Martin Mozina

The frequency of adverse drug reaction related admissions according to method of detection, admission urgency and medical department specialty

BackgroundAdverse Drug Reactions (ADRs) have been regarded as a major public health problem since they represent a sizable percentage of admissions. Unfortunately, there is a wide variation of ADR related admissions among different studies. The aim of this study was to evaluate the frequency of ADR related admissions and its dependency on reporting and method of detection, urgency of admissions and included medical departments reflecting department/hospital type within one study.MethodsThe study team of internal medicine specialists retrospectively reviewed 520 randomly selected medical records (3%) of patients treated in the medical departments of the primary city and tertiary referral governmental hospital for certain ADRs causing admissions regarding WHO causality criteria. All medical records were checked for whether the treating physicians recognised and documented ADRs causing admissions. The hospital information system was checked to ensure ADR related diagnoses were properly coded and the database of a national spontaneous reporting system was searched for patients with ADRs included in this study.ResultsThe established frequency of admissions due to certain ADRs recognised by the study team and documented in medical records by the treating physicians was the same and represented 5.8% of all patients (30/520). The frequency of ADR causing admissions detected by employing a computer-assisted approach using an ICD-10 coding system was 0.2% (1/520), and no patient admitted due to ADRs was reported to the national reporting system (0/520). The recognized frequency of ADR related admissions also depends on the departments specialty (p = 0.001) and acceptance of urgently admitted patients (p = 0.001). Patients admitted due to ADRs were significantly older compared to patients without ADRs (p = 0.025). Gastrointestinal bleeding due to NSAID, acetylsalicylic acid and warfarin was the most common ADR that resulted in admission and represented 40% of all certain ADRs (12/30) according to WHO causality criteria.ConclusionADRs cause 5.8% of admissions in medical departments in the primary city and tertiary referral hospital. The physicians recognise certain ADR related admissions according to WHO causality criteria and note them in medical records, but they rarely code and report ADRs. The established frequency of ADR related admissions depends on the detection method, department specialty and frequency of urgently admitted patients.

Polydipsia as another mechanism of hyponatremia after 'ecstasy' (3,4 methyldioxymethamphetamine) ingestion.

Acute symptomatic hyponatremia after ecstasy (3,4 methyldioxymethamphetamine; MDMA) ingestion is well documented and has been attributed to the syndrome of inappropriate antidiuretic hormone (SIADH). We report the case of an 18-year-old woman who took five tablets of ecstasy in a suicide attempt and drank 1700 ml water at the Emergency Department (ED). The laboratory findings obtained 5 h after ingestion showed a serum sodium concentration of 130 mmol/l, plasma osmolality of 264 mOsm/kg, urinary osmolality of 335 mOsm/kg and natriuresis of 101 mmol/l. The plasma arginine vasopressin level by radioimmunoassay was 33.7 pmol/l 5 h after ingestion. A gas chromatography-mass spectrometry assay confirmed MDMA in blood samples, with serum concentrations of 0.87 mg/l on arrival. This case report strongly suggests that MDMA reduces serum sodium levels through the dual pathways of SIADH and polydipsia. Accordingly, we believe that hyponatremia may be prevented in ED patients after MDMA ingestion by the early restriction of water intake.

Prolonged hypoglycaemia after insulin lispro overdose.

Insulin lispro has a more rapid onset and a shorter duration of hypoglycaemic action than regular insulin. We report a 39-year-old woman, with no previous medical history, who injected 300 U of the insulin lispro (Humalog) in an attempted suicide. Half an hour later, she was found comatose and brought to our emergency department. On arrival, she was comatose, with capillary glucose of 0.4 mmol/L. She awoke after a 50 ml intravenous bolus of 50% glucose. A continuous infusion of 10% glucose was started. Intermittent hypoglycaemia with neurological signs requiring treatment with 50% glucose was recorded three times during subsequent hospitalization, the last episode being 11 h after insulin injection. The plasma insulin level 4 h after injection was 1465 mU/L, and 18 h after injection was 11 mU/L. Hypoglycaemia after an insulin lispro overdose may last for more than 11 h. Repeated hypoglycaemia after an insulin overdose could be avoided with a glucose infusion rate equivalent to the maximal glucose disposal rate.

Urinary serotonin level is associated with serotonin syndrome after moclobemide, sertraline, and citalopram overdose

Introduction. Altered mental status, autonomic dysfunction, and neuromuscular abnormalities are a characteristic triad of serotonin syndrome. No laboratory tests confirm the diagnosis of serotonin syndrome. Case report. A 35-year-old woman took moclobemide, sertraline, and citalopram in a suicide attempt. She was conscious with mild tachycardia, hypertension, and tachypnea one hour after ingestion. In the second hour after ingestion diaphoresis, mydriasis, horizontal nystagmus, trismus, hyperreflexia, clonus, and tremor appeared. She became agitated and unresponsive. In the third hour after ingestion she became comatose and hyperthermic. She was anesthetized, paralyzed, intubated, and ventilated for 24 hours. Serum moclobemide, sertraline, and citalopram levels were above therapeutic levels. The serum serotonin level was within normal limits and the urinary 5-hydroxyindoleacetic acid:creatinine ratio was below the average daily value. The urinary serotonin:creatinine ratio was increased on arrival (1 mg/g). Discussion and conclusion. The urinary serotonin level is increased in serotonin syndrome due to a monoamine oxidase inhibitor and selective serotonin-reuptake inhibitors overdose. It is possible that urinary serotonin concentration could be used as a biochemical marker of serotonin syndrome.

Poisoning with rivastigmine

CASE REPORT A 59-year-old man with a noncontributory medical history was found comatose and soiled after having urinated and defecated while unconscious. During transport to the Emergency Department (ED) he had two seizures that resolved spontaneously. On arrival, he was somnolent and he vomited. He had miosis, nystagmus, and excessive salivary and bronchial secretions. Breathing was shallow at a respiratory rate of 28 per minute between apneic pauses. Diffuse crackles were heard in his lungs. His tympanic temperature was 33.5 C, pulse 79 beats per minute, supine blood pressure 180/ 90 mmHg, and SpO2 76% on room air. The patient was intubated, suctioned, and ventilated. Atropine 3 mg intravenously cleared the bronchial secretions. Gastric lavage was performed and activated charcoal was given 1 hour after presentation. Gastric content had a normal smell. His initial laboratory test results were serum sodium 135 mmol/L, potassium 3.0 mmol/L, BUN 4.5 mmol/L, creatinine 65 mmol/L, glucose 12.9 mmol/L, and bicarbonate 26 mmol/L. Plasma butyrylcholinesterase was 6.0 mkat/L (normal 60–190 mkat/L). An electrocardiogram showed a sinus tachycardia and a brain CT scan revealed no pathological changes. Between 5 and 13 hours after presentation he had three periods of bradycardia (30 beats per minute), which were reversed with atropine 1 mg each time. Artificial ventilation was stopped 23 hours after presentation and he was extubated 3 hours later. After extubation his physical examination was unremarkable, lungs were clear, and cholinergic signs were absent. He reported that he had taken 48 tablets of Exelon (288 mg of rivastigmine) and 28 tablets of Cipramil (280 mg of citalopram) in a suicide attempt 5 hours before he was found. The drugs belonged to his mother who has Alzheimer’s disease. A toxicological screening of gastric content by gas chromatography–mass spectrometry (incapable of detecting rivastigmine) was positive only for citalopram. During the rest of his hospitalization he felt dizziness and fatigue, but his physical examination was otherwise unremarkable. Plasma butyrylcholinesterase gradually returned to normal values in 5 days (Fig. 1). Red blood cell acetylcholinesterase was not measured. The patient was discharged after psychiatric evaluation on the fifth day.