[Atypical presentation of rhabdomyolysis due to hypokalaemia induced by diuretics abuse: Case report from Sierra Leone.]

Rhabdomyolysis results from acute necrosis of skeletal muscle fibres and consequent leakage of muscle constituents into the circulation. Its association with anything different than trauma in the Emergency Room is not that frequent. We present the case of a 47-year-old male, hypertensive, that developed weakness and incapability to walk without help, finding on the blood biochemistry that he had developed a rhabdomyolysis due to hipokalemia after abusing of diuretics.

La rabdomiólisis es el resultado de la necrosis de las fibras musculoesqueléticas y la consiguiente fuga de constituyentes musculares a la circulación. Su asociación con algo diferente a un trauma en la sala de emergencias no es tan frecuente. Presentamos el caso de un varón de 47 años, hipertenso, con historia de abuso de diuréticos, desarrollando debilidad e incapacidad para caminar por sus propios medios, encontrando en la bioquímica sanguínea que había padecía rabdomiólisis por hipocalemia.

Adverse drug reactions and deliberate self-poisoning as cause of admission to the intensive care unit: a 1-year prospective observational cohort study.

OBJECTIVE: The aim of the present study was (1) to determine the prevalence of intensive care unit (ICU) admissions due to an adverse drug reaction (ADR), and (2) to compare affected patients with patients admitted to the ICU for the treatment of deliberate self-poisoning using medical drugs. DESIGN: Prospective observational cohort study. SETTING: Fourteen bed medical ICU including an integrated intermediate care (IMC) section at a tertiary referral center. PATIENTS: A total of 1,554 patients admitted on 1 January 2003 to 31 December 2003. RESULTS: Ninety-nine patients were admitted to the ICU with a diagnosis of ADR (6.4% of all admissions), 269 admissions (17.3%) were caused by deliberate self-poisoning. Patients admitted for treatment of ADR had a significantly higher age, a longer treatment duration in the ICU, a higher SAPS II score, and a higher 6-month mortality than those with deliberate self-poisoning. Most patients (71.7%) suffering from ADR required advanced supportive care in the ICU while the majority of patients (90.7%) with deliberate self-poisoning could be sufficiently treated in the IMC area. All diagnostic and therapeutic procedures in the ICU except mechanical ventilation were significantly more often performed in patients with ADR. CONCLUSIONS: This study provides further evidence that ADR is a frequent cause of admission to medical ICUs resulting in a considerable use of ICU capacities. In the present setting patients with ADR required longer and more intense medical treatment in the ICU than those with deliberate self-poisoning.

Acute oxcarbazepine, benazepril, and hydrochlorothiazide overdose with alcohol.

An epiletic patient, suffering from partial complex seizures and hypertension, ingested approximately 42 g of oxcarbazepine (OXC) and an undefined number of tablets containing an association of benazepril and hydrochlorothiazide along with some glasses of wine. Four hours later he was brought to the emergency room. He was stuporous and gradually became unconscious. Therefore he was intubated and, approximately 6 hours after the overdose, transferred to the intensive care unit, where he underwent a 4-hour hemodialysis. Even if this procedure did not accelerate the elimination of the prodrug nor its active metabolite (monohydrocarbazepine), 3 hours after the end of dialysis the patient was fully recovered.

Determination of furosemide in whole blood using SPE and GC-EI-MS.

A simple and rapid method was validated to determine furosemide in whole blood. The experimental work was performed so that all validation parameters are considered simultaneously in a one-day assay protocol. A solid-phase extraction procedure using BondElut-LRC Certify columns was used to extract this compound from blood samples, while ketoprofen was used as an internal standard. The extracts were analyzed by gas chromatography-electron ionization-mass spectrometry after on-column derivatization with trimethylanilinium hydroxide (0.2M in methanol). Calibration curves were prepared daily, between 0.10 and 5.00 microg/mL, and the correlation coefficients were above 0.9910. The calculated limits of detection and quantitation were 0.010 and 0.045 microg/mL, respectively. Control samples at low, medium, and high concentrations (0.30, 0.75, and 3.00 microg/mL) of furosemide of an independent source were measured in the same day. Precision and trueness, calculated in terms of relative standard deviation (%), were less than 15% for all concentration levels. The relative recoveries calculated for the three levels of the control samples were 104%, 89%, and 91%, respectively. In general, a sensitive, specific, and reliable procedure has been developed for the determination of furosemide in whole blood samples and was found suitable for the application in postmortem forensic toxicology routine analysis.

Concealed administration of frusemide simulating Bartter syndrome in a 4.5-year-old boy.

A 4.5-year-old boy was admitted to three different hospitals because of a tendency towards dehydration and polyuria, along with normal blood pressure, hypochloraemia, hypokalaemia, metabolic alkalosis and an impaired urinary concentrating ability. A renal biopsy failed to reveal juxtaglomerular hyperplasia. The clinical and laboratory findings failed to improve despite supplementation with potassium chloride and treatment with indomethacin. The urine was found to contain frusemide. The parents denied any drug administration to the boy. The child is now doing well more than 1 year after separation from his mother. Since ingestion of diuretic cannot be differentiated from true Bartter syndrome by blood and urinary electrolyte measurements alone, a diuretic screen is warranted in children with findings consistent with Bartter syndrome.

[Drugs as a cause of death. A prospective quality assurance project in a department of medicine]. / Legemidler som årsak til dødsfall. Et prospektivt kvalitetssikringsprosjekt i en medisinsk avdeling.

This study is part of a prospective quality assurance project in a Norwegian county hospital. The major aims of the study were to estimate the number of drug-related deaths; assess whether these were recognized by the clinicians, and (if not) discuss why the clinicians had difficulties in recognizing drug-related deaths. A panel of two internists, one pathologist, one pharmacologist and one pharmacist evaluated all inpatients deaths over a six-month period. Among 3,082 hospitalized patients, 169 died. Of these deaths, 20 were classified as probably (nine) or possibility (11) drug-related. Only two of the deaths were recognized as such by the clinicians in the ward. The reasons for the clinicians failure to recognize adverse drug reactions include frequent presence of multiple diseases, polypharmacy and inadequate guidelines on how to look for adverse reactions to drugs. A two-year survey aimed at studying these aspects in depth is in progress.

Poisoning with antihypertensive drugs: diuretics and potassium supplements.

Diuretics are widely prescribed to treat hypertension and oedema. The increasing use of these drugs opens the possibility of an increase in deliberate or accidental self-poisoning. However, experience with overdosage and toxicity with the diuretics remains very limited. In general, supportive therapy by the reduction of gastrointestinal absorption, monitoring of vital signs and the correction of hypertension and electrolyte abnormalities are indicated.

[Edema caused by diuretic abuse]. / Edema por abuso de diuréticos.

We present the case of an "idiopathic" edema induced by the chronic use of diuretics in a 44-years-old patient. The patient showed a significant secondary hyperaldosteronism which have been erroneousley labelled as primary in previous studies. The pathogenicity of the idiopathic edema and its relation to diuretic abuse are discussed.