Spinal hematoma has been described in autopsies since 1682 and as a clinical diagnosis since 1867. It is a rare and usually severe neurological disorder that, without adequate treatment, often leads to death or permanent neurological deficit. Epidural as well as subdural and subarachnoid hematomas have been investigated. Some cases of subarachnoid spinal hematoma may present with symptoms similar to those of cerebral hemorrhage. The literature offers no reliable estimates of the incidence of spinal hematoma, perhaps due to the rarity of this disorder. In the present work, 613 case studies published between 1826 and 1996 have been evaluated, which represents the largest review on this topic to date. Most cases of spinal hematoma have a multifactorial etiology whose individual components are not all understood in detail. In up to a third of cases (29.7%) of spinal hematoma, no etiological factor can be identified as the cause of the bleeding. Following idiopathic spinal hematoma, cases related to anticoagulant therapy and vascular malformations represent the second and third most common categories. Spinal and epidural anesthetic procedures in combination with anticoagulant therapy represent the fifth most common etiological group and spinal and epidural anesthetic procedures alone represent the tenth most common cause of spinal hematoma. Anticoagulant therapy alone probably does not trigger spinal hemorrhage. It is likely that there must additionally be a "locus minoris resistentiae" together with increased pressure in the interior vertebral venous plexus in order to cause spinal hemorrhage. The latter two factors are thought to be sufficient to cause spontaneous spinal hematoma. Physicians should require strict indications for the use of spinal anesthetic procedures in patients receiving anticoagulant therapy, even if the incidence of spinal hematoma following this combination is low. If spinal anesthetic procedures are performed before, during, or after anticoagulant treatment, close monitoring of the neurological status of the patient is warranted. Time limits regarding the use of anticoagulant therapy before or after spinal anesthetic procedures have been proposed and are thought to be safe for patients. Investigation of the coagulation status alone does not necessarily provide an accurate estimate of the risk of hemorrhage. The most important measure for recognizing patients at high risk is a thorough clinical history. Most spinal hematomas are localized dorsally to the spinal cord at the level of the cervicothoracic and thoracolumbar regions. Subarachnoid hematomas can extend along the entire length of the subarachnoid space. Epidural and subdural spinal hematoma present with intense, knife-like pain at the location of the hemorrhage ("coup de poignard") that may be followed in some cases by a pain-free interval of minutes to days, after which there is progressive paralysis below the affected spinal level. Subarachnoid hematoma can be associated with meningitis symptoms, disturbances of consciousness, and epileptic seizures and is often misdiagnosed as cerebral hemorrhage based on these symptoms. Most patients are between 55 and 70 years old. Of all patients with spinal hemorrhage, 63.9% are men. The examination of first choice is magnetic resonance imaging. The treatment of choice is surgical decompression. Of the patients investigated in the present work, 39.6% experienced complete recovery. The less severe the preoperative symptoms are and the more quickly surgical decompression can be performed, the better are the chances for complete recovery. It is therefore essential to recognize the relatively typical clinical presentation of spinal hematoma in a timely manner to allow correct diagnostic and therapeutic measures to be taken to maximize the patient's chance of complete recovery.

Spinal hematoma: a literature survey with meta-analysis of 613 patients

Thirty patients were treated surgically for spinal epidural hematoma (SEH). Twelve of these cases resulted from spinal surgery, seven from epidural catheters, four from vascular lesions, three from anticoagulation medications, two from trauma, and two from spontaneous causes. Pain was the predominant initial symptom, and all patients developed neurological deficits. Eight patients had complete motor and sensory loss (Frankel Grade A); six had complete motor loss but some sensation preserved (Frankel Grade B); and 16 had incomplete loss of motor function (10 patients Frankel Grade C and six patients Frankel Grade D). The average interval from onset of initial symptom to maximum neurological deficit was 13 hours, and the average interval from onset of symptom to surgery was 23 hours. Surgical evacuation of the hematoma was performed in all patients; 26 of these improved; four remained unchanged, and no patients worsened (mean follow up 11 months). Complete recovery (Frankel Grade E) was observed in 43% of the patients and functional recovery (Frankel Grades D or E) was observed in 87%. One postoperative death occurred from a pulmonary embolus (surgical mortality 3%). Preoperative neurological status correlated with outcome; 83% of Frankel Grade D patients recovered completely compared to 25% of Frankel Grade A patients. The rapidity of surgical intervention also correlated with outcome; greater neurological recovery occurred as the interval from symptom onset to surgery decreased. Patients taken to surgery within 12 hours had better neurological outcomes than patients with identical preoperative Frankel grades whose surgery was delayed beyond 12 hours. This large series of SEH demonstrates that rapid diagnosis and emergency surgical treatment maximize neurological recovery. However, patients with complete neurological lesions or long-standing compression can improve substantially with surgery.

Surgical management of spinal epidural hematoma: relationship between surgical timing and neurological outcome

We reviewed 44 cases of ischemia and infarction of the spinal cord at two university hospitals. Three patients experienced transient ischemic attacks. Etiologies of completed strokes were diverse and included rupture and surgical repair of aortic aneurysms, aortic dissection, aortic rupture and thrombosis, global ischemia, anterior spinal artery embolism, repair and thrombosis of spinal arteriovenous malformations, hematomyelia, epidural hematoma, cervical osteophytosis, celiac plexus block, systemic lupus erythematosus, coagulopathy, and decompression sickness. Motor function improved in 12 patients, was substantial in only one, and occurred largely within the first 2 to 4 weeks. Favorable ambulatory outcome correlated with improving neurologic examinations and relatively preserved strength in hip abductors and knee extensors. More extensive deficits without initial improvement portended a more severe prognosis. Autonomic dysfunction, pain, paresthesia, and depression were common and impeded recovery in some patients. The mean level of deficit was at T-8 and in cases of global ischemia was at T-9, which leads us to dispute the classical view of a midthoracic watershed zone of ischemic vulnerability near T-4.

Spinal cord infarction Etiology and outcome

The spontaneous spinal epidural hematoma. A study of the etiology.

OBJECTIVE: We clarify the factors affecting postoperative outcomes in patients who have suffered spontaneous spinal epidural hematomas. METHODS: We review 330 cases of spontaneous spinal epidural hematomas from the international literature and three unpublished cases of our own. Attention was focused on sex, age, medical history, mortality, size and position of the hematoma, vertebral level of the hematoma, preoperative neurological condition, operative interval, and postoperative result. RESULTS: Sex, age, and size and position of the hematoma did not correlate with postoperative outcome. Mortality correlated highly with cervical or cervicothoracic hematomas, especially in patients with cardiovascular disease and those undergoing anticoagulant therapy. Incomplete preoperative sensorimotor deficit correlated highly with favorable outcomes (P < 0.0005), and recovery was significantly better when decompression was performed in < or = 36 hours in patients with complete sensorimotor loss (P < 0.05) and in < or = 48 hours in patients with incomplete sensorimotor deficit (P < 0.005). CONCLUSION: The critical factors for recovery after spontaneous spinal epidural hematoma are the level of preoperative neurological deficit and the operative interval. The vertebral level of the hematoma did not correlate with postoperative results, which suggests that local compression, rather than vascular obstruction, is the main factor in producing neurological deficit.

Operative treatment of spontaneous spinal epidural hematomas : a study of the factors determining postoperative outcome

Preoperative neurological status in predicting surgical outcome of spinal epidural hematomas

The anterior spinal artery syndrome in three patients is described and from the literature 60 additional patients were collected. Motor recovery in the following groups of patients was noted: (1) Partial loss of motor function and pain sensation--70.4 per cent (19/27); (2) Complete motor loss but partial loss of pain--83.3 per cent (5/6); (3) Paresis but pain sensation absent--66.7 per cent (6/9); and (4) Absent motor function and pain--38.9 per cent (7/18). Motor recovery was also found to vary according to aetiology: (A) Unknown cause--92.9 per cent (13/14); (B) Post-infection or vaccination--88.9 per cent (8/9); (C) Anterior spinal artery occlusion--33.3 per cent (3/9); (D) Spinal cord angioma--20 per cent (2/10); and (E) Aortic lesion--20 per cent (1/5). Patients with sparing of motor function or pain sensation below the lesion do better than those without both functions. Neurological return also varies with the aetiology of the syndrome.

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Anterior spinal artery syndrome and its natural history

Thirteen patients with motor complete but sensory incomplete lesions following vertebral and spinal cord injuries are described. Sensory dissociation was present with more impairment of pain than touch or proprioception. The loss of pain sensation was complete in seven patients, but was incomplete in the other six subjects four of whom showed major motor recovery. The major point of interest of this study is to show that patients who retain not only touch but also pain sensation have a definitely better prognosis for neurological recovery.

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Post-traumatic acute anterior spinal cord syndrome.

A 58-year-old man sustained C4-C5 post-traumatic myelopathy with C3-C4 subluxation, slight compression of C3 vertebral body, C4 spinous process fracture and C6 compression fracture. He subsequently developed syringomyelia from C4 to C6, which was shunted into the subarachnoid space. Postoperatively, there was some but insignificant improvement of his symptoms although a postoperative metrizamide spinal computerised tomography showed complete drainage of the cyst. This patient died 1 year later. Autopsy examination of the spinal cord showed extensive damage of the posterior half of the cord at C3-C4 but the damage was much less extensive from C4 to C6 (where the syrinx was located), affecting mainly the right dorsal column at C4 and the right dorsal column and right anterior horn at C5-C6. In this patient, the syrinx developed in the partially damaged segments of the cord at the level of the spinal fractures and complete drainage of the cyst was not followed by satisfactory relief of his symptoms.

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A case of post-traumatic syringomyelia. Neuropathological findings after 1 year of cystic drainage.

Complete motor tetraplegia with incomplete sensory loss was caused by spontaneous epidural bleeding from an arteriovenous malformation in the cervical region. There was a family and personal history of cutaneous hemangioma.

Dominic Foo

Papers

Preoperative neurological status in predicting surgical outcome of spinal epidural hematomas

Anterior spinal artery syndrome and its natural history

Post-traumatic acute anterior spinal cord syndrome.

A case of post-traumatic syringomyelia. Neuropathological findings after 1 year of cystic drainage.

Spontaneous cervical epidural hemorrhage, anterior cord syndrome, and familial vascular malformations: Case report