(061) A Case Report and Literature Review of Paroxysmal Sympathetic Hyperactivity for Consultation-Liaison Psychiatrists
Abstract: Learning Objectives:
< !1.To inform clinicians about the current etiologies and diagnostic criteria of paroxysmal sympathetic hyperactivity.
Background/significance:
Identifying and tailoring treatment to hyperactive delirium is often complicated by complex medical comorbidities and multiple sedating medication regimens in the critical care unit. Here we present a case of refractory paroxysmal sympathetic hyperactivity (PSH) and highlight the pathophysiology, barriers to diagnosis, and theoretical treatment, in hopes of empowering consultation-liaison psychiatrists to recognize and recommend appropriate treatment.
Case:
51-year-old male presented with septic shock secondary to liver abscess, severe acute respiratory distress, and AKI. Due to worsening respiratory status, he was cannulated for venous-venous ECMO and sedated with propofol, hydromorphone (HM), midazolam, and dexmedetomidine (DEX). On HD29 CL psychiatry began guanfacine 1.5mg TID and valproic acid 1000mg. On HD33 patient was clinically improving and weaned off propofol and midazolam. On HD34 the patient sustained several cerebrovascular accidents and by HD36 developed spontaneous unprovoked vital sign abnormalities unresponsive to boluses of propofol, hydromorphone, and haloperidol. On HD39 patient was placed back on propofol, HM, DEX and continued requiring several classes of PRN medications to control sympathetic hyperactivity. On HD40 patient was diagnosed with PSH with a PSH-Assessment Measure of 14. Phenobarbital, pregabalin, and other short acting β-blockers were utilized for acute episodes, but PSH remained refractory to treatment. By HD46 the patient’s ARDs had significantly worsened leading to withdrawal of care.
Discussion:
PSH is disordered regulation of the autonomic nervous system manifesting with spontaneous episodes of motor and sympathetic activity in various combinations (Baguley, 2008). The PSH Assessment Measure can help guide clinicians as to likelihood of PSH (Baguley, 2014). Pathophysiologically, there is a disconnect of regions of sympathetic activation from regions of sympathetic inhibition (Meyfroidt, 2017). Episodes are characterized by sharp increases in catecholamines and adrenocorticotropic hormone. Pharmacologic treatment includes rapid onset and short half-life medications not traditionally used to manage agitation associated with delirium. Therefore, it is imperative to diagnose and implement treatment that improves long-term recovery potential.
Conclusion:
Given the medical complexity of critical care patients, CL psychiatrists should remain vigilant for PSH and feel confident recommending pharmacologic options typically considered outside of our classic armamentarium.
References: 1.Baguley IJ, Heriseanu RE, Cameron ID, Nott MT, Slewa-Younan S. A critical review of the pathophysiology of dysautonomia following traumatic brain injury. Neurocrit Care. (2008) 8:293–300. doi: 10.1007/s12028-007-9021-3 2.Baguley IJ, Perkes IE, Fernandez-Ortega JF, Rabinstein AA, Dolce G, Hendricks HT, et al. Paroxysmal sympathetic hyperactivity after acquired brain injury: consensus on conceptual definition, nomenclature, and diagnostic criteria. J Neurotrauma. (2014) 31:1515–20. doi: 10.1089/neu.2013.3301