Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

- Rogue Medic

Excited Delirium Strikes without Warning – Part I

In the February issue of JEMS, Dr. Keith Wesley has a very important article about excited delirium and in custody deaths.

According to the U.S. Department of Justice, 47 states and the District of Columbia reported 1,095 arrest-related deaths from 2003–2005.[1]

Assuming that the 2003-2005 means January 01, 2003 through to December 31, 2005, that means 1,095/3 years or 365 in custody deaths per year. Almost an average of one a day. 2004 was a leap year with 366 days. Maybe leap days exert a protective effect against excited delirium. 🙄

Before the proliferation of such less-lethal techniques as CEDs, pepper spray and bean bag rounds, many subjects who were this aggressive met their death from the use of lethal force.[1]

In custody death is nothing new. These deaths just seem less preventable when they are the result of GSWs (Gun Shot Wounds), rather than the now he’s alive – now he’s dead – and he stays dead presentation that is typical for these patients.

Current research reveals excited delirium patients have abnormally altered levels of several neurochemicals in their brain—the most important being dopamine.(4)[1]

This can happen even among those not taking stimulant drugs.

Elevated levels of dopamine cause agitation, paranoia and violent behavior. Heart rate, respiration and temperature control are also affected by dopamine levels with elevation resulting in tachycardia, tachypnea and hyperthermia. For this reason, hyperthermia is a hallmark of excited delirium.[1]

Kind of like hyperventilation syndrome on crack cocaine.

As dopamine levels rise, in combination with the stimulant effects of drugs, the patient’s metabolic activity increases. This results in hyperthermia. The patient becomes acidotic as a result of muscle activity, which has been documented to elevate creatinine phosphokinase—a protein released from muscle death. Metabolic acidosis results in hyperkalemia, which can precipitate dysrhythmias. Therefore, when cardiac arrest occurs, it does so in an environment of severe acidosis and hyperkalemia.(6)[1]

Therefore, when cardiac arrest occurs, it does so in an environment of severe acidosis and hyperkalemia.

A study in Los Angeles reviewed 18 consecutive witnessed arrests from excited delirium. Despite receiving immediate ALS care, all patients died.(8)[1]

Despite receiving immediate ALS care, all patients died.

It may be a good idea to start treatment with calcium (chloride is preferred, but gluconate can work, too).

Why calcium?

1. If this is a case of hyperkalemia, there is no more effective initial treatment than calcium.

2. If this is a case of hyperkalemia, there is nothing that works as quickly as calcium.

3. Even with immediate ALS (Advanced Life Support), nobody seems to be able to resuscitate these patients, so there does not appear to be anything to lose. How can calcium possibly make things any worse?

The resuscitation rate for witnessed arrests should at least equal the resuscitation rate for the community as a whole. These patients do not respond to conventional ACLS (Advanced Cardiac Life Support). Therefore, these patients should not be treated as conventional cardiac arrest patients.

Given the expectation that these patients are hyperkalemic, is it responsible to treat these patients as anything other than hyperkalemic?

If hyperkalemia is left untreated, a sine-wave pattern, idioventricular rhythms, and asystolic cardiac arrest may develop.203,204[2]

ACLS Modifications in Management of Severe Cardiotoxicity or Cardiac Arrest Due to Hyperkalemia
Treatment of severe hyperkalemia aims at protecting the heart from the effects of hyperkalemia by antagonizing the effect of potassium on excitable cell membranes, forcing potassium into cells to remove it promptly from the circulation, and removing potassium from the body. Therapies that shift potassium will act rapidly but are temporary and thus may need to be repeated. In order of urgency, treatment includes the following:

Stabilize myocardial cell membrane:
· Calcium chloride (10%): 5 to 10 mL (500 to 1000 mg) IV over 2 to 5 minutes or calcium gluconate (10%): 15 to 30 mL IV over 2 to 5 minutes[3]

That is the initial treatment for hyperkalemia. That is what EMS should focus on.

Some people will say that we should start with sodium bicarbonate. Ignore them. They do not know what they are talking about. Every responsible organization should make it clear that calcium is the initial treatment for unstable hyperkalemia.

When cardiac arrest occurs secondary to hyperkalemia, it may be reasonable to administer adjuvant IV therapy as outlined above for cardiotoxicity in addition to standard ACLS (Class IIb, LOE C).[3]

Otherwise, there is no reason to believe that these patients will be resuscitated. Similarly, we should focus on calcium when treating cardiac arrest with dialysis patients.

To be continued in Excited Delirium Strikes without Warning – Part II.

Footnotes:

[1] Excited Delirium Strikes without Warning
by Keith Wesley, MD, FACEP
JEMS February 2011 Issue
Tuesday, February 1, 2011
Article

[2] Hyperkalemia
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 12: Cardiac Arrest in Special Situations
Part 12.6: Cardiac Arrest Associated With Life-Threatening Electrolyte Disturbances
Free Full Text From Circulation with link to Free Full Text PDF Download

[3] ACLS Modifications in Management of Severe Cardiotoxicity or Cardiac Arrest Due to Hyperkalemia
2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Part 12: Cardiac Arrest in Special Situations
Part 12.6: Cardiac Arrest Associated With Life-Threatening Electrolyte Disturbances
Hyperkalemia
Free Full Text From Circulation with link to Free Full Text PDF Download

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