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 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.