemiparesis predominantly on the lower limb. Pressure sore of the skin was found on the right flank and over the sacral region. Axillary temperature was 39.6°C and his minimal amount of urine looked concentrated after catheterisation. Arterial blood gases showed severe metabolic acidosis and hyperkalaemia. Apart from sinus tachycardia 12-lead ECG was normal.\nThe urgent computer tomography scan of the head and the cervical spine could not show any pathology. Soon after the diagnostic procedures the patient became very agitated and eventually endotracheal intubation had to be performed with rapid sequence induction after which the patient was transferred to the intensive care unit (ICU). Routine intensive care with mechanical ventilation, continuous propofol and morphine sedation, and standard monitoring was commenced.\nImmediately after ICU admission arterial and central venous catheters were inserted and fluid resuscitation was started with crystalloid infusion. Cerebrospinal fluid (CSF), bronchial secretions, urine samples, and blood cultures were taken for microbiological examination and combined imipenem (500 mg tds); amikacin (1000 mg qd) antibiotic therapy was initiated. Due to the oliguria, severe metabolic acidosis, and hyperkalaemia, a hemodialysis catheter was inserted and intermittent venous-venous hemodiafiltration (IVVHDF) was started.\nAnalysis of the CSF sample revealed no leukocytosis; total protein level and the CSF to serum glucose were also normal. The appearance of the spinal fluid was clear and the latex agglutinin rapid diagnostic tests for N. meningitidis, S. pneumoniae, and H. influenzae were all negative. According to toxicology, ethanol was not detected in the serum but amphetamine was present in the urine sample.\nRoutine laboratory tests revealed acute kidney injury (creatinine: 395 μmol/L, blood urea nitrogen: 21.5 mmol/L) most likely due to rhabdomyolysis indicated by extremely high creatinine kinase (). The rest of the most relevant laboratory parameters is summarised in . Patient rendered an APACHE II score of 34 points.\nMicrobiology did not confirm infection from the CSF, blood and urine samples, and in the view of the full clinical picture, and laboratory profile antibiotics were stopped after 24 hours.\nThe patient's general condition stabilised and on day 3 he was extubated. He remained agitated, which was treated successfully by iv. haloperidol boluses. The right sided hemiparesis also improved gradually with physiotherapy in which symptom was supposed to be the consequence of the prolonged immobilisation on the ground before hospital admission. However, he remained anuric and required daily IVVHDF for the rest of his stay in ICU. On day ten he was discharged with stable vital parameters and no focal neurological signs.
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 [].