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 70-year-old woman with a 9-year history of PD was admitted to the emergency department (ED) with a 1-day history of altered consciousness, fever, and convulsive movements. She was already bedridden (Hoehn and Yahr scale 5) and had left hand tremor. Her medications included carbidopa/levodopa (25 mg/100 mg per oral [PO] three times a day) and memantine (10 mg PO twice a day). Her family member informed us that she had taken her antiparkinsonian medications regularly before admission to the ED and that she had recurrent diarrhea with poor oral intake 1 week before the ED visit. After the recurrent diarrhea 1 week before the ED visit, the left hand tremor was aggravated. At admission, her vital signs included a blood pressure of 100/60 mmHg, temperature of 39.0°C, respiratory rate of 24 breaths/min, and heart rate of 138 beats/min. A physical examination showed hot and wet skin, rigidity of extremities, and left hand tremor. The patient showed seizure-like movements accompanied by leftsided eye deviation and muscle contraction 30 minutes after admission to the ED. The results of an arterial blood gas analysis showed respiratory alkalosis (pH 7.51, PaCO2 22 mmHg, PaO2 148 mmHg, and HCO3- 18.3 mEq/L) via O2 face mask 10 L. The initial laboratory results showed a white blood cell count of 16.2 × 103/L, sodium at 146 mEq/L, blood urea nitrogen (BUN) at 34.4 mg/dl, creatinine at 0.6 mg/dl, creatinine kinase(CK) at 41 U/L, and C-reactive protein (CRP) < 0.5 mg/dl. The computed tomography (CT) scan of the chest and abdomen did not show any abnormal findings. The brain CT showed severe brain atrophy with communicating hydrocephalus, but the cerebrospinal fluid examination result was normal. An electroencephalogram showed no epileptiform abnormalities. There were no cultured bacteria in the patient’s blood or urine. Six hours after admission, the patient showed high fever (> 40°C). The blood pressure of this patient was 90/50 mm/Hg despite administering 1.5 L of 0.9% NaCl over 4 hours. At 12 hours after admission, blood pressure was decreased (systolic blood pressure of 40 mmHg) and her respiration was shallow. Then, we decided intubation and mechanical ventilation support, and the patient was given a vasopressor (norepinephrine 0.6 μg/kg/h IV). Central venous catheterization was performed via the right subclavian vein and central venous pressure was 3 mmHg. To control the fever, dantrolene sodium (40 mg IV) and a cooling blanket were used; as a result, her temperature decreased to 36°C 15 hours after admission. At 14 hours after admission, the laboratory results indicated sodium at 149 mEq/L, BUN at 63.3 mg/dl, creatinine at 1.6 mg/dl, serum procalcitonin (PCT) at 25.63 ng/ml, and myoglobin at 970.8 ng/ml but showed no elevated CRP (). Based on a presumptive diagnosis of severe pseudomembranous colitis due to a history of antibiotic use (ceftriaxone 2 g for 5 days) 1 month before and elevated PCT, oral vancomycin was given once. Urine output was decreased (< 0.4 ml/kg/h), and hence, continuous venovenous hemodiafiltration (CVVHDF) with Multifiltrate® (Fresenius Medical Care, Bad Homburg, Germany) for acute kidney injury and oligouria was applied at 20 hours after admission. At 43 hours after admission, the laboratory results showed elevated CK (274 U/L) and decreased PCT levels (9.79 ng/ml). Clostridium difficile and its toxins were not detected in the stool and results of polymerase chain reaction assays were negative. There was improvement in the renal function tests and oligouria, so CVVHDF was stopped at 56 hours after admission. Based on a diagnosis of MS in PD on the 4th hospital day (HD), the patient received antiparkinsonian drugs that had been taken previously via a Levin tube. The frequency of the left hand tremor decreased, and her consciousness recovered to its previous condition. Weaning and extubation were performed on the 12th HD. After conservative treatment, she was discharged on the 22nd HD after recovery to her previous condition before admission.