APIK Journal of Internal Medicine

CASE REPORT
Year
: 2019  |  Volume : 7  |  Issue : 4  |  Page : 134--136

Intramedullary spinal tuberculosis in pregnancy: A rare case report


Shridhar Patil, Sangram Biradar 
 Department of Medicine, M R Medical College, Kalaburagi, Karnataka, India

Correspondence Address:
Dr. Sangram Biradar
Department of Medicine, M R Medical College, Kalaburagi, Karnataka
India

Abstract

Tuberculosis (TB) is an infectious disease which has the pulmonary form as the most common presentation. The spinal column is involved in <1% of all cases of TB. Dissemination of the disease is common in immunocompromised patients, but immunodeficiency related to pregnancy severe enough to cause dissemination of the mycobacteria is rare to date; there has been conflicting evidence on the maternal and neonatal complications of TB in pregnancy. Intramedullary tuberculoma (IMT) is a rare form of spinal TB; spinal TB leading to paraplegia is uncommon in pregnancy and is a diagnostic and therapeutic challenge. Medical therapy is the mainstay of treatment for IMT though there are surgical options for selective patients. We report a case of tubercular paraplegia presenting at 34 weeks of gestation, which lead to paraplegia.



How to cite this article:
Patil S, Biradar S. Intramedullary spinal tuberculosis in pregnancy: A rare case report.APIK J Int Med 2019;7:134-136


How to cite this URL:
Patil S, Biradar S. Intramedullary spinal tuberculosis in pregnancy: A rare case report. APIK J Int Med [serial online] 2019 [cited 2021 Jul 29 ];7:134-136
Available from: https://www.ajim.in/text.asp?2019/7/4/134/269572


Full Text



 Introduction



Tuberculosis (TB) is one of the oldest known infectious diseases that have seen a resurgence in recent years. TB is estimated to be even more prevalent in pregnant women than the general population.[1] Spinal TB presents commonly as tuberculous spondylitis or arachnoiditis. Intramedullary spinal tuberculomas are rare;[2] intramedullary tuberculoma usually occurs at young age, with most common location in the thoracic spinal cord.[3] There are many causes of spinal cord compression such as hematoma and infection. Bone infection can be initiated by two other mechanisms, particularly in the vertebrae: direct extension through the lymphatics from a caseous paravertebral lymph node and direct local hematogenous or lymphatic extension from a neighboring bone. As bone is destroyed progressively by pressure necrosis and formation of a cold abscess, a nearby joint may become involved.[4] However, case of intramedullary tuberculoma with disseminated intracranial lesion is very rare constituting only 0.2%–0.5% of all central nervous system tuberculomas.

 Case Report



A 27-year-old second gravida, with previous one spontaneous abortion, presented to our institute at 34 weeks of gestation with sudden onset, progressive weakness in both lower limbs with urinary retention of 6-day duration. Her medical, antenatal, and past histories were unremarkable except a history of dull aching backache for 6 months which was not progressive and had not been evaluated earlier; her neurological deficit was progressed in 6 days and she was unable to walk even with support. There was no past history of pulmonary TB or contacts with TB patients.

On neurological examination, her sensorium was diminished; she was drowsy and responded to verbal commands. The Glasgow Coma Scale was E5 M3 V3. The tone of the bilateral upper limb was normal; in lower limbs, the tone decreased in the proximal and distal group of muscles. Power was 1/5 in both lower limbs. Deep tendon reflexes were absent in both limbs. Plantars were bilateral extensor, neck rigidity was present, and fundus examination of both the eyes was normal.

In the hospital course, the weakness progressed to 0/5, with loss of touch and pain sensations in both lower limbs. There was loss of pupillary reaction to light in the right eye with development of papilledema in both the eyes. On per abdominal examination, the uterus was 34-week size with decreased perception of fetal movements with absent fetal heart sounds which was later confirmed it to be intrauterine device by ultrasonography.

With all aseptic precautions, the dead macerated fetus was induced and delivered on the next day of admission.

Investigations

Cerebrospinal fluid analysis showed appearance – clear; total count – 160; differential count – only lymphocytes; protein – 750; sugar – 10; and adenosine deaminase – 127.

Her complete blood count, renal profile, liver function tests, human immunodeficiency virus, Venereal Disease Research Laboratory test, and hepatitis B surface antigen were negative. Her chest X-ray appeared normal, erythrocyte sedimentation rate was 90, and the Mantoux was reactive.

MRI whole spine-T2 hypointense lesion and T1 hyperintense lesion in the cord at the level of D11-12 vertebra with surrounding edema were possibly suggestive of intramedullary tuberculoma. T1 contrast (gd) showed peripheral enhancement [Figure 1], [Figure 2], [Figure 3].{Figure 1}{Figure 2}{Figure 3}

MRI brain – T2/fluid-attenuated inversion recovery (FLAIR) hyperintensity – noted involving right medial temporal lobe, insular cortex, and right hemipons showing diffusion restriction, was suggestive of acute infarct. FLAIR hyperintensities noted in the right parietal sulcus spaces and right Sylvian fissure were suggestive of meningitis [Figure 4] and [Figure 5].{Figure 4}{Figure 5}

The patient was started on four drugs antitubercular therapy (ATT): isoniazid (300 mg), rifampicin (450 mg), pyrazinamide (1500 mg), and ethambutol 800 mg. In addition, pyridoxine (40 mg) and dexamethasone (1 mg/kg tid) were administered. The response to ATT could not be assessed as the patient died due to meningoencephalitis with septic shock after the 3rd day of admission.

 Discussion



It has been described in young immunocompromised as well as immunocompetent individuals.[5] These patients often have a history of contact to patients with TB or an extracranial focus of TB. It can also occur solely, in the absence of extracranial focus or pulmonary involvement. In the series of intramedullary tuberculomas reported by Mac Donnel et al.,[6] 38% of the patients had no evidence of tuberculous disease elsewhere.

The signs and symptoms of spinal TB include “night cries” and restless sleep, a low-grade daily fever, and a peculiar position (such as torticollis with cervical lesions) or gait. Findings on physical examination may include marked “guarding” because of dorsal muscle spasm, pain when the back is “pounded,” a deformity (such as gibbus), or reflex changes (including clonus).[4]

Typical MRI characteristics of intramedullary tuberculoma are hypo- or isointense to cord in T1-weighted sequence with only an indirect sign of focal cord expansion and heterogeneous intensity on T2-weigted image with central hypointensity and peripheral hyperintensity, which is described as target sign. Peripheral enhancement is a characteristic feature of tuberculoma on postcontrast images.[4] The central hypointensity on T2-weighted image is suggestive of caseating necrosis. Intramedullary tuberculoma can occur in combination with tuberculous spondylodiscitis and tuberculous arachnoiditis.

In our case, chest X-ray and abdominal ultrasound were normal. The patient was immunocompetent. Typical MRI characteristics of ring enhancement, T2 target sign, and associated meningeal enhancement favored intramedullary tuberculoma. Although typical MRI imaging features such as homogeneous postcontrast enhancement are common in immunocompromised patients, they may also occur in immunocompetent patients as in our case and also reported in other case reports.[4] Imaging characteristics of intramedullary tuberculoma, T2 target sign, ring enhancement, or homogeneous enhancement may vary depending on the immune response more than the immune status.

MRI is the best diagnostic tool to determine the location,[3] number, and size of the lesions and to assess response to antituberculous chemotherapy in follow-up imaging. In cases manifesting with typical MR imaging features, ATT and follow-up imaging can avoid other intervention procedures. In the absence of typical imaging characteristics, biopsy and histopathological correlation is essential. Optimum neurologic outcome is possible with microsurgical technique in patients with significant cord compression symptoms or neurological deficit. In addition to surgical treatment, chemotherapy with antituberculous drugs should be instituted as soon as the diagnosis is made to achieve the best neurologic outcome.[2],[3]

 Conclusion



For spinal cord compressions, tuberculomas should be kept as one of the differential diagnoses as TB is common in India and is most often misdiagnosed.

From the above imaging, we conclude that intramedullary spinal tuberculoma is the cause for spinal cord compression in our case.

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.

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