Paroxysmal sympathetic hyperactivity in a child with stroke: a case report

Autor: Jay Bhagwat Jomalkar, Vineetha Vijayan, Avanti Rajendra Saoji, Abhinaya Vaidyanathan, Praveen Unki, Santosh Kondekar, Surbhi Rathi, Chandrahas T. Deshmukh
Jazyk: angličtina
Rok vydání: 2023
Předmět:
Zdroj: Egyptian Pediatric Association Gazette, Vol 71, Iss 1, Pp 1-5 (2023)
Druh dokumentu: article
ISSN: 2090-9942
DOI: 10.1186/s43054-023-00184-9
Popis: Abstract Background Paroxysmal sympathetic hyperactivity (PSH) is the result of dysregulated autonomic function with sympathetic symptoms characterised by increased heart rate, respiratory rate, blood pressure and temperature with abnormal posture, which predominately occur periodically but can be persistent in severe cases. Common causes that present in similar fashion such as infectious process (bacteremia, meningitis, etc.); non-PSH neurological deterioration (increased intracranial pressure, intracranial haemorrhage, intracranial oedema, seizures, encephalitis); pulmonary embolism; thyrotoxicosis, alcohol or drug withdrawal; neuroleptic malignant syndrome; serotonin syndrome; and malignant hyperthermia need to be excluded before diagnosing PSH. The earlier the diagnosis made, the better the prognosis. Case presentation We report a case of a 3-year-old male child who was a diagnosed case of Tetralogy of Fallot presented with left focal seizure with secondary generalisation. Child also had respiratory complaints prior to convulsion. He had developed signs of raised intracranial pressure. Blood culture sent to rule out infective endocarditis was negative. CT brain showed bilateral diffuse cortical infarct. Child developed signs and symptoms of PSH such as fever, tachycardia, tachypnoea, hypertension, diaphoresis, dystonia and bilateral completely dilated pupils. Other common causes such as infective endocarditis, increased intracranial pressure, intracranial oedema, intracranial haemorrhage, seizure, encephalitis and infectious processes (bacteremia, meningitis and infective endocarditis) were ruled out. The diagnosis of PSH was made and started on propranolol along with clonidine. Child responded well to the treatment. Conclusion The complex pathophysiology of PSH warrants extensive work-up to rule out other common causes. The outcome of our patient shows the importance of early diagnosis and multidisciplinary treatment for better outcome.
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