Abstract and Introduction
Following acute multiple trauma, hypothalamic stimulation of the sympathetic nervous system and adrenal glands causes an increase in circulating corticoids and catecholamines, or a stress response. In individuals with severe traumatic brain injury or a Glasgow Coma Scale score of 3-8, this response can be exaggerated and episodic. A term commonly used by nurses caring for these individuals to describe this phenomenon is storming. Symptoms can include alterations in level of consciousness, increased posturing, dystonia, hypertension, hyperthermia, tachycardia, tachypnea, diaphoresis, and agitation. These individuals generally are at a low level of neurological activity with minimal alertness, minimal awareness, and reflexive motor response to stimulation, and the storming can take a seemingly peaceful individual into a state of chaos. Diagnosis is commonly made solely on clinical assessment, and treatment is aimed at controlling the duration and severity of the symptoms and preventing additional brain injury. Storming can pose a challenge for the nurse, from providing daily care for the individual in the height of the storming episode and treating the symptoms, to educating the family. Careful assessment of the individual leads the nurse to the diagnosis and places the nurse in the role of moderator of the storming episode, including providing treatment and evaluating outcomes.
After acute trauma, an immediate sympathetic surge provides the needed rapid response to compensate for the effects of the injury (Keller & Williams, 1993; Neil-Dwyer, Cruickshank, & Doshi, 1990; Stanford, 1994). The outward expressions of this surge are hypertension (HTN), hyperthermia, pupillary dilatation, tachycardia, cardiac arrhythmias, profuse sweating, an increased release of glucose, and an increased basal metabolic rate (Cartlidge & Shaw, 1981; Stanford). Some individuals suffering severe traumatic brain injury (TBI) have demonstrated a spontaneous episodic exaggerated stress response, or storming (Baguley, Nicholls, Felmingham, Crooks, Gurka, & Wade, 1999; Boeve, Wijdicka, Benarroch, & Schmidt, 1998; Bricolo, Turazzi, Alexandre, & Rizzuto, 1984; Bullard, 1987; Do, Sheen, & Brumfield, 2000; Hackl et al., 1991; Horntagl et al., 1980; Keller & Williams; Klug et al., 1984; Neil-Dwyer, Cruickshank, & Doshi; Pranzatelli, Palvlakis, Gould, & DeVivo, 1991; Rosner, Newsome, & Becker, 1984; Rossitich & Bullard, 1988; Russo & O'Flaherty, 2000; Strum, 2002; Thorley, Wertsch, & Klingbeil, 2001). Strum speculates that 15%-33% of individuals who suffer severe TBI will demonstrate storming, a poor prognostic indicator (Boeve et al.; Do, Sheen, & Brumfield; Pranzatelli et al.; Rossitich & Bullard; Strum).
Sympathetic storming tends to be associated with lower neurological functional level and can be caused by injury or pressure created by tumors, hydrocephalus, or subarachnoid hemorrhage, though it is most commonly seen in the TBI population (Baguley et al., 1999; Boeve et al., 1998; Do, Sheen, & Brumfield, 2000; Darnell & Arbit, 1993; Keller & Williams, 1993; Russo & O'Flaherty, 2000; Strum, 2002; Thorley et al., 2001). This article specifically addresses sympathetic storming after TBI and reviews history, proposed etiology, clinical presentation, assessment parameters, differential diagnosis, treatment, family education, and the role of the nurse.
J Neurosci Nurs. 2004;36(1) © 2004 American Association of Neuroscience Nurses
Cite this: Riding Out the Storm: Sympathetic Storming after Traumatic Brain Injury - Medscape - Feb 01, 2004.