PLID by Rezaul Karim sirsefgvffedrfgg.pptx

PLID by Rezaul Karim sirsefgvffedrfgg.pptx

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  ACUTE LUMBAR INTERVERTEBRALDISC PROLAPSE (PLID) PROF. DR. MD. REZAUL KARIM SPINE & ORTHOPAEDIC SURGEON NITOR
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  DISC AND SPINEANATOMY • The intervertebral disc has a complex structure; the nucleus pulposus has an organized matrix, which is laid down by relatively few cells. • The central gelatinous nucleus is contained around the periphery by the collagenous anulus, the cartilaginous anulus and the cartilage endplates cephalad and cauded • The anulus has a lamellar structure with interconnections between adjacent layers of collagen fibrils.
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  NATURAL HISTORY OFDISC DISEASE • Dysfunction- Age 15 to 45 years old It is characterized by circumferential and radial tears in the disc anulus and localized synovitis of the facet joints. • Instability- Age 35- to 70-year-old. It is characterized by internal disruption of the disc, progressive disc resorption, degeneration of the facet joints with capsular laxity, subluxation, and joint erosion
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  NATURAL HISTORY OFDISC DISEASE • Stabilization- Age of the patients older than 60 years. In this stage, the progressive development of hypertrophic bone around the disc and facet joints leads to segmental stiffening or frank ankylosis
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  NATURAL HISTORY OFDISC DISEASE
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  NATURAL HISTORY OFDISC DISEASE • Each spinal segment degenerates at a different rate. • As one level is in the dysfunction stage, another may be entering the stabilization stage. • Disc herniation in this scheme is considered a complication of disc degeneration in the dysfunction and instability stages. • Spinal stenosis from degenerative arthritis in this scheme is a complication of bony overgrowth compromising neural tissue in the late instability and early stabilization stages
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  NATURAL HISTORY OFDISC DISEASE • The primary benefit of surgery has been noted to occur early in the first year after surgery, but with time the statistical significance of the improvement appears to be lost. • Nonprogressive neurological deficits (except cauda equina syndrome) can be treated nonoperatively with expected improvement clinically. • If surgery is necessary, it usually can be delayed 6 to 12 weeks to allow adequate opportunity for improvement.
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  NATURAL HISTORY OFDISC DISEASE •The natural history of degenerative disc disease is one of recurrent episodes of pain followed by periods of significant or complete relief
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  • Severe nervecompression shown by MRI or CT correlates with symptoms of distal leg pain; • However, mild-to-moderate nerve compression disc degeneration or bulging, and central stenosis do not correlate significantly with specific pain patterns
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  • Acute discherniation (prolapse, rupture) is a result of underlying disc degeneration. • It occurs most commonly in the fourth to fifth decades of life, • It is more common in men than women (3:1 ratio) and occurs mostly at L4/5 and L5/S1 disc levels. • Risk factors include smoking, heavy lifting especially with torsional stress, strenuous physical activity, and occupational driving. ACUTE INTERVERTEBRAL DISC PROLAPSE
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  • A ‘protrusion’is a posteriorly bulging disc with the outer annulus intact. • When rupture occurs, fibro- cartilaginous disc material is extruded posteriorly (extrusion) through the posterior longitudinal ligament; • when disc material breaks free to lie in the canal, it is termed sequestration . • A large central rupture may cause compression of the cauda equina
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  • A posterolateralrupture presses on the nerve root proximal to its point of exit through the intervertebral foramen; • Thus a herniation at L4/5 will compress the fifth lumbar nerve root, and a herniation at L5/ S1, the first sacral root.
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  • Acute backpain at the onset of disc herniation probably arises from disruption of the outermost layers of the annulus fibrosus and stretching or tearing of the posterior longitudinal ligament. • Nerve root irritation causes pain in the buttock which may be referred or radiate down the posterior thigh and calf (sciatica). • Local inflammatory response with oedema aggravates the symptoms.
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  • Pressure onthe nerve root itself causes paresthesia and/or numbness in the corresponding dermatome, as well as weakness and depressed reflexes in the muscles supplied by that nerve root
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  Clinical features • Acutedisc prolapse may occur at any age but it is uncommon in the very young and the very old • A common presentation is acute severe back pain which improves, followed by the development of buttock and leg pain (sciatica) a few days later • Both backache and sciatica are made worse by coughing or straining. • Paresthesia or numbness in the leg or foot, and occasionally muscle weakness may occur
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  Clinical features Cauda equinacompression is rare but may cause urinary retention and perineal numbness Urinary retention or incontinence can be due to pressure on the cauda equina. Faecal incontinence or urgency, and impotence
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  On Examination • Thepatient usually stands with a list to one side (sciatic scoliosis) • Sometimes the knee on the painful side is held slightly flexed to relax tension on the sciatic nerve; • Straightening the knee makes the skew back more obvious. • All back movements are restricted, and during forward flexion the list may increase.
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  On Examinatin • Palpationmay find tenderness in the midline and paravertebral muscle spasm.
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  On Examination • Straight-legraising is restricted and painful on the affected side; • Dorsiflexion of the foot
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  On Examination • Bowstringingof the lateral popliteal nerve may accentuate the pain • A crossed straight-leg raise test, if present, is highly specific for a disc prolapse. • With a high or mid-lumbar prolapse the femoral stretch test may be positive.
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  • Neurological examination •Muscle weakness (and, later, wasting), • Diminished reflexes and sensory loss corresponding to the affected level. • L5 impairment causes weakness of knee flexion and big toe extension as well as sensory loss on the outer side of the leg and the dorsum of the foot. • Normal reflexes at the knee and ankle are characteristic of L5 root compression.
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  • Paradoxically, theknee reflex may appear to be increased, because of weakness of the antagonists (which are supplied by L5). • S1 impairment causes weak plantarflexion and jerk and sensory loss along the lateral border of the foot. • Occasionally an L4/5 disc prolapse compresses both L5 and S1. • Cauda equina compression causes urinary retention and sensory loss over the sacrum.
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  Imaging • X-rays arehelpful to exclude bony pathology and reassure the clinician and patient. • MRI is the default investigation for spinal pathology and has replaced other imaging modalities . • Where there are contraindications to MRI (such as MRI incompatible pacemaker) a CT myelogram is indicated.
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  Differential diagnosis • Space-occupyinglesions (SOL), • Epidural abscess, • Tumours, • Epidural haematoma, • Stenosis and • Intradural pathology may present with sciatic symptoms. • Piriformis syndrome (compression neuropathy):- Direct sciatic nerve compression in the pelvis and upper thigh
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  Treatment • Around 90%of symptomatic lumbar disc herniations will improve over 6 weeks irrespective of the advice or treatment given. • All the usual conservative treatment modalities are symptomatic and have not been shown to change the natural history
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  Treatment • NON-INTERVENTIONAL TREATMENTS Commonlyprescribed non-interventional treatments are: • Bedrest, • heat, • ice,
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  Treatment • NON-INTERVENTIONAL TREATMENTS •Short course of analgesics, • non-steroidal anti-inflammatory drugs (NSAIDs), • antidepressants and muscle relaxants • Massage, spinal manipulation, spinal traction, acupuncture, advice to stay active, exercise therapy
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  Treatment INTERVENTIONAL TREATMENTS The followingmodalities of treatment are available but cannot be recommended on the current evidence: • Epidural corticosteroids • Automated percutaneous discectomy • Laser discectomy • Percutaneous disc decompression
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  Treatment INTERVENTIONAL TREATMENTS • Chemonucleolysisdissolution of the nucleus pulposus by percutaneous injection of a proteolytic enzyme (chymopapain). • Controlled studies have shown that this is less effective (and potentially more dangerous) than surgical removal of the disc material
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  Indication of surgery INTERVENTIONALTREATMENTS Absolute indication - cauda equina compression syndrome – this is an emergency. Relative indications are • Neurological deterioration or progressive neurological deterioration • Persistent pain and • Failed adequate conservative treatment
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  Indication of surgery Surgicalprocedure are • Fenestration & Discectomy • Laminectomy & discectomy, • Laminotomy & discectomy, • Microdiscectomy • Endoscopic discectomy
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  Procedure • The ligamentumflavum is removed on the relevant side, • If necessary, with some margin of the bordering laminae and medial third of the facet joint. • The dura and nerve root are retracted towards the midline and the disc bulge or extrusion/sequestration is displayed.
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  Procedure • With anintact annulus an annulotomy is performed and the disc material removed. • A far lateral disc protrusion cannot be visualized through the interlaminar approach and usually needs an extraforaminal approach.
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  Complication Complications include • Epiduralbleeding, • Dural tears, • Nerve root injury and • Incomplete removal of prolapsed disc fragments
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  Complication • Epidural bleedingis minimized by positioning the patient prone with the abdomen free thus minimizing venous pressure. • The major postoperative complication is disc space infection, but fortunately this is rare. • Recurrent prolapse with sciatica is more common (5−11% incidence) and may require revision decompression surgery
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  Rehabilitation • After recoveryfrom an acute disc rupture, or disc removal, the patient is mobilized and needs to limit physical exertion until 6−8 weeks to allow the annular defect to scar up and minimize re-prolapse. • Nonimpact exercises are usually safe.
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  outcome • The recentSpine Patient Outcomes Research Trial (SPORT) showed clinical and economic superiority of surgical versus non-operative care for lumbar disc herniation after 4 years.
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  PERSISTENT POSTOPERATIVE BACKACHEAND SCIATICA Persistent symptoms after operation may be due to: (1) Recurrent disc prolapse (typified by recurrence of sciatica after successful discectomy); (2) Residual disc material in the spinal canal; (3) Disc prolapse at another level;
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  PERSISTENT POSTOPERATIVE BACKACHEAND SCIATICA Persistent symptoms after operation may be due to: (4) Postoperative discitis; (5) Nerve root compression by a hypertrophic facet joint or a narrow lateral recess (‘root canal stenosis’). After careful investigation, any of these may call for re-operation; but second procedures do not have a high success rate – third and fourth procedures still less