A report of probable paroxysmal sympathetic hyperactivity syndrome in a patient with necrotizing fasciitis
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A report of probable paroxysmal sympathetic hyperactivity syndrome in a patient with necrotizing fasciitis Sarah Fraser, MD . Daniel H. Ovakim, MD
Received: 28 December 2019 / Revised: 15 April 2020 / Accepted: 17 April 2020 Ó Canadian Anesthesiologists’ Society 2020
To the Editor, Paroxysmal sympathetic hyperactivity (PSH) is a well described syndrome of increased sympathetic nervous system activity, typically seen following traumatic brain injury, with rare reports in the setting of central nervous system infection, brain malignancy, and anoxic brain injury following cardiac arrest.1–3 We wish to share an unusual case following disseminated Group B Streptococcus infection. A 51-yr-old man with a medical history notable only for hypertension was vacationing in Jamaica when he developed unilateral knee pain and swelling. This prompted his early return to Canada and presentation to the emergency department where he was diagnosed with septic arthritis in his left knee and necrotizing fasciitis in his left leg and right arm. Synovial fluid and blood cultures were positive for Group B Streptococcus. He was admitted to the intensive care unit (ICU) and underwent several surgical debridement procedures to control the infection. His course in the ICU was complicated by septic shock, acute kidney injury requiring continuous renal replacement therapy, Candida albicans fungemia, and prolonged mechanical ventilation. After 12 ICU days, the patient’s clinical status had stabilized, his candidemia had cleared,
S. Fraser, MD Department of Medicine, University of British Columbia, Victoria, BC, Canada D. H. Ovakim, MD (&) Department of Emergency & Critical Care Medicine, Island Health Authority, Vancouver, BC, Canada e-mail: [email protected] Department of Medicine, University of British Columbia, Vancouver, BC, Canada
he had transitioned to intermittent hemodialysis, and he was successfully extubated. He remained in the ICU because of ongoing hydromorphone and dexmedetomidine infusions and heavy nursing requirements for wound care and dressing changes. Other than a brief (\ 30 sec) desaturation episode (SpO2 \ 75%), there was no documented hypoxemia that could have precipitated anoxic brain injury. On ICU day 14, two days after extubation, and within one hour of an uneventful dressing change, the patient acutely became tachycardic, hypertensive, diaphoretic, hyperthermic, and hypertonic with extensor posturing. This episode resolved with an increase in both the opioid and dexmedetomidine infusions. For several days, he continued to experience at least one similar episode daily, each lasting 20–45 min. A particularly severe episode presented with a respiratory rate of 40 breathsmin-1, drenching diaphoresis, severe hypertension (systolic 253 mmHg), tachycardia at 142 beatsmin-1, and hyperthermia (Tmax 38.6°C). While these episodes typically followed dressing changes, turns, or bathing, several developed without an identifiable trigger and were not preceded by reductions in opioid doses. In anticipation of
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