|Year : 2021 | Volume
| Issue : 1 | Page : 21-22
Prompt identification of loss of voice in a child can save a life, Guillian-Barre syndrome with vocal cord paralysis in a young boy
Kaushambi Basu, Rupa Biswas
Department of Pediatric Medicine, Calcutta National Medical College, Kolkata, West Bengal, India
|Date of Submission||05-Nov-2020|
|Date of Acceptance||12-Dec-2020|
|Date of Web Publication||31-Mar-2021|
Dr. Kaushambi Basu
Akshara Lotus Garden, Baguiati, Kolkata, West Bengal
Source of Support: None, Conflict of Interest: None
Guillain-Barré syndrome presenting as bilateral vocal cord paralysis is extremely rare in the paediatric age group. We report an unusual case of GBS in which the patient manifested loss of voice resulting from bilateral vocal cord paralysis with lower limb weakness. In conclusion, we emphasize that early recognition of atypical presentations of GBS warrants complete evaluation and institution of prompt and appropriate management.
Keywords: Guillain-Barre syndrome, intravenous immunoglobulin, vocal cord paralysis
|How to cite this article:|
Basu K, Biswas R. Prompt identification of loss of voice in a child can save a life, Guillian-Barre syndrome with vocal cord paralysis in a young boy. J Public Health Prim Care 2021;2:21-2
|How to cite this URL:|
Basu K, Biswas R. Prompt identification of loss of voice in a child can save a life, Guillian-Barre syndrome with vocal cord paralysis in a young boy. J Public Health Prim Care [serial online] 2021 [cited 2022 Jun 30];2:21-2. Available from: http://www.jphpc.com/text.asp?2021/2/1/21/312695
| Introduction|| |
Guillain-Barré syndrome (GBS) is an inflammatory demyelinating polyneuropathy associated with progressive ascending motor weakness and areflexia. However, GBS presenting as bilateral vocal cord paralysis is extremely rare with only few cases reported in the literature.,,,, Herein, we report an unusual case of GBS in which the patient manifested hoarseness resulting from bilateral vocal cord paralysis in a 9 year-old boy.
| Case Report|| |
A 9-year-old male patient was referred from a peripheral health facility to our hospital with complaints of acute onset of difficulty in speech and weakness of both lower legs. The patient had been in his usual state of good health until 48 hours before seeking treatment, when he developed hoarseness of voice, followed by gradual loss of speech. He also gradually developed inability to bear weight on his lower legs. His medical history was unremarkable. He had no history of preceeding cough, cold, loose stools, vaccination, trauma, honey or canned food intake, animal bite or surgery/instrumentation.
On physical examination, his vital signs revealed a blood pressure of 110/75 mm Hg, respiratory rate of 20 breaths/min, and temperature of 36.5°C. Oxygen saturation was 96% in room air. He was noted to have an inspiratory sound while attempting to speak with increased work of breathing. He had symmetric and adequate chest rise, equal breath sounds bilaterally with no added sounds. There was tenderness to palpation of lower extremities.
Neurological examination revealed no ophthalmoplegia, ptosis, facial palsy but gag reflex was absent. Motor examination revealed power of lower extremities as 2/5 and upper extremities 3/5.Tone was normal in both upper and lower extremities. His deep tendon reflexes were absent in the lower extremities but normal in the upper extremities. No sensory or autonomic disturbances were elicited. Bladder and bowel control was preserved. Shortly after admission to the paediatric intensive care unit, he started having increased oral secretions and respiratory distress ensued as he was not able to handle his secretions well. Decision for intubation and mechanical ventilation was taken. Direct laryngoscopy, while intubating the boy, was performed which revealed that there was minimal movement of the left vocal cord and no movement of the right cord. By this time, he also developed weakness of both his upper extremities. An ophthalmological exam revealed no evidence of papilledema to suggest increased intracranial pressure. A clinical diagnosis of Guillian - Barre Syndrome was suggested and treatment with Intravenous Immunoglobulin (IvIg) was started at 1gm/kg/day over 2 days along with supportive treatment and parenteral nutrition. Investigations done in the meantime included complete blood count, serum electrolytes, Urea, Creatinine, Urine Routine & Microscopic examination and Culture Sensitivity which were essentially normal. After about 5 days of assisted ventilation, the patient improved neurologically and was extubated. MRI Brain and Spine was done which were normal. Flexible laryngoscopy was, however, not performed due to the prevailing SARS-CoV2 pandemic. Cerebro-spinal fluid examination done on 10th day of illness revealed albumin-cytological dissociation (cells-nil, protein-110mg/dl). Nerve Conduction studies (NCS) revealed axonal & demyelinating type of sensory polyradiculopathy (lower limbs more affected than upper limbs). About 10 days post-extubation, he was able to feed himself, sit assisted and could speak just few words in a soft voice. He was discharged after a 4 weeks' hospital stay, with advice of physiotherapy and follow up. At the follow-up OPD 2 weeks later, he could walk unassisted into the clinic and had regained his voice as well.
| Discussion|| |
The disease is characterized by an acute inflammatory polyneuropathy with a rapidly progressive, symmetric weakness and areflexia. The weakness in GBS characteristically begins distally, though 15% to 20% of cases in children can begin with proximal patterns.
Cranial nerve involvement is more common in children than in adults. The clinical course is rapid with maximal deficits emerging within 4 weeks. Ataxia, which is a relatively common feature in paediatric GBS cases, results from weakness rather than cerebellar dysfunction. Respiratory failure is a rare but feared complication of the disease and frequently a cause of death. In the present case, however, though respiratory distress was the initial presenting symptoms, it was probably the result of vocal cord paralysis rather than intercostal and accessory breathing muscle weakness. However, a review of the aetiologies of vocal cord paralysis attributed some adult cases to neuromuscular dysfunction secondary to GBS.
GBS presenting as bilateral vocal cord paralysis is extremely rare, with only few cases having been reported in the literature, none from India., Some cases of bilateral vocal cord paralysis developing during the course of treatment have also been reported.,,,,,
Guillain–Barré syndrome (GBS) is the most common cause of rapidly evolving, flaccid weakness with associated areflexia in children. The incidence of GBS in children is currently 0.60 cases per 100,000 children younger than 15 years. Long-term outcome in children does not correlate with severity of the acute neurologic manifestations but rather with young age and rapid progression during an acute attack. Historically, 70% had complete recovery and 20% nearly complete recovery with just mild weakness in one or more muscle groups. Mortality in childhood GBS is quite low, resulting mostly from respiratory failure. These deaths can also be prevented if rapidly diagnosed and intensively monitored for respiratory failure and autonomic dysfunction. Early detection and prompt treatment of vocal cord paralysis as a part of the clinical spectrum of GB Syndrome can also prevent fatal complications.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Panosian MS, Quatela VC. Guillain-Barré syndrome presenting as acute bilateral vocal cord paralysis. Otolaryngol Head Neck Surg 1993;108:171-3.
Godiwala N, Steele RW. A toddler with stridor and leg weakness. Clin Pediatr (Phila) 2010;49:809-11.
Rodrigues JF, Nair CPV. Upper airway obstruction in Guillain-Barré syndrome. Chest 1984;86:147-8
Holinger LD, Holinger PC, Holinger PH. Etiology of bilateral abductor vocal cord paralysis: A review of 389 cases. Ann Otol Rhinol Laryngol 1976;85:428-36.
Mattucci KF, Chodosh PL. Vocal cord paralysis in Guillian-Barre syndrome. Eye Ear Nose Throat Mon 1970;49:318-21.
Raman PG, Mehta RS. “Post infective polyradiculoneuropathy with bilateral recurrent laryngeal nerve palsy”. J Assoc Physicians India 1987;35:534-5.
Yoskovitch A, Enepekides DJ, Hier MP, Black MJ. Guillain-Barré syndrome presenting as bilateral vocal cord paralysis. Otolaryngol Head Neck Surg 2000;122:269-70.
Dong Hoon Lee, Chang Joon Lee, John Jae Woon Lee and Joon Kyoo Lee Guillain-Barré Syndrome Presenting as Bilateral Vocal Cord Paralysis. Korean J Otorhinolaryngol-Head Neck Surg 2013;56:169-71
Cerisola-Cardoso A, Capote-Moreira G, Scavone-Mauro C. Guillain-Barré syndrome in paediatrics. Different forms of presentation and difficulties involved in reaching an early diagnosis. Rev Neurol 2007;44:725-32.
Ryan MM. Guillain-Barré syndrome in childhood. J Pediatr Child Health 2005;41:237-41.