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BACKGROUND

Episodes of acute agitation in children and adolescents can range from a state of unrest and anxiety with low frustration tolerance to a state of fear, anger, and/or pain expressed through verbal or physical aggression. An episode of agitation can pose a significant safety risk to the agitated youth, nearby patients, family members, and hospital staff. Thus identifying an episode of acute agitation at its earliest stage is desirable. There are nonpharmacological and pharmacological interventions that can be used to reduce agitation. If there is imminent risk of harm to self and/or others, and there is no less restrictive intervention available to prevent or interrupt harm, medication and/or physical restraints are indicated. This chapter discusses the assessment, management, and prevention of acute agitation in the pediatric population.

ETIOLOGY

Agitation and aggression can have biological and/or psychosocial contributors. Accordingly, a thorough clinical evaluation in the context of both a medical and social history, and treatment of identified contributing factors, is required for all agitated patients.1

Risk factors for acute agitation include a recent history of agitation, impaired cognitive functioning/brain injury, delirium, recent psychosocial stressors and loss, substance use/withdrawal, specific medication side effects (psychotropic medications, steroids, etc.), a prior history of violence or assault as a victim and/or perpetrator, a prior history of physical restraint, acute medical illness, pain, worsening of a chronic medical condition, and various psychiatric and developmental disorders (Figure 138-1). Agitation can occur in multiple psychiatric conditions, including attention deficit hyperactivity disorder (ADHD), post-traumatic stress disorder (PTSD), bipolar disorder, autism spectrum disorders, agitated unipolar depression, impulse control disorders, disruptive behavior disorders, childhood psychosis, and developmental disorders. Agitation is not a marker for a specific diagnosis; rather, agitation manifests across multiple psychiatric disorders and is often indicative of illness severity. It is unclear whether agitation is the same across psychiatric disorders in quality, cause, and treatment response.2

FIGURE 138-1.

Risk identification algorithm.

Multiple studies support the characterization of two subtypes of aggression: impulsive aggression (IA) and planned aggression (PA). Epidemiological research shows differences between IA and PA in both antecedent events and developmental trajectories (IA is associated with poor peer relationships, inadequate problem-solving skills, and a history of physical abuse; PA is associated with aggressive role models who positively value violent behavior). Animal studies indicate that IA and PA are linked to different patterns of brain activation.2 The orbitofrontal cortex, medial prefrontal cortex, hypothalamus, and amygdala are proposed brain systems involved in the modulation of aggression and impulsivity. Behavioral and pharmacological interventions can be effective in reducing aggressive behavior, regardless of subtype, although IA is often more amenable to pharmacological interventions.3 Much of the information presented in this chapter relates to the impulsive subtype of aggression, which is referred to as acute agitation.

CLINICAL PRESENTATION

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