6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
A) Prehospital gastrointestinal decontamination is not recommended because of potential for CNS depression, seizures, and cardiovascular instability.
6.5.2) PREVENTION OF ABSORPTION
A) SUMMARY 1) Consider gastric lavage after ingestion of a potentially life-threatening amount of poison if it can be performed soon after ingestion (generally within 1 hour) and the airway is protected. Consider activated charcoal in patients with a potentially toxic ingestion who are awake and able to protect their airway. Because of the potential for abrupt onset of hemodynamic instability or seizures, consider intubating the patient to protect the airway first. Most effective when administered within one hour of ingestion.
B) ACTIVATED CHARCOAL 1) Flecainide has been shown to bind to activated charcoal, which prevents further absorption (Nitsch et al, 1987). Repeated charcoal administration and gastric lavage may be effective in severe flecainide poisonings due to gastrointestinal metabolism and entero-enteric circulation (Nitsch, 1992). 2) CHARCOAL ADMINISTRATION a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
3) CHARCOAL DOSE a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005). 1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
b) ADVERSE EFFECTS/CONTRAINDICATIONS 1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
C) GASTRIC LAVAGE 1) INDICATIONS: Consider gastric lavage with a large-bore orogastric tube (ADULT: 36 to 40 French or 30 English gauge tube {external diameter 12 to 13.3 mm}; CHILD: 24 to 28 French {diameter 7.8 to 9.3 mm}) after a potentially life threatening ingestion if it can be performed soon after ingestion (generally within 60 minutes). a) Consider lavage more than 60 minutes after ingestion of sustained-release formulations and substances known to form bezoars or concretions.
2) PRECAUTIONS: a) SEIZURE CONTROL: Is mandatory prior to gastric lavage.
b) AIRWAY PROTECTION: Place patients in the head down left lateral decubitus position, with suction available. Patients with depressed mental status should be intubated with a cuffed endotracheal tube prior to lavage.
3) LAVAGE FLUID: a) Use small aliquots of liquid. Lavage with 200 to 300 milliliters warm tap water (preferably 38 degrees Celsius) or saline per wash (in older children or adults) and 10 milliliters/kilogram body weight of normal saline in young children(Vale et al, 2004) and repeat until lavage return is clear.
b) The volume of lavage return should approximate amount of fluid given to avoid fluid-electrolyte imbalance.
c) CAUTION: Water should be avoided in young children because of the risk of electrolyte imbalance and water intoxication. Warm fluids avoid the risk of hypothermia in very young children and the elderly.
4) COMPLICATIONS: a) Complications of gastric lavage have included: aspiration pneumonia, hypoxia, hypercapnia, mechanical injury to the throat, esophagus, or stomach, fluid and electrolyte imbalance (Vale, 1997). Combative patients may be at greater risk for complications (Caravati et al, 2001).
b) Gastric lavage can cause significant morbidity; it should NOT be performed routinely in all poisoned patients (Vale, 1997).
5) CONTRAINDICATIONS: a) Loss of airway protective reflexes or decreased level of consciousness if patient is not intubated, following ingestion of corrosive substances, hydrocarbons (high aspiration potential), patients at risk of hemorrhage or gastrointestinal perforation, or trivial or non-toxic ingestion.
6.5.3) TREATMENT
A) SUPPORT 1) MANAGEMENT OF MILD TO MODERATE TOXICITY: Treat seizures with benzodiazepines. Manage mild hypotension with IV fluids.
2) MANAGEMENT OF SEVERE TOXICITY: Treat ventricular dysrhythmias with sodium bicarbonate, correct electrolyte abnormalities, and perform cardioversion for unstable rhythms. Consider intravenous lipid therapy early for patients with ventricular dysrhythmias or hypotension. Antidysrhythmic drugs are generally not effective, and some (procainamide, disopyramide, encainide, sotalol, propafenone) should be avoided. Consider extracorporeal support (cardiopulmonary bypass, extracorporeal membrane oxygenation, aortic balloon pump) early in unstable patients. Treat torsades de pointes with magnesium and overdrive pacing. Intubate patients with hemodynamic instability, dysrhythmias or CNS depression. Treat hypotension initially with IV fluids, then vasopressors if necessary. Treat seizures with benzodiazepines, add propofol or barbiturates if seizures persist.
B) MONITORING OF PATIENT 1) Monitor vital signs frequently, obtain serial ECGs, and institute continuous cardiac monitoring.
2) Monitor serum electrolytes and acid/base balance.
3) Monitor for seizures and CNS depression following substantial overdoses.
4) While flecainide concentrations can be measured, they are not rapidly available and not useful to guide overdose treatment. A therapeutic level is estimated at 0.2 to 1 mcg/mL; levels greater than 1.5 mcg/mL may be considered toxic.
C) VENTRICULAR ARRHYTHMIA 1) SUMMARY: Initial treatment with sodium bicarbonate boluses to decrease the amount of sodium channel blockade. Frequent ECGs and continuous cardiac monitoring. Monitor arterial blood gases to target pH 7.45 to 7.55. Ventricular tachycardia induced by flecainide has been difficult to treat and refractory to conventional antidysrhythmic drug therapy, cardioversion, and ventricular pacing. Minimize aggravating conditions for dysrhythmias (eg, electrolyte abnormalities, hypoxia). Avoid drugs with similar sodium channel blocking effects. Antidysrhythmics are rarely effective. Consider overdrive transvenous pacing. Avoid procainamide and disopyramide as they may worsen flecainide-induced dysrhythmias. Institute cardiopulmonary bypass, extracorporeal membrane oxygenation, or intra-aortic balloon pump early for patients with persistent hemodynamic instability. The goal is to support the patient hemodynamically while the flecainide is metabolized. 2) Dysrhythmias induced by flecainide have been very difficult to treat and refractory to conventional antiarrhythmic drug therapy, cardioversion, and ventricular pacing (Spivack et al, 1984). a) Cardioversion was effective in two patients with ventricular tachyarrhythmias (Wehr et al, 1985).
b) Blood pressure and adequate heart rate were maintained in a 42-year-old man who ingested an unknown large amount of flecainide with a pacemaker and catecholamines (Gotz et al, 1991).
3) SODIUM BICARBONATE a) By blocking fast sodium channels, flecainide overdoses result in markedly widened QRS complex and a widened QT interval as well as hypotension. Intravenous hypertonic sodium bicarbonate has been shown to reduce QRS duration and ventricular dysrhythmias in a dog model and several human case reports of flecainide overdose (Levechio et al, 1996; Sholar et al, 1996; Murad et al, 1996). 1) Administer an initial IV dose of 2 mEq/kg in patients with dysrhythmias or QRS widening, repeated as needed with careful monitoring of ECG and ABGs. Target blood pH is 7.45 to 7.55. Continuous sodium bicarbonate infusion may be given in addition to boluses, but boluses appear to be most effective in increasing blood pH.
b) CASE REPORT: A 34-year-old woman with a history of paroxysmal supraventricular tachycardia developed cardiovascular collapse, altered level of consciousness, and severe metabolic acidosis after ingesting 4500 mg of flecainide (serum flecainide concentration 3.6 mg/L). She was successfully treated with supportive therapy that included several boluses of sodium bicarbonate (total 450 mEq over 3 hours) without recourse to invasive modalities such as cardiopulmonary bypass or extracorporeal therapies. Laboratory results showed elevated sodium concentration (peaked at 151 mmol/L) and the base excess at 6.8 mmol/L (Devin et al, 2007). c) CASE REPORT: Lovecchio et al (1998) reported successful use of hypertonic sodium bicarbonate (8.4% boluses) 100 mEq in 2 patients with hypotension (resistant to normal saline infusions) and QRS widening. In a 38-year-old woman who had ingested 1,000 mg flecainide, 2 boluses of 100 mEq of 8.4% sodium bicarbonate, followed by a bicarbonate drip (150 mEq bicarbonate in 1 L of 5% dextrose in water at 150 mL/hr) increased her blood pressure to 120/70 mmHg and resulted in a narrowing of her QRS complex to 128 msec. The patient was transferred to psychiatric care 36 hours later (Lovecchio et al, 1998). d) CASE REPORT: A 33-year-old woman presented to the emergency department with mental status changes following an overdose ingestion of flecainide. After presentation, the patient developed ventricular tachycardia that progressed to cardiac arrest and was successfully resuscitated following defibrillation and administration of 6 ampules of sodium bicarbonate. The patient was intubated, at which time a sodium bicarbonate infusion (300 mEq/hour) and lipid emulsion therapy were initiated. An ECG revealed a heart rate of 109 beats/min, a PR interval of 236 msec, a QTc interval of 439 msec, and an initial QRS interval of 92 msec widening to 156 msec. Narrowing of the QRS interval occurred with repeat sodium bicarbonate doses (11 ampules), but attempts to wean the patient from the sodium bicarbonate or lipid emulsion infusions resulted in recurrent unstable ventricular tachycardia (VT). Following transfer to the intensive care unit, the patient developed VT cardiac arrest and, after several resuscitative attempts and subsequent return of spontaneous circulation, the patient was placed on extracorporeal membrane oxygenation (ECMO), resulting in a return to neurologic baseline and subsequent discharge on hospital day 12 (Brumfield et al, 2015). e) DOGS: In 7 dogs with flecainide-induced ventricular tachycardias and prolonged QRS complexes, hypertonic sodium bicarbonate, in 3 doses of 3 mEq/kg/dose, was effective in all dogs in reducing the QRS complexes and producing significant reduction in ventricular beats (Salerno et al, 1995). 4) LIDOCAINE a) LIDOCAINE/INDICATIONS 1) Ventricular tachycardia or ventricular fibrillation (Prod Info Lidocaine HCl intravenous injection solution, 2006; Neumar et al, 2010; Vanden Hoek et al, 2010).
b) LIDOCAINE/DOSE 1) ADULT: 1 to 1.5 milligrams/kilogram via intravenous push. For refractory VT/VF an additional bolus of 0.5 to 0.75 milligram/kilogram can be given at 5 to 10 minute intervals to a maximum dose of 3 milligrams/kilogram (Neumar et al, 2010). Only bolus therapy is recommended during cardiac arrest. a) Once circulation has been restored begin a maintenance infusion of 1 to 4 milligrams per minute. If dysrhythmias recur during infusion repeat 0.5 milligram/kilogram bolus and increase the infusion rate incrementally (maximal infusion rate is 4 milligrams/minute) (Neumar et al, 2010).
2) CHILD: 1 milligram/kilogram initial bolus IV/IO; followed by a continuous infusion of 20 to 50 micrograms/kilogram/minute (de Caen et al, 2015). c) LIDOCAINE/MAJOR ADVERSE REACTIONS 1) Paresthesias; muscle twitching; confusion; slurred speech; seizures; respiratory depression or arrest; bradycardia; coma. May cause significant AV block or worsen pre-existing block. Prophylactic pacemaker may be required in the face of bifascicular, second degree, or third degree heart block (Prod Info Lidocaine HCl intravenous injection solution, 2006; Neumar et al, 2010).
d) LIDOCAINE/MONITORING PARAMETERS 1) Monitor ECG continuously; plasma concentrations as indicated (Prod Info Lidocaine HCl intravenous injection solution, 2006).
5) AMIODARONE a) Amiodarone should only be used with extreme caution. b) AMIODARONE/INDICATIONS 1) Effective for the control of hemodynamically stable monomorphic ventricular tachycardia. Also recommended for pulseless ventricular tachycardia or ventricular fibrillation in cardiac arrest unresponsive to CPR, defibrillation and vasopressor therapy (Link et al, 2015; Neumar et al, 2010). It should be used with caution when the ingestion involves agents known to cause QTc prolongation, such as fluoroquinolones, macrolide antibiotics or azoles, and when ECG reveals QT prolongation suspected to be secondary to overdose (Prod Info Cordarone(R) oral tablets, 2015).
c) AMIODARONE/ADULT DOSE 1) For ventricular fibrillation or pulseless VT unresponsive to CPR, defibrillation, and a vasopressor therapy give an initial dose of 300 mg IV followed by 1 dose of 150 mg IV. For stable ventricular tachycardias: Infuse 150 milligrams over 10 minutes, and repeat if necessary. Follow by a 1 milligram/minute infusion for 6 hours, then a 0.5 milligram/minute. Maximum total dose over 24 hours is 2.2 grams (Neumar et al, 2010).
d) AMIODARONE/PEDIATRIC DOSE 1) Infuse 5 milligrams/kilogram as a bolus for pulseless ventricular tachycardia or ventricular fibrillation; may repeat twice up to 15 mg/kg. Infuse 5 milligrams/kilogram over 20 to 60 minutes for perfusing tachycardias. Maximum single dose is 300 mg. Routine use with other drugs that prolong the QT interval is NOT recommended (Kleinman et al, 2010).
e) ADVERSE EFFECTS 1) Hypotension and bradycardia are the most common adverse effects (Neumar et al, 2010).
f) Ventricular tachycardia refractory to parenteral antiarrhythmic agents and pacing responded to rapid IV infusion of amiodarone (Sagie et al, 1988). g) CASE REPORT: Following the ingestion of 2000 mg flecainide, a 45-year-old woman developed therapy-resistant ventricular fibrillation with cardiopulmonary arrest. After 64 minutes of CPR and advanced life support, a 300 mg amiodarone bolus was administered. She developed effective spontaneous rhythm and resumed breathing. Amiodarone was continued as an infusion for 72 hours (900 mg in the first 48 hr, reduced to 600 mg/24 hr prior to discontinuation) (Siegers & Board, 2002). 6) ISOPROTERENOL a) ANIMAL STUDIES: ECG abnormalities and ventricular tachycardia were partially alleviated by administration of isoproterenol to nine dogs intoxicated by flecainide (Avitall et al, 1991). There are no studies of the efficacy of isoproterenol after flecainide overdose in humans. b) ISOPROTERENOL INDICATIONS 1) Used for temporary control of hemodynamically significant bradycardia in a patient with a pulse; generally other modalities (atropine, dopamine, epinephrine, dobutamine, pacing) should be used first because of the tendency to develop ischemia and dysrhythmias with isoproterenol (Neumar et al, 2010).
2) ADULT DOSE: Infuse 2 micrograms per minute, gradually titrating to 10 micrograms per minute as needed to desired response (Neumar et al, 2010).
3) CAUTION: Decrease infusion rate or discontinue infusion if ventricular dysrhythmias develop(Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
4) PEDIATRIC DOSE: Not well studied. Initial infusion of 0.1 mcg/kg/min titrated as needed, usual range is 0.1 mcg/kg/min to 1 mcg/kg/min (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
7) SODIUM LACTATE a) Infusion of molar sodium lactate in high doses to 3 patients with flecainide intoxication (cardiovascular collapse, wide QRS) resulted in rapid clinical and electrocardiographic improvement. The molar sodium lactate may displace flecainide from its receptor sites or may alter the action of flecainide on the fast sodium channels (Chouty et al, 1987).
D) TORSADES DE POINTES 1) SUMMARY a) Withdraw the causative agent. Hemodynamically unstable patients with Torsades de pointes (TdP) require electrical cardioversion. Emergent treatment with magnesium (first-line agent) or atrial overdrive pacing is indicated. Detect and correct underlying electrolyte abnormalities (ie, hypomagnesemia, hypokalemia, hypocalcemia). Correct hypoxia, if present (Drew et al, 2010; Neumar et al, 2010; Keren et al, 1981; Smith & Gallagher, 1980).
b) Polymorphic VT associated with acquired long QT syndrome may be treated with IV magnesium. Overdrive pacing or isoproterenol may be successful in terminating TdP, particularly when accompanied by bradycardia or if TdP appears to be precipitated by pauses in rhythm (Neumar et al, 2010). In patients with polymorphic VT with a normal QT interval, magnesium is unlikely to be effective (Link et al, 2015).
2) MAGNESIUM SULFATE a) Magnesium is recommended (first-line agent) for the prevention and treatment of drug-induced torsades de pointes (TdP) even if the serum magnesium concentration is normal. QTc intervals greater than 500 milliseconds after a potential drug overdose may correlate with the development of TdP (Charlton et al, 2010; Drew et al, 2010). ADULT DOSE: No clearly established guidelines exist; an optimal dosing regimen has not been established. Administer 1 to 2 grams diluted in 10 milliliters D5W IV/IO over 15 minutes (Neumar et al, 2010). Followed if needed by a second 2 gram bolus and an infusion of 0.5 to 1 gram (4 to 8 mEq) per hour in patients not responding to the initial bolus or with recurrence of dysrhythmias (American Heart Association, 2005; Perticone et al, 1997). Rate of infusion may be increased if dysrhythmias recur. For persistent refractory dysrhythmias, a continuous infusion of up to 3 to 10 milligrams/minute in adults may be given (Charlton et al, 2010).
b) PEDIATRIC DOSE: 25 to 50 milligrams/kilogram diluted to 10 milligrams/milliliter for intravenous infusion over 5 to 15 minutes up to 2 g (Charlton et al, 2010).
c) PRECAUTIONS: Use with caution in patients with renal insufficiency.
d) MAJOR ADVERSE EFFECTS: High doses may cause hypotension, respiratory depression, and CNS toxicity (Neumar et al, 2010). Toxicity may be observed at magnesium levels of 3.5 to 4.0 mEq/L or greater (Charlton et al, 2010).
e) MONITORING PARAMETERS: Monitor heart rate and rhythm, blood pressure, respiratory rate, motor strength, deep tendon reflexes, serum magnesium, phosphorus, and calcium concentrations (Prod Info magnesium sulfate heptahydrate IV, IM injection, solution, 2009).
3) OVERDRIVE PACING a) Institute electrical overdrive pacing at a rate of 130 to 150 beats per minute, and decrease as tolerated. Rates of 100 to 120 beats per minute may terminate torsades (American Heart Association, 2005). Pacing can be used to suppress self-limited runs of TdP that may progress to unstable or refractory TdP, or for override refractory, persistent TdP before the potential development of ventricular fibrillation (Charlton et al, 2010). In a case series overdrive pacing was successful in terminating TdP associated with bradycardia and drug-induced QT prolongation (Neumar et al, 2010).
4) POTASSIUM REPLETION a) Potassium supplementation, even if serum potassium is normal, has been recommended by many experts (Charlton et al, 2010; American Heart Association, 2005). Supplementation to supratherapeutic potassium concentrations of 4.5 to 5 mmol/L has been suggested, although there is little evidence to determine the optimal range in dysrhythmia (Drew et al, 2010; Charlton et al, 2010).
5) ISOPROTERENOL a) Isoproterenol has been successful in aborting torsades de pointes that was resistant to magnesium therapy in a patient in whom transvenous overdrive pacing was not an option (Charlton et al, 2010) and has been successfully used to treat torsades de pointes associated with bradycardia and drug induced QT prolongation (Keren et al, 1981; Neumar et al, 2010). Isoproterenol may have a limited role in pharmacologic overdrive pacing in select patients with drug-induced torsades de pointes and acquired long QT syndrome (Charlton et al, 2010; Neumar et al, 2010). Isoproterenol should be avoided in patients with polymorphic VT associated with familial long QT syndrome (Neumar et al, 2010). b) DOSE: ADULT: 2 to 10 micrograms/minute via a continuous monitored intravenous infusion; titrate to heart rate and rhythm response (Neumar et al, 2010). c) PRECAUTIONS: Correct hypovolemia before using; contraindicated in patients with acute cardiac ischemia (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013). 1) Contraindicated in patients with preexisting dysrhythmias; tachycardia or heart block due to digitalis toxicity; ventricular dysrhythmias that require inotropic therapy; and angina. Use with caution in patients with coronary insufficiency (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
d) MAJOR ADVERSE EFFECTS: Tachycardia, cardiac dysrhythmias, palpitations, hypotension or hypertension, nervousness, headache, dizziness, and dyspnea (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013). e) MONITORING PARAMETERS: Monitor heart rate and rhythm, blood pressure, respirations and central venous pressure to guide volume replacement (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013). 6) OTHER DRUGS a) Mexiletine, verapamil, propranolol, and labetalol have also been used to treat TdP, but results have been inconsistent (Khan & Gowda, 2004).
7) AVOID a) Avoid class Ia antidysrhythmics (eg, quinidine, disopyramide, procainamide, aprindine), class Ic (eg, flecainide, encainide, propafenone) and most class III antidysrhythmics (eg, N-acetylprocainamide, sotalol) since they may further prolong the QT interval and have been associated with TdP.
E) FAT EMULSION 1) Intravenous lipid emulsion (ILE) has been effective in reversing severe cardiovascular toxicity from local anesthetic overdose in animal studies and human case reports. Several animal studies and human case reports have also evaluated the use of ILE for patients following exposure to other drugs. Although the results of these studies are mixed, there is increasing evidence that it can rapidly reverse cardiovascular toxicity and improve mental function for a wide variety of lipid soluble drugs. It may be reasonable to consider ILE in patients with severe symptoms who are failing standard resuscitative measures (Lavonas et al, 2015). 2) The American College of Medical Toxicology has issued the following guidelines for lipid resuscitation therapy (LRT) in the management of overdose in cases involving a highly lipid soluble xenobiotic where the patient is hemodynamically unstable, unresponsive to standard resuscitation measures (ie, fluid replacement, inotropes and pressors). The decision to use LRT is based on the judgement of the treating physician. When possible, it is recommended these therapies be administered with the consultation of a medical toxicologist (American College of Medical Toxicology, 2016; American College of Medical Toxicology, 2011): a) Initial intravenous bolus of 1.5 mL/kg 20% lipid emulsion (eg, Intralipid) over 2 to 3 minutes. Asystolic patients or patients with pulseless electrical activity may have a repeat dose, if there is no response to the initial bolus.
b) Follow with an intravenous infusion of 0.25 mL/kg/min of 20% lipid emulsion (eg, Intralipid). Evaluate the patient's response after 3 minutes at this infusion rate. The infusion rate may be decreased to 0.025 mL/kg/min (ie, 1/10 the initial rate) in patients with a significant response. This recommendation has been proposed because of possible adverse effects from very high cumulative rates of lipid infusion. Monitor blood pressure, heart rate, and other hemodynamic parameters every 15 minutes during the infusion.
c) If there is an initial response to the bolus followed by the re-emergence of hemodynamic instability during the lowest-dose infusion, the infusion rate may be increased back to 0.25 mL/kg/min or, in severe cases, the bolus could be repeated. A maximum dose of 10 mL/kg has been recommended by some sources.
d) Where possible, LRT should be terminated after 1 hour or less, if the patient's clinical status permits. In cases where the patient's stability is dependent on continued lipid infusion, longer treatment may be appropriate.
3) CASE REPORT: A 72-year-old woman presented to the hospital after ingesting approximately 1500 mg flecainide, 150 mg of oxazepam and 150 mcg of levothyroxine in a suicide attempt. Upon arrival, the patient was hypotensive (70/50 mmHg), tachypneic (RR 30) and had a normal heart rate (HR 55 bpm). ECG revealed a widening of the QRS complex longer than 0.2 sec and prolongation of the QT interval. The patient received aggressive supportive care with fluid resuscitation (750 mL of 4.2% sodium bicarbonate with hydroxyethyl starch 1500 mL), mechanical ventilation, and up to 6 mg/h of epinephrine before she was transferred to a hospital that would provide further circulatory assistance. During transfer, the patient was started on intravenous lipid emulsion at 1.5 ml/kg bolus, followed by a 0.25 mg/min infusion. The patient's clinical status improved within 30 minutes of lipid emulsion. When she arrived at the other hospital, her BP had improved (111/80 mmHg), her HR was 75 bpm and ECG revealed marked shortening of the QRS complexes. The patient was admitted to an intensive care unit without the implementation of circulatory assistance, and despite developing aspiration pneumonia, she eventually recovered without long term medical deficit(Moussot et al, 2011). 4) CASE REPORT: A 52-year-old woman, with a history of paroxysmal atrial fibrillation, Gitelman syndrome with hypokalemia, and depression, presented with an out-of-hospital cardiac arrest. Prior to presentation, the patient had been unresponsive. An ECG, performed by paramedics, revealed a wide complex QRS complex and severe bradycardia, requiring external pacing. The patient subsequently developed pulseless electrical activity which resolved with successful cardiopulmonary resuscitation. At presentation, the patient was tachycardic and hypotensive (90/55 mmHg), despite vasopressor therapy. Laboratory analysis revealed severe hypokalemia (1.7 mmol/L), a bicarbonate concentration of 16 mmol/L, a lactic acid concentration of 10 mmol/L, and a flecainide concentration of 4.13 mcg/mL (reference range 0.2 to 1 mcg/mL). Intravenous lipid emulsion therapy and extracorporeal life support (ECLS) were initiated. Within a few hours after beginning ECLS therapy, The patient experienced hemodynamic and rhythm stabilization. ECLS was weaned off over the next 24 hours, and the patient recovered and was discharged (Sivalingam et al, 2013). 5) CASE REPORT: A 33-year-old woman presented to the emergency department with mental status changes following an overdose ingestion of flecainide. After presentation, the patient developed ventricular tachycardia that progressed to cardiac arrest and was successfully resuscitated following defibrillation and administration of sodium bicarbonate. The patient was intubated, at which time a sodium bicarbonate infusion and lipid emulsion therapy (20% lipid emulsion 100 mL IV bolus (1.5 mL/kg), followed by an IV infusion at 900 mL/hour (approximately 12 mL/kg/hour)) were initiated. An ECG revealed a heart rate of 109 beats/min, a PR interval of 236 msec, a QTc interval of 439 msec, and an initial QRS interval of 92 msec widening to 156 msec. Narrowing of the QRS interval occurred with repeat sodium bicarbonate doses, but attempts to wean the patient from the sodium bicarbonate or lipid emulsion infusions resulted in recurrent unstable ventricular tachycardia (VT). Following transfer to the intensive care unit, the patient developed VT cardiac arrest and, after several resuscitative attempts and subsequent return of spontaneous circulation, the patient was placed on extracorporeal membrane oxygenation (ECMO), resulting in a return to neurologic baseline and subsequent discharge on hospital day 12 (Brumfield et al, 2015). 6) CASE REPORT/ADOLESCENT: A 13-year-old girl developed first degree AV block (PR interval 215 ms), right bundle branch block (QRS duration 164 ms), and a QTc interval of 452 ms after ingesting 900 mg of flecainide, 25 mg of bisoprolol, and 225 mg of aspirin. Despite supportive therapy, including administration of IV fluids, IM glucagon (for bisoprolol ingestion), IV sodium bicarbonate and IV magnesium sulfate, the patient experienced VF arrest approximately 2.5 hours post presentation (1 hour after presenting to the ED). After she was successfully resuscitated, a 70-mL IV bolus of 20% lipid emulsion (ILE) (1.5 mL/kg) was administered followed by 225 mL (0.25 mL/kg/min) over 20 minutes. Over the next 8 hours, following ILE, she continued to experience cardiac instability (ie, sinus tachycardia alternating with right bundle branch block, torsade de pointes, a Brugada-like syndrome, coarse ventricular tachycardia, and ventricular standstill). With continued IV sodium bicarbonate and inotropic support, the patient's cardiac status stabilized within 12 hours post-presentation, and she was eventually discharged with no apparent sequelae (Mukhtar et al, 2015). 7) CASE REPORT/CHILD: A 17-month-old girl developed lethargy, hypotension (64/41 mmHg), and wide complex tachycardia (QRS 162 msec) following inadvertent administration of 100 mg flecainide instead of the intended 17 mg. Intravenous lipid emulsion was started approximately 11 minutes after arrival to the emergency department with a 1 mL/kg bolus followed by an infusion of 165 mL/hour (0.25 mL/kg/min). At 26 minutes post-arrival, the patient was also given a 2 mEq/kg IV bolus of 4% sodium bicarbonate. Three minutes later, the patient's blood pressure improved to 104/63 mmHg and her QRS complex and QTc intervals were 62 msec and 356 msec, respectively. The rest of her hospital course was uneventful (Lookabill et al, 2015). 8) CASE REPORT/CHILD: A 12-month-old boy presented to the emergency department with hypotension (60/40 mmHg), delayed capillary refill and weak central pulses. His medication history included flecainide for management of supraventricular tachycardia. An ECG indicated wide complex tachycardia (133 bpm). His serum flecainide concentration at presentation was 2.57 mcg/mL (reference 0.2 to 1 mcg/mL). After receiving IV fluids and 2 synchronized cardioversion attempts, the patient converted to sinus tachycardia with a wide QRS complex and intermittent episodes of non-sustained ventricular tachycardia. Treatment included IV sodium bicarbonate and norepinephrine, and a 1.5 mL/kg bolus of 20% intravenous lipid emulsion (ILE), followed by a 0.25 mL/kg/hour continuous infusion over a 2-hour period. Thirty minutes after the completion of the infusion, ventricular tachycardia (145 bpm) recurred, and the 20% ILE infusion was restarted, along with administration of sodium bicarbonate and normal saline boluses. Within 20 minutes of beginning the second course of ILE, the patient's cardiovascular status improved with conversion to a wide complex sinus rhythm. Continuation of ILE and sodium bicarbonate for an additional 18 hours resulted in development of a narrow complex rhythm (Szadkowski et al, 2015). F) CARDIOPULMONARY BYPASS OPERATION 1) Yasui et al (1997) report the successful use of peripheral cardiopulmonary bypass support (CBS) in a flecainide overdose to maintain perfusion of the liver in order to facilitate clearance of the flecainide. CBS through the right femoral artery and vein was maintained at 4 L/min in a 20-year-old woman with an initial flecainide serum level of 5.45 mcg/mL. Prior to CBS, aggressive resuscitation attempts with hypertonic saline and transvenous pacing were unsuccessful. Cardiac rhythm improved after 2 hours of CBS to an idioventricular rhythm with narrow QRS complexes, and systolic blood pressure rose to 80 to 100 mmHg. Due to persistent hemorrhage at the cannulation site, CBS was stopped after 10 hours. During CBS, flecainide serum levels rapidly decreased, to a half-life of 6 hr. The substantial reduction in flecainide levels during CBS and effective cardiac rhythm and blood pressure were sustained. Within 10 hr of CBS, flecainide levels decreased to nonlethal levels.
2) CASE REPORT: Corkeron et al (1999) reported the successful use of extracorporeal circulatory support using cardiopulmonary bypass (CPB) in a 20-year-old patient following ingestion of 3000 to 4000 mg flecainide. Prior to CPB the patient showed resistance to increasing doses of adrenalin infusions. CPB was started approximately 5 hours after admission to the ED. Rapid clinical improvement was noted with improved peripheral perfusion, which preceded drug levels falling to the therapeutic range. CPB was weaned progressively and stopped 30 hours after initiation (Corkeron et al, 1999).
G) ACUTE LUNG INJURY 1) ONSET: Onset of acute lung injury after toxic exposure may be delayed up to 24 to 72 hours after exposure in some cases. 2) NON-PHARMACOLOGIC TREATMENT: The treatment of acute lung injury is primarily supportive (Cataletto, 2012). Maintain adequate ventilation and oxygenation with frequent monitoring of arterial blood gases and/or pulse oximetry. If a high FIO2 is required to maintain adequate oxygenation, mechanical ventilation and positive-end-expiratory pressure (PEEP) may be required; ventilation with small tidal volumes (6 mL/kg) is preferred if ARDS develops (Haas, 2011; Stolbach & Hoffman, 2011). a) To minimize barotrauma and other complications, use the lowest amount of PEEP possible while maintaining adequate oxygenation. Use of smaller tidal volumes (6 mL/kg) and lower plateau pressures (30 cm water or less) has been associated with decreased mortality and more rapid weaning from mechanical ventilation in patients with ARDS (Brower et al, 2000). More treatment information may be obtained from ARDS Clinical Network website, NIH NHLBI ARDS Clinical Network Mechanical Ventilation Protocol Summary, http://www.ardsnet.org/node/77791 (NHLBI ARDS Network, 2008)
3) FLUIDS: Crystalloid solutions must be administered judiciously. Pulmonary artery monitoring may help. In general the pulmonary artery wedge pressure should be kept relatively low while still maintaining adequate cardiac output, blood pressure and urine output (Stolbach & Hoffman, 2011). 4) ANTIBIOTICS: Indicated only when there is evidence of infection (Artigas et al, 1998). 5) EXPERIMENTAL THERAPY: Partial liquid ventilation has shown promise in preliminary studies (Kollef & Schuster, 1995). 6) CALFACTANT: In a multicenter, randomized, blinded trial, endotracheal instillation of 2 doses of 80 mL/m(2) calfactant (35 mg/mL of phospholipid suspension in saline) in infants, children, and adolescents with acute lung injury resulted in acute improvement in oxygenation and lower mortality; however, no significant decrease in the course of respiratory failure measured by duration of ventilator therapy, intensive care unit, or hospital stay was noted. Adverse effects (transient hypoxia and hypotension) were more frequent in calfactant patients, but these effects were mild and did not require withdrawal from the study (Wilson et al, 2005). 7) However, in a multicenter, randomized, controlled, and masked trial, endotracheal instillation of up to 3 doses of calfactant (30 mg) in adults only with acute lung injury/ARDS due to direct lung injury was not associated with improved oxygenation and longer term benefits compared to the placebo group. It was also associated with significant increases in hypoxia and hypotension (Willson et al, 2015). H) SEIZURE 1) Administer benzodiazepines (IV lorazepam 1 to 5 mg) for initial control. Consider phenobarbital or propofol if seizures are not controlled with benzodiazepines. 2) SUMMARY a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
3) DIAZEPAM a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
b) PEDIATRIC DOSE: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
4) NO INTRAVENOUS ACCESS a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
5) LORAZEPAM a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
c) PEDIATRIC DOSE: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2010; Chin et al, 2008).
6) PHENOBARBITAL a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
7) OTHER AGENTS a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012): 1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).
I) HYPOTENSIVE EPISODE 1) SUMMARY a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
2) DOPAMINE a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
3) NOREPINEPHRINE a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005). b) DOSE 1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
4) EPINEPHRINE a) ADULT 1) BOLUS DOSE: 1 mg intravenously/intraosseously every 3 to 5 minutes to treat cardiac arrest (Link et al, 2015).
2) INFUSION: Prepare by adding 1 mg (1 mL of 1:1000 (1 mg/mL) solution) to 250 mL D5W, yielding a concentration of 4 mcg/mL, and infuse this solution IV at a rate of 1 mcg/min to 10 mcg/min (maximum rate) (Lieberman et al, 2010). Used primarily for severe hypotension (systolic blood pressure 70 mm Hg), or anaphylaxis associated with hemodynamic or respiratory compromise, may also be used for symptomatic bradycardia if atropine and transcutaneous pacing are unsuccessful or not immediately available (Peberdy et al, 2010).
b) PEDIATRIC 1) CARDIOPULMONARY RESUSCITATION: INTRAVENOUS/INTRAOSSEOUS: OLDER INFANTS/CHILDREN: 0.01 mg/kg (0.1 mL/kg of 1:10,000 (0.1 mg/mL) solution); maximum 1 mg/dose. May repeat dose every 3 to 5 minutes (Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sorrentino, 2005). ENDOTRACHEAL: OLDER INFANTS/CHILDREN: 0.1 mg/kg (0.1 mL/kg of 1:1000 (1 mg/mL) solution). Maximum 2.5 mg/dose (maximum total dose: 10 mg). May repeat every 3 to 5 minutes (Kleinman et al, 2010; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008). Follow ET administration with saline flush or dilute in isotonic saline (1 to 5 mL) based on the child's size (Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
2) INFUSION: Used for the treatment of refractory hypotension, bradycardia, severe anaphylaxis. DOSE: 0.1 to 1 mcg/kg/min, titrate dose; start at lowest dose needed to reach desired clinical effects. Doses as high as 5 mcg/kg/min may sometimes be necessary. High dose epinephrine infusion may be useful in the setting of beta blocker poisoning (Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
c) CAUTION 1) Extravasation may cause severe local tissue ischemia (Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008); infusion through a central venous catheter is advised.
J) BRADYCARDIA 1) ATROPINE/DOSE a) ADULT BRADYCARDIA: BOLUS: Give 0.5 milligram IV, repeat every 3 to 5 minutes, if bradycardia persists. Maximum: 3 milligrams (0.04 milligram/kilogram) intravenously is a fully vagolytic dose in most adults. Doses less than 0.5 milligram may cause paradoxical bradycardia in adults (Neumar et al, 2010). b) PEDIATRIC DOSE: As premedication for emergency intubation in specific situations (eg, giving succinylchoine to facilitate intubation), give 0.02 milligram/kilogram intravenously or intraosseously (0.04 to 0.06 mg/kg via endotracheal tube followed by several positive pressure breaths) repeat once, if needed (de Caen et al, 2015; Kleinman et al, 2010). MAXIMUM SINGLE DOSE: Children: 0.5 milligram; adolescent: 1 mg. 1) There is no minimum dose (de Caen et al, 2015).
2) MAXIMUM TOTAL DOSE: Children: 1 milligram; adolescents: 2 milligrams (Kleinman et al, 2010).
2) ISOPROTERENOL INDICATIONS a) Used for temporary control of hemodynamically significant bradycardia in a patient with a pulse; generally other modalities (atropine, dopamine, epinephrine, dobutamine, pacing) should be used first because of the tendency to develop ischemia and dysrhythmias with isoproterenol (Neumar et al, 2010).
b) ADULT DOSE: Infuse 2 micrograms per minute, gradually titrating to 10 micrograms per minute as needed to desired response (Neumar et al, 2010).
c) CAUTION: Decrease infusion rate or discontinue infusion if ventricular dysrhythmias develop(Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
d) PEDIATRIC DOSE: Not well studied. Initial infusion of 0.1 mcg/kg/min titrated as needed, usual range is 0.1 mcg/kg/min to 1 mcg/kg/min (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
3) PACEMAKER a) Insertion of a transvenous pacemaker should be considered early the course of patients with persistent bradycardia (Hanley et al, 1998).
K) MYOCARDIAL DYSFUNCTION 1) INTRA-AORTIC BALLOON PUMP a) An intra-aortic balloon pump has been used during the acute phase of flecainide overdose associated with severe myocardial depression (Timperley et al, 2005). 1) CASE REPORT: Following an overdose of flecainide (24 hour post-ingestion serum level 2340 mcg/L; normal 200-700 mcg/L), a 47-year-old woman with a history of hypertension and paroxysmal atrial fibrillation presented with a 4-hour history of severe central chest pain. On admission, she was unresponsive with a GCS of 6 and had a heart rate of 70 bpm and blood pressure of 60/40 mmHg. ECG revealed atrial fibrillation and broad QRS complexes (320 ms) with a sine wave appearance. She was treated with thrombolysis (IV alteplase) for a presumptive diagnosis of an acute myocardial infarction. Echocardiogram revealed cardiogenic shock with severely impaired left ventricular function, and angiography showed normal coronary arteries. Following the use of an intra-aortic balloon pump and inotropic support, she improved over 48 hours, with QRS duration and left ventricular function returning to normal (Timperley et al, 2005).
L) EXTRACORPOREAL MEMBRANE OXYGENATION 1) CASE REPORT: Auzinger & Scheinkestel (2001) reported the successful use of extracorporeal membrane oxygenation (ECMO) to treat a 30-year-old man following an overdose of 6000 mg flecainide. ECMO was started approximately 4 hours after the overdose when no clinical improvement was seen following fluid resuscitation, high dose epinephrine infusion and transvenous pacing. ECMO was continued for 26 hours when stable cardiac function with decreasing pump flow and almost normalized conscious state were noted. Flecainide blood concentration had decreased to 3.4 mcmol/L (1611 ng/L) by 32 hours (Auzinger & Scheinkestel, 2001).
2) CASE REPORT: A 52-year-old woman, with a history of paroxysmal atrial fibrillation, Gitelman syndrome with hypokalemia, and depression, presented with an out-of-hospital cardiac arrest. Prior to presentation, the patient had been unresponsive. An ECG, performed by paramedics, revealed a wide complex QRS complex and severe bradycardia, requiring external pacing. The patient subsequently developed pulseless electrical activity which resolved with successful cardiopulmonary resuscitation. At presentation, the patient was tachycardic and hypotensive (90/55 mmHg), despite vasopressor therapy. Laboratory analysis revealed severe hypokalemia (1.7 mmol/L), a bicarbonate concentration of 16 mmol/L, a lactic acid concentration of 10 mmol/L, and a flecainide concentration of 4.13 mcg/mL (reference range 0.2 to 1 mcg/mL). Intravenous lipid emulsion therapy and extracorporeal life support (ECLS) were initiated. Within a few hours after beginning ECLS therapy, The patient experienced hemodynamic and rhythm stabilization. ECLS was weaned off over the next 24 hours, and the patient recovered and was discharged (Sivalingam et al, 2013).
3) CASE REPORT: A 33-year-old woman presented to the emergency department with mental status changes following an overdose ingestion of flecainide. After presentation, the patient developed ventricular tachycardia that progressed to cardiac arrest and was successfully resuscitated following defibrillation and administration of sodium bicarbonate. The patient was intubated, at which time a sodium bicarbonate infusion and lipid emulsion therapy were initiated. An ECG revealed a heart rate of 109 beats/min, a PR interval of 236 msec, a QTc interval of 439 msec, and an initial QRS interval of 92 msec widening to 156 msec. Narrowing of the QRS interval occurred with repeat sodium bicarbonate doses, but attempts to wean the patient from the sodium bicarbonate or lipid emulsion infusions resulted in recurrent unstable ventricular tachycardia (VT). Following transfer to the intensive care unit, the patient developed VT cardiac arrest and, after several resuscitative attempts and subsequent return of spontaneous circulation, the patient was placed on extracorporeal membrane oxygenation (ECMO), resulting in a return to neurologic baseline and subsequent discharge on hospital day 12 (Brumfield et al, 2015).
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