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A 4-year-old with abdominal pain, refusal to walk
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The guest columnist this month is Nazia A. Jones, MD, with assistance from William A. B. Dalzell, MD, and Jennifer Crotty, MD, of the departments of pediatrics and pediatric infectious diseases of the Brody School of Medicine, East Carolina University.
A 4-year-old male came to the ED with 3 days of fever, abdominal pain and refusal to walk. Eight days earlier, he had developed abdominal pain and low-grade fever, for which he was seen at the local ED and diagnosed with otitis media and prescribed amoxicillin.
Nazia A. Jones
He saw his pediatrician the following day and was instructed to take acetaminophen for pain and fever, and polyethylene glycol for constipation, the presumed cause of the abdominal pain, but he returned to the ED with worsening abdominal pain 2 days later. Despite an unremarkable CT scan of the abdomen, he was evaluated by the surgical team, found to have signs of peritonitis on physical exam and taken to the operating room for an exploratory laparotomy, revealing only mesenteric lymphadenitis. His appendix was removed, and he was discharged from the hospital the following day, afebrile and tolerating oral fluids.
James H. Brien
After discharge, he continued to complain of worsening abdominal pain, had refusal to walk and began spiking higher fevers during the next 2 days. As his symptoms progressed, complaining of pain with all movement with decreased oral intake, he was brought back to the ED for further evaluation.
On physical examination, he was talking coherently but extremely irritable and resistant to examination. He complained of pain regardless of touch. He was febrile with cervical tenderness, nuchal rigidity and refusal to turn his head to the right. Generalized abdominal tenderness was present with well-healing surgical incision sites from the recent exploratory laparotomy. He was uncooperative for the rectal tone exam, but reflexes were brisk (4+) throughout with sustained clonus on the right and four beats on the left. Tone appeared to be increased and sensory examination was intact to touch in the upper and lower extremities.
An MRI of the spine is shown in Figures 1 and 2.
Source: Brien JH
Serum white blood cell count (WBC) was elevated at 43,000/mcL with 81% neutrophils and C-reactive protein (CRP) 310 mg/L. Due to concern for meningitis, a lumbar puncture was performed that yielded cloudy, purulent and slow-flowing cerebrospinal fluid (CSF) that took 30 minutes to collect 2 mL. CSF results showed WBC 8,350/mcL with 74% neutrophils, 1,350/mcL red blood cells, protein >1,500, and a low glucose of 31 mg/dL (serum glucose 108 mg/dL), and the Gram stain was negative for bacteria. He was treated with dexamethasone and empiric antibiotics (ceftriaxone, vancomycin and piperacillin/tazobactam) while cultures were pending. CT scan of the head was unremarkable. An MRI of the spine is shown in Figures 1 and 2.
Admission screening nasal swab for methicillin-resistant Staphylococcus aureus (MRSA) was positive, and later blood cultures also grew MRSA.
What’s Your Diagnosis?
A. Tuberculous meningitis
B. Spinal epidural abscess
C. Staphylococcal bacterial meningitis
D. Guillain-Barré syndrome
Answer: MRI of the spine revealed a holocord spinal epidural abscess (B) extending from C1 to S3.
The MRI shows in Figure 1 shows a large, rim-enhancing collection in the epidural space, extending from C1 through the thoracic spine. Figure 2 shows a large epidural phlegmon and abscess extending from thoracic and lumbar segments of the spine to the sacrum.
The patient was emergently taken to the operating room for laminectomy and abscess decompression, revealing 10 mL of pus drained from the cervical region and 40 mL of pus from the thoracic region. A drain was left at the cervical level and the wound was copiously irrigated with antibiotic solution. MRSA grew from the wound culture. A peripherally inserted central catheter (PICC) line was placed and the patient was treated with linezolid and daptomycin (Cubicin, Cubist Pharmaceuticals) for 7 weeks and rifampin for synergy for 4 weeks. He showed excellent clinical improvement as well as decline in erythrocyte sedimentation rate (ESR) from 109 mm/hour to 14 mm/hour. The patient’s neurodevelopmental status returned to near baseline, with occasional bladder incontinence.
Spinal epidural abscess (SEA) is a rare but potentially fatal illness that requires a heightened clinical awareness for prompt diagnosis and treatment. S. aureus is the most frequently isolated pathogen. Most cases are due to hematogenous spread from a remote focal infection, such as of the skin, soft tissue, urinary or respiratory tract. SEA can occur discontinuously at several levels of the spine. In much rarer cases, it occurs throughout the spine, documented in the literature as holospine or holocord SEA. IV drug use, spinal procedures, surgical interventions and medical conditions such as diabetes, Crohn disease and chronic renal failure are all risk factors for SEA, and most cases are associated with at least one of these risk factors.
Considering a diagnosis of SEA in the differential diagnosis is crucial for early detection and optimal outcome. Patients with SEA often have multiple visits to the ED before the diagnosis is made. This case highlights the importance of maintaining a high index of suspicion for SEA, even in patients without established risk factors who may present with fever, pain with movement, back pain, refusal to bear weight and neurologic deficits such as focal weakness, radiculopathy, myelopathy, bladder dysfunction and loss of rectal tone. The cause of neurological impairment is usually due to direct mechanical compression by the abscess. Neurological deficits may occur more frequently at late stages of the disease and can ultimately lead to paralysis, which is likely irreversible if present for more than 24 hours. MRI is the gold standard for diagnosis of SEA because CT has lower sensitivity, specificity and accuracy than MRI. Inflammatory markers such as CRP and ESR are generally elevated, however, they are nonspecific. These can be helpful in monitoring effectiveness of antibiotic therapy. CSF pleocytosis and high protein and lactate are typical, but again, not specific to SEA. Peripheral blood culture is helpful in isolating the causative organism and selecting appropriate antibiotics.
Figure 3. Focal neurologic signs that may develop include cranial nerve palsies due to the primary location of the infection at the base of the brain.
Official recommendations regarding management of SEA in the pediatric population are lacking and surgical intervention is controversial. Treatment for SEA in clinical practice has generally been surgical decompression and drainage in combination with antibiotics. Substantial neurological improvement occurs after surgical decompression. CT-guided needle drainage is a less invasive option compared with laminectomy for abscess drainage. Nonsurgical management should be considered in patients without neurological deficits and with extensive comorbid conditions that preclude safely undergoing surgery. Close monitoring, following inflammatory markers and repeat MRI may be necessary if management is nonsurgical. The duration of antibiotic therapy is usually at least 4 to 6 weeks. Final neurological outcome correlates closely with the severity and duration of neurological deficits before surgery.
Staphylococcal meningitis (C) is very uncommon without co-factors, such as shunts or other devices. One would expect a much more rapid clinical presentation with gram-positive cocci seen on the CSF Gram stain.
Tuberculous meningitis (A) is uncommon in the United States but can certainly occur and present very gradually or fairly acutely. According to the excellent chapter on Mycobacterium tuberculosis in Principals and Practice of Pediatric Infectious Diseases, 4th edition, written by Infectious Diseases in Children Editorial Board member
Guillain-Barré syndrome (GBS) is a group of autoimmune disorders that may be preceded by a febrile illness, but typically not an acute febrile illness per say, but rather a poly-neuropathy with ascending paralysis. It is usually not confused with meningitis. The CSF findings may share an elevated protein, but there is little to no pleocytosis with GBS, as well as a negative Gram stain and normal glucose.
Columnist Comments
I want to thank Dr. Nazia Jones for contributing this excellent case, and for her discussion of spinal epidural abscess. Dr. Jones is a senior pediatric resident at the Brody School of Medicine at ECU in Greenville, N.C. She graduated from the University of South Carolina School of Medicine. In the fall of 2014, she will be joining a private practice in Columbia, S.C. This submission would not have been possible without the mentorship of Dr. William A. B. Dalzell and Dr. Jennifer Crotty.
More Medical History
Last month, I introduced some of you to the great Persian physician Rhazes, the “Father of Pediatrics.” This month, I thought we would go back a bit closer to the beginning of recorded medicine and review the origin of the symbol of medicine: the Staff of Asclepius. The line between historic fact and Greek mythology appears to be blurred in the case of Asclepius. According to the writings of Homer, and supported by the National Library of Medicine, Asclepius was an actual person, who was the most notable physician in Greece during a time of approximately 1200 B.C. The mythological Asclepius was the son of a mortal mother (Koronis) and the god Apollo. Due to Koronis being unfaithful to Apollo, his twin sister, Artemis, killed her prior to the birth of Asclepius; however, Apollo rescued him from the body of Koronis as she burned on the funeral pyre. Apollo then turned the baby over to the centaur Chiron to raise and educate the child about medicine. He learned fast, but of course, there probably was not much to know in those days. I doubt Asclepius had to memorize the Krebs cycle. Anyway, his reputation became such that he inspired many followers (Asclepiads), who later claimed to be biological descendants, inheriting the same mystical powers of healing. History (mythology) subsequently transformed Asclepius into the god of medicine, and Aesculapian temples were built as places of worship and healing centers; the forerunners of hospitals. All depictions of Asclepius are shown with him holding a staff or rod with a snake wrapped around it. The staff could serve as many things, from a walking stick to a weapon. The snake has deep roots in the healing arts, as they were used for their presumed medicinal powers. It has been written that some patients who came to the temple for help were required to sleep in a room with a non-poisonous snake in hopes that the spirit of Asclepius would appear in a dream to cure their ailment(s). Whatever the real story may be, adopting the symbol of a staff with a single serpent wrapped around it, is derived from Asclepius, and has stood the test of time as the true symbol of medicine in the minds of most academic medical historians.
Figure 4. Dr. Brien's Army jacket seen above.
This symbol also has roots in Greek mythology as the symbol of Mercury or a messenger. However, as a symbol, it had mystical powers to soothe the suffering of those dying. There is also a connection with Apollo, who gave a Caduceus to his step-brother, Hermes, as a token of friendship. It has also been associated with trade and commerce. However, its use as a symbol of medicine is probably not technically appropriate, but has also stood the test of time, even if by mistake. Inappropriate as it might be, I wore this symbol every work day for more than 20 years, as this is the symbol used by the US Army Medical Corps, and is part of the uniform (figure 4, my old Army jacket). Just like the improper use of language, it becomes proper and accepted over time. The word “ain’t” was not in Webster’s Dictionary when I was in school.
Please keep in touch, and let me know if these bits of history are worthwhile.
Starke JR. Mycobacterium tuberculosis. In: Long SS, ed. Principals and Practice of Pediatric Infectious Diseases, 4th ed. Philadelphia, Pa.: Elsevier; 2012.
James H. Brien, DO, is vice chair for education in the department of pediatrics at McLane Children’s Hospital at Scott & White/Texas A & M College of Medicine in Temple, Texas. He is also a member of the Infectious Diseases in Children Editorial Board. Brien can be reached at: jhbrien@aol.com.
Disclosure: Brien reports no relevant financial disclosures.