Identification and Management of Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury

Zheng, Ruizhe; Lei, Zhong-Qi; Yang, Runze; Huang, GQ; Zhang, Guangming

doi:10.3389/fneur.2020.00081

Cited by 54 publications

(81 citation statements)

References 92 publications

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“…[6][7][8] Medical treatments for PSH include combinations of µ-opioid receptor agonist (morphine), non-selective ß-receptor blocker (propranolol), α 2 -receptor agonist (clonidine), GABA-receptor agonist (gabapentin), dopaminereceptor antagonist (bromocriptine) and benzodiazepines (diazepam) to abort or minimize PSH episodes via inhibition of sympathetic flow, afferent sensory process and effector end organ response. [6][7][8][11][12][13][14] Early diagnosis and optimized treatment is believed to shorten ICU stay, facilitate patient recovery and minimize physical disability. In conclusion, 'clinical scoring' was used to dignose PSH, since there was no any confirmatory test.…”

Section: Discussionmentioning

confidence: 99%

<p>Diagnosis and Treatment of Paroxysmal Sympathetic Hyperactivity in Medical ICU, University of Gondar Hospital, Northwest Ethiopia: A Case Report</p>

Bekele

Mesfin

Hailu

et al. 2020

IMCRJ

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Background Paroxysmal sympathetic hyperactivity (PSH) is a neurologic syndrome characterized by paroxysmal and simultaneous occurrence of hypertension, hyperpyrexia, tachycardia, tachypnea, diaphoresis and dystonic posturing due to surge in sympathetic outflow after acquired brain injuries. Diagnosis of PSH is made using the paroxysmal sympathetic hyperactivity-assessment measure (PSH-AM) score, which comprises “clinical features severity” (CFS) score and “diagnosis likelihood tool” (DLT) score. Case presentation A 35-year-old woman diagnosed to have echo-proven chronic rheumatic heart disease for 25 years. Percutaneous balloon mitral valvotomy was done 6 weeks previously for severe mitral stenosis. Left atrial thrombus was detected after the procedure and anticoagulant (warfarin) was initiated. She presented with severe headache and repeated vomiting of 1 day duration on arrival to the hospital. She had frequent seizure attacks with subsequent loss of consciousness on third day of admission. Diagnosis of status epilepticus secondary to intracranial hemorrhage due to warfarin toxicity was made after CT-scan revealed acute subdural hematoma and ventricular bleeding. Then she was transferred to medical intensive care unit (ICU), intubated and put on mechanical ventilator. Anti-epileptic drugs, antibiotics, vitamin K and fresh frozen plasma were given. She developed paroxysms of hypertension, tachycardia, tachypnea, hyperpyrexia, diaphoresis and decerebrate posturing after 7 days of neurological insult. She had normal inter-ictal EEG tracing during cyclic autonomic surge. CFS score was 11 and DLT score was 10. In sum, PSH-AM score was 21, suggested “probable” diagnosis of PSH. Morphine, diazepam, propranolol and gabapentin were given in combination to treat PSH. Severity of autonomic storm started to improve on second week of ICU admission. On the third week of admission, her clinical condition deteriorated suddenly, she developed asystole and died of cardiac arrest despite cardiopulmonary resuscitation (CPR). Conclusion 'Clinical scoring' was used used to diagnose PSH, since there was no any confirmatory test. Cocktail of drugs were required to treat catecholamine surge in PSH.

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Section: Discussionmentioning

confidence: 99%

<p>Diagnosis and Treatment of Paroxysmal Sympathetic Hyperactivity in Medical ICU, University of Gondar Hospital, Northwest Ethiopia: A Case Report</p>

Bekele

Mesfin

Hailu

et al. 2020

IMCRJ

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“…TBI causes paroxysmal sympathetic hyperactivity (PSH) manifested by increases in sympathetic activity involved in heart rate, blood pressure, respiratory rate and other. PSH has been reported in 33 % patients suffering from severe TBI and associated with poorer outcome (16,17). Hypoxia and hypotension following TBI are recognized as a signifi cant secondary disorder associated with a poor outcome (18).…”

Section: Physiological Factorsmentioning

confidence: 99%

The initial factors affecting in-hospital mortality rate of patients undergoing surgery for post-traumatic extra-axial hematomas

Kulesza¹,

Mazurek²,

Szmygin³

et al. 2020

BLL

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INTRODUCTION: Traumatic brain injury (TBI) is one of the most important causes of disability and death among young adults and referred to as "silent" epidemic. The most frequent consequences of a TBI are extra-axial hematomas, comprising of acute subdural (SDH) and epidural hematoma (EDH). Most of the factors affecting the mortality have been analyzed in a wide group of TBI. The aim of this study is to identify factors affecting in-hospital mortality in patients undergoing surgery for acute traumatic subdural and epidural hematoma. PATIENTS AND METHODS: The study included 128 patients operated on due to extra-axial hematomas. Twenty-eight patients were operated on for EDH and 100 on for SDH. Patients were treated at the Department of Neurosurgery Medical University in Lublin, during almost three years. The following factors were analyzed: demographic data, physiological factors, laboratory factors, computed tomography scan characteristics and time between the trauma and the surgery. All the factors were correlated with in-hospital mortality rate. RESULTS: The univariate analysis has confi rmed the infl uence of many factors affecting the in-hospital mortality. CONCLUSION: It is interesting that factors such as GSC score, systolic blood pressure, respiratory rate and glycemia were associated with in-hospital mortality rate with highly statistically signifi cant differences (Tab. 3, Fig. 2, Ref. 40).

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“…Both the onset and the duration of the episodes are variable, ranging from less than 2 weeks to many months; in some cases, residual dystonia and spasticity persist chronically after the sympathetic storms subside. Notably, PSH may clinically resemble other entities such as malignant catatonia or neuroleptic malignant syndrome and may share triggers such as neuroleptic agents [15]. However, the temporal dissociation between motor signs such as mutism, posturing, staring, immobility, rigidity and autonomic signs such as tachycardia and hypertension allow distinction between NMS and PSH.…”

Section: Introductionmentioning

confidence: 99%

Storms and silence: a case report of catatonia and paroxysmal sympathetic hyperactivity following cerebral hypoxia

2020

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Background Delayed Post Hypoxic Leukoencephalopathy (DPHL) is a syndrome that occurs after hypoxia, and can present with a variety of neuropsychiatric symptoms, including catatonia and paroxysmal sympathetic hyperactivity (PSH). The gold standard for the treatment of catatonia is electroconvulsive therapy (ECT). However, ECT can exacerbate the paroxysms of sympathetic hyperactivity and complicate recovery from DPHL. The treatment of PSH is not well established. Case presentation We present a case of a patient with multiple opiate overdoses who presented with altered mental status. He was diagnosed with catatonia and subsequently treated with ECT. His clinical condition worsened, and a revised diagnosis of PSH was established. The patient’s condition improved with medical management. Conclusion This case highlights the need to distinguish between these two related symptom clusters, as the incidence of DPHL and opioid overdose related neuropsychiatric problems increase. This distinction can greatly influence the course of treatment, and the need to consider alternative treatments.

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Identification and Management of Paroxysmal Sympathetic Hyperactivity After Traumatic Brain Injury

Cited by 54 publications

References 92 publications

<p>Diagnosis and Treatment of Paroxysmal Sympathetic Hyperactivity in Medical ICU, University of Gondar Hospital, Northwest Ethiopia: A Case Report</p>

<p>Diagnosis and Treatment of Paroxysmal Sympathetic Hyperactivity in Medical ICU, University of Gondar Hospital, Northwest Ethiopia: A Case Report</p>

The initial factors affecting in-hospital mortality rate of patients undergoing surgery for post-traumatic extra-axial hematomas

Storms and silence: a case report of catatonia and paroxysmal sympathetic hyperactivity following cerebral hypoxia

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