DOI: 10.1097/01.ana.0000211029.64667.8b
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PMID: 17198106
Issn Print: 0898-4921
Publication Date: 2007/01/01
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Excerpt
Stridor as a result of vocal cord paralysis secondary to neurologic problems is a known entity.1 Meningomyelocele and Chiari malformations in pediatrics are often reported to be associated with stridor as presenting symptom. The compression of hind brain and herniation along with brain dysgenesis has been related to it.2 Resolution of the symptom follows decompression of associated hydrocephalus, which is an indirect cause of stridor.3,4 In our neurosurgical intensive care unit, we recently encountered an 18 months female child who developed respiratory distress accompanied by stridor. The neonatal history of the child was remarkable for birth by lower segment cesarean section with birth weight of 2 kg and was admitted to Pediatrics Department of our hospital with neonatal jaundice. The jaundice subsided within 2 weeks but the child developed fever and convulsions. Cerebrospinal fluid (CSF) analysis was suggestive of tubercular meningitis. By 23rd day of life the child developed hydrocephalus, for which a ventriculo-peritoneal shunt was performed. At seventh month, the child underwent shunt revision surgery for blocked ventricular end of shunt catheter. The shunt was blocked again at 9 months. This time the lower end of shunt was exteriorized. After few days the child became drowsy. CSF analysis showed increased protein and cellular response, suggestive of bacterial meningitis. A computerized tomography of the head showed bilateral ventriculomegaly, the left ventricle being dilated more than right. The shunt was removed and a left cerebral catheter reservoir was placed under general anesthesia. The right ventricle got compartmentalized and started enlarging. This time a right cerebral catheter reservoir was placed. Regular CSF taps were done. After fever subsided and CSF reports became normal, bilateral shunt placements was planned.
Presently, at 18 months of age, the child was admitted again with respiratory distress accompanied by stridor. Direct laryngoscopy revealed sluggish movements of the vocal cords bilaterally indicating palsy. Nebulization with steroid and adrenaline was started. As the computed tomographic scan showed gross hydrocephalus, immediate decision to tap CSF from the previously placed cerebral catheter reservoirs was made (Fig. 1). It was noted that no sooner 30 to 35 mL of CSF was drained, the cry of the child had improved and stridor disappeared. Over the next few days, the child developed recurrent attacks of stridor, which improved only after CSF tapping. As the symptoms reverted successfully after CSF tapping, the need for intubation or tracheostomy was never felt. Within a week, however, the child showed respiratory and neurologic deterioration and died on the fifth day of admission after cardiac arrest from which she could not be revived. Davis and Ross5 suggest that vocal cord palsies are caused by high intracranial pressure. The probable mechanism is not destruction of brain stem cells but rather stretching, compression, or ischemia of the vagus nerves during their course from the nuclei ambigui to the jugular foramen, as this would resolve, bringing a return of vocal cord function, as the intracranial pressure decreases through conservative or operative management.5 Similar mechanisms may have occurred in our case also. Repeated tapping of CSF resolved stridor in our patient. Unlike other cases reported in literature, our patient suffered postmeningitic hydrocephalus and presented with stridor. We suggest that stridor be recognized as a sign of raised intracranial pressure in neurosurgical patients. The sign may not only be associated with congenital malformations (Arnold-Chiari, myelomeningocele) and central nervous system catastrophes (cerebral trauma, infarct), but also with meningitis resulting in hydrocephalus.
