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Cauda Equina Syndrome M. Creech Feb 2012. Outline Definition Epidemiology Pathophysiology Presentation Imaging Treatment Outcomes.

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Presentation on theme: "Cauda Equina Syndrome M. Creech Feb 2012. Outline Definition Epidemiology Pathophysiology Presentation Imaging Treatment Outcomes."— Presentation transcript:

1 Cauda Equina Syndrome M. Creech Feb 2012

2 Outline Definition Epidemiology Pathophysiology Presentation Imaging Treatment Outcomes

3 Definition Cauda equina: “horse’s tail” –refers to the terminal portion of the spinal cord and roots of the spinal nerves beginning at the L1 Cauda Equina Syndrome (CES): –is a compression of some or all of the nerve roots of the cauda equina – symptoms: bowel and bladder dysfunction saddle anesthesia varying degrees of loss of lower extremity sensory and motor function

4 Epidemiology Causes for CES –DISC HERNIATION (1-6% of operated discs are CES) –Trauma –Tumor –Spinal stenosis –Epidural hematoma/abscess Iatrogenic causes: –Lumbar spine surgery –Durotomy –Annuloplasty –Gel- foam –Epidural fat graft placement –Spinal manipulation Spector et al. JAAOS 2008;16:

5 Pathophysiology Conus medularis: –Caudal end of spinal cord btwn T12 to L2 Filum terminale attaches conus to coccyx Cauda equina is collection of peripheral nerves L1-S5 –Contained in dural sac in lumbar spinal canal Lesions of cauda equina result in: –Lower motor neuron lesion –Weakness, loss of sensation, decreased reflexes

6 CES: Bladder dysfunction S2-4 parasympathetic (empty bladder by contract detrusor, and relax internal sphincter) T11-L3 sympathetic hypogastric plexus (retain urine by detrusor relaxation, sphincter contraction) S2-4 Somatic (pudendal nerve) controls external sphincter Reflex arc disrupted by lower motor neuron lesion: –resultant loss of sensation and motor fxn causes retention and overflow incontinence, as unable to void voluntarily

7 3 Main Causes of CES: 1.Mechanical Compression 2.Ischemia 3.Venous overflow (compartment syndrome)

8 Mechanical Compression Exposed nerve roots No epineurium, No perineurium Only endoneurium Increased susceptibility to trauma

9 Mechanical compression Compressing nerve roots also reduces nutrition Animal studies (canine model) demonstrated decreased nutrition by reducing both blood flow and nutrient diffusion from the surrounding cerebrospinal fluid Delamarter; Spine 1991

10 Ischemia Most important observation: watershed area of hypo vascularity around cauda equina Primary blood supply of anterior spinal artery, and paired dorsolateral spinal aa Nerve roots supplied by distal and proximal radicular artery = anastomosis Tentative blood supply that is susceptible to damage Parke JBJS A 1981: anatomic studyParke JBJS A 1981: anatomic study

11 Venous Congestion (Compartment Syndrome) Mechanical pressure causes intraneural edema Directly causes nerve damage Secondary injury due to increase in intraneural pressure, when greater than the nerve root perfusion pressure ischemia occurs Animal studies (porcine) showed 2 level compression worse than 1 –Preventing outflow Rydevik et al Clin Orthop Relat Res 1992

12 Pathophysiology CES: post-operative spine surgery lumbar discectomy: retraction or hematoma reports suggest spinal stenosis and edema cause venous congestion and resultant CES usually <24hrs, can be 7d before develops reported CES after arthrodesis for spondylolisthesis, which was detected late 2-7d (5/12 recovered), thought routine urinary catheter (and lack of awareness by surgeon) delayed diagnosis. Delamarter et al Spine 1991

13 Pathophysiology Peri-op anticoagulation: suggested to start LWMH 2 hrs post lumbar puncture, later or avoid if a “traumatic” bloody tap. wait 8-12hrs after LMWH before inserting spinal needle CHEST guidelines: Elective spine surgery: recommends against mechanical or chemical anticoagulation, recommends mobilization Resuming pre-op anticoagulants after 48-72hrs Weighting risk of post-op bleed/ CES vs need for anticoag Recommend: no loading dose or bridging anticoag

14 Presentation Hx: LBP &/or bilateral leg pain (progressively worsening nature) Acute vs insidious onset Inquire about bowel or bladder habits –difficulty voiding, urinary incontinence, and/ or loss of bowel control high index of suspicion of anticoagulated or post operative pts

15 Presentation PE: Myotomes Dermatomes Reflexes Sensation to pinprick in perianal region (S2-S4 dermatomes), discrimination btwn pinprick/ light touch req’d –typically preserved sensation to pressure and light touch

16 Presentation Rectal examination: assess tone and voluntary contracture of external anal sphincter Decreased rectal tone early finding of CES Anal wink test –Tactile stimulus cause contraction of anal sphincter muscles and also flexion –The stimulus is detected by nociceptors in perineal skin and causes a reflex arc involving the pudendal nerve (S2-4) –Absence of reflex indicates interruption of reflex arc Bulbocavernosus reflex

17 Segmental polysynaptic reflex with crossover in S1-4 Apply pressure to glans penis or clitoris and/or traction on the Foley catheter Normal response involves contraction of the anal sphincter Absence of reflex indicates spinal shock

18 Presentation Symptoms: LBP, or groin or perineal pain Bilateral sciatica, leg weakness, sensory deficits Loss of bowel or bladder fxn Signs: lower extremity weakness hypo/ areflexia, sensory deficits, perineal hypoesthesia or saddle anesthesia, loss of bowel or bladder function Saddle anesthesia: late finding/ poor prognosis Bladder dysfxn (required for dx) Difficulty initiating flow > retention> overflow (often have prodrome of sciatica/ LBP) LBP: often severe, or resolving, bilateral sciatica is most associated with CES

19 Presentation Acute: Sudden severe LBP, sciatica, urinary retention requiring catheterization, motor weakness of LE, and perineal anesthesia –most commonly from acute central disc herniation Insidious: Recurrent episodes of LBP over weeks to years, followed by gradual onset sciatica, sensorimotor loss, and bowel and bladder dysfunction –most commonly with spinal stenosis Kostuik et al. JBJS 1986, Spector et al AAOS 2008

20 Presentation previous LBP confuses CES dx, and delays treatment –acute presentation 1.1d until decompression –insidious presentation 3.3d (17/31 had unilateral sciatica) sensory deficit in the perineal area (partial, complete, unilateral, or bilateral) was most important prognostic indicator Missing the diagnosis delays tx. Widely varying presentation causes delayed recognition 44 cases: 24 pts had delayed dx by 9d avg –(pt related causes 17%; MD related 83%)

21 Imaging Clinical diagnosis! Emergent imaging used to help determine characteristics and to plan approach to surgery In post-op pts, may Rx surgically without imaging if not available or if MRI preop MRI is preferred modality Myelography and CT if MRI not possible/ available

22 Treatment Surgical exploration and decompression of any compressive lesions –if medically stable Micro discectomy, or wide laminectomy, discectomy, and open inspection of nerve roots Goals: minimize manipulation of nerves; may require larger laminectomy than uncomplicated disk herniation

23 Treatment Can this wait until the morning? Retrospective reviews indicate optimal outcomes if decompressed within 48hrs –no benefit between 24hrs vs 48hrs –After 48hrs since presentation, recovery decreases Shown by: Ahn, Spine 2000 Shapiro, Neurosurgery 1993 Kostuik, JBJS 1986 Shapiro, Spine 2000

24 Outcomes Initial report was bleak: –1966 Schaeffer; recovery unlikely (5pts) Reports improved over time: –17/22 regained urinary fxn; 13/17 motor recovery, 14/21 sensory recovery, 13/15 regained perianal sensation –Urodynamics: at 8w ranged post-void residuals, and essentially full recovery by 8-12mo for 9/11 pts (4 did not recover) –Sexual dysfunction 26-50%; loss of sensation, urinary incontinence –Chronic LBP associated with worse recovery of urinary and rectal function –Increased age correlated w poor sexual function recovery –Surgery within 48hrs improved recovery for B/B fxn, sensory and motor deficits. No difference for pain and sexual fxn

25 Thank you. OITE

26 A man has a T5 Burst fracture. Examination reveals 0/5 motor strength in both lower extremities in all groups. He has no light touch or pinprick sensation in his lower extremities or trunk. He has decreased rectal tone but has an intact perianal sensation and bulbocavernosus reflex. According to ASIA what is the classification of spinal cord injury? 1. ASIA A, complete 2. ASIA A, incomplete 3. ASIA B, complete 4. ASIA B, incomplete 5. ASIA C, incomplete

27 4. ASIA B, incomplete

28 Figure 1 and 2 show MRI scans of a 62 year old male with 1 year hx of worsening low back pain and bilateral leg pain. His leg pain is greater than his back pain and increases in severity when he walks more than 5 mins. He has normal bowel and bladder. Conservative management has failed. Appropriate treatment include; 1. computer-assisted axial traction 2. interspinous process spacer placement 3. L4/5 laminectomy with posterior spine arthrodesis 4. Complete laminectomy at L4 with bilateral NR decompression 5. anterior discectomy and interbody fusion at L4/5

29

30

31 4. Complete laminectomy at L4 with bilateral NR decompression

32 A 51-year-old male with a extensive cardiac history including insertion of pacemaker reports difficulty with urination and numbness in his bilateral buttock. His symptoms began 12 hours ago. What is the next step in management? 1. MRI of the spine 2. CT myelogram of the lumbar spine 3. Epidural steroid injection 4. Physical therapy, NSAIDs, and outpatient followup 5. High dose methylprednisone

33 4. CT Myelogram of lumbar spine

34 A 49-year-old male presents with saddle anesthesia, lower extremity weakness, and urinary retention. When must surgical decompression be done to improve bladder and motor recovery? 1. less than 24 hours after symptom onset 2. less than 48 hours after symptom onset 3. less than 60 hours after symptom onset 4. less than one week after symptom onset 5. less than two weeks after symptom onset

35 2. less than 48 hours after symptom onset

36 Thank you

37 Neurogenic Shock Abnormal Hemodynamics: 1. Hypotension 2. Bradycardia 3. Peripheral vasodilation Resulting from autonomic dysfunction and the interruption of sympathetic nervous system. Usually in injuries above T6, secondary to the disruption of the sympathetic outflow from T1-L2 and to unopposed vagal tone, leading to a decrease in vascular resistance

38 Spinal Shock Complete loss of all neurologic function, including reflexes and rectal tone, below a specific level that is associated with autonomic dysfunction. State of transient physiologic (rather than anatomic) reflex depression of cord function below the level of injury Flaccid paralysis, including of the bowel and bladder, is observed, and sometimes sustained priapism develops. Usually resolves in hrs


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