Depending on the vascular area affected, a spinal cord infarction can present with a variety of symptoms. According to the literature, it is a rare disease with an estimated incidence of 0.003% of all events and 0.3-2% of all strokes [1,2].
In most cases, the etiology is not identified. Causes can be categorized into iatrogenic and non-iatrogenic; The former may be due to aortic surgery or injury from other surgical procedures, while non-iatrogenic causes include trauma, atherosclerosis, arteriovenous malformations, thrombotic/fibrocartilaginous emboli, polycythemia vera, vertebral hyperextension, myelitis, infections, and/or neoplasms [1,3].
This case report aims to describe a rare case of acute spinal cord ischemia syndrome with atypical presentation and its treatment, particularly treatment and etiological investigation.
A 39-year-old white male with a history of cigarette smoking, occasional cannabinoid use, and hypertension presented to the emergency department (ED) with spontaneous constrictive pain in the right posterior thoracic region that began acutely one hour prior to admission and radiated to the interscapular region and upper extremities to elbows, with a pain rating of 8/10, with no history of prior trauma.
On admission to the emergency department, the patient had a blood pressure of 192/113 mmHg, a pulse rate of 130 beats per minute, a regular rhythm, a temperature of 36.8 °C, and a respiratory rate of 14 breaths per minute. Physical examination was normal, with cardiac auscultation without murmurs, pulmonary auscultation was symmetric with no adventitious murmurs, and no peripheral edema. The neurological examination showed no focal deficits. Electrocardiogram (ECG) showed sinus rhythm with ST depression in leads V4-V6. A complete blood count and basal metabolic panel were normal with no elevation in inflammatory parameters (C-reactive protein of 3.2 mg/L) and no elevation in cardiac biomarkers (troponin I, creatinine phosphokinase, and myoglobin) at hours zero and six. In addition, he had a B-type natriuretic peptide level of 43 pg/ml. A transthoracic echocardiogram was performed with documentation of moderate concentric left ventricular hypertrophy without other abnormalities. To rule out an aortic dissection, a computed tomography angiography (angio-CT scan) of the thorax, abdomen and pelvis (Fig 1) was performed and showed no anomalies. The patient was admitted for clinical monitoring because of persistent symptoms.
On the second day of hospitalization, the patient began to develop neurological deficits and decreased muscle strength in the left lower extremity and both hands with altered sensitivity in the region corresponding to the T9-T12 dermatomes, associated with acute urinary retention. Neurological examination revealed myotic pupils, low light reactivity, difficulty in bilateral handgrip, 3/5 muscle strength in the left lower extremity, decreased abdominal sensitivity below T5, and bilateral hyporeflexia. Due to the use of morphine for pain control, naloxone was administered without reversal of symptoms and physical examination findings. An urgent angio CT scan (Fig 2) performed, which showed a lesion area extending from C5 to D2 and affecting mainly the left anterior and lateral spaces, suggesting a subacute ischemic spinal cord infarction. Due to subacute development and a National Institutes of Health Stroke Scale (NIHSS) score of 3, the patient did not undergo thrombolysis or thrombectomy. Dual antiplatelet therapy (DAPT) and a high-potency statin were initiated. Electromyography performed five days after the first event showed increased F-wave latency levels in both the upper and lower extremities, findings likely related to involvement of the proximal motor portion of the spinal reflex arc. In addition, there was bilateral evidence of non-recent mild neurogenic dysfunction at the level of C7, with no activation of voluntary motor units at C8, also bilateral. In addition, hyporeflexia was noted in the upper extremities distal to C7, and areflexia in the lower extremities and at the sensory level at T3. Taken together, these findings indicated medullary dysfunction.
A subsequent etiological investigation was performed. Specific blood tests ruled out autoimmune disease or hypercoagulable conditions as antinuclear and antineutrophil cytoplasmic antibodies, lupus anticoagulant and antiphospholipid antibodies were negative; C protein, S protein, antithrombin III, fibrinogen and VIII factors were normal; and prothrombin gene and factor V Leiden mutations were identified. In addition, the lipid profile was normal (total cholesterol, 171 mg/dL, high-density lipoprotein (HDL) cholesterol, 28 mg/dL, low-density lipoprotein (LDL) cholesterol, 95 mg/dL, triglycerides, 237 mg /dL) and glycated hemoglobin was 5.5%. Although previously described as hypertensive, the patient maintained a controlled blood pressure profile throughout the hospitalization without the introduction of antihypertensive drugs. Cranioencephalic and neuraxial magnetic resonance imaging (MRI) (Fig 3) confirmed the diagnosis and showed no vascular malformations. Carotid and vertebral echo Doppler were performed and revealed normal luminal permeability without atherosclerotic disease. A transesophageal echocardiogram ruled out a patent foramen ovale, septal defects, or vegetations. During admission, the patient was monitored electrocardiographically for 72 hours with no evidence of arrhythmias.
During the hospital stay, he was complicated by nosocomial pneumonia without associated respiratory failure after completing antibiotic therapy with clinical improvement. The patient began rehabilitation treatment for bladder training for recurrent urinary retention after an attempt to remove a urinary catheterization and motor training for quadriplegia grade D on the Asia Impairment Scale with neurological C6 level with left side predominance and a hand grip deficit that disabled him Grasping objects without altered proprioceptive sensitivity. The patient was discharged after 15 days of hospitalization and referred to a motor and functional rehabilitation center.
SCI is often overlooked in the emergency department due to its low incidence [1]. In almost 70% of non-specific chest pain it may be the initial presentation and in these cases it is localized at the level of the ischemic lesion [4]. Bladder dysfunction is present in more than half of cerebral strokes but rarely in myocardial infarction; However, when it is present, it is usually associated with urinary retention [5].
Predisposing conditions include aortic aneurysms, venous thromboembolism, coagulopathies, and aortic surgery [4]. The cardiovascular risk factor that appears to be associated with this disease is atherosclerosis, although due to its infrequent occurrence it remains unclear [2,6]. It has been described as a case of embolization from a patent foramen ovale [7]. Classic risk factors such as high blood pressure and diabetes mellitus are associated with a more severe myocardial infarction [2].
Symptoms often develop within hours. Biphasic ictus is observed in almost 50% of patients; usually a referred pain between the shoulders that precedes acute or transient symptoms of spinal cord sensory deficit. The peak of symptoms can last from 35-45 minutes to 24 hours [2]. Initial imaging (CT scan or MRI) may be normal for several days [3,8].
There are no guidelines for treating medullary strokes and they should be treated like cerebral strokes [2]. Antiplatelet therapy, anticoagulants when clinically warranted, and control of cardiovascular risk factors are the main strategies. Other approaches may be necessary and should be considered on an individual basis, such as B. steroids to reduce marrow edema and/or drainage of cerebrospinal fluid. There is no data based on clinical studies to support the use of fibrinolysis [3,8].
Symptom severity at presentation is the prognostic factor with a more long-term predictive value [1]. Men and young adults tend to show more severe symptoms; however, they tend to improve faster. Rehabilitation programs usually have a favorable outcome. Autonomic dysfunction and chronic pain are reported in most patients at follow-up [2,4].
Diagnosing spinal cord infarction is very difficult due to its low incidence and the variety of symptoms that may be present on admission. Biphasic ictus and normal initial imaging, as seen in this case, could be another factor contributing to the delay in diagnosis and therefore management and treatment. Despite a long and exhaustive study, idiopathic events are common.
Antiplatelet/anticoagulant therapy, control of cardiovascular risk factors, and rehabilitation are the main management and follow-up strategies for these patients. Although anxious, this entity usually has a better long-term outcome.
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