Daniel Pan, BA
Medical Student
University of Pittsburgh School of Medicine
Pittsburgh, Pennsylvania, United States
Siulam Koo, DO
Fellow Physician
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania, United States
Patricia Maina, MD
Resident Physician
University of Pittsburgh Medical Center
Pittsburgh, Pennsylvania, United States
Gary Galang, MD
Physician
UPMC
Pittsburgh, Pennsylvania, United States
Ventriculoperitoneal shunt malfunction; Posttraumatic hydrocephalus; Ventriculoperitoneal shunt infection
Case Description:
A healthy 16-year-old male presented as a level 1 trauma with grade 3 diffuse axonal injury and multi-compartmental hemorrhages requiring craniectomy, ventricular shunt placement, and cranioplasty. He was admitted to inpatient rehabilitation (IPR) in a minimally conscious state 2 months later. During IPR, the patient emerged, making significant functional improvements, but exhibited paroxysmal sympathetic hyperactivity (PSH) episodes of fevers, tachycardia, and hypertension immediately after downtitration of sympatholytics such as propranolol and bromocriptine. Basic infectious workup was negative, and neuroimaging revealed increased left-sided ventricular caliber. Invasive neurosurgical shunt investigation revealed Staphylococcus epidermidis colonization and distal shunt obstruction. The patient underwent shunt revision followed by systemic antibiotics, and subsequently made exponentially greater gains in speech production, swallow, initiation, and ambulation. His sympatholytics were successfully downtitrated, and he was discharged home with family support.
Discussions:
PSH, due to excitation from the structural disconnect of inhibitory pathways, is diagnosed after ruling out causes with overlapping presentations (e.g. septicemia) and typically resolves within weeks of acute traumatic brain injury (TBI). This case of PSH months after injury was unusual – the first we heard of – as this patient was improving and traditional workup was unremarkable except for ventricular dilation, which could be due to gray matter atrophy after injury. Only invasive diagnostics, including mechanical evaluation and cultures, were able to identify sympathetic hyperactivity due to shunt malfunction and occult infection, rather than ongoing inhibitory pathway damage. The patient made greater gains after proper treatment, solidifying this unconventional diagnosis.
Conclusions:
In TBI patients with ventricular shunts, obstruction and occult infection can be causes of sympathetic hyperactivity and sympatholytic hypersensitivity, even without functional or clinical decline. The standard PSH assessment algorithm can then easily be unrevealing, so all possible etiologies in these scenarios should be considered to guide necessary treatment.
