Anesth Analg 2001;92:358-361
© 2001 International Anesthesia Research Society
PEDIATRIC ANESTHESIA
Bilateral Vocal Cord Palsy After Ventricular Drainage in a Child
Lionel Davis, FRCA, and
Nick Ross, FRCS*
Departments of Paediatric Anaesthesia and *Neurosurgery, Royal London Hospital, London, UK
Address correspondence and reprint requests to Lionel Davis, FRCA, Department of Paediatric Anaesthesia, Royal London Hospital, Whitechapel Rd., London E1 1BB, United Kingdom.
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Abstract
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Implications: Vocal cord palsies are caused by high intracranial pressure and normally improve with treatment. Our case report implies that stridor after drainage of a hydrocephalus, in susceptible patients, can be a result of worsening of vocal cord palsies.
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Introduction
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Bilateral vocal cord palsy (BVCP), and thus stridor, is a recognized complication of increased intracranial pressure (ICP), particularly in children with a Chiari malformation (1,2) in whom the stridor typically resolves with ventricular-peritoneal (VP) shunting. We describe a child in whom insertion of a VP shunt caused a worsening of a BVCP, necessitating securing of the upper airway by means of a surgical tracheostomy and transfer to a pediatric intensive care unit (PICU). We believe this to be the first report in which BVCP followed a neurosurgical procedure that decreased ICP.
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Case Report
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A 7-yr-old 32-kg male presented to his local emergency room (ER) after suffering a fall at home sustaining a minor head injury. There had been no loss of consciousness although he did develop hiccoughs and was described by his parents as having "difficulty in breathing." A brainstem tumor, later identified as an astrocytoma, had been diagnosed 7 mo previously and he had been treated with radiotherapy with little benefit. During treatment he had received numerous general anesthetics for imaging and radiotherapy without ill effect. His postradiotherapy magnetic resonance imaging showed that there had been progression of the tumor and a more pronounced distortion of the fourth ventricle as shown in Figure 1. Although he had been functioning well at home since the end of treatment, he had a left hemiparesis since his initial presentation and some degree of bulbar palsy with swallowing and gaze difficulties but no reported dyspnea.
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Figure 1. Sagittal magnetic resonance imaging scan preinsertion of ventricular-peritoneal shunt with posterior fossa tumor indicated by arrow.
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On examination in the emergency department, heart rate was 118 bpm, arterial blood pressure increased at 141/75 mm Hg, respiratory rate 20 breaths/min, and pulse oximetry showed 100% while the patient was breathing room air. There were no abnormalities on examination of his cardiovascular system, and despite the parental reports of respiratory difficulty, his chest was clear, he was breathing gently, and no stridor was noted. His Glasgow Coma Scale score was 15, he was responsive and talking, albeit in a hoarse voice that his parents did not recognize as normal. He had some mild left facial weakness and some dribbling of saliva. His left upper and lower limbs were noted to be hypertonic and there was a 5 cm boggy area over the left parieto-occipital area. Several hours after arriving in the emergency department he had a generalized tonic-clonic convulsion lasting for 1 min that responded to diazepam 7.5 mg administered IV. A computed tomography scan at this time demonstrated evidence of hydrocephalus and intracerebral edema but no evidence of any hemorrhage.
He was admitted to our pediatric neurosurgical unit, and because of his recent deteriorating neurological status, which was thought to be caused by an expanding hydrocephalus, as well as his acute neurosurgical symptoms, he was scheduled for insertion of a VP shunt under general anesthesia the next day. On his preoperative anesthetic assessment, he was described as obeying commands and talking appropriately, but only answering yes or no questions. As before, there was no report of any stridor. Anesthesia was induced using fentanyl and thiopental and tracheal intubation was facilitated using atracurium; laryngoscopy was described as Grade I (Cormack and Lehane (3) classification). An uncuffed internal diameter 5.5 mm endotracheal tube was passed with ease and a substantial air leak was noted making intermittent positive pressure ventilation difficult. This was improved with the placement of a loosely inserted throat pack. General anesthesia was maintained with intermittent positive pressure ventilation using nitrous oxide and isoflurane in oxygen. The patient remained stable throughout the course of the general anesthetic, and the neuromuscular blockade was reversed with neostigmine and atropine at the end of the procedure. When the patient demonstrated eye opening, spontaneous ventilation, and movement of his right side, the throat pack and the endotracheal tube were removed. Immediately on extubation of the trachea, the patient demonstrated a harsh inspiratory stridor that was not improved with nebulized epinephrine. After an hour, considering there was no improvement and that the child was showing signs of tiring, his trachea was reintubated with the same size endotracheal tube as before, after administration of propofol 90 mg. Laryngoscopy at that time revealed a normal pharynx and slightly hyperemic cords with both cords open. Vital signs continued to be stable with clear breath sounds bilaterally and a return to the level of consciousness of that before general anesthesia. As the patient was allowed to awaken, he regained purposeful movements and was allowed to remove the endotracheal tube himself. Immediately, as before, there was a harsh inspiratory stridor that was resistant to treatment with nebulized epinephrine. On this occasion the patient was sedated, his trachea reintubated and arrangements made to transfer to a neighboring PICU for prolonged ventilation and definitive treatment. A postoperative computed tomography scan, as compared with the preoperative one, showed good shunt position with ventricles shrunken in size and no evidence of intracranial bleeding.
The patient spent 2 days in a PICU, during which time there were two additional attempts to extubate his trachea, both resulting in the immediate onset of stridor. On day 4 of his PICU stay he was taken to the operating room for formal direct laryngoscopy and tracheostomy. The former showed glottic granulomas and fixed vocal cords indicating BVCP. A size 4 Shiley uncuffed tracheostomy tube was inserted without difficulty and he was transferred to the general pediatric ward the next day.
One week after tracheostomy he was transferred back to our hospital. Within 2 wk, however, he showed respiratory and cardiovascular deterioration (decreasing saturations, increasing FIO2, tachycardia, and hypertension) caused by aspiration pneumonia and rapid growth of his tumor, necessitating admission to the intensive care unit. Shortly afterward he was taken to the operating room for craniotomy and debulking of his tumor in an effort to improve the quality of what little life he had left, but unfortunately no clinical benefit was gained and he died just 5 wk after the onset of symptoms.
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Discussion
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Vocal cord palsy (VCP) in children can be either unilateral or bilateral. BVCP will in general be diagnosed earlier and is more likely to present with stridor and cyanosis than unilateral VCP, where the presenting symptom is likely to be hoarseness or voice change (4). Central nervous system congenital malformations (e.g., Arnold-Chiari deformity) (1,2) and central nervous system catastrophes (e.g., cerebral infarct, perinatal asphyxia, cerebral trauma) are more likely to cause BVCP (5), the severity being related to the degree of pressure applied to the brainstem.
Children with BVCP are more likely to require tracheostomy and these are unlikely to be decannulated unless palliative surgery such as VP shunting is performed. Those children with unilateral VCP are surprisingly still at risk, albeit less than those with BVCP, of needing tracheostomy; stridor and feeding problems still being present in 59% and 50% of unilateral VCP respectively, but are more easily decannulated if they proceed to tracheostomy and have an overall better verbal communication quality at long-term follow-up (4).
Increased ICP, whatever the cause, can result in BVCP. The probable mechanism is not destruction of brainstem 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 ICP decreases through conservative or operative management. This is demonstrated by a rare case report of BVCP after a severe blunt head injury that caused a posterior fossa epidural hematoma and occipital bone fracture (6). The ICP, initially normal, increased to 50 mm Hg on day 2 and was resistant to medical treatment. As in our case report, the diagnosis was made when coarse inspiratory stridor occurred after repeated attempts to extubate the trachea after nearly two weeks of intensive care. A tracheostomy was performed and rehabilitation proceeded without further complication with return to normal laryngeal function after a month. This head injury differed from our patient, as the posterior fossa hematoma would have naturally resolved with time whereas the tumor in our child continued to grow preventing decannulation.
In our case report, the child was known before the operation to have a large posterior fossa mass, increased ICP, and bulbar signs with hoarseness representing a presumed unilateral VCP. Postoperatively, the initial diagnosis on encountering the severe inspiratory stridor was to attribute it to edema of the larynx secondary to passage of an endotracheal tube. However, this was unlikely, as there had been a substantial leak on initial intubation of the trachea, necessitating use of a throat pack to establish intermittent positive pressure ventilation. In addition, there was no improvement whatsoever with nebulized epinephrine and steroids. The conclusion that the stridor was caused by the patient’s unilateral VCP becoming a BVCP was surprising as the patient’s hydrocephalus had been successfully drained ( Fig. 2) and this would be expected to normalize an increased ICP. Even if there remained a mechanical compression from a very aggressive tumor on the brainstem, insertion of a VP shunt would not, on initial consideration, be expected to make any pressure effects worse on the vagal nuclei or nerves. It is unlikely that the BVCP was already in evolution preoperatively and the placement of the VP shunt merely a coincidence, as there was such a marked change the child’s airway immediately on wakening. If the stridor had been caused by growth of the tumor, BVCP would have developed gradually over time; that it happened so precipitously and exactly after the VP shunt insertion leads us to suspect that the VP shunt caused the BVCP.
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Figure 2. Sagittal magnetic resonance imaging scan postinsertion of ventricular-peritoneal shunt showing upward progression of the tumor (indicated by black arrow) and ventricles shrunk to normal size (white arrow).
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There is only one previous report of a VCP in a child after drainage of an intracerebral fluid collection when a Dandy-Walker cyst-to-peritoneal (CP) shunt insertion caused a unilateral VCP in an infant aged four months (7). He regained normal vocal cord movements 10 days later when the CP shunt was repositioned. The authors postulated that the decompression of the cyst could have placed traction on the vagus nerve that would have resolved with time.
The BVCPs in our case report can be explained by the large brainstem astrocytoma, seen in the magnetic resonance imaging scan (Figs. 1 and 2) as a significant posterior fossa mass lesion. There was concurrent expansion of the pons, fourth ventricle displacement, compression, and incipient upward transtentorial herniation. We postulate that insertion of the VP shunt caused a decrease in supratentorial pressure and may have facilitated upward transtentorial herniation allowing the brainstem to move upwards. The net effect of this would have been to put traction on the lower cranial nerves, including the vagus nerves, whose function was already compromised by the mass effect of the tumor, resulting in an acute deterioration and BVCP. Comparison of sagittal magnetic resonance imaging scan before and after insertion of the VP shunt confirms this upwards herniation. The superior colliculus is 5.5 cm above the posterior margin of the foramen magnum before insertion and moved upwards by 5 mm afterward.
In summary, we present a child who developed BVCP after a successful placement of a VP shunt that had not resolved by the time of his death five weeks later. We postulate that successful drainage of a supratentorial ventricle facilitated vagal deterioration via upward herniation of the brainstem and stretching of the lower cranial nerves.
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References
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Accepted for publication October 24, 2000.
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Abstract
Introduction
