Successful use of extracorporeal life support and hemadsorption in the context of venlafaxine intoxication requiring cardiopulmonary resuscitation: a case report

A 17-year-old female patient was admitted to a regional hospital for mixed intoxication with a presumed intake of 24 g of venlafaxine (both immediate and extended-release preparations) and unknown amounts of oxycodone, zolmitriptan and itinerol B6. The patient had been treated with venlafaxine by her outpatient psychiatrist for severe depression with suicidal ideation for two weeks prior to the event. An inpatient psychiatric stay had already been planned. Approximately five hours after taking the medication, the patient was found somnolent and brought to the hospital by ambulance. Due to the severity of the intoxication with the risk of developing hemodynamic instability, the patient was immediately transferred to the intensive care unit.

Shortly after that, recurrent generalized seizures occurred. Due to a status epilepticus, the patient was then analgosedated and intubated. After tracheal intubation, progressive hemodynamic deterioration occurred with sinus tachycardia up to 140 bpm, hypotension with systolic blood pressure of 70 mmHg and centralization (prolonged capillary refill time > 3 s). Figure 1 shows the ECG on the day of admission with sinus tachycardia and a prolongation of the cQT-time. Echocardiography revealed severely impaired left ventricular function (EF 10–15%) with hypokinetic left ventricle, apical and midventricular akinesia with normal right ventricular function. Pericardial effusion was excluded. Arterial blood gas analysis showed metabolic acidosis (pH 7.28) and a serum lactate of 7.8 mmol/l. Despite extended catecholamine therapy with high-dose norepinephrine, dobutamine and adrenaline, the patient could not be stabilized and cardiopulmonary resuscitation due to cardiac arrest was initiated. After 2.5 h (150 min) of mechanical resuscitation, extracorporeal life support (ECLS) system was established on-site with subsequent air-bound transfer to a tertiary hospital.

Fig. 1figure 1

ECG on day of admission with sinus tachycardia and prolonged cQT 441 ms. Running speed 25 mm/s

Shortly after arrival at the tertiary hospital, a large volume of tablets (filling one-third of the stomach) was removed during primary decontamination via gastroscopy. The gastric mucosa was slightly hemorrhagic. A total of 55 g of activated charcoal was applied for additional adsorption. Because of a distended abdomen with subileus, repetitive administration was withheld. Laboratory chemistry revealed disseminated intravascular coagulation (DIC) and acute liver failure with transaminase elevation (max. AST 4226 U/l, max. ALT 3224 U/l), drop in coagulation factor V (Factor V: < 10%), INR elevation (max. INR 5.9) and lactic acidosis (Lactate max. 9.8 mmol/l, pH min. 7.27), leading to the administration of N-acetylcysteine following Prescott schema for four days despite negative paracetamol serum levels. Sonographically, the liver was well perfused without obstructive intra- or extrahepatic cholestasis. The patient was anuric with acute kidney injury (AKIN stage 3, max. creatinine 331mcmol/l) and required continuous hemodiafiltration from day five. Toxicological screening in urine and blood detected the metabolites of oxycodone, tramadol, nicotine and lidocaine, venlafaxine, metoprolol, metoclopramide, naloxone, and caffeine. In addition, iatrogenic amoxicillin, midazolam and levetiracetam metabolites were found. The initial compound venlafaxine/desmethylvenlafaxine plasma concentration was markedly elevated (maximum 52.53 µmol/l) but reduced significantly (9.60 µmol/l) within the first 24 h under initiated ECLS therapy with CytoSorb® filter. The adsorption filter (CytoSorb®, blood flow 300 ml/min) was changed three times over 72 h and removed after three days of therapy as recommended by the manufacturer. Figure 2 shows the course of venlafaxine/desmethylvenlafaxine plasma concentration and LV-EF (left ventricular ejection fraction) graphically. Balanced hemodynamic management using volume and low-dose epinephrine (0.1 µg/kg/min) to promote inotropy, as well as high ECLS blood flow (maximum 5 l/min), were used to maintain sufficient mean arterial pressure. A 900 ml serous left pleural effusion was drained following the correction of coagulation on day four. Already at admission, microbiological sampling was performed after documented aspiration and the established antimicrobial therapy with amoxicillin/clavulanic acid was continued. Despite negative bacterial detection, antimicrobial therapy was escalated to piperacillin/tazobactam on day eight due to respiratory deterioration and increasing inflammatory parameters (CRP peak level 154 mg/l).

Fig. 2figure 2

On the left Y-axis in blue, plot of the time course of compound plasma concentration of venlafaxine. On the right Y-axis in green, time course of left ventricular ejection fraction (LV-EF) in percent. On the upper X-axis days since ingestion are displayed. Below the X-axis, plot using bars of the duration of use of ECLS, Cytosorb®, and hemofiltration. ECLS extracorporeal life support, CRRT continuous renal replacement therapy

The patient’s health condition progressively improved over the next few days. In addition to an increased blood pressure amplitude over 20 mmHg, serial transthoracic echocardiograms (TTE) documented improved cardiac function and sufficient ejection fraction (EF) of approximately 35% under ECLS blood flow of 3–4 l. Electrocardiographically, cQT peaked at 507 ms with no arrhythmias. Three days post-admission, levosimendan (0.1mcg/kg/min) perfusion (25 mg) was followed by weaning and removal of the ECLS system. Hepatic function recovered and after 7 days of high-volume hemodiafiltration, acid–base and fluid hemostasis were restored. The patient was transferred back to the peripheral hospital on day 11 after symptom onset and completely recovered there neurologically and cardiopulmonarily. The discharge to inpatient psychiatric treatment was organized 31 days after intoxication due to persistent suicidality.

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