Epidural abcess a case presentation

Dr. Ramy Mostafa Abdelkader,Msc

Clinical fellow in Emergency medicine

Case presentation

8/11/2016 Not just back pain

Not just back pain

Disclosures

I have no conflict of interest or

disclosure in relation to this

presentation

Learning Objectives

i. Case based discussion about LBP presentations and differential diagnosis

ii. Role of proper imaging in diagnosis

iii. Current Updates In Emergency Medicine management

68 years old female

Known HTN, 30yrs h/o intermittent LBP, 2wks ago

exacerbation of LBP admitted abroad, given NSAIDs, had

MRI LSS showing L3/4 L4/5 disc bulges and discharged,

from 3ds her pain became worse and now she is unable

to move .

What questions would you like to ask

regarding her history?

Patient Presentation to ER

lower limb weakness, loss of sensation plus

urinary retention and burning sensation of 3

days duration.

Till the last week the patient was mobile and

admitted to hospital in her country due to back

pain and got NSAIDs and steroids on regular

basis then discharged .

fell down at home due to Lower Limb loss of

power followed by fever and urinary retention

with drippling.

History continued

Vitals & Measurements T: 36.8 °C (Oral) HR: 72 (Monitored) RR:

19 BP: 130/58 SpO2: 98% WT: 90 kg

Past History

Hypertension

Chronic dermatitis

Chronic low back pain

Family History

Positive in her parents for hypertension

Procedure/Surgical History

Never

Medications

bisoprolol, 5.0 mg, Oral, Daily

celecoxib, 200.0 mg, Oral, BID

valsartan, 160.0 mg, Oral, Daily

Prednisolone 5 mg, Oral , Daily

Allergies

No Known Allergies

Social History

Tobacco

Details: Never smoker

Review of Systems Constitutional: History of fever, No chills.

Respiratory: shortness of breath, No cough, No wheezing.

Cardiovascular: No chest pain, No palpitations.

Gastrointestinal: no nausea, no vomiting, diarrhea, No

heartburn.

Genitourinary: dysuria and urinary urgency. Then developed

anuria

Musculoskeletal: low back pain, no joint pain, muscle pain.

Neurologic: Alert Generalized weakness

Physical Exam General: the patient looks tired and in pain but fully

conscious afebrile and vitally stable

HEENT: No pharyngeal erythema.

Respiratory: Lungs are clear to auscultation.

Cardiovascular: Normal rate, No murmur, Good pulses equal in all extremities.

No pedal edema

Abdomen: Soft, Non-tender .

Back exam: lumbosacral spinal tenderness

P/R exam: normal anal tone

Neurological: sensation lost up to umblicus

motor power 1/5 in both lower limbs

reflexes -ve

Gait couldn’t be assessed

• POCUS: full bladder and bilateral mild

Hydronephrosis

• Urinary Catheter Insertion

• Urine Microscopy/reflex culture

• Complete blood count

• Complete metabolic panel

• Coagulation profile

• Inflammatory markers

• Septic work up including blood C/S

and CXR

• MRI thoraco-lumbar

spine(with/without contrast?)

• Neurosurgeon consultation

• Start IV antibiotic and adequate

analgesia

Lab Results :

Cr932, Ur51.20, K+6.2, Na130, WBCs16.4,

ESR77, CRP198, bicarbonate 15.6,lactate 2.1

At that time ECG was requested

POC Urine analysis:

+3 RBCs

+3 wbcs

Nitrite +ve

What is your

Working diagnosis

Cauda equine

AKI + hyperkalemia

UTI

What will you do first?

• Patient shifted to Bay 1 (monitoring

for Hyperkalemia?!)/Dialysis line.

• Neurosurgeon want MRI once

patient is stable .

• Nephrologist wants to do

Hemodialysis & official Ultrasound

(ATN from NSAIDS given for pain or

post obstructive Uropathy due

to Urinary retention).

• Hemodialysis was done first (and

once)

• Patient is Delayed disposition as Bay 1

specialist and consultant refused to

admit the patient to AMU as

requested by the nephrologist (in his

notes) Until MRI is done.

• Patient developed fever (38.1 C during

her stay in ED)

• MRI done after 18 hours in ED

MRI reportImpression of the radiologist:

Extensive precontrast T1 hyperintense (subacute blood versus proteinaceous

material like pus) thoracolumbar spinal canal extramedullay collection with distal

spinal cord compression and cord signal change and crowding of cauda equina.

MRI Spine whole

There is T1 hyperintense extramedullary intraspinal collection surrounding the spinal cord which is seen

predominantly anteriorly from C6 to T11 levels and posteriorly from T5 to S2 level. There are also small

posterior loculated areas at T1-T3 on the right side and anterior collections from L4 - S2.

The posterior epidural fat is visualized in many areas where the collection is present and this feature suggest

that the collection is likely subdural in location, but exact differentiation between epidural and subdural is not

really possible in this noncontrast study. Contrast was not given due to severely elevated creatinine and

extremely low GFR

There is spinal cord compression which is most prominent at T11 and T2 levels extending superiorly to T10

and inferiorly to L1 levels. The lower spinal cord shows T2 hyperintensity.

Within the lumbar canal, there is crowding and mild compression of the nerve roots of the cauda equine due to

mass effect from the collection. Cervical spine shows mild degenerative changes most prominent at C5-6 and

C6-7 levels with mild disc bulges and right-sided uncovertebral DJD at C5-6. Mild disc bulges are also seen at

L2-3, L3-4 and L4-5 with slight ventral canal indentation, but not significant.

Multiple incidental hemangiomas are seen most prominent at T4, T7, T8, L3 and S1 levels. No evidence of

vertebral marrow or disc injury or infection.

Impression:

Extensive precontrast T1 hyperintense (subacute blood versus proteinaceous material like pus) thoracolumbar

spinal canal extramedullay collection with distal spinal cord compression and cord signal change and crowding

of cauda equina.

Spinal Epidural abscess

for Urgent intra-operative drainage

• MRI was done but without contrast and showed

long segment spinal epidural collection ( ?abscess)

with a compression mainly anteriorly above D 10

and posteriorly from the level of the 11 and below.

MRI also shows abnormal cord signal (ischemia) at

same levels.

Spinal Epidural AbscessSpinal epidural abscess (SEA) is a collection of pus or inflammatory

granulation between the dura mater and the vertebral column.[1] Currently the

annual incidence rate of SEAs is estimated to be 2.5-3 per 10,000 hospital

admissions. Incidence of SEA is on the rise, due to factors such as an aging

population, increase in use of invasive spinal instrumentation, growing number

of patients with risk factors such as diabetes and intravenous drug use.[1] SEAs

are more common in posterior than anterior areas,[2] and the most common

location is the thoracolumbar area, where epidural space is larger and contains

more fat tissue.[3] SEAs are more common in males, and can occur in all ages,

although highest prevalence is during the fifth and seventh decades of life.[1]

Spinal Epidural Abscess.

Why Care?

Irreversible paralysis in up to 22% of

patients, not because of bacterial

virulence but due to delayed diagnosis.4

50% of patients are initially

misdiagnosed.5 Paralysis lasting greater

than 24 hours is irreversible

Spinal epidural abscess: Intracranial epidural abscess

prevalence is 9:1

Predisposing factors

Trauma,

• prior surgery, or spinal procedures.

• Immunocompromised states

Pregnancy

• Diabetes mellitus (Type I or II)

• Bacteremia: (endocarditis, lung or

abdominal abscess, or previous septic

episodes)

Osteomyelitis

Acupuncture

IV drug use

Alcoholism

Chronic renal failure (Hemodialysis)

• The leading bacterial pathogen causing spinal epidural abscess

(SEA) is S. aureus, which accounts for about two-thirds of cases

caused by pyogenic bacteria

• Various other bacteria can also produce the infection.

• Mycobacterium tuberculosis is a more frequent cause of epidural

abscesses in parts of the developing world 1,2,4,5

Causative Organisms

As the pyogenic inflammation progresses and the

abscess extends longitudinally in the epidural space,

damage to the spinal cord can be caused by one or

more of the following mechanisms 6

●Direct compression

●Thrombosis and thrombophlebitis of nearby veins

●Interruption of the arterial blood supply

●Bacterial toxins and mediators of inflammation

Pathogenesis

DiagnosisThinking of spinal epidural abscess (SEA) is the key to diagnosis.

Is by Classic Triad

• Fever

• Spine pain (local spinal tenderness)

• Neurologic deficit

Differential Diagnosis

• Spinal Radiculopathy /

polyradiculopathy

• Bacterial meningitis.

• Osteomyelitis

• Spinal tumor / spinal hematoma.

• Multiple Sclerosis

• Spinal cord infraction (radiating pain

along involved nerve roots similar to the

pain seen with a spinal abscess.

LABORATORY FINDINGS

— Routine laboratory studies are seldom

helpful in the diagnosis of spinal epidural

abscess (SEA).

ESR is usually elevated in both SEA (90%)

and vertebral osteomyelitis,

the leukocyte count may be elevated or

normal 7

Approach to diagnosis• Magnetic resonance imaging (MRI)

the preferred test is MRI with Contrast because it is often

positive early in the course of the infection

• Computed tomography (CT) scanning with intravenous

contrast is an acceptable alternative to MRI if MRI is not

immediately available9

MANAGEMENTCombination of aspiration, drainage, and antibiotic

therapy

Early consulting the neurosurgeon is

mandated once SEA is suspected.

Appropriate empiric parenteral regimens include:

●Vancomycin for empiric coverage of MRSAPLUS●Either cefotaxime or ceftriaxone

The indications and timing for operative management of spinal epidural abscess: literature

review and treatment algorithm. Neurosurg Focus 37(2):E8:1-8, 2014

Quick Hits on Spinal Epidural Abscesses:

– bacteria can gain access to epidural space via

hematogones spread or direct inoculation into spinal canal

(e.g. during spinal or epidural procedures/surgery)

– risk factors include epidural catheters, diabetes mellitus,

alcoholism, HIV, bacteremia, IVDU

– Staph aureus is responsible for two-thirds of cases

caused by pyogenic bacteria

– MRI is the imaging test of choice for diagnosis; a less

sensitive/specific alternative is CT w/ contrast

– clear indications for urgent surgical interventions include

acute/progressive neurological deficits, spinal instability, or

disease progression despite antibiotics

Any Questions

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5. Darouiche RO, Hamill RJ, Greenberg SB, et al. Bacterial spinal epidural abscess. Review of 43 cases and literature survey.

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Thank you

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Presented by

Dr. Ramy Mostafa Abdelkader, MSc

Clinical fellow in Emergency medicine