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| CASE REPORTS |
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| Year : 2023 | Volume
: 38
| Issue : 1 | Page : 91-99 |
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Long-segment myelitis after traumatic paraplegia in COVID-19 positive patient: An unusual case report
Ravindra Mohan1, Yashvardhan Sharma2, Akanksha Singh3, Shailendra Singh1, Arpit Singh1
1 Department of Orthopedics, KGMU, Lucknow, India
2 Department of Orthopedics, Sarojini Naidu Medical College, Agra, India
3 Department of Pathology, KGMU, Lucknow, Uttar Pradesh, India
| Date of Submission | 18-Nov-2022 |
| Date of Acceptance | 28-Nov-2022 |
| Date of Web Publication | 20-Apr-2023 |
Correspondence Address:
Ravindra Mohan
Department of Orthopedics, KGMU, Lucknow, Uttar Pradesh
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/jbjd.jbjd_40_22
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has devastated the mankind globally, and countless lives have been lost all around the world. This disease has been linked to various extrapulmonary symptoms and consequences in addition to typical respiratory illness. This case highlights a probable neurological complication of SARS-CoV-2 infection. A 28-year-old healthy man, sustained wedge compression of D12 vertebra following road traffic accident, presented with paraplegia. One week following admission, the patient had a progressive neurological deterioration and developed high grade fever with weakness in both upper limbs. The patient developed quadriplegia 10 days after admission. Magnetic resonance imaging (MRI) brain and spine were done. MRI brain was normal, whereas MRI spine showed D11-D12 anterolisthesis with cord compression with T2 hyperintensity of cervical cord. His SARS-CoV-2 reverse transcriptase polymerase chain reaction turned out to be positive. We hereby report a case of posttraumatic long-segment myelitis with coronavirus disease 2019 as a probable etiology. Keywords: COVID-19, myelitis, paraplegia
How to cite this article:
Mohan R, Sharma Y, Singh A, Singh S, Singh A. Long-segment myelitis after traumatic paraplegia in COVID-19 positive patient: An unusual case report. J Bone Joint Dis 2023;38:91-9 |
How to cite this URL:
Mohan R, Sharma Y, Singh A, Singh S, Singh A. Long-segment myelitis after traumatic paraplegia in COVID-19 positive patient: An unusual case report. J Bone Joint Dis [serial online] 2023 [cited 2023 Jun 7];38:91-9. Available from: http://www.jbjd.in/text.asp?2023/38/1/91/374428 |
| Background | |  |
The coronavirus disease 2019 (COVID-19) was first reported in Wuhan, China, in December 2019.[1] It is caused by a new type of enveloped RNA coronavirus-B named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). SARS-CoV-2 enters the human body through angiotensin converting enzyme type 2 (ACE2) receptors on the surface of cells of humans.[2] It typically presents with fever and respiratory symptoms. However, this disease has also been linked to a wide range of extrapulmonary symptoms as well as neurological manifestations. Neurological complications of COVID-19 are well recognized and affect both the central nervous system (CNS) and the peripheral nervous system. The neurological features reported in the literature include headache, dizziness, anosmia, taste disturbances, cerebrovascular accident, Guillain-Barré syndrome, acute encephalitis, and acute transverse myelitis.[3],[4] The virus reaches the CNS through hematogenous or neural proliferation. Spinal cord cells also express ACE2 receptors on their surface. However, the implication of spinal cord neurons in the pathogenesis of COVID-19 is still unknown. Subacute posttraumatic ascending myelopathy (SPAM) is a rare complication after spinal cord injury, which is defined as neurological deterioration involving four or more vertebral segments above the initial injured site. It usually occurs within the first few weeks after the injury and was first described by Frankel.[5] A typical SPAM magnetic resonance imaging (MRI) shows a hyperintense signal on T2-weighted image, a heterogeneous intramedullary signal on T1-weighted image, and an expanded spinal cord typically without a syringe. Neurological deterioration ascending from the thoracolumbar spine to the cervical spine is distinctly rare. Here, we present an extremely rare case of traumatic paraplegia with COVID-19, who suddenly developed quadriplegia after initial high fever, suggesting that the CNS may be targeted as well by SARS-CoV-19.
| Case Presentation | | |
A previously healthy 28-year-old man presented to our emergency unit with bilateral lower limb weakness following a road traffic accident 2 days prior to presentation. On examination, he was thin built with respiratory rate of 15 breaths per minute, oxygen saturation of 98% on room air, blood pressure of 114/78 mm Hg, heart rate of 90 beats per minute, and temperature of 36.9°C. Cranial nerve examinations including fundus were within normal limits. Upper limb power was normal (MRC Grade 5), whereas both lower limbs had grade 0 power. Tendon reflexes were absent in both lower limbs. There was decreased anal tone and absent perianal sensations on digital rectal examination. He had a sensory level at D12 with spinal tenderness at lower thoracic region. Rest of the systemic examinations was normal. X-rays of the cervical, dorsal, and lumbar spine were ordered, which revealed a wedge compression fracture of the D12 vertebra [Figure 1][Figure 2][Figure 3]. The patient was diagnosed as a case of traumatic paraplegia complete below D12 with bowel and bladder involvement (ASIA Impairment Scale Grade A). Routine blood investigations [Table 1] were within normal limits, and COVID-19 reverse transcriptase polymerase chain reaction (RT-PCR) was negative. Focussed assessment with sonography in trauma (FAST) showed a mild left-sided pleural effusion. Conservative treatment was started, and the patient’s hospital stay remained uneventful for the initial few days.
The patient was planned for surgical fixation of the spine and was posted in the elective theater. On the preanesthetic check-up, the patient was found to have bilateral chest crepitations with decreased air entry and was declared unfit for surgery by the anesthesia team. A respiratory medicine reference was done. USG-guided pleural fluid aspiration was advised, and the patient was posted for pleural fluid tap in the Department of Interventional Radiology. USG screening revealed a left-sided pleural effusion of approximately 10 mL and a right-sided effusion of around 5–7 mL through the abdominal window, but the pleural tap could not be performed as the patient was unable to sit for the procedure.
On posttraumatic day 7, the patient developed high grade fever (102–104 F), which was transiently relieved on paracetamol infusion. He also complained of chest pain and headache with tingling and numbness in both upper limbs along with dyspnea at rest. A high resolution ultrasonography (HR-USG) thorax was performed, which showed a left-sided pleural collection of 80 mL with no right-sided collection. On neurological examination, the paraplegic level had risen to the C8 level with hypoesthesia in bilateral upper limbs. Methyl-prednisolone and empirical antibiotics were started.
On posttraumatic day 10, the patient developed quadriplegia. MRI brain and whole spine were performed [Figure 4][Figure 5][Figure 6][Figure 7]. MRI brain did not reveal any abnormality, whereas MRI spine showed diffuse expansion of spinal cord extending from C2 to D12 with T2 hyperintensity of cervico-dorsal cord with wedge compression of D12 vertebral body, bilateral D11-D12 facet joint dislocation, and retropulsion of fracture fragment. There was no improvement in patient’s fever, and routine investigations were repeated along with SARS-CoV-2 RT-PCR test.
Blood tests revealed a slightly raised C-reactive protein (24 mg/L), elevated erythrocyte sedimentation rate (44 mm/h), total leukocyte count of 6200/mm3, hemoglobin of 8.7 g/dL, hematocrit of 23.8%, and decreased serum sodium levels (119.2 mmol/L). MRI brain did not reveal any abnormality, whereas MRI spine showed D11-D12 anterolisthesis with cord compression with T2 hyperintensity of cervical cord. His SARS-CoV-2 RT-PCR turned out to be positive, and the patient was shifted to the COVID-19 intensive care unit (ICU) where he received treatment as per the institutional COVID-19 protocols.
Patient remained admitted in the COVID-ICU for 6 days during which there was no improvement in his neurological condition and he remained quadriplegic. After 6 days of COVID-ICU stay, his SARS-CoV-2 RT-PCR turned to be negative and he was shifted to the post-COVID ward the following day after a second negative RT-PCR report. The patient had developed bed sores during his stay in the COVID ward for which daily dressing was done. The patient was discharged from the post-COVID ward after 3 days on request, and further follow-up could not be done.
| Outcomes and Follow-up | | |
The patient expired at home 15 days after discharge.
| Discussion | | |
The common symptoms associated with COVID-19 infection include fever, cough, fatigue, and dyspnea. The various neurological complications of COVID-19 are well recognized. Common symptoms reflecting CNS involvement include headache, anosmia, agitation, delirium, and altered consciousness. SARS-CoV-2 binds strongly to ACE2 receptors found in the heart, lungs, CNS, and skeletal muscles. Viral replication and an increased ACE2 receptor activation in the CNS trigger a systemic inflammatory response, resulting in increased permeability of the blood–brain barrier and immune-mediated inflammation of the CNS. Interleukin-6, a proinflammatory cytokine, has been implicated in this response. Paterson et al.[6] described the postulated mechanisms causing the various neurological syndromes associated with SARS-CoV-2. These include direct viral neuronal injury[7],[8],[9] and the host’s secondary hyperinflammation syndrome, either individually or in combination.[10] The latency period between SARS-CoV-2 infection and the onset of the neurological symptoms is unknown in most instances because of asymptomatic COVID-19. The neurological complications of viral infections can be either parainfectious, i.e., due to direct viral neurotropism, or postinfectious, i.e., resulting from immune-mediated reactions against the virus.[11]
We have presented a case of posttraumatic long-segment myelitis in a COVID-19 positive patient. We postulate that this presentation was most likely due to an immune-mediated inflammatory response rather than direct invasion of SARS-CoV-2 into the CNS. However, we could not carry out a cerebrospinal fluid (CSF) analysis for the detection of SARS-CoV-2 RNA.
| CONCLUSION/LEARNING POINTS | | |
This review confirms that long-segment myelitis is a possible neurological complication associated with COVID-19 infection.
A close assessment of the paraplegic level should be performed daily so that neurological deterioration can be detected at the earliest.
Research to pick out the responsible antigen(s) and the immunopathogenesis of COVID-19-associated myelitis must be encouraged.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
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| 11. | Reichard RR, Kashani KB, Boire NA, Constantopoulos E, Guo Y, Lucchinetti CF Neuropathology of COVID-19: A spectrum of vascular and acute disseminated encephalomyelitis (ADEM)-like pathology. Acta Neuropathol 2020;140:1-6. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]
[Table 1]
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