Pathophysiology
Excited delirium syndrome (ExDS) is often triggered by drug use of stimulants or hallucinogens as well as psychiatric illness. The drugs often include cocaine, methamphetamine, PCP, LSD, bath salt and synthetic marijuana. It can also be triggered by psychiatric illnesses including schizophrenia and bipolar disorder.
Cocaine is often the drug that is thought to be associated with excited delirium. It was first recognized in the 1980s when there was a spike in ExDS cases. Cocaine works by increasing the amount of dopamine in the central nervous system synapses. Dopamine is the main neurotransmitter in reward pathways which is the reason that cocaine produces extreme euphoria. Cocaine is also a sympathomimetic drug meaning that is is able to manipulate the sympathetic nervous system. Think fight or flight. It causes the abnormal "flight response". This includes tachycardia, tachypnea, hypertension, dilated pupils and increased alertness. These symptoms are often seen in patients with ExDS.
Research has shown that excessive dopamine signaling in the central nervous system has been seen in ExDS. Dopamine has the ability to alter the brain's temperature regulation syndrome which explains the extreme hyperthermia seen in ExDS. Along with cocaine, schizophrenia also alters central dopamine signaling which could explain why schizophrenia patients alone can be at risk for ExDS.
Cocaine is often the drug that is thought to be associated with excited delirium. It was first recognized in the 1980s when there was a spike in ExDS cases. Cocaine works by increasing the amount of dopamine in the central nervous system synapses. Dopamine is the main neurotransmitter in reward pathways which is the reason that cocaine produces extreme euphoria. Cocaine is also a sympathomimetic drug meaning that is is able to manipulate the sympathetic nervous system. Think fight or flight. It causes the abnormal "flight response". This includes tachycardia, tachypnea, hypertension, dilated pupils and increased alertness. These symptoms are often seen in patients with ExDS.
Research has shown that excessive dopamine signaling in the central nervous system has been seen in ExDS. Dopamine has the ability to alter the brain's temperature regulation syndrome which explains the extreme hyperthermia seen in ExDS. Along with cocaine, schizophrenia also alters central dopamine signaling which could explain why schizophrenia patients alone can be at risk for ExDS.
Sudden Cardiac Arrest in ExDS Patients
Excited delirium can cause acidosis, rhabdomyolysis (destruction of muscle cells) and secondary trauma. Studies show that approx. 10% of ExDS patients go into cardiac arrest.
One of the main concerns in ExDS is metabolic acidosis most likely a result of the excessive exertion seen in these patients that results in the formation of lactic acid. The body's way to compensate for the metabolic acidosis is to increase respiratory rate and blow off the excess CO2 in their respiratory system thus attempting to reduce the acidosis the patient is experiencing. Restraining patients in positions that impair ventilation can worsen acidosis since they are unable blow off the excess CO2. Restraining patients at all may also worsen metabolic acidosis because it may cause patients ability to fight more against the restraints and produce more lactic acid.
Rhabdomyolysis which is the breakdown of muscles is often seen in ExDS. The hyperthermia, agitation and extreme exertion is thought to be responsible for this. As the muscles break down, potassium is released into the system and can produce hyperkalemia in patients. Acute kidney injury may happen due to the increase in myoglobin in the bloodstream. Hypovolemia may also happen because of the extravisation of fluid into the injured muscle.
In the 10% of patients where cardiac arrest occurs, they often experience a brief period of tranquility prior to the arrest and it is something to take into consideration. It has also been found post autopsy that many patients who die of excited delirium have significant cardiovascular diseases. Autopsies often show that patients have severe atherosclerosis and diabetes. Many patients also have cardiomyopathy as a result from chronic cocaine and amphetamine abuse.
When attempting resuscitation of these patients we need to take into consideration the metabolic acidosis, hypoxia and hypovolemia. We may also need to consider pre existing cardiovascular diseases.
One of the main concerns in ExDS is metabolic acidosis most likely a result of the excessive exertion seen in these patients that results in the formation of lactic acid. The body's way to compensate for the metabolic acidosis is to increase respiratory rate and blow off the excess CO2 in their respiratory system thus attempting to reduce the acidosis the patient is experiencing. Restraining patients in positions that impair ventilation can worsen acidosis since they are unable blow off the excess CO2. Restraining patients at all may also worsen metabolic acidosis because it may cause patients ability to fight more against the restraints and produce more lactic acid.
Rhabdomyolysis which is the breakdown of muscles is often seen in ExDS. The hyperthermia, agitation and extreme exertion is thought to be responsible for this. As the muscles break down, potassium is released into the system and can produce hyperkalemia in patients. Acute kidney injury may happen due to the increase in myoglobin in the bloodstream. Hypovolemia may also happen because of the extravisation of fluid into the injured muscle.
In the 10% of patients where cardiac arrest occurs, they often experience a brief period of tranquility prior to the arrest and it is something to take into consideration. It has also been found post autopsy that many patients who die of excited delirium have significant cardiovascular diseases. Autopsies often show that patients have severe atherosclerosis and diabetes. Many patients also have cardiomyopathy as a result from chronic cocaine and amphetamine abuse.
When attempting resuscitation of these patients we need to take into consideration the metabolic acidosis, hypoxia and hypovolemia. We may also need to consider pre existing cardiovascular diseases.
Recognition of Excited Delirium Syndrome
According to the 2009 ACEP White Paper, patients may present with the following symptoms/behaviors. The frequency of occurrence is in parentheses. These are all noted in the PA 2017 ALS protocols.
- Exceptional/abnormal pain tolerance (100%)
- Tachypnea (100%)
- Tactile hyperthermia (95%)
- Unusual strength (90%)
- Police noncompliance (90%)
- Lack of tiring against restraint (90%)
- Inappropriate clothing for environmental temperature (70%)
- Violent and paranoid behavior
- Rapid development of symptoms
- Rapidly fluctuating periods of calm and then delirium
Treatment Per PA Protocols
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