Laurentiu Sorodoc

Lipid emulsion therapy in cardiodepressive syndrome after diltiazem overdose—case report

We present a case of diltiazem overdose in which the patient ingested 5.6 g in an apparent suicide attempt. She was admitted in the emergency department 2 hours postingestion with cardiodepressive syndrome. She was treated with gastric lavage, activated charcoal, intravenous fluids, calcium, and epinephrine, without improvement in vital signs. We gave her an infusion of 20% intralipid, leading to a favorable evolution. The patient was stable hemodynamically and metabolic in the following 24 hours. She was alert and oriented and was extubated in the second day. She was discharged after 4 days in a good state and without any neurologic deficits.

Is MARS system enough for A.phalloides-induced liver failure treatment?

Patients with Amanita phalloides-induced liver failure (LF) have a high mortality, despite significant advances in intensive care managemet. Our study evaluated the effect of Molecular Absorbents Recirculating System (MARS) comparative with optimal intensive care (OIC) in adults with this condition, in the absence of liver transplantation (LT). Six consecutive patients (women, range 16—61 years) affected by A.phalloides-induced LF were treated with OIC (3 patients) and MARS (3 patients). Laboratory parameters and hepeatic encephalopaty were evaluated 15 min before and 24 hours following each MARS treatment. Three 6-hour sessions per patient were performed in MARS group, with a statistically significant decrease in ammonia (p value 0.011), alaninaminotransferase (ALT) and prothrombin time (PT) (p value 0.004). Two patients had a significant rebound in bilirubin (+116%; p value 0. 04) 24 hours following MARS. Mortality in MARS group was 66.7%. Survival rate in OIC was 0%. Negative prognostic markers: lack of PT and hepatic encephalopaty improvement, rebound in bilirubin, and delay of MARS therapy initiation. No significant adverse reactions occurred during MARS. MARS is an effective depurative therapy in adults with A.phalloides-induced LF, but alone is not enough. Survival is predicted by the results of the initial MARS, amount of mushroom consumed, and time from toxin exposure.

Epidemiology of acute drug poisoning in a tertiary center from Iasi County, Romania

The aim of this retrospective epidemiological study was to investigate the demographical, etiological and clinical characteristics of acute drug poisonings in Iasi County, Romania. All patients were referred and admitted in the Toxicology Clinic of “Sf. Ioan” Emergency Clinic Hospital Iasi, Romania. Between 2003 and 2009, 811 cases of acute drug poisonings were recorded, counting for 28.43% from the total number of poisonings. The majority of these poisonings resulted in mild (51.94%) and medium (28.35%) clinical forms, while 19.71% were coma situations. In all, 63.51% of patients originated from urban areas, 39.94% were unemployed and the patients were predominantly women (66.46%). A high percentage (97.27%) were suicide attempts, using only one type of drug (65.88%) and the 21–30 years group (29.8%) records the highest incidence, for both women and men. The most frequently involved drugs were benzodiazepines 13.69%, anticonvulsive drugs 8.63%, barbiturates 8.51% and cardiovascular drugs 5.92%. Drugs combinations were recorded in 32.92% of cases and 1.2% were combinations between drugs and other substances. Mortality was the outcome in 0.3% of the total registered number of acute drug poisonings. This study underlines that in order to provide a proper management of these situations, a Regional Poison Information Center is absolutely necessary.

Cardiac Troponin T and NT-proBNP as Biomarkers of Early Myocardial Damage in Amitriptyline-Induced Cardiovascular Toxicity in Rats:

The main objective of this study was to investigate whether cardiac troponin (cTn) and N-terminal, protein B-type natriuretic peptide (NT-proBNP) can be useful as indicators for amitriptyline cardiotoxicity which is a known drug having sublethal toxic cardiac effects. At the same time, this study looked at detecting potential histopathological changes specific to irreversible cardiac injuries in a rat model of amitriptyline cardiotoxicity. Male Wistar rats were randomly divided into 2 groups, control (saline) group and amitriptyline group (100 mg/kg body weight intraperitoneally, equivalent for lethal dose at 50%). Blood was collected 30 minutes after the administration. The cTn was measured using 3 different methods (2 methods designed for human use and a sandwich enzyme immunoassay specific for rat cTnT). The brain natriuretic peptide was measured by 2 different methods (1 for human and 1 specific for rats). Electrocardiography showed that the QRS complex (P < .0001) and the QT interval (P = .002) were significantly prolonged for amitriptyline-treated animals. Troponin T and NT-proBNP had significantly increased levels in all the rats but showed positive results only when using rat-specific quantitative measurement. In certain rats, the histopathological examination identified a few small foci of acute myocardial necrosis. In conclusion, elevation of cTnT and NT-proBNP are early indicators of cardiotoxicity, yet the significance of irreversible myocardial damage in amitriptyline cardiotoxicity needs to be further understood.

Toxic and Drug-Induced Changes of the Electrocardiogram

There are numerous toxins and drugs that can cause, in overdose, electrocardiogram (ECG) changes, even in patients without history of cardiac pathology. The diagnosis and management of patients with an abnormal ECG encountered in a specific toxicity can challenge experienced physicians. One must have serious knowledge of basic cardiac physiology, in order to understand the ECG changes associated with various drugs and toxins. The main mechanisms involved include membrane – depressant action (sodium channel blockers, slow calcium channel blockers, outward potassium (K+) channel blockers, and sodium-potassium adenosine-triphosphatase blockers), and action on autonomic nervous system and its sites of cardiovascular action (beta-adrenergic blockers and other sympathetic-inhibitors, sympathomimetic, anticholinergic and cholinomimetic substances). Many toxins and medications have actions that involve more than one of these mechanisms, including hypoxia, electrolyte and metabolic imbalances, and thus may result in a combination of electrocardiographic changes. In resting state, the myocardial cell membrane is impermeable to positively charged sodium ions (Na+). The Na+/K+ ATPase maintains a negative electric potential of approximately 90 mV in the myocyte. The rapid opening of Na+ channels and massive Na+ influx (phase 0 of action potential) explains depolarization of the cardiac cell membrane (fig.1), causing the rapid upstroke of the cardiac action potential, which is conducted through the ventricles and is expressed as the QRS complex of the ECG. The closure of Na+ channels and the transient opening of Ito K+ efflux channels (phase 1) mark the peak of the action potential. Then, phase 2 of the action potential occurs when the opening of slow calcium (Ca2+) channels produces an influx of positive ions with a steady maintenance of the membrane potential and myocardial contraction continues. The end of the cardiac cycle is marked by the closure of the Ca2+ channels and the activation of the K+ efflux channels, which allow the action potential to return to its resting potential of – 90 mV (phase 3). This K+ efflux from the myocardial cell is directly responsible for the QT interval on the ECG (Holstege et al., 2006). During phase 4 of the cardiac cell action potential, some cardiac fibers allow sodium ions to enter the cell, increasing the resting membrane potential, known as spontaneous diastolic depolarization. When the threshold in membrane potential is reached, the Na+ channels open and another action potential is generated.

Acute pancreatitis after nifedipine and acetaminophen poisoning — case report

The incidence of drug-induced pancreatitis is rare. There have been several reports of acute pancreatitis as a complication in acute poisoning with drugs or toxins. We present a case of a young woman with acute pancreatitis secondary to an overdose of nifedipine and acetaminophen in a suicide attempt. We excluded other causes of acute pancreatitis by clinical history, serum toxicology, serology, and abdominal imaging. The most likely underlying pathophysiological mechanism was ischemic injury of the pancreas secondary to severe collapse induced by nifedipine and possible acetaminophen-induced direct pancreatotoxicity. The pancreatitis resolved with treatment that included continuous veno-venous haemofiltration in an intensive care unit. Emergency and intensive care units should be aware of this unusual complication of such poisoning. To our knowledge, this is the first reported association between massive nifedipine overdose and acute pancreatitis.

Profile of adult acute cholinesterase inhibitors substances poisoning – a 30 years analysis

Abstract Objectives: The objective of this study was to assess the pattern and outcome of acute cholinesterase inhibitors substances (CIS) poisoning cases, in a cohort from a regional tertiary care hospital. Methods: cases admitted in the Toxicology Clinic of “Sf. Spiridon” Emergency Clinic Hospital Iasi, Romania between 1983 and 2013 were studied. Results: a total number of 606 patients were included. The reason for exposures was intentional in 70% of cases and the commonest route of poisoning was oral in 92.2%. The highest percent of cases was females (56.4), the age group 20-29 (25.4%) and the majority (66.7%) coming from rural areas, 28.2% being agricultural workers. 36.6% of cases were severe clinical forms. Overall mortality rates were 3.8%, more than half of the death patients (65.2%) had concomitant alcohol intake. It was a significant statistical association between decrease level of serum cholinesterase on admittance and severe forms (p 0.000) and between survival and deaths groups (p 0.000). The pattern of poisoning described by our retrospective study suggests that CIS poisoning are mainly preventable. The main effective goals for prevention are restriction in free accessibility to toxic pesticides, together with sustained efforts in education concerning the life-threatening danger of pesticide poisoning.