Non-traumatic paraplegia developing in pregnancy is rare phenomenon with only sporadic reports [1, 2, 3]. Spontaneous development of spinal epidural hematoma (SEH) without any predisposing factor is rare and even more sporadic in pregnancy. The etiologies of SEH include hypertension, vascular malformation, neoplasia, and use of anticoagulant medications ^[4]. High clinical suspicion of this rare condition is necessary for better outcome of both mother and baby. Usual clinical presentation includes neck pain, pain in the interscapular area or back pain that progresses to paraparesis or quadriparesis depending on the location of hematoma. Immediate diagnosis and treatment are of utmost importance for better outcome. Standard treatment includes urgent operative decompression of the hematoma and conservative management and close monitoring for patients who show spontaneous recovery in short period of time. Delivery of the baby may be carried out in the same setting or at a later date depending of the gestational age. Here, we report a rare case of spontaneous SEH in a 35 weeks pregnant lady who presented with acute onset paraplegia.

A 28-year pregnant female G1P0L0 presented with sudden onset upper back pain and associated weakness of bilateral lower limbs of 8 days duration. There was no history of trauma, fever, seizure, or altered sensorium. There was no history of bleeding disorders since childhood or intake of any anticoagulant, or tuberculosis. On examination, she was afebrile, vitals were stable. BP 110/80 mm of Hg, pulse of 84/min., and the abdomen distended corresponding to the 35 weeks gestational age. Fetal heart rate was 140/min and fetal movement could be appreciated. The neurological examination showed complete paraplegia (MRC-0/5 in both limbs) with a sensory level of D6. The bladder was catheterized and perianal sensation was absent. A magnetic resonance imaging (MRI) was done for further evaluation that showed elongated T2 and T1 hyperintense lesion (over a length of 3.5 cm and maximum thickness 8 mm) in posterior epidural region extending from D3 to D5 vertebral level. Signal of the lesion was not suppressed on fat suppressed image. The lesion was displacing the thecal sac and spinal cord anteriorly causing cord compression and increased T2 signal of the spinal cord at this level (Fig. 1). Vertebral bodies and intervertebral disc spaces appeared normal. Diagnosis of subacute posterior epidural hematoma causing compressive myelopathy was made based on MRI. Routine biochemical investigations revealed Hb-12 g/mL, TLC of 11,400, sodium of 142 meq/l, potassium of 4.5 meq/l, and platelet of 2.5 lacs/cmm. The patient had a normal bleeding time, prothrombin time and was negative for Protein C, Protein S, or Antiphospholipid antibody. Her TSH was raised to 102 mlU/l at the time of admission. The mother was given steroidsfor lung maturation of the fetus and after 48 h, a caesarean section (CS) was done and baby delivered. With escalating dose of thyroxine, laminectomy and decompression of spinal canal done and hematoma drained. The baby was normal while the mother was started on physiotherapy and electrical stimulation. At 6 months post-surgery, there is improvement in 2 grade MRC and one grade sensory. The patient is ambulatory on a wheel chair.

SEH is a rare cause of spinal cord compression and spinal emergency seen in 0.3–0.9% of all epidural space-occupying lesions ^[5]. Post-traumatic SEH is common in men having ankylosing spondylitis or rheumatoid arthritis. Non-traumatic SEH is usually seen in patients having congenital or acquired bleeding disorders, spinal arteriovenous malformations, hemorrhagic tumors, and in hypertensive patients ^[4]. In patients without any predisposing factors, possible etiopathogenesis could be acute increase of the spinal epidural venous pressure. Epidural veins are more susceptible to congestion during pregnancy ^[6]. Krishnan and Kartikueyan. reported a case in a 27 weeks gestation lady that was decompressed in lateral position with D3-7 laminectomy. Kaushal et al. reported a 35 weeks pregnant female with tuberculolsis leading to paraplegia that was managed with conservatively with medication. Eventually she had a normal labor and complete recovery of her paraplegia. Kulkarni et al. encountered a hypokalemia paraplegia in 45 weeks pregnant woman. She needed medical termination of pregnancy with correction of her electrolytes. Mohanty et al. found an aggressive hemangioma causing paraparesis in term pregnant lady presenting for CS. She recovered eventually without surgery [1, 2, 3, 7]. Clinical symptoms vary depending on the location and the severity of compression. Our case showed with typical MRI findings with T1 and T2 hyperintense hematoma extending from D3 to D5 that corresponded to the clinical localization. Most patients present with acute onset back pain depending on the site of hematoma. This symptom is present in 80 to 89% of SEH. Progressive motor weakness and sensory loss may be seen below the level of cord compression ^[8]. MRI is the diagnostic modality of choice for diagnosis of SEH. MRI can accurately localize the hematoma and its extent, stage of hematoma, cord compression, and myelopathic changes in the spinal cord if any. Acute hemorrhage appears hypointense on T2WI and isointense on T1WI and at times difficult to identify. But increased epidural space causing compression of thecal sac gives a clue. Subacute hemorrhage appears hyperintense on both T1 and T2WI due to the presence of methaemoglobin. Hyperintensity on T1 fat saturated image excludes any fat containing lesion ^[9]. Clinical presentation is also variable. In SEH, presentation is acute, however fat containing lesion such as lipoma or dermoid usually has an insidious onset of symptom. Epidural CSF leak may present with paraparesis and MRI can show increased epidural space. However, MRI shows CSF signal intensity in the increased epidural space ^[10]. Clinical details, level of epidural hemorrhage and management of previously reported cases are described in Table 1. Early decompression is required to release compression over the spinal cord and to prevent permanent damage and its long-term sequelae. The management also depends on the gestational age of the fetus at the time of presentation. In term pregnancy, CS followed by laminectomy is preferred; whereas laminectomy with evacuation of hemorrhage is done if the fetus is preterm. Furthermore, if the patient presents only with pain without weakness, close follow-up is necessary to look for spontaneous resolution or progression of hematoma [1, 6, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30]. Our patient was treated successfully by delivery of the baby by CS and release of cord compression by D3-D5 laminectomy.

Spontaneous SEH in pregnancy is a rare clinical condition with acute presentation. Clinical suspicion is necessar y for early management. MRI is the investigation of choice. Early decompression is required to avoid complications.

Diagnosis of a case of acute onset paraplegia is challenging. Most common cause for the same is dorsal cord compression. MRI is the investigation of choice to see the status of the spinal cord and extent of involvement. Also, it does not use ionizing radiation and thus relatively safe in pregnancy. Early diagnosis and management are necessary to avoid detrimental consequences.