Short Description

This algorithm outlines the steps to guide the lay rescuer to efficiently identify and manage a person with cardiac arrest due to an opioid overdose.

Algorithm at a Glance

• The lay rescuer identifies when an individual may have had an opioid overdose.
• In cardiac arrest, the rescuer begins high-quality CPR while waiting for a defibrillator/AED and naloxone.
• Naloxone is administered as soon as it is available and then every 4 minutes as needed.
• CPR and monitoring are maintained continuously.

Goals for the Management of Adult Patients with Opioid Overdose

The lay rescuer will be able to:

• Recognize an opioid-associated life-threatening emergency
• Provide appropriate treatment for an opioid-associated emergency

Adult Opioid Emergency for Lay Rescuers Algorithm

Box 1: The Patient is Assessed and EMS Activated

The layperson rescuer calls for help and sends someone for an AED and naloxone. The layperson checks to determine if the patient is responsive.

Box 2: Is the Patient Breathing Normally?

If the patient is breathing normally, the rescuer proceeds to Box 3. If breathing is NOT normal (gasping or no breathing), they proceed to Box 5.

Box 3: Supporting the Patient

The layperson rescuer maintains an open airway and prepares the patient for transport to the ED. The rescuer should consider the administration of naloxone if available.

Box 4: Continuous Monitoring

While waiting for EMS, the layperson continues to monitor the patient’s breathing and level of consciousness until EMS arrives for transport.

Box 5: Does the Patient Have a Pulse?

If the patient is not breathing, the layperson rescuer provides high-quality CPR and administers naloxone when available. If not trained to provide rescue breaths, the lay rescuer performs hands-only CPR and uses the AED when available.

Administering Naloxone in BLS

Respiratory Arrest

In a patient with likely opiate toxicity with a pulse but respiratory arrest, provide naloxone via IM or IV route with BLS care and resuscitation. (Class Iib, Evidence level C-EO).

Cardiac Arrest

In a patient with likely opiate toxicity without a palpable pulse begin with routine resuscitation with CPR, rather than naloxone. Naloxone IV or IM can be administered if this will not delay CPR, especially if there is doubt about cardiac arrest. (Class Iib, Evidence level C-EO). However, naloxone administration or evaluation of response to naloxone should not delay other higher level care. (Class I, Evidence level C-EO). Patients should be provided higher levels of medical services as needed, even if there is a response to naloxone. (Class Iib, Evidence level C-EO).

Administering Naloxone in ACLS

If respiratory arrest is evident, support the airway and ventilation and provide naloxone. (Class I, Evidence level C-LD).Bag mask ventilation scan be provided until reversal of respiratory arrest, and intubation and other advanced technique should be pursued if naloxone is ineffective

Cardiac Arrest

Follow the typical treatment of cardiac arrest with compressions and ventilations. No recommendations regarding naloxone use in ACLS is available.

ROSC

Monitor patients until ROSC or normal breathing have resumed. Ensure normal mentation and vital signs. (Class I, Evidence level C-LD). If opiate toxicity recurs, repeated naloxone dose can be given. (Class Iia, Evidence level C-LD). For patients with life-threatening toxicity or use of long-lasting opiates, it is prudent to observe the patient for longer periods. Additionally, naloxone may be offered in a post-arrest setting to reverse the action of long-lasting opiates. (Class Iib, Evidence level C-EO).

Benzodiazepines

Flumazenil is an antagonist to benzodiazepines in the neurologic system and can oppose neurologic and respiratory depression associated with benzodiazepine toxicity. However, benzodiazepine toxicity should be ensured the medication should not be administered routinely for a coma. Flumazenil should not be given to all coma patients. (Class III; harmful, Evidence level B). Adverse events include seizure (in dependent patients) as well as arrhythmia, hypotension, and seizure when benzodiazepine ingestion is combined with tricyclic antidepressants and other medications.

Carbon Monoxide

This is the most common cause of accidental death from toxins (aside from intentional drug abuse). Carbon monoxide decreases the oxygen-carrying function of hemoglobin and causes direct damage to the brain and heart. There is a high risk of permanent brain damage in survivors. Cardiac arrest associated with carbon monoxide has a very ominous prognosis even if ROSC is attained. However, patients should be managed using the typical treatment of cardiac arrest.  

Hyperbaric Oxygen

This therapy may be beneficial in improving neurologic function following toxicity with carbon monoxide. However, the research is controversial, with some studies showing no benefit. The treatment has little severe side effects and may benefit patients in the acute setting when there is severe toxicity. (Class Iib, Evidence level C). It is reasonable to offer transfer to a setting that can provide the therapy following ROSC if the transport is not considered overly risky. It is important to note that following carbon monoxide toxicity, there is also a prolonged risk of cardiovascular complications regardless of treatment options. 

Methemoglobinemia

This occurs due to an increased level of methemoglobin or iron oxidized forms of hemoglobin in the blood. These forms do not transport oxygen and cause a significant decrease in oxygen delivery to the tissue. There are congenital forms (abnormality in metabolizing methemoglobin to hemoglobin or abnormal non-oxygen carrying forms of hemoglobin) as well as acquired forms due to medical or chemical toxicities. The congenital forms are usually mild but may become symptomatic when individuals are exposed to oxidizing agents. Very mild cases may be asymptomatic; however, clinical cases can lead to central cyanosis that does not respond to oxygen administration. Medications that cause this syndrome are:

• Dapsone
• Nitrates (nitroglycerin, nitrofurantoin, isosorbide dinitrate)
• Anesthetics (lidocaine, benzocaine, prilocaine, procaine)
• Sulfonamides (Bactrim)
• Ciprofloxacin, quinine, metoclopramide, phenazopyridine, phenobarbital, phenelzine, aniline dyes
• Benzene derivatives

These medications or chemical can increase hemoglobin oxidization from 10 to 100 times normal and leads to oxidized forms of hemoglobin that the body cannot metabolically mange. Deoxyhemoglobin levels of 5g/dL are clinically significant. A level below 30% of methemoglobin in a healthy individual is usually clinically insignificant; however, levels between 30-50% will cause cardiac and neurologic impairment such as headaches, tachycardia, weakness, and dyspnea. When levels rise above 50%, patients may have stupor, respiratory depression, seizures, arrhythmias as well as acidosis. Levels between 60-70% are often fatal, and above this level, methemoglobinemia is universally fatal. Note that patients with underlying medical conditions, including anemia, pulmonary, or cardiovascular disease, may be more susceptible. Symptoms usually occur between 20-60 minutes following exposure, and the methemoglobin half-life is 55 minutes.

Arterial blood gasses (ABGs) will not be accurate in patients with methemoglobinemia or other hemoglobin types as ABGs uses the oxygen partial pressure to calculate oxygen saturation, assuming normal hemoglobin. To determine accurate results in these cases, co-oximetry is needed. This uses the absorption of light at various wavelengths to determine the amount of different types of hemoglobin- normal hemoglobin, carboxyhemoglobin, and methemoglobin.

Treatment for mild cases is with stopping the inciting medication or chemical.  Significant cases with signs of hypoxemic tissue will require treatment based on clinical presentation and blood levels of methemoglobin. Treat patients with methylene blue, using 1-2 mg/kg of 1% solution slowly. Patients may need hyperbaric oxygen or exchange transfusion if severe symptoms arise. Ensure continuous monitoring. 

Metabolic Acidosis

Cyanide

Cyanide is a ubiquitous chemical from industrial sources, jewelry cleaning and electroplating solutions as well as a by-product of sodium nitroprusside and amygdalin. It is also a common by-product of fires, and patients with smoke inhalation are at risk of exposure. Additionally, chronic exposure can occur with cyanide rich foods such as cassava or apricot seed.  The typical symptoms include depression of the neurologic system, hypotension, metabolic acidosis, and nares soot. 

Patients may develop cardiac arrest, hypotension, seizures, lactic acidosis, and central apnea. Treatment of cardiac arrest or significant cardiac compromise is with the cyanide scavenger drug: IV hydroxocobalamin, sodium nitrate/inhaled amyl nitrate with subsequent sodium thiosulfate IV. Sodium nitrate and hydroxocobalamin act rapidly. However, nitrites can cause methemoglobin to form, leading to hypotension. On the other hand, hydroxocobalamin is safer, especially in pediatric patients and smoke inhalation. Sodium thiosulfate is a useful adjunct as it improves the effects of the cyanide scavenger. Its main side effect is emesis. The recommended treatment is hydroxocobalamin either in combination with sodium thiosulfate or without. (Class I, Evidence level B).

Salicylates

Toxicity with salicylates may be acute with ingestion over 150mg/kg or chronic with repeated supratherapeutic doses over 100mg/kg each day. Salicylates are widely available at pharmacies or drug stores for a host of indications.

The effects of acute salicylate toxicity include hyperventilation as well as respiratory alkalosis. Cellular ATP is decreased, and metabolic acidosis can occur. Typical symptoms included hyperventilation, nausea, emesis, fever, hearing loss, and decreased consciousness. Patients may also progress to seizures, tachycardia, and dehydration. Laboratory evaluation of ABGs, anion gaps as well as salicylate level can aid in diagnosis. With progression, patients may develop rhabdomyolysis and organ failure.

Patients experiencing chronic toxicity may have less pronounced symptoms such as confusion, dehydration, seizures, and hypotension. Patients may be elderly, and obtaining the diagnosis may be difficult. Treatment includes the administration of activated charcoal, diuresis, and hemodialysis.

• Administer activated charcoal if evidence of adequate bowel function or contraindication. Repeat as needed until clinical improvement
• Diurese using sodium bicarbonate and potassium chloride. This increases urine pH and excretion of salicylate. This can prevent renal failure associated with rhabdomyolysis. 
• Monitor level of salicylate frequently in acute toxicity
• Administer hemodialysis if severe or chronic toxicity. Patients with seizures, respiratory or renal failure, and change in mental status are at higher risk. 
• Administer glucose replacement if a change in mental status even when normoglycemic. 
• Provide supportive care included benzodiazepines to manage seizures as well as cooling in the case of fevers. 
• Toxicity done intentionally from self-harm or malicious intent should be managed in the emergency room. Obtain guidance from a toxicology center.