A 24-year-old woman was admitted to the emergency department after ingesting ∼8000 mg (153.8 mg/kg) of acetaminophen in 12 h. She arrived at the emergency room after closely spaced ingestion of 4 tablets every 3 h for a total of 16 tablets from 08:00 to 22:00. On admission, the patient was mentally alert, although she suffered from epigastric pain, nausea, and vomiting. Vital signs upon arrival at our emergency department were as follows: blood pressure, 110/80 mm Hg; pulse rate, 66 times/min; respiratory rate, 20 times/min; and body temperature, 37.0°C. The patient reported direct tenderness around the epigastric area. However, she did not show signs of rebound tenderness or costovertebral angle tenderness.\nN-acetylcysteine was administrated for 20 h, ∼13 h after the first intake of acetaminophen by the patient. C-reactive protein (CRP), glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and white blood cell (WBC) counts were normal. However, PCT was measured at 31.89 ng/mL at ∼60 h after the first intake of acetaminophen by the patient. Acetaminophen drug level was <5.0 μg/mL at ∼27 h after the first intake of acetaminophen. All laboratory results are summarized in Table . An ultrasound did not reveal any abnormal hepatic parenchymal echogenicity or bile duct dilatation. There were no indications suggesting the probability of infection such as rigor or fever. The patient was discharged from the hospital without complications four days after she was first admitted to the emergency department.
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.