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 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.