Riding Out the Storm: Sympathetic Storming after Traumatic Brain Injury

Denise M. Lemke

Disclosures

J Neurosci Nurs. 2004;36(1) 

In This Article

Consequences of Prolonged Sympathetic Output

Prevention of secondary injury is a primary goal in the treatment of TBI. Effects of prolonged sympathetic overactivity (hyperthermia, hyperglycemia, increased basal metabolic rate, hyperhydrosis, dystonia, and increased circulating catecholamines) can increase the risk of secondary brain injury (Baguley et al., 1999; Horntagl et al., 1980; Keller & Williams, 1993; Rosner, Newsome, & Becker, 1984; Stanford, 1994; Strum, 2002). Careful monitoring of the individual is needed to prevent potential problems.

Extreme or prolonged hyperthermia and increased basal metabolic rate with hyperglycemia can result in further neuronal dysfunction, hypoxia, and possible cell death (Baguley et al., 1999; Strum, 2002). Intramuscular (IM) or intravenous (IV) chlorpromazine (Thorazine) can be helpful with severe hyperthermia. Chlorpromazine suppresses hypothalamic activity, diminishing piloerection and allowing for cooling, and can rapidly reduce the core temperature (Strum, 2002). Chlorpromazine can be used in conjunction with acetaminophen and cooling blankets (Strum). Insulin may be required to regulate serum blood glucose within a normal range, and frequent monitoring of blood glucose is required to document trends and determine insulin dosing.

Energy needs can be increased by 100%-200% in the presence of storming (Baguley et al., 1999; Horntagl et al., 1980; Rosner, Newsome, & Becker, 1984; Stanford, 1994; Strum, 2002). The drastic increase in metabolism leads to protein wasting and a catabolic state. This places the individual at risk for weight loss. Weight loss causes a decrease in muscle mass. With dystonia, there is increased risk for contractures, potential for injury, skin breakdown, and further atrophy. These can limit the potential for rehabilitation. Nursing care should be directed at measures such as providing nutritional support, use of splints, padded rails, passive range of motion, and judicious skin care to reduce the risk of problems.

The increased metabolic rate and the presence of hyperhydrosis increase the risk of dehydration and skin breakdown. Dehydration can decrease the ability to mobilize secretions, increasing the risk for pneumonia. An electrolyte imbalance can also occur from prolonged dehydration without adequate fluid replacement. Assessment parameters include close monitoring of serum electrolytes, serum albumin, 24-hour fluid status, and weight. Ongoing dietary involvement can provide the needed adjustment of caloric, protein, and water intake to prevent problems.

Cardiovascular risks can be much higher. Prolonged sympathetic overactivity can result in ECG changes including decreased T wave amplitudes, biphasic T waves, rising ST segments, and ST depression (Horntagl et al., 1980; Keller & Williams, 1993). Sustained sympathetic stimulation can lead to heart damage, which begins as focal myocytolysis related to sustained levels of catecholamines (Horntagl et al.). This can lead to myocardial damage and, if severe, theoretically death (Horntagl et al.; Strum, 2002). Given the variety of symptoms and severity, careful assessment is needed to prevent complications, though the presence of storming does not always warrant care within the ICU setting.

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