A case of dengue fever complicated by acute transverse myelitis

Abstract

Dengue infection is now known to have varied neurological complications, involve central as well as peripheral nervous system. Only few isolated cases of acute transverse myelitis (ATM) have been reported. In this paper, we report a case of a 15-year-old female who developed acute onset quadriparesis following a dengue virus infection. Magnetic resonance imaging of the spinal cord disclosed signal-intensity abnormalities from C2 to T3. A diagnosis of ATM was considered. Because of the very rapid involvement of upper cervical cord, respiratory paralysis ensues. The patient condition necessitated her to be put on mechanical ventilation. Intravenous methylprednisolone was also given, but eventually patient expired.

Keywords: Acute transverse myelitis, Dengue fever, quadriparesis

How to cite this article:
Gutch M, Jain N, Kumar S, Modi A. A case of dengue fever complicated by acute transverse myelitis. Ann Trop Med Public Health 2013;6:251-3

 

How to cite this URL:
Gutch M, Jain N, Kumar S, Modi A. A case of dengue fever complicated by acute transverse myelitis. Ann Trop Med Public Health [serial online] 2013 [cited 2020 Nov 23];6:251-3. Available from: https://www.atmph.org/text.asp?2013/6/2/251/116498

 

Introduction

Dengue infection and its complications have a great toll on morbidity and mortality. Approximately, 50-100 million cases of dengue infection occur each year throughout the world. [1] The overall mortality in dengue infection is 1-5% without treatment and less than 1% with adequate treatment; however severe disease carries a mortality of 26%. [2],[3] In dengue infection, neurological involvement are being frequently reported, the common entities are delirium, drowsiness, depression, coma, extreme irritability, psychosis, dementia, amnesia, hypokalemic paralysis and meningo-encephalitis. However, sporadic cases of Guillain-Barre syndrome, Miller-Fisher syndrome, optic neuritis, neuromylitis optica, phrenic neuropathy, long thoracic neuropathy, oculomotor palsy, maculopathy and fatigue syndrome have been described by Murthy. [4] However, the involvement of spinal cord in dengue viral infection has rarely been mentioned. There have been only fourpreviously reported cases of transverse myelitis in association with dengue infection. [5] Here author reports a rapidly progressive transverse myelitis developed in a patient following a dengue infection, eventually patient died due to progressive brain stem involvement and respiratory paralysis.

Case History

A 15-year-old female admitted with high grade fever and generalized body pain for 2 days. She also complained ofprogressively increasing weakness of both the lower limbs since last day that progressed to upper limbs at the time of admission. There were no symptoms of sensory deficit and bladder-bowel involvement. There was no history of recent vigorous exercise or a high carbohydrate meal. At the time of admission, she was completely bedridden, muscle power in the upper and lower limbs was 1/5 (MRC scale) and generalized areflexia was evident on motor examination. There was no respiratory distress at the time of presentation. There was no evidence of diplopia, ptosis or difficult deglutition. Other systems were completely normal.

Laboratory parameters showed normal complete blood picture, blood sugars, electrolytes and kidney functions test. Liver-related enzymes were elevated but with normal bilirubin and clotting parameters. Cerebrospinal fluid analysis was done which showed total cell count of 5 (all lymphocytes) with normal protein and sugar. IgM Dengue was positive in CSF. Because of the rapidly progressive weakness, magnetic resonance imaging (MRI) of the spinal cord was done on 2 nd day to exclude compressive or inflammatory disease which showed finding of suggestive of acute transverse myelitis (ATM) [Figure 1]a and b.

Figure 1: (a) Sagittal T2-weighted MR image of the cervicothoracic spine shows an area of intramedullary high signal intensity from C2-T4 level suggestive of acute transverse myelitis. (b) AxialT2WMR image at the level of C3-4 shows a small area of isointensity relative to the cord in the center of the large intramedullary hyperintensity

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During the hospital course, she also developed sensory impairment in both lower extremities on day 2. On day 3, she developed retention of urine, fecal incontinence, and loss of sensation below neck level with sign of respiratory distress. She was given ventilatory support. But despite of well support, patient expired on 4 th day of ventilatory support due to progressive respiratory failure.

Discussion

ATM is characterized by bilateral spinal cord dysfunction presenting as upper and lower extremity weakness with or without sensory symptoms and bladder dysfunction. It typically manifests over a period of hours to 1week. ATM has been described after infections with large numbers of viral infections, commonly implicated are Epstein-Barr virus, cytomegalovirus, herpes simplex virus infections, rubella, chickenpox, coxsackie virus infectious mononucleosis, measles and seldomly by HIV. [6] Our patient had no evidence of a systemic disease (like lupus, leukemia), neither she had a history of contact with a potentially

infective agent of the spinal cord (e.g., borreliosis, cat-scratch disease, toxocariasis, schistosomiasis).

Transverse myelitis is a clinical syndrome which can be associated with a number of different conditions. It is, therefore, necessary to identify a direct infection, a systemic disease or an autoimmune (postinfectious or postvaccinal) process. [7]

The differential diagnosis of an acute pathology of the spinal cord comprises a wide range of conditions [8] that are bacterial abscesses, spinal cord tumors, vascular malformations and haematomas can be usually ruled out by image methods. Here, the diagnosis of dengue fever was considered because of the presence of IgM antibody by Capture-ELISA during the febrile period.

The clinical picture of ATM includes partial or complete paraplegia or quadriplegia, decrease or loss of deep reflexes, sensory impairment and varying degrees of bladder and bowel disturbance. Usually the full-blown disease is reached within four weeks after onset, but in most cases the peak occurs in the first week with the level of involvement set at the onset. [9] In a few patients, however, the disease has an ascending course with risk of asphyxia when upper cervical segments (C3-C5) are involved. In the present case, the onset was sudden and the cervical spinal cord immediately involved.

The neuropathogenesis of the central nervous system involvement in dengue infection has been poorly understood; both direct infection and postinfectious immune-mediated neural injury have been postulated. The development of neurologic symptoms in close association with the initial dengue infection (peri-infectious) and flaccid paraplegia are attributed to direct viral invasion of the nervous tissue, whereas the late appearance of neurologic disorders (postinfectious) and spastic paraplegia are considered immunologically mediated neural injury. [5] Direct invasion of the central nervous system by the dengue virus is supported by the isolation of the dengue virus antigen from CSF and spinal cord tissue in the cases of TM immediately following dengue infection. [10]

Treatment of ATM is a matter of controversy in the literature. [11] There is insufficient evidence to determine the utility of corticosteroids in alleviating TM attacks. Despite the absence of evidence, administration of high-dose IV methylprednisolone

(1 g daily for 3 to 7 days) is typically the first treatment offered to hasten recovery, reduce disease activity, and restore neurologic function. [12],[13] Plasma exchange may be considered in patients with ATM who fail to improve after corticosteroid treatment. There is insufficient evidence to support or refute the efficacy of other therapies. [12] The prognosis of ATM is variable and residual symptoms are common.

To conclude, in countries endemic to dengue, it is prudent to investigate for dengue infection in patients with fever and acute neurological manifestations.

References

 

1. WHO. World Health Organization Report of the Internal Consultation, 18-20 October 1999. Geneva: WHO; 2000.
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3. WHO. Dengue Guidelines for Diagnosis, Treatment, Prevention and Control. 10-11 Geneva: WHO; 2009.
4. Murthy JM. Neurological complication of dengue infection. Neurol India 2010;58:581-4.
5. Salgado CD, Weisse ME. Transverse myelitis associated with probable cat-scratch disease in a previously healthy pediatric patient. Clin Infect Dis 2000;31:609-11.
6. Linssen WH, Gabreëls FJ, Wevers RA. Infective acute transverse myelopathy. Report of two cases. Neuropediatrics 1991;22:107-9.
7. Lahat E, Pillar G, Ravid S, Barzilai A, Etzioni A, Shahar E. Rapid recovery from transverse myelopathy in children treated with methylprednisolone. PediatrNeurol 1998;19:279-82.
8. Jeffery DR, Mandler RN, Davis LE. Transverse myelitis. Retrospective analysis of 33 cases, with differentiation of cases associated with multiple sclerosis and parainfectious events. Arch Neurol 1993;50:532-5.
9. Solomon T, Dung NM, Vaughn DW, Kneen R, Thao LT, Raengsakulrach B, et al. Neurological manifestations of dengue infection. Lancet 2000;355:1053-9.
10. Seet RC, Lim EC, Wilder-Smith EP. Acute transverse myelitis following dengue virus infection. J ClinVirol 2006;35:310-2.
11. Victor M, Ropper AH. Diseases of the spinal cord. In : A0 dams RD Victor M, editors. Principles of Neurology. 7 th ed. New York : M0 cGraw Hill; 2001.
12. Scott TF, Frohman EM, De Seze J, Gronseth GS, Weinshenker BG, Therapeutics and Technology Assessment Subcommittee of American Academy of Neurology. Evidence-based guideline : c0 linical evaluation and treatment of transverse myelitis : r0 eport of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 2011;77:2128-34.
13. Leão RN, Oikawa T, Rosa ES, Yamaki JT, Rodrigues SG, Vasconcelos HB, et al. Isolation of dengue 2 virus from a patient with central nervous system involvement (transverse myelitis). Rev Soc Bras Med Trop 2002;35:401-4.

Source of Support: None, Conflict of Interest: None

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DOI: 10.4103/1755-6783.116498

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