Vision loss after lumbar epidural steroid injection.Colleague's E-mail is Invalid. Your message has been successfully sent to your colleague. MD ; Ajimal, Gurjit S. Address correspondence and reprint requests proviron only for pct Eric P. Visual loss associated with retinal hemorrhages after laparoscopy performed under general anesthesia has been previously inection in the anesthesiology literature . This complication has been reported only once after an epidural steroid injection in the anesthesia literature . We report a case of acute monocular vision loss secondary to multiple retinal hemorrhages after a lumbar vizion steroid injection.
Vision loss after lumbar epidural steroid injection. - PubMed - NCBI
Neurological deficits after epidural steroid injection ESI are rare but occur despite meticulous technique. Some neurologic deficits reverse spontaneously, others reverse only with timely interventions, and some are permanent. Assess the immediate diagnostic and treatment steps to undertake when a patient experiences a severe neurologic deficit so that the best neurologic recovery can be obtained. The literature was systematically reviewed for case reports and case series describing neurologic deficit after ESI.
From these reports, the mechanism, temporal onset, permanence or reversibility of the deficit, and assessment and management were recorded and analyzed. Thirty-three cases of neurological deficits were identified: Temporal onset of differential diagnoses subdural and intrathecal injection, hematoma, and vascular punctures overlap.
Faced with deficits after ESI that do not resolve, the physician will need access to MRI, or similar radiographic studies, and subsequent neurosurgical consultation and facilities if MRI results indicate a decompressible lesion. Respiratory insufficiency with quadriplegia and loss of consciousness can occur, and in the worst of scenarios, the physician would also need the capability to ventilate the patient.
Spinal cord infarction associated with transforaminal TF epidural steroid injection ESI has focused clinical attention on neurological deficits subsequent to ESI [1,2]. Alterations in procedural technique to lessen the risk of this complication have been suggested [1—3].
The occurrence of neurological deficits after any elective procedure is devastating and deserves clinical attention. Permanent neurological deficits can alter an individual's mobility, sphincter control, and ability to care for oneself. Additional handicaps imposed on the individual by permanent neurological deficits include loss of employment, financial insecurity, social restriction, and complicating medical and depressive illnesses [4—7].
To date, no work is available that details the clinical course and prognosis of neurological deficits of any etiology subsequent to ESI. Retrospective chart reviews to describe the incidence and types of complications subsequent to ESI have been published [8—15] Table 1. Most adverse reactions are minor, but potentially serious neurological complications like epidural hematoma  , radicular injury  , and transient limb weakness  are mentioned.
Details about the specific incidence of these more serious complications as well as the clinical course of these events are not described. The purpose of this article is to collect and analyze case reports of neurological deficits subsequent to ESI in order to describe their time course, etiology, permanence or reversibility, neurological level, and prognosis. The strategy of assimilating case reports to inform a clinical impression of rare medical events is not novel.
Spinal hematomas  and epidural abscesses  of all etiologies have been studied in this manner. More specific to pain medicine, Hooten and colleagues  , who reviewed cases of discitis after spinal-area injections, suggest that case report literature contain the majority of information about infectious complications of spinal injections.
This current review of case report literature collects and analyzes cases that resulted in the chief complaint or clinical presentations of neurological signs and symptoms after ESI; it then analyzes clinical progression from symptom presentation and tries to identify trends in temporal onset, differential diagnoses, evaluation and treatment, and prognosis.
Neurological deficits include alteration or loss of consciousness LOC , or alteration or loss of sensory—motor function in one or more limbs. An important limitation of this methodology includes inconsistent or lack of reporting of clinical information among disparate case reports .
An added burden of small series, commented on by Hooten and colleagues, is that findings must be interpreted with caution . Unreported or inconsistent data points in individual cases augment the handicap of small sample size. Identification of clinical features of neurological deficits subsequent to ESI should expedite patient care when this complication occurs. Although the expert interventional pain physician may believe severe adverse events after ESI related to the neurological system have an empiric treatment, some of these events have delayed presentations to which the first physician responder is in the emergency department of a community hospital [19—22].
Moreover, catastrophic adverse neurological events immediately after ESI quickly recruit emergency physicians, intensivists, diagnostic radiologists, and neurological or spinal surgeons [23—25]. A clinical framework to treat neurological deficits after ESI benefits the patient and assists a spectrum of health care providers.
Additional cases were found by reviewing cited references. After a cursory review of the cases, six more search terms were queried: The goal was to include cases that mimic the clinical experience of a patient presenting with neurological deficits any time during or after an ESI.
Definition of terms is required. Neurological deficit, as used in this article, reflected the patient's chief complaint and objective signs or weakness or sensory loss or in the case of LOC, the overwhelming clinical presentation. Transient pain experienced during a procedure but not associated with allodynia or weakness was not considered a neurological deficit or the onset of a neurological deficit. The patient was placed in the category of the highest level of deficit manifested: Neurological deficits, which presented immediately during injection, postinjection , intermediately recovery room or later that day , or late days after injection in temporal relationship to the ESI, were included in this study.
Hypotension was not an exclusion criterion. Vasovagal events can result in LOC. It is understood that they are hemodynamic events that can result in alteration of neurological function. For this article, any etiology of neurological deficit was investigated; permanent neurological injury did not have to occur. On the other hand, a study of the severity of vasovagal symptoms was not the goal of this article. Only one case describes hypotension associated with LOC .
This case is also the only reversible case of LOC . Subdural or intrathecal injection is postulated . Hypotension and bradycardia are not exclusion criteria for occurrences of quadriplegia and paraplegia because these hemodynamic findings occur in acute spinal cord injury of other etiologies .
Excluded were case reports describing 1 procedures other than ESI e. Also excluded were cases involving injury to or abnormality of supporting structures of the neuroaxis but having a normal neurological exam [30,31] , or infections of the neuroaxis in which the chief complaint was related to systemic complaints fever or localized pain [18,32—35].
In these cases, the onset of neurological deficits was subsequent to other prominent signs. Deficits of the special senses visual loss [36—39] were also excluded. Information collected from the case reports included 1 anatomic approach: Appendices 1 and 2 Onset of neurological deficits were based on objective exam findings and were arbitrarily defined as during injection, just after injection or up to 30 minutes , in the recovery period but prior to discharge or 30 minutes to 3 hours , after discharge the same day or 3 hours to 24 hours , and greater than 24 hours.
After a cursory review of the cases, five other designations needed to be defined: The reversibility or permanence of a neurological lesion was absolute in some cases. However, cases in which the neurological deficit improved partially required a set point between reversible and permanent. ASIA impairment scales  were determined for patients with tetraplegia and paraplegia. Four other categories exist to describe motor function: Infarctions included diagnosis demonstrated on radiographic or postmortem findings.
An MOL included epidural or subdural collections with well-defined borders pathologically occupying an anatomic space. Except where otherwise noted, Fisher's exact test with two-tailed P value  evaluated relationships among nominal or categorical nonparametric events and conditions. Mann—Whitney U-test  evaluated ordinal data related to temporal onset of neurological deficits. Thirty-three case reports, dated between and , describe neurological deficits after ESI: The first division of cases occurred along the quality of permanence or reversibility.
Nineteen presenting deficits remained permanent [3,19,23—25,43—45,48—53, 56] while fourteen were reversible neurological deficits [20—22,26,27,46—48,54,55,57,58] Table 2.
The average age of the permanent group was 51 years SD 11 years , and the average age of the reversible group was 53 years SD 12 years. The permanent and reversible groups were then subdivided into four levels of neurological deficits: Severe sequelae included four deaths [19,23,24,43] , three intubations [24,25,43] , and the need to access higher levels of care. Differences between groups include the average year of publication: The range of publication was 16 years — for both groups, but possible differences in procedural technique as well as mode of diagnostic testing were analyzed to assess for different eras of care.
The distribution of TF vs IL approaches differed between the permanent and reversible groups. There were significantly more TF approaches in the permanent group and significantly more IL approaches in the reversible group.
Unknown values resulted in a loss of data and a loss of clinical information. Initial imaging showed a radiographic lesion 13 of 18 times [19,23,24,43,44,48,49,52,56]. Of the five initially negative scans, four developed radiographic lesions on follow-up studies [3,45,50,53]. Only one patient had negative initial and follow-up neuroimaging . Six patients in this group were imaged, and all initial studies revealed pathology: The distribution of diagnoses causing deficits between the permanent group and the reversible group was analyzed by comparing one diagnostic etiology to the combination of all other etiologies.
The rates of recovery for the two largest diagnostic groups—infarction and MOL—were compared. The etiology of neurological deficits and its distribution in the permanent or reversible group; P value reflects the distribution of the specific etiology in the permanent and reversible groups vs all other etiologies combined. This subject had negative initial and 6-month magnetic resonance images . A fourth patient may have two factors contributing to his neurological deficit.
The mechanism of injury in this permanent-deficit case was postulated to be vascular injection and spinal infarction by the case's authors, and spinal infarction was considered the mechanism of injury in this review .
Modest motor improvement occurred, however, after urgent discectomy, suggesting MOL contributed to the neurological deficit. The temporal distribution of each diagnosis was compared with the combined temporal distribution of all other cases not in that diagnostic group. The 10th case, a cerebellar infarction and herniation, presented after discharge, and the 11th infarction occurred during injection. In three of four cases, neurological deficits due to neural trauma presented after 24 hours Table 4.
Vital signs, to evaluate the possibility of vasovagal and subdural injection in LOC cases, were reported in only three of six cases. Vital signs were stable in two cases of permanent altered consciousness that led to death [23,24]: In the third LOC case, which was the only reversible case, hypotension was noted and subdural injection was postulated .
The fifth case, due to delayed cerebellar infarction and herniation, reported a patient being discharged home  ; one presumption is that vital signs were stable at the time of discharge.
The sixth case of LOC did not report vital signs . This sample size is insufficient to assess the prognostic significance of hypotension vs normotension associated with LOC after ESI. In cases reporting on spinal paralysis, only one author used ASIA terminology to describe spinal cord injury .
Several authors reported on both sensory—motor level and rectal tone, which allows calculation of an ASIA impairment scale [25,45,57—49,51,54].
The LOC and quadriplegia categories are combined when discussing treatment and outcome because both levels of injury had marked morbidity and mortality in the permanent group. The LOC patients died within 24 hours of their injections [23,24]. The quadriplegia patients died after 2  to 4 weeks  due to complications of their courses.