Calming the Storm: Dysautonomia for the Pediatrician

Identification and Management of Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury

“…The presence of these symptoms was related to some unexpected events, such as higher overall mortality, longer recovery time, higher risk of infection, and other worse outcomes (7). Meanwhile, some unforeseen comorbidities, such as cardiac involvement, weight loss, heterotopic ossification, and immunodepression, invariably accompany the core symptoms of PSH (40)(41)(42)(43). For instance, resting energy expenditure in the paroxysmal state was three times higher than baseline, and weight loss was 25-29% in patients when entering the rehabilitation stage (3).…”

“…Currently, many reports have presented empirical evidence for the early identification of PSH after TBI. Although PSH cannot be diagnosed accurately by laboratory examination, a diagnosis of exclusion should rule out the following: infectious disease (e.g., pneumonia or sepsis), drug-induced disease (e.g., fever or neuroleptic malignant syndrome), rhabdomyolysis, dehydration, seizures, pulmonary embolism, or deep vein thrombosis (43). In TBI patients, negative microbial cultivation of blood, cerebrospinal fluid, airway secretion, or urine provides clues for exclusion.…”

“…Traditional views hold that obstacles to the development of PSH treatment are the following: (1) insufficient understanding of brain regions, (2) no definite relationship between neurotransmitters or hormones and clinical symptoms, (3) lack of standardized measures to assess the curative effect, and (4) insufficient evidence from clinical trials regarding the benefits of intervention for long-term outcomes (2,3,10,65,66). However, significant progress has been made in the management of this complication with the goals of avoiding the triggering event, relieving excessive sympathetic nerve activity, and alleviating adverse effects (3,43,65). Prior to treatment, the first step is discerning the necessity and urgency of which symptoms need to be priority processed (43).…”

“…However, significant progress has been made in the management of this complication with the goals of avoiding the triggering event, relieving excessive sympathetic nerve activity, and alleviating adverse effects (3,43,65). Prior to treatment, the first step is discerning the necessity and urgency of which symptoms need to be priority processed (43). For instance, the key step in treatment of PSH patients with hyperhidrosis is sufficient fluid replacement, rather than control of the sympathetic outbreak, because dehydration will reduce consciousness, and either positive pharmacotherapy or external cooling is critical for hyperthermia, as fever is inherently harmful (19).…”

“…Then, different types of core symptoms that are involved in the different phase of PSH should be determined. How to apply pharmacotherapy and supplementary treatment in the interval phase and whether to adopt supportive therapy during the rehabilitation stage are the most common problems faced by clinicians, by far (3,43). Previous experience holds that there is a sympathetic positive feedback loop in patients with long-term duration that is impossible to disrupt, making treatment all the more difficult (67).…”