Atypical Presentations of Epidural Abscess in Intravenous Drug Abusers HEATHER PRENDERGAST, MD, DAVID JERRARD, MD, JEANNE O'CONNELL, MD Two cases of epidural abscess in afebrile intravenous drug abusers are presented, Both patients presented for evaluation of back pain that developed only after having moved heavy household items. One patient admitted to not having used intravenous drugs in at least 2 years. These cases are presented to illustrate the atypical fashion in which epidural abscess may present. (Am J Emerg Med 1997;15:158-160, Copyright © 1997 by W.B. Saunders Company) Epidural abscess is a well-known complication of intravenous drug abuse. Most commonly in this group of patients cutaneous disruption coupled with poor hygiene allows hematogenous bacterial seeding of the epidural space. Because of the anatomy of the epidural space, the usual sites for proliferation of these abscesses are the lower thoracic and proximal lumbar region of the vertebral column. Ordinarily, patients with epidural abscess will report spontaneous onset of back pain and fever. We report two cases of extensive epidural abscess in afebrile patients who had no back pain prior to minor back trauma. One patient had not used intravenous drugs in more than 2 years.
CASE 1 A 42-year-old black man presented to the emergency department (El)) with a complaint of low back pain. He reported that 3 days earlier he had helped a friend move a sofa, during which he lost his balance and injured his back. He reported no back pain prior to the incident. He reported no extremity weakness in the ensuing days since the accident. He admitted to a history of intravenous abuse of drugs such as heroin but had not used any drugs in over 2 years. He reported no fevers or chills. He denied any medical problems including diabetes, hypertension, or cardiac disease. He reported no family or personal history of sickle cell disease. On examination, the patient appeared to be in a mild amount of pain. His temperature was 36.5°C; blood pressure, 140/80 mm Hg; pulse, 86 beats/rain; and respiratory rate, 20 breaths/min. He was tender in a paralumbar distribution only at a level of L3-L4. His motor strength was 5/5 throughout. Knee and ankle reflexes were +2. There were no sensory abnormalities noted. He was able to ambulate well. He complained of no radicular pain. The patient was given the diagnosis of musculoskeletal back pain and was dis-
From the Division of Emergency Medicine, University of Maryland Medical Center, Baltimore. Manuscript received September 6, 1995, returned October 17, 1995; revision accepted November 23, 1995. Address reprint requests to Dr Jerrard, Emergency Medicine, University of Maryland Medical Center, 22 South Greene St, Baltimore, MD 21201. Key Words: Epidural abscess, atypical presentation. Copyright © 1997 by W.B. Saunders Company 0735-6757/97/1502-001355.00/0 158
charged on 800 mg of ibuprofen three times daily and 10 mg of cyclobenzaprine three times daily. He returned to the ED 2 days later complaining of increasing weakness in his legs and increasing lower lumbar back pain. He denied any paresthesias. His temperature was 38°C; respiratory rate, 20 breaths/min; pulse, 88 beats/min; and blood pressure, 150/80 mm Hg. He denied any symptoms such as cough, myalgias, or rhinorrhea. He denied bowel or bladder incontinence.Again, he was questioned about his intravenous drug abuse history. This time he denied any sort of needle use in well over 5 years. He also denied any recent infections. On examination, he was found to be in significantly more pain than 2 days earlier. His pain was still paralumbar in location. Reflexes were unchanged. Motor strength was 4/5 throughout. Rectal tone was normal. Laboratory tests revealed a white blood cell count of 18,600. Differential was 86 segs, 6 bands, 8 lymphs. Lumbar radiographs were normal. The patient underwent emergent magnetic resonance imaging (MRI), which showed epidurai abscess not only at the L1-L3 level but also at the T8-T9 level, an area where he had never complained of pain. The patient was admitted to the neurosurgical service and underwent emergent total laminectomy and drainage. The patient remained in the neurosurgical intensive care unit for 2 days before being transferred to the floor. His hospital course was remarkable for his regaining of full motor strength in his lower extremities. The patient walked out of the hospital 2 weeks after surgery. Abscess cultures grew Staphylococcus aureus.
CASE 2 An obese 46-year-old black man presented to our ED complaining of lower back pain 3 days after having helped a friend move a refrigerator. He denied back pain prior to moving the refrigerator. He denied any weakness or paresthesias. He admitted to occasional intravenous drug abuse, his last use having been approximately 2 weeks before this ED presentation. He denied fevers or chills. He also denied any medical problems such as diabetes, hypertension, cardiac disease, or sickle cell disease. The patient was in a moderate amount of pain. His blood pressure was 160/88 nun Fig; pulse, 82 beats/min; respirations, 20 hreaths/min; and temperature, 36.8°C. The patient had 5/5 motor strength throughout both lower extremities and was tender in a paralumbar distribution from L2-L4. There was no midline tenderness noted. Reflexes were +2 throughout. The patient ambulated well. He was discharged on 800 mg of ibuprofen three times daily and 10 mg of cyclobenzaprine three times daily. He returned to the ED approximately 2 days later unable to move both legs. He had been unable to move his legs for approximately 24 hours. He denied bowel or bladder incontinence. His temperature was 38.5°C; pulse, 80 beats/rain; respiratory rate, 22 breaths/ min; and blood pressure, 160/70 mm Hg. The patient had no reflexes and was unable to move his legs. Rectal tone was diminished. Laboratory data revealed a white blood cell count of 19,400. The differential revealed 84 segs, 10 bands, 6 lymphs. Plain radiographs of the lumbar vertebrae showed no abnormal findings. On further questioning at this time, the patient reported no recent bouts of pharyngitis, urinary tract infection, or dental manipulation.
PRENDERGAST ET AL • ATYPICAL EPIDURAL ABSCESS
Emergent MRI was performed, which showed a large epidural abscess (3 cm × 3 cm) encompassing L2-L4 level. The patient underwent emergency total laminectomy and drainage. Abscess cultures ultimately grew S aureus. At a 6-month follow-up, the patient still had complete plegia of lower extremities.
DISCUSSION Epidural abscess is a relatively uncommon disease with a previously reported incidence of 1 per 10,000 admissions.l,a However, in recent years the incidence has increased to an estimated 1.9 to 2.8 cases per 10,000 admissions. 3 Factors responsible include the growing use of epidural catheterization for pain relief and an upsurge in intravenous drug abuse. Defined as a bacterial infection in the epidural space with accumulation of purulent material or infected granulation tissue, this entity was first described by Morgagni in the 16th century. 4 The classic presentation, still in effect today, was described by Heusner in 1948 as a continuum of four phases. 5 The first phase is characterized by spinal ache or midline back pain, soon accompanied by localized tenderness and fever. Phase lI is characterized by the development of root or radicular pain, often associated with fever and peripheral leukocytosis. Phase II usually follows phase I by 2 to 3 days. Headache and nuchal rigidity may also be found during this stage. 6 Phase III usually follows phase II by approximately 4 days and is characterized by weakness of voluntary muscles and bowel and bladder sphincter tone, as well as by sensory abnormalities such as ascending anesthesia. Phase IV is marked by progression of weakness to paralysis. This progression may be rapid--within 24 hours for nearly one third of patients. 7 Once paralysis has occurred, the rate of full neurological recovery, even with immediate surgery, has been dismal. Heusner 5 reported that of 158 cases of epidural abscess, not 1 of 39 patients who had been paralyzed for longer than 48 hours regained motor function. Those having no paralysis at the time of surgery uniformly recovered. In 1973, Hancock 8 described a series of 48 patients with paralysis at the time of surgery, only 41% of whom had any degree of neurological recovery following drainage. 8 The devastating sequelae of an epidural abscess is the direct result of cord compression as well as epidural and intraspinous thrombosis of arteries and veins. 6 It is believed that these vascular lesions most significantly contribute to the rapid progression from phase III to IV. 9 In the majority of cases infection reaches the epidural space via two primary routes, direct extension and hematogenous spread from cutaneous diseases, pneumonia, dental abscesses, and urinary tract infections. 2 There have been reports of abscesses occurring as a result of minor trauma and lymphatic spread, l° Patients at an increased risk of developing epidural abscess include alcoholics, intravenous drug abusers, patients with malignancies, diabetics, chronic dialysis patients, and those who are steroid dependent. ~ It has been proposed that an elevated erythrocyte sedimentation rate (ESR) in a diabetic with back pain may be pathognomenic for epidural abscess? 2 At this point, no recommendations can be made as to the reliability of the ESR as a screening test because no studies have determined its sensitivity.
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The spectrum of organisms causing epidural abscess is becoming more diverse with gram-negative infection on the increase. 2 Other organisms implicated include Mycobacterium species. ~ However, the most common organism is S aureus, with a reported incidence of 64% to 90%. 3,~ An acute epidural abscess should be suspected in any patient with back pain and fever, particularly so in a patient who has abused drugs intravenously. The differential diagnosis should include the inflammatory myelopathies such as transverse myelitis and acute myelitis, vertebral disease, intervertebral disc disease, tumors compromising the spinal canal, and meningitis. These entities will usually differ from epidural abscess in character, but ancillary studies will be needed to definitively rule out the existence of epidural abscess. 9 For cases in which there is a heightened suspicion of an epidural abscess, radiologic imaging is indicated. Plain radiographs are usually normal unless there is concomitant vertebral osteomyelitis. Myelography is almost always positive but has largely been abandoned because of the risk of intradural spread of infection. H MRI appears to be superior for early recognition and anatomic localization of the infection. 13,14 Computed tomography (CT) is less sensitive than MRI and may fail to identify not only the extent of the abscess but the abscess itself. 14,~5MRI is equally as sensitive as CT myelography in detecting epidural abscess but has the further advantage of distinguishing other entities in the differential diagnosis, such as disc herniation, spinal tumor, syrinx, spinal herniation, and infarct, as well as transverse myelitis.16 MRI will define spinal cord compression and the status of the cord. It will also determine the extent of the abscess and exclude a drainable paraspinal fluid collection. If MRI is absolutely not available, CT myelography may be used. CT myelography has the inherent risks of an invasive procedure. Efforts should be directed toward transferring the patient to a center that has MRI capability.~7 Once confirmed, the mainstay of treatment remains surgical intervention with decompression laminectomy. There are reports of patients being managed medically with mixed results. 2,3,1° Antibiotic regimens have varied but most seem to have included an aminoglycoside along with a semisynthetic penicillin. Vanocomycin, if methicillin-resistant staphylococcus is a concern, may be used. To date, however, there is no consensus in the published literature on the efficacy or advisability of nonsurgical approaches in managing spinal epidural abscesses. On occasion, the neurosurgery literature has called for a more liberal use of nonsurgical therapy. Most specifically, those situations include lack of neural compression from mass effect, as well as obtaining satisfactory culture of the infectious agent. 18On the other hand, literature from infectious disease specialists has maintained that surgical intervention is the treatment of choice.t5 The current published literature does not support the widespread use of nonsurgical therapy for spinal epidural abscess. Steroids are not warranted. Back pain and fever in an intravenous drug abuser clearly dictates that epidural abscess be at the forefront of a practitioner's differential diagnosis. However, as the nature and dramatic outcome of these two cases show, the presence of epidural abscess may not at all times during development
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AMERICAN JOURNAL OF EMERGENCY MEDICINE • Volume 15, Number 2 • March 1997
be heralded by fever and back pain. As in these cases, symptomatology such as back pain may initially be ascribed to temporally related trauma. Curiously, although the abscesses were well formed and, in one case, had multiple locations, neither patient reported back pain prior to the recent trauma. Although it was known that both patients were intravenous abusers of drugs, the time of onset of back pain and in what context, coupled with the lack of fever, determined the initial treatment. Ultimately, though, in every case back pain and fever will be present coincidentally. The first case raises an additional issue with regards to time elapsed since last intravenous drug use and the point at which the likelihood of epidural abscess becomes less plausible in a patient with a remote history of intravenous drug use and back pain with or without fever. The patient's initial admission was that he had not used intravenous drugs in more than 2 years, but he changed this on revisit to encompass a much longer period of drug-free living. Drug testing was not done. Extensive review of the literature has failed to demonstrate work showing a "safe" period of drug-free living beyond which fever and back pain no longer necessitate MRI testing.
SUMMARY All undiagnosed epidural abscesses will lead to paralysis and, ultimately, death. Classically, the history of nontraumatic back pain, fever, and intravenous drug abuse have been compelling reasons to pursue the diagnosis of epidural abscess. Back pain from any etiology in a patient with a history of intravenous drug use should still arouse suspicion for the possibility of epidural abscess. Back pain, fever, and a history of intravenous drug abuse absolutely necessitate, most ideally, MRI evaluation. Complete recovery without neurological deficit is dependent on early diagnosis and treatment.
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