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Management of Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury
Introduction
Paroxysmal sympathetic hyperactivity (PSH) is a dysautonomic syndrome characterized by paroxysmal and episodic increases in sympathetic and motor activity ( ). PSH occurs after severe acquired brain injury of diverse etiology, and core clinical features of PSH include tachycardia, hypertension, tachypnea, hyperthermia, diaphoresis, and increased motor activity ( ). Additional clinical features may include agitation, mydriasis, decreased level of consciousness, horripilation, and flushing. Most reported cases of PSH follow traumatic brain injury (TBI), stroke, and anoxic brain injuries ( ); however, case reports of patients with PSH have also included etiologies such as hydrocephalus ( ) and encephalitis ( ). Although the clinical presentation is similar across etiologies ( ), we will focus on PSH after TBI.
Nomenclature
The syndrome that we refer to as PSH has been known by at least 31 other names in the published literature ( ); common terms include dysautonomia, sympathetic storm, diencephalic or autonomic seizures, autonomic dysfunction or storm, and paroxysmal autonomic instability with dystonia. The Consensus Working Group proposed that the term PSH accurately and specifically describes the syndrome without making an assumption about the underlying pathology driving the symptoms and thus should be the term used to unify literature on the syndrome ( ).
Incidence
In the first seven days post-TBI, autonomic arousal is very common; the incidence in an ICU population of individuals with severe TBI reached 92% ( ). However, not all of the individuals with autonomic arousal experience it to a pathological level. PSH incidence estimates range from 8% to 33% in the moderate-severe TBI population ( ), though the higher estimates are likely inflated due to inconsistencies in diagnostic criteria (eg, diagnosis at time of admission to hospital; ) and inclusion criteria (eg, febrile patients in the ICU; ). Incidence of PSH in patients with moderate-severe TBI who survive to rehabilitation is estimated to be 5.3% ( ). Reports of PSH in the pediatric literature are rarer, but estimates of incidence in children with acquired brain injury range from 9.7% ( ) to 14% ( ).
Diagnostic Criteria
A previous literature review yielded nine unique sets of diagnostic criteria for PSH ( ); the authors called for the establishment of standard diagnostic criteria by expert consensus. In 2014, the aforementioned Consensus Working Group identified 11 criteria for the diagnosis of PSH ( ). In this chapter we classify these 11 criteria by precipitating factor, episode onset, frequency/duration, clinical features, differentiation, and management ( Table 9.1 ). Likelihood of PSH diagnosis is based on the number of diagnostic criteria met, as well as the severity of the clinical features (eg, tachycardia or tachypnea); failure to meet all diagnostic criteria does not imply lack of PSH. PSH is a diagnosis of exclusion; alternative diagnoses to be ruled out include infection, seizures, edema, deep vein thrombosis, pulmonary emboli, hypoxia, thyroid storm, myocardial infarction, drug withdrawal, pain, anxiety, neuroleptic malignant syndrome, malignant hyperthermia, lethal catatonia, Cushing reflex, and spinal cord injury ( ).
Table 9.1
Diagnostic Criteria for PSH ( )
| Category | Diagnostic Criteria |
|---|---|
| Precipitating factor | Antecedent acquired brain injury |
| Episode onset | Episodes are paroxysmal in nature |
| Frequency/duration | Features persist ≥3 consecutive days |
| Features persist ≥2 weeks postinjury | |
| ≥2 episodes daily | |
| Clinical features | Clinical features occur simultaneously |
| Sympathetic overreactivity to normally nonpainful stimuli | |
| Absence of intraparoxysmal parasympathetic features during episodes | |
| Differentiation | Features persist despite treatment of alternative differential diagnoses |
| Lack of alternative explanations | |
| Management | Medication administered to decrease sympathetic features |
Risk Factors
The majority of published literature on PSH consists of case reports, so understanding of risk factors for PSH is limited. However, published cohort studies suggest that younger age ( ), male sex ( ), and increased severity of injury (eg, presence of diffuse axonal injury, brainstem injuries, preadmission hypoxia; ) may be risk factors for PSH after TBI.
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