Paroxysmal sympathetic hyperactivity following acute diffuse brain swelling due to traumatic brain injury: a case report with good clinical outcome

Abstract

Background Paroxysmal sympathetic hyperactivity (PSH) may occur after acquired brain injury. The clinical presentation of PSH results from increased sympathetic overdrive, including transient paroxysms of tachycardia, hypertension, hyperventilation, hyperthermia, dystonic posturing, and excessive sweating. The exact pathophysiology of PSH, however, remains unclear, and no definitive treatment is available. Herein, the authors report a case of PSH in a male patient who experienced acute brain swelling after acquired head injury, for which a good clinical outcome was achieved due to multimodal treatment. The ensuing discussion also addresses the pathophysiology of PSH. Case presentation An 18-year-old man was transported to the authors’ hospital after experiencing a traumatic brain injury. On admission, computed tomography revealed cerebral herniation due to diffuse brain edema in the left parietal lobe. Emergency decompressive craniotomy and internal decompression were performed. After surgery, anti-edema therapy (glycerol and mannitol) was continued. Ten days postoperatively, PSH was diagnosed in accordance with the PSH assessment score (20 points). Vecuronium, fentanyl, morphine, propofol, dexmedetomidine, and a calcium channel blocker were administered; however, the drug effect was insufficient. Thirty-two days postsurgery, the patient gradually recovered from the adrenergic symptoms of PSH, and head computed tomography performed 32 days after surgery revealed improvement in diffuse brain edema. Ultimately, the patient fully recovered and lived independently at home. Conclusions Considering the pathophysiology of PSH, cerebral contusion, acute brain swelling, and secondary mechanisms of brain injury may trigger sympathetic nerve-enhancing regions and cause hyperexcitation of the sympathetic nervous system, resulting in PSH. The outcome of the present case demonstrates that PSH can be reversed if it is identified early and before it becomes irreversible, that is, post the development of hypoxic encephalopathy or widespread brain damage. Appropriate management, including decompression craniotomy for brain swelling and multidisciplinary treatment, leads to good clinical outcomes.

The Role of Dexmedetomidine in Paroxysmal Sympathetic Hyperactivity: A Systematic Review

“…Following screening and appraisal, 13 pieces of literature were included in this systematic review, comprising 5 cohort analyses and 8 case reports of 178 patients diagnosed with PSH (Table 3). [11][12][13][14][15][16][17][18][19][20][21][22][23] Etiologies included TBIs, ICHs, autoimmune encephalitis, anoxic/ischemic brain injury, and hypoglycemia. Dexmedetomidine was administered to 48 (27%) patients for the acute treatment of PSH and 50 (28%) patients for prophylaxis.…”

“…The efficacy of dexmedetomidine in PSH treatment was evaluated in 12 studies, with 4 cohort analyses and 8 case reports. 11,[13][14][15][16][17][18][19][20][21][22][23] Reductions in paroxysm severity and frequency were observed in 44 of 48 patients after therapy. 11,[13][14][15][16][17]19,20,21 Etiologies of TBIs, ICHs, anoxic/ischemic brain injury, and autoimmune encephalitis were documented within this group.…”

“…11,[13][14][15][16][17][18][19][20][21][22][23] Reductions in paroxysm severity and frequency were observed in 44 of 48 patients after therapy. 11,[13][14][15][16][17]19,20,21 Etiologies of TBIs, ICHs, anoxic/ischemic brain injury, and autoimmune encephalitis were documented within this group. Dexmedetomidine was infused at 0.1-1.0 mcg/kg/h for durations of 3-7 days with or without 1-mcg/kg loading doses.…”

“…11,[14][15][16][17]19,23 PSH etiologies of the 4 patients who failed dexmedetomidine therapy include anoxic/ischemic brain injury, TBIs, and hypoglycemia. 15,16,21,22 Infusions of 200 mcg/day and 0.1-0.3 mcg/ kg/h were utilized in this group. 15,21 Prophylactic use of dexmedetomidine was compared with other sedatives (midazolam, propofol, and diazepam) in 1 study of 90 postsurgical patients with TBIs.…”

“…15,16,21,22 Infusions of 200 mcg/day and 0.1-0.3 mcg/ kg/h were utilized in this group. 15,21 Prophylactic use of dexmedetomidine was compared with other sedatives (midazolam, propofol, and diazepam) in 1 study of 90 postsurgical patients with TBIs. 12 Fifty patients were administered dexmedetomidine as a 0.08-mcg/kg loading dose followed by 0.25-0.75-mcg/ kg/h infusions with a goal duration of 5 days; the mean total treatment duration dose was 6.08 ± 2.95 mcg.…”