Abstract
The identification and treatment of paroxysmal sympathetic hyperactivity (PSH) still present a significant challenge. We assessed the efficacy of pharmacological agents in treating PSH symptoms and the validity of the diagnostic scales in a cohort of Hispanic patients. A retrospective chart review of cases from a single hospital was conducted in 464 records. Exclusion criteria included underlying conditions such as severe infection. Only nine patients remained in the cohort after examining their clinical records, corresponding to the following diagnoses: traumatic brain injury, subdural hemorrhage, anoxic or ischemic encephalopathy, pneumocephalus, and cerebral palsy. Using the PSH likelihood scale, six of the nine patients were identified with a score of 17 or higher, corresponding to a “probable” PSH, and three patients obtained a score between 8 and 16, corresponding to a “possible” PSH diagnosis. The top three classes of medications used were beta-blockers, antipyretics, and opioids. Benzodiazepines and neuromodulators were also frequently used in patients with trauma, but not in the ones with non-traumatic injuries. Interestingly, 75% of the patients have prescribed levothyroxine as a home medication after the PSH presentation. Medication administration did not follow a specific pattern, suggesting high variability in the management of PSH within our setting, requiring further research. Our results suggest that the pituitary axis might be involved in the progression of PSH. Establishing a specific medical code (e.g., ICD-10) describing PSH as a single entity is essential for appropriate identification and management.
Highlights
Excessive sympathetic nervous system activity can develop after severe acquired brain injury.The sympathetic discharge can have a striking presentation with paroxysmal tachycardia, arterial hypertension, tachypnea, hyperthermia, and decerebrate posturing occurring in response to afferent stimulation [1]
The initial report obtained from the hospital included 464 encounters that fit the diagnostic criteria for the presence of four or more of the symptoms related to paroxysmal sympathetic hyperactivity (PSH), after applying exclusion
We found that all patients received beta-blockers, which is the first line of treatment for tachycardia
Summary
Excessive sympathetic nervous system activity can develop after severe acquired brain injury.The sympathetic discharge can have a striking presentation with paroxysmal tachycardia, arterial hypertension, tachypnea, hyperthermia, and decerebrate posturing occurring in response to afferent stimulation [1]. Excessive sympathetic nervous system activity can develop after severe acquired brain injury. Clinical features resembling paroxysmal sympathetic hyperactivity (PSH). Paroxysmal Sympathetic Hyperactivity in Hispanics hyperthyroidism, pulmonary embolism, substance withdrawal, serotonin syndrome, sepsis, pheochromocytoma, neuroleptic malignant syndrome, or malignant hyperthermia. Initial description, the same syndrome has had over 31 different labels Some of these labels were descriptive (e.g., dysautonomia, autonomic storms, or sympathetic storms), some referred to an assumed epileptic mechanism (e.g., autonomic seizures), and some to the site of damage [e.g., hypothalamic storms; [3,4,5]]. The current consensus is that autonomic hyperactivity in PSH concerns only the sympathetic nervous system [1, 6, 7]. The absence of a clear definition or terminology for PSH was probably a consequence of its under-recognition, despite its relatively high incidence after severe brain damage [8, 9], the well-recognized association with morbidity [1, 10], and increased health- care and societal costs [11]
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