Article, Emergency Medicine

Paroxysmal sympathetic hyperactivity after near-hanging

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American Journal of Emergency Medicine

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Paroxysmal sympathetic hyperactivity after near-hanging?,??,?


Paroxysmal sympathetic hyperactivity (PSH) isa relatively common early complication after severe brain injury. It is characterized by episod- ic generalized sympathetic hyperactivity. We herein present a case of a 29-year-old woman who developed PSH after near-hanging with uncer- tainty of cardiac arrest. The patient attempted suicide by hanging herself. Her mother found her pulseless and in a deep coma and started chest compressions. Upon arrival at our hospital, spontaneous breathing was restored and her vital signs stabilized; however, she remained in a deep coma. After admission to the intensive care unit, generalized tonic-clonic convulsions developed and her body temperature increased to 39.2 ?C despite Surface cooling. We presumed that she had been in car- diac arrest when her mother discovered her and initiated 24-hour ther- apeutic hypothermia (TH) and 24-hour rewarming. After rewarming, her temperature increased to 38.7 ?C again despite the disappearance of her convulsions, and she suddenly exhibited a decerebrate posture, muscle stiffness, pupillary dilatation, Elevated blood pressure, and tachy- cardia by repeated extrinsic stimulation. She was diagnosed with PSH, and medical treatment and fever management were begun. The PSH began to resolve, and she was transferred to another hospital for rehabil- itation in a Persistent vegetative state without PSH on the 42nd hospital day. In this case, TH was utilized for Anoxic brain injury after near- hanging with uncertain cardiac arrest. A clinical course of PSH after near-hanging is presented with a brief review of TH indication.

Paroxysmal sympathetic hyperactivity (PSH) is a recently recog- nized syndrome characterized by episodic high fever, diaphoresis, tachycardia, tachypnea, hypertension, papillary dilation, and muscle hy- peractivity. Traumatic brain injury is the most common etiology of PSH, followed by anoxic brain injury [1-3]. We herein present a case of PSH following anoxic brain injury caused by near-hanging.

A 29-year-old woman attempted suicide by hanging herself. Her mother found her pulseless and in deep coma and started chest com- pressions. When an ambulance service arrived at the scene 8 minutes later, the patient was still in a deep coma and her pupil diameter was

5.0 mm bilaterally with no light reaction. She was not spontaneously breathing, but her Radial artery was palpable. En route to our hospital, spontaneous breathing was restored with bag-bulb mask ventilation. On arrival 30 minutes after the emergency call, her Glasgow Coma Scale score was 3 and her pupils were reactive. Her other vital signs were stable (blood pressure, 114/60 mmHg; heart rate, 127 beats/ minute; respiratory rate, 16 breaths/minute; SpO2, 100% under Oxygen administration at 5 L/minute). Her blood gas analysis results were as

? Competing interests: None.

?? Funding sources: None.

? Acknowledgements: None.

follows: pH, 7.354; pCO2, 26.4 mmHg; pO2, 415.1 mmHg; HCO3,

14.4 mmol/L; BE, -9.7 mmol/L; lactate, 10.33 mmol/L. No abnormalities were found on brain computed tomography (Fig. 1). When she was admitted to the intensive care unit, Therapeutic hypothermia was not initially indicated.

The patient remained in a coma, and 3 hours after arrival, a focal con- vulsion appeared in her mouth and neck and spontaneously ceased. Two hours after this initial focal seizure, generalized tonic-clonic convulsions developed and her body temperature increased to 39.2 ?C despite sur- face cooling. Intravenous diazepam was repeatedly administered, but the effect was temporary. Initiation of TH at 34 ?C was planned, but her mother hesitated regarding this as aggressive treatment. Therefore, the patient did not undergo general anesthesia for TH until 13 hours after arrival. Valproic acid (1200 mg/day) was also administered to stop the convulsions. After 24-hour TH and 24-hour rewarming, the pa- tient remained in a coma without visible convulsions. Magnetic reso- nance imaging on the fifth hospital day revealed diffuse cortical ischemia predominantly in the occipital lobes (Fig. 2). Her body temper- ature increased to 38.7 ?C again, and she suddenly exhibited a decere- brate posture, muscle stiffness, pupillary dilatation, elevated systolic blood pressure at 150 mmHg, and tachycardia of 120/bpm upon postur- al change. These episodes developed whenever attempting a body posi- tion change or oral care and continued for about 20 minutes. Electroencephalography revealed low-voltage, diffuse slow-wave activ- ities, but no epileptogenic discharge. We began treatment with gabapentin (1200 mg/day) and fever management under a diagnosis

Fig. 1. No abnormalities in the parasagittal watershed region were found on computed tomography upon presentation.

0735-6757/(C) 2014

Fig. 2. diffusion-weighted imaging on the fifth hospital day (a-c) showing diffuse brain injury, most prominently in the posterior parietal and occipital cortices.

of PSH. Atenolol (50 mg/day) was added on the seventh hospital day, and bromocriptine (7.5 mg/day) was added to treat the persistent PSH. On the tenth hospital day, the PSH began to resolve, and only tachy- cardia and pupillary dilation were seen once or twice daily with stimu- lation. No increased blood pressure, diaphoresis, or decerebrate posture occurred, although the tachycardia and pupillary dilation remained. On the 42nd hospital day, she was transferred for rehabilita- tion in a persistent vegetative state without PSH.

Our patient developed biphasic fever elevation soon after arrival and again after rewarming of TH. The first episode of hyperthermia together with the convulsions suggested severe brain injury, and the second episode was triggered by stimuli and accompanied by sympathetic hy- peractive dysfunction, meeting the criteria for PSH. Notably, high fever after TH may be a PSH symptom and should be treated. Although effec- tive treatment of PSH may be challenging, control of the fever and ad- ministration of medication to mitigate the sympathetic storm are mandatory to avoid secondary brain injury.

Hyperthermia is a common occurrence in patients following brain injury. Secondary injury such as excitotoxicity, free radical generation, inflammation, apotosis, and genetic responses to the injury may also de- velop [4]. TH is recommended and widely used for comatose adult pa- tients with return of spontaneous circulation after out-of-hospital cardiac arrest [5] and neonatal Hypoxic-ischemic encephalopathy [6]. TH may mitigate anoxic brain injury due to near-hanging, but there is controversy regarding whether TH should be applied for near-hanging victims without cardiac arrest [7-9]. Because asphyxic cardiac arrest causes more severe and widespread injury than does ventricular fibrillation-induced cardiac arrest of the same duration [10], there is a rationale for early TH application for patients without confirmed cardiac arrest. Delayed TH induction has little benefits. Several recent studies have shown that patients who underwent TH after hanging-induced cardiac arrest had Good neurologic outcomes and suggested a potential benefit of TH even in Unconscious patients after near-hanging without cardiac arrest at the scene [11,8,12]. Regrettably, TH initiation was de- layed in our patient; the high fever and generalized convulsions obvi- ously exacerbated her brain injury. TH, if indicated, should be rapidly applied for comatose patients after near-hanging. Further prospective studies are crucial to establish a treatment strategy of TH for anoxic brain injury and PSH.

Atsushi Fujiwara, MD? Hitoshi Kobata MD, PhD

Osaka Mishima Emergency Critical Care Center

?Corresponding author. Department of Anesthesiology Osaka Medical College, 2-7 Daigaku-Machi, Takatsuki Osaka 569-8686, Japan

Tel.: +81 72 683 1221; fax: +81 72 684 6552

E-mail address: [email protected]


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