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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 1  |  Issue : 1  |  Page : 8-9

Bell's palsy in a child with acute viral hepatitis C infection


1 Department of Pediatrics, Dr. Ram Manohar Lohia Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
2 Department of Pediatrics, Chandan Hospital, Lucknow, Uttar Pradesh, India

Date of Submission11-Jun-2020
Date of Decision21-Oct-2020
Date of Acceptance06-Nov-2020
Date of Web Publication27-Feb-2021

Correspondence Address:
Dr. Neha Thakur
Department of Pediatrics, Dr. Ram Manohar Lohia Institute of Medical Sciences, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ipcares.ipcares_3_21

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  Abstract 

Background: Bell's palsy is the most common form of facial paralysis in children. Etiology of facial paralysis can be both congenital and acquired. Acquired facial paralysis in most cases is due to viral infections. Hepatitis C infection leading to Bell's palsy is an unusual complication which has not been reported until now. Clinical Description and Management: A 4 month's old male child was admitted with fever, vomiting, refusal to feed, and icterus. His investigations revealed anemia with neutrophilic leukocytosis and deranged liver function tests. Hepatitis C antibody test was reactive. On 5th day of admission, right-sided Bell's palsy was noticed. There were no other signs of neurological deficit. Parental testing revealed hepatitis C antibodies in mother. The child was managed conservatively. He responded to treatment and symptoms subsided within 1 week of its onset. Conclusion: This case report highlights an unusual complication of hepatitis C infection in children. Prognosis in this case was good as the child recovered spontaneously.

Keywords: Hepatitis, infant, jaundice


How to cite this article:
Thakur N, Rai N. Bell's palsy in a child with acute viral hepatitis C infection. Indian Pediatr Case Rep 2021;1:8-9

How to cite this URL:
Thakur N, Rai N. Bell's palsy in a child with acute viral hepatitis C infection. Indian Pediatr Case Rep [serial online] 2021 [cited 2021 May 8];1:8-9. Available from: http://www.ipcares.org/text.asp?2021/1/1/8/310228

Bell's palsy is a neuropathy of the seventh cranial nerve, also known as the facial nerve. It is characterized by the sudden onset of unilateral temporary paralysis of the facial muscles, due to seventh cranial nerve dysfunction. It is one of the most frequent forms of facial paralysis in children aged 1–15 years with a likely incidence of about 6.1 cases per year per 100,000.[1] The prognosis is favorable with more than 70% affected individuals recovering spontaneously.[1] Bell's palsy can be either congenital or acquired. Among the acquired infections Epstein –Barr virus, Herpes zoster, Haemophilus influenzae, and Mycobacterium tuberculosis are important causative agents.[2] As far as hepatitis is concerned, Bell's palsy has been reported in a child post hepatitis B vaccination,[3] but literature search did not reveal any case reports of Bell's palsy as a complication of hepatitis C infection. Jaundice, malaise, anorexia, and vomiting are the most common presenting signs and symptoms of acute viral hepatitis C. Majority undergo spontaneous resolution. Complications are mostly related to chronic hepatitis C infection such as portal hypertension, cirrhosis, and hepatocellular carcinoma. Neurological complications have not been reported until now. This case presents an uncommon complication of Bell's palsy posthepatitis C infection which resolved spontaneously.


  Clinical Description Top


A 4-month-old boy presented with fever for 7 days, vomiting for 4 days, refusal to feed for 3 days, and yellowish discoloration of eyes and skin for 3 days. The child was apparently healthy prior to the onset of these symptoms. He was born by normal vaginal delivery at term to a primigravida mother. The child was exclusively breast fed till admission. His postnatal and neonatal period was uneventful. He had been immunized appropriately as per age. On examination, the child was irritable, pale, and icteric with hepatosplenomegaly. He did not have any clinically significant lymphadenopathy. There was no bleeding from any site. Rest of the systemic examination was normal.

Management and Outcome

Hematological investigation showed hemoglobin of 13.7 g/dL, total leukocyte count of 4.000 × 103/μL (polymorphs 45%, lymphocyte 55%) and platelet count of 250 × 103/μL. His liver function test was deranged with serum bilirubin level of 8 mg/dL and raised serum ALT level (389 IU/L). Renal function test, serum electrolytes, and blood coagulation studies were normal. Ultrasound abdomen showed hepatosplenomegaly. HCV antibody test was positive whereas serological tests for other viruses such as EBV, Hepatitis A, E, B, and HIV were negative. A diagnosis of acute viral hepatitis C was made. On 5th day of admission, the child developed sudden onset of facial asymmetry with features of complete lower motor neuron type left facial nerve paralysis. It was not associated with motor, sensory, or any other cranial nerve involvement. There were no active HSV or herpes zoster lesions anywhere in the body or in the oral mucosa. Otoscopic examination was normal. A diagnosis of acute viral hepatitis C with left sided Bell's palsy was made. As the child was diagnosed with acute viral hepatitis C serological tests for both parents were also sent. Mother's test came out to be positive but father was negative. On examination, the mother was asymptomatic with normal systemic examination. Her liver function tests were also normal. On further history taking, she gave the history of blood transfusion in her second trimester of pregnancy. The child was managed with intravenous fluids, antipyretics, multivitamin supplementation, and hepatoprotective drugs such as L-ornithine and L-aspartate supplementation. The child showed response to treatment. The facial asymmetry resolved after a week of its onset. It coincided with the resolution of jaundice. At 2 weeks' postadmission, the child was discharged with no signs of Bell's palsy and resolving icterus. The liver enzymes had started to normalize. The baby became active and started accepting feeds.


  Discussion Top


Sir Charles Bell, a Scottish surgeon in 1821 first described Bell's palsy[4] as weakness of facial nerve. It still remains the commonest cause of facial nerve weakness in children. Pediatric facial nerve palsy can be either idiopathic (Bell's palsy), congenital or acquired. Birth trauma or various syndromes such as Moebius syndrome, Goldenhar syndrome, Syringobulbia, and Arnold–Chiari syndrome are important congenital causes. Surgery is the treatment of choice for many children presenting with a permanent congenital facial palsy.[2],[5] Hereditary myopathies, such as myotonic dystrophy and myasthenia, are important genetic causes of facial nerve paralysis.[2] Acquired facial nerve palsy is mostly due to infectious causes. Of the infectious causes, herpes simplex, Epstein–Barr virus, and Varicella zoster are important. There have been case reports of facial palsy associated with the presence of vesicular lesions on skin or in the external auditory canal.[6],[7] Bell's palsy post vaccination with Hepatitis B has also been reported.[3] There has not been a single case report of an infant developing Bell's palsy as a complication of acute viral hepatitis C. Our case had developed acute viral hepatitis at 4 months of age followed by development of Bell's palsy. We did not find any signs and symptoms of other etiologies of Bell's palsy in our child. Recent studies have shown the role of intraaxonal signal molecules such as SARM1, mitochondrial permeability, and cell-mediated immune response against myelin sheath to be the key immunopathological mechanism for the development of bell's palsy post viral infection.[8],[9] The child symptoms resolved spontaneously and coincided with his normalization of liver enzymes and resolution of signs and symptoms of viral hepatitis C.

Hence, to conclude, Bell's palsy is a neuropathy of the seventh cranial nerve. It has a number of causes both congenital and acquired. Autoimmune etiology is the most probable underlying mechanism of infectious cause of Bell's palsy. Hepatitis C infection can cause Bell's palsy as seen in this child. Prognosis was good as child recovered spontaneously.



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

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Özkale Y, Erol I, Saygi S, et al. Overview of pediatric peripheral facial nerve paralysis: Analysis of 40 patients. J Child Neurol 2015;30:193-9.  Back to cited text no. 1
    
2.
Pavlou E, Gkampeta A, Arampatzi M. Facial nerve palsy in childhood. Brain Dev 2011;33:644-50.  Back to cited text no. 2
    
3.
Alp H, Tan H, Orbak Z. Bell's palsy as a possible complication of hepatitis B vaccination in a child. J Health Popul Nutr 2009;27:707-8.  Back to cited text no. 3
    
4.
Zandian A, Osiro S, Hudson R, et al. The neurologist's dilemma: A comprehensive clinical review of Bell's palsy, with emphasis on current management trends. Med Sci Monit 2014;20:83-90.  Back to cited text no. 4
    
5.
Al Tawil K, Saleem N, Kadri H, et al. Traumatic facial nerve palsy in newborns: Is it always iatrogenic? Am J Perinatol 2010;27:711-3.  Back to cited text no. 5
    
6.
Sima NH, Saidha PK, Sreenivas V. Pediatric Ramsay Hunt syndrome: A rare clinical entity. Indian J Otol 2016;22:217-9.  Back to cited text no. 6
  [Full text]  
7.
Ciorba A, Corazzi V, Conz V, et al. Facial nerve paralysis in children. World J Clin Cases 2015;3:973-9.  Back to cited text no. 7
    
8.
Conforti L, Gilley J, Coleman MP. Wallerian degeneration: An emerging axon death pathway linking injury and disease. Nat Rev Neurosci 2014;15:394-409.  Back to cited text no. 8
    
9.
Galluzzi L, Blomgren K, Kroemer G. Mitochondrial membrane permeabilization in neuronal injury. Nat Rev Neurosci 2009;10:481-94.  Back to cited text no. 9
    




 

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