Delirium
Answer: D.
This patient is experiencing a subcategory of delirium called excited delirium (or agitated delirium). A similar syndrome called “Bell’s mania” was described in the late 1800s in institutionalized patients. The literature becomes somewhat silent on this presentation in the 1950s with the advent of antipsychotic medications. Since de-institutional policies were enacted in the 1980s, a steady increase in what is now called excited delirium syndrome (ExDS) has been documented.
ExDS is characterized by delirium, agitation, and hyperadrenergic autonomic dysfunction, typically in the setting of acute on chronic drug abuse or serious mental illness. These patients are reported to have superhuman strength and to be susceptible to further agitation by external stimulus. A summary of typical findings follows:
This patient is experiencing a subcategory of delirium called excited delirium (or agitated delirium). A similar syndrome called “Bell’s mania” was described in the late 1800s in institutionalized patients. The literature becomes somewhat silent on this presentation in the 1950s with the advent of antipsychotic medications. Since de-institutional policies were enacted in the 1980s, a steady increase in what is now called excited delirium syndrome (ExDS) has been documented.
ExDS is characterized by delirium, agitation, and hyperadrenergic autonomic dysfunction, typically in the setting of acute on chronic drug abuse or serious mental illness. These patients are reported to have superhuman strength and to be susceptible to further agitation by external stimulus. A summary of typical findings follows:
Modified from source: ACEP Task Force on Excited Delirium Syndrome, 2009
The diagnosis and treatment of delirium is always medical, and the morbidity and mortality of ExDS is significantly higher than in other delirious patients. Although a thorough history and physical examination are important in the diagnosis and total management of this man (A), he must be controlled now. The emergency physician must intervene immediately in order to support a favorable outcome. Sedation with midazolam can be given via the intranasal, intramuscular, or intravenous routes; this may be a good adjunct in gaining some control for definitive IV access. Haloperidol and diphenhydramine may be given initially IM, if an IV is not readily available. Although all of these medications may be given by mouth or intraosseously, these routes are impractical and will likely to agitate the patient more, respectively.
Serotonin syndrome is also characterized by autonomic hyperactivity. The Hunter Criteria are sensitive and specific for serotonin syndrome; the patient should have at least one of the following: spontaneous clonus; inducible clonus AND agitation or diaphoresis; ocular clonus AND agitation or diaphoresis; tremor AND hyperreflexia; hypertonia AND temperature above 38 ºC AND ocular clonus or inducible clonus. This is a clinical diagnosis and important to discern, as inadvertently adding a serotonergic agent such as fentanyl or atypical antipsychotics such as olanzapine and risperdone may exacerbate the presentation.
Based on retrospective data, ExDS has been linked to sudden death, often associated with prolonged ‘hog-tie’ or ‘hobble-position’ or electroshock weapons (i.e. Taser use) (D). Despite observational data, the true etiology and risk factors for ExDS are unclear. However, consensus recommendations include avoidance of prone positioning during restraint, as this does not allow for proper chest rise and oxygenation/ventilation, and the ExDS patient is particularly prone to dysrhythmias (as well as lack of regard for self-preservation). Risk of death in ExDS is likely increased with physiologic stress – all efforts should be made for minimizing inciting stressors and for rapid control of symptoms and signs of ExDS.
Acute psychosis from untreated schizophrenia or bipolar disorder or psychotropic withdrawal or non-adherence may mimic ExDS (B). The ExDS patient, however, presents in an exaggerated manner, and will likely manifest a marked lactic acidosis and rhabdomyolysis not commonly seen otherwise (see above table).
The risk of death is likely increased with physiologic stress. Attempts to minimize such stress are needed in the management of these patients. Other causes of agitation and sudden death include Takutsubo’s cardiomyopathy (Broken Heart Syndrome, caused by severe emotional distress), Cannon’s Voodoo Death (“cursed” patients who become agitated and fulfill their belief in their impending death), Lethal Catatonia (hyperkinetic type, with slow onset, agitation, fever, exhaustion, death) and Sudden Unexplained Death in Epilepsy (SUDEP). Although the differential diagnosis must remain open (C, as in Takutsubo cardiomyopathy), the emergency physician must secure the patient’s (and staff’s) security and initiate therapy based on limited information.
Other causes of acute violent behavior are hypoglycemia (rapidly ruled out at the bedside), heat stroke (which does not typically include profound acidosis as it does here), and encephalitis, among others.
The diagnosis and treatment of delirium is always medical, and the morbidity and mortality of ExDS is significantly higher than in other delirious patients. Although a thorough history and physical examination are important in the diagnosis and total management of this man (A), he must be controlled now. The emergency physician must intervene immediately in order to support a favorable outcome. Sedation with midazolam can be given via the intranasal, intramuscular, or intravenous routes; this may be a good adjunct in gaining some control for definitive IV access. Haloperidol and diphenhydramine may be given initially IM, if an IV is not readily available. Although all of these medications may be given by mouth or intraosseously, these routes are impractical and will likely to agitate the patient more, respectively.
Serotonin syndrome is also characterized by autonomic hyperactivity. The Hunter Criteria are sensitive and specific for serotonin syndrome; the patient should have at least one of the following: spontaneous clonus; inducible clonus AND agitation or diaphoresis; ocular clonus AND agitation or diaphoresis; tremor AND hyperreflexia; hypertonia AND temperature above 38 ºC AND ocular clonus or inducible clonus. This is a clinical diagnosis and important to discern, as inadvertently adding a serotonergic agent such as fentanyl or atypical antipsychotics such as olanzapine and risperdone may exacerbate the presentation.
Based on retrospective data, ExDS has been linked to sudden death, often associated with prolonged ‘hog-tie’ or ‘hobble-position’ or electroshock weapons (i.e. Taser use) (D). Despite observational data, the true etiology and risk factors for ExDS are unclear. However, consensus recommendations include avoidance of prone positioning during restraint, as this does not allow for proper chest rise and oxygenation/ventilation, and the ExDS patient is particularly prone to dysrhythmias (as well as lack of regard for self-preservation). Risk of death in ExDS is likely increased with physiologic stress – all efforts should be made for minimizing inciting stressors and for rapid control of symptoms and signs of ExDS.
Acute psychosis from untreated schizophrenia or bipolar disorder or psychotropic withdrawal or non-adherence may mimic ExDS (B). The ExDS patient, however, presents in an exaggerated manner, and will likely manifest a marked lactic acidosis and rhabdomyolysis not commonly seen otherwise (see above table).
The risk of death is likely increased with physiologic stress. Attempts to minimize such stress are needed in the management of these patients. Other causes of agitation and sudden death include Takutsubo’s cardiomyopathy (Broken Heart Syndrome, caused by severe emotional distress), Cannon’s Voodoo Death (“cursed” patients who become agitated and fulfill their belief in their impending death), Lethal Catatonia (hyperkinetic type, with slow onset, agitation, fever, exhaustion, death) and Sudden Unexplained Death in Epilepsy (SUDEP). Although the differential diagnosis must remain open (C, as in Takutsubo cardiomyopathy), the emergency physician must secure the patient’s (and staff’s) security and initiate therapy based on limited information.
Other causes of acute violent behavior are hypoglycemia (rapidly ruled out at the bedside), heat stroke (which does not typically include profound acidosis as it does here), and encephalitis, among others.