Cardiac arrest s/p ingestion
58yF w/ unknown PMHx arrives via EMS in cardiac arrest. Per EMS, patient called 911 stating that she wanted to kill herself. When they arrived they found her pulseless on the floor with a bag of medications beside her, all containing at least some pills. No drugs, liquids, alcohol or other items found strewn beside her. Medications found in her bag her bag, some in multiples, listed alphabetical order: Baclofen, Gabapentin, Hydromorphone, Hydroxyzine, Ibuprofen, Methocarbamol, Simvastatin
EMS initiated ACLS, placing an ETT and a L tibial IO, w/ 2 rounds of epinephrine and 2mg Narcan administered, with a total of 15-25 mins of prearrival CPR.
On arrival to ED in persistent PEA arrest, ACLS was continued with adjunct medications given as deemed appropriate. Approximately 5-10 minutes after arrival, after several rounds of ACLS, ROSC was achieved. Hypothermia protocol started, epinephrine drip started for persistent hypotension, and an ECG was obtained.
Gen: Nonresponsive, inubtated
HEENT: No abrasions/lacerations/echymoses to scalp or face. Pupils dilated b/l, nonreactive, white sclera. Lacerations to internal mucosa of inferior lip, and to anterior tongue, oozing blood
7.0 ETT visualized through cords, 21 cm at lips.
Neck: no echymoses or crepitus
Chest: Breath sounds CTAB w/ manual ventilation, palpable broken ribs, no heart sounds
Abdomen: soft nondistended no ecchymosis or lividity
Extremities: no palpable pulses, no gross deformity, no track marks or lacerations noted
RRR and LAFB. Rate 132. PR 210, QRS 192, QTc 605
What do you think caused cardiac arrest? By what mechanism or mechanisms? (There may be multiple answers)
Hydroxyzine likely caused an arrhythmia through cardiac sodium channel blockade.
Apart from epinephrine, what adjunct therapeutics would you consider during ACLS and afterward in this case? Should intralipid be administered?
Sodium Bicarbonate is the antidote for sodium channel blockade and should be administered. Intralipid may be administered in this case but its routine use is controversial.
What other interventions could you consider in this case?
Consider gastric decontamination
Though multiple drugs can be implicated in arrest, we postulate hydroxyzine as the culprit here, though other medications on the list may have potentiated the arrest if ingested
Hydroxyzine is a first generation H1-antagonist. While classical antimuscarinic effects take place at mild and moderate overdoses, severe overdoses can be complicated by sodium channel blockade that can manifest in a wide complex unstable tachycardia. QTc prolongation can also occur, likely due to hydroxyzine binding the HERG potassium channel. Both abnormalities were noted on the post-ROSC ECG. By a similar mechanism, seizures can also be precipitated by severe overdose, and there was some evidence (lip laceration) that this patient may have sustained a seizure.
Hydromorphone can cause respiratory arrest and opiates can precipitate hypotension, but would not cause a wide-complex tachyarrhythmia. Further, the time course of events seems to argue against this agent’s responsibility.
One can create a long list of toxicological antidotes but unfortunately there is no single cocktail to administer to every toxicological arrest that comes through the door. In our case, the indicated adjunct is Sodium Bicarbonate, to help overcome sodium channel blockade. This was given in boluses and then a drip with narrowing of the QRS seen on post ROSC ECG.
Though the ingested opioid is less likely the main cause of cardiac arrest, Naloxone may be a reasonable choice and is recommended in any cardiac arrest with known opioid ingestion. Additionally post-ROSC hypotension may be a result of the ingested opioid Hydromorphone, which could respond favorably to reversal.
The usage of intravenous fat emulsion (ILE), branded as Intralipid, is evolving and controversial. While originally discovered as a therapy in cases of IV local anesthetic toxicity, enthusiasm has led to its use in a more widespread manner, in particular with cardiotoxic Calcium Channel Blocker and Beta-Blocker overdose.
Evidence is extremely limited, however, both in ILE’s indications and its dosing. Though there are several proposed mechanisms for how the 20% free fatty acid mixture limits drug toxicity, the prevailing theory is the “lipid sink model” in which lipid soluble drugs are trapped and contained by the emulsion, reducing the amount distributing into tissue.
Even as case reports continue to be published reporting success in ILE use for a wide range of toxic overdoses, including for anticholinergics, expert opinion and recommendations have (as of Fall 2016) shifted away from indicating ILE in life threatening toxicity except in cases of IV local anesthetic toxicity. There remains a neutral recommendation in cases of cardiac arrest. The considerations for this recommendation include a large-scale review of all available evidence of ILE administration by drug class. There has even been concern that ILE administration in cases of oral overdose could increase toxicity by increasing absorption of a drug from the GI tract.
In our case ILE was administered but was not recommended by toxicology after consultation.
If ILE is administered, dosage is as follows:
Initial bolus: 1.5 ml/kg ideal body weight over 1 minute
Repeat bolus up to two times if refractory
Maximum 10ml/kg over first 30 minutes.
GI decontamination is an intervention that should be considered in every oral poisoning, though efficacy remains controversial.
Historically, syrup of ipecac was commonly used to induce emesis in acute ingestion and was sold in small quantities over-the-counter for first aid kit use. The use of Ipecac is no longer recommended by any expert organization after accumulated evidence failed to demonstrate any benefit to the intervention, one that has potential side effects.
Gastric lavage is another former mainstay of decontamination that remains popular in developing countries but has largely fallen by the wayside in the US except in limited circumstances. The ingestion must have been within the previous hour – so that pills may still be within the stomach – and the patient must have a protected airway. Data does not support the procedure’s efficacy and the risks of the procedure are serious. GL does not necessarily lead to complete decontamination, is potentially distracting in its time and labor intensiveness, and has a number of serious risks including water toxicity, esophageal damage (especially in cases of corrosive ingestion), airway compromise and aspiration. The procedure requires the passage of a very large orogastric 36-40 gauge tube, historically called an Ewald tube, into the stomach followed by serial administration of fluids and aspiration of contents. After ROSC in our patient, this procedure was attempted as the patient was intubated and met the timeframe of ingestion, but it was subsequently aborted when resistance was met in passing the tube – a contraindication to continuing.
Activated charcoal administration is the choice intervention for decontamination. Administered charcoal prevents toxin absorption by binding them to its vast total surface area, with subsequent safe passage through the GI tract into the feces. It can also increase elimination of toxins that undergo enterohepatic cycling. Similar to other discussed interventions, there is no evidence demonstrating clear clinical benefit to the therapy.
Expert opinion again recommends its use if administered within 1 hour of ingestion (can be done after lavage), but some studies suggest later administration may still significantly decrease drug absorption. Downsides to activated charcoal are poor palatability (difficult to flavor as flavors are adsorbed), frequent post-administration vomiting, and potential aspiration w/ severe complications. Administration to intubated patients via NG tube results in fewer complications. The black cakey material that forms in the mouth when charcoal is administered can also potentially complicate future attempts at intubation, and will certainly prevent endoscopy, so if endoscopy is foreseen (such as in caustic ingestions), AC is contraindicated. Dosing is 1 g/kg (25-100g typical dose) in adults and .5-2 g/kg in children.
In our case, activated charcoal administration was attempted but aborted after resistance was felt in the NG tube.
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