After reading this note you will be able to recognise the clinical picture of spinal cord compression, list the common local aetiologies, order and interpret the essential investigations, grade severity and outline the immediate and definitive management steps – remembering to verify drug choices and local protocols against the Kenya MoH guideline and your hospital formulary.
Definition
A syndrome in which an extrinsic lesion (tumour, infection, haemorrhage, inflammatory mass, bone fragment, disc material) exerts pressure on the spinal cord, producing progressive neurological dysfunction that can be reversible if decompressed promptly.
Anatomy and physiology you need
- Spinal cord: extends to L1‑L2 in adults; central grey matter (motor) surrounded by white matter (sensory tracts).
- Epidural space: fat and venous plexus – common site for metastatic deposits and epidural abscesses.
- Dura mater & arachnoid: tight, limit expansion → small increase in volume produces large rise in intrathecal pressure.
- Vascular supply: anterior spinal artery (motor pathways) and paired posterior spinal arteries (sensory pathways); compromise leads to ischemic component.
- Segmental innervation: cervical lesions → quadriparesis, respiratory compromise; thoracic → trunk sensory level, autonomic dysfunction; lumbar → lower‑limb weakness, bowel/bladder involvement.
Causes and risk factors
| Category | Common aetiologies in Kenya | Key risk factors |
|---|---|---|
| Metastatic disease | Breast, prostate, lung, Kaposi sarcoma | Advanced cancer, HIV‑associated malignancies |
| Infectious | Tuberculous epidural abscess, pyogenic abscess (Staph aureus), fungal (Cryptococcus) | HIV, uncontrolled diabetes, recent spinal procedures |
| Traumatic | Vertebral fracture, disc herniation | Road‑traffic accidents, falls, mining injuries |
| Hematologic | Sickle cell vaso‑occlusive infarcts, marrow expansion | Sickle cell disease, severe anaemia |
| Inflammatory / rheumatic | Ankylosing spondylitis (vertebral fusion), rheumatoid pannus | Chronic inflammatory arthritis |
| Tropical / other | Cerebral malaria cerebral sequestration (rare spinal involvement), schistosomiasis (granuloma) | High malaria burden, endemic schistosomiasis |
| Iatrogenic | Post‑operative epidural haematoma, radiation fibrosis | Recent spine surgery, radiotherapy |
Pathophysiology
Extrinsic lesion → mechanical compression of cord → ischemia (arterial/venous compromise) → axonal injury → edema (vasogenic + cytotoxic) → increased intrathecal pressure → progressive demyelination & neuronal loss → clinical deficits.
Clinical features
| Domain | Key questions / findings | Why it occurs |
|---|---|---|
| Onset & tempo | When did symptoms start? <br> Was the onset sudden, sub‑acute (days‑weeks) or chronic (months)? | Rapid compression (e.g., epidural abscess, fracture) gives abrupt deficits; slower processes (TB, metastatic tumour) allow gradual progression and possible spinal deformity. |
| Pain | Location (neck, mid‑back, lower back)? <br> Radiation to shoulders, arms, abdomen or legs? <br> Is the pain worse with movement or lying still? | Compression irritates the dura and nerve roots → axial pain. Radicular pain follows the dermatomal distribution of the involved cord segment. Mechanical instability amplifies pain on movement. |
| Motor weakness | Do you have difficulty lifting objects, climbing stairs, walking, or using your hands? <br> Is the weakness symmetric or one‑sided? | Anterior horn cell and corticospinal tract involvement produce paresis. Cervical lesions affect upper limbs first; thoracic lesions affect trunk/legs; lumbar lesions may spare the arms. |
| Sensory change | Any numbness, tingling, “pins‑and‑needles” or loss of sensation? <br> Which areas are affected – trunk, limbs, perineum? | Dorsal column (vibration, proprioception) and spinothalamic tract (pain, temperature) are compressed. A “sensory level” (sharp demarcation) indicates the spinal segment involved. |
| Autonomic dysfunction | Any urinary urgency, frequency, retention or incontinence? <br> Bowel habit change? <br> Sexual dysfunction? | Sacral autonomic fibres run on the ventral surface of the cord; compression leads to neurogenic bladder/bowel and erectile dysfunction. |
| Gait & balance | Do you feel unsteady, sway, or have difficulty turning? | Posterior column loss of proprioception and corticospinal tract involvement cause ataxic gait and spasticity. |
| Systemic clues | Fever, night sweats, weight loss? <br> History of TB, HIV, recent trauma, malignancy, sickle‑cell crises? | Infective (TB, pyogenic abscess) or neoplastic causes often have constitutional symptoms; trauma points to fracture; sickle‑cell disease predisposes to vertebral infarction. |
| Red‑flag features | Rapid progression (<24 h), severe pain, new bladder dysfunction, fever, recent spinal procedure? | Suggests emergency compression (e.g., epidural haematoma, abscess) requiring urgent decompression. |
Examination
| Finding | Interpretation |
|---|---|
| Spinal tenderness | Localised bony or soft‑tissue pain → fracture, infection, tumour. |
| Motor exam (strength grading, tone) | Upper motor neuron signs (spasticity, hyperreflexia, Babinski) indicate cord involvement above the level of the lesion; lower motor neuron signs (flaccidity, fasciculations) suggest anterior horn cell or nerve root compression. |
| Sensory level | Sharp demarcation of loss of pin‑prick, temperature, or proprioception defines the highest affected spinal segment. |
| Proprioceptive loss (position sense, vibration) | Posterior column compression → gait ataxia, positive Romberg. |
| Reflexes (deep tendon, plantar) | Hyperreflexia and extensor plantar response = corticospinal tract involvement; absent reflexes below the lesion may reflect spinal shock early on. |
| Sphincter tone (perineal sensation, anal wink) | Sacral cord involvement → neurogenic bladder/bowel. |
| Upper limb signs (e.g., Hoffmann’s, clonus) | Cervical cord compression. |
| Lower limb signs (e.g., ankle clonus) | Thoracic or lumbar cord compression. |
| Systemic exam (fever, lymphadenopathy, skin lesions) | Clues to infectious or malignant aetiology. |
Differential diagnosis
| Condition | Points toward it | Distinguishing features |
|---|---|---|
| Epidural abscess | Fever, back pain, recent infection or IV drug use, HIV | MRI shows rim‑enhancing collection; rapid neuro decline; elevated ESR/CRP |
| Tuberculous spondylitis (Pott’s) | Chronic back pain, weight loss, TB exposure, HIV | MRI: vertebral body destruction with paravertebral abscess; slow onset; positive TB tests |
| Metastatic vertebral tumour | Known primary cancer, night pain, weight loss | MRI: focal marrow replacement, often multiple levels; CT shows lytic/blastic lesions |
| Traumatic fracture / dislocation | Recent trauma, focal tenderness, deformity | Plain X‑ray/CT shows bony disruption; often acute severe pain |
| Herniated disc (large central) | Mechanical back pain, radiculopathy, no systemic signs | MRI: disc protrusion without vertebral body destruction; symptoms often limited to one level |
| Hematoma (spontaneous or post‑procedural) | Anticoagulation, recent epidural injection, coagulopathy | MRI: acute blood signal; rapid onset; no infection signs |
| Sickle‑cell vaso‑occlusive infarction of vertebrae | Sickle‑cell disease, vaso‑occlusive crisis | MRI: marrow edema, often multiple levels; improves with disease‑specific therapy |
| Rheumatologic inflammatory disease (e.g., ankylosing spondylitis) | Young male, chronic inflammatory back pain, HLA‑B27 | X‑ray: sacroiliac fusion; MRI shows enthesitis, not focal compression |
Investigations
| Test | What it answers | Typical result interpretation |
|---|---|---|
| MRI spine (T1, T2, STIR, post‑gadolinium) | Location, extent, cause (abscess, tumour, fracture) | Hyperintense cord edema; rim‑enhancing lesion = abscess; vertebral body collapse = TB or tumour |
| Plain radiograph (AP & lateral) | Bony alignment, fractures, gross lytic lesions | Vertebral collapse, step‑off, calcified discitis |
| CT scan (with contrast if needed) | Fine bony detail, surgical planning | Cortical breach, pedicle involvement, calcified tumour |
| Full blood count & ESR/CRP | Inflammation or infection | Elevated ESR/CRP → infection or TB; leukocytosis → pyogenic abscess |
| Blood cultures | Bacteremia source | Positive cultures → pyogenic abscess; negative in TB |
| TB investigations (GeneXpert, sputum, urine PCR) | Mycobacterial infection | Positive GeneXpert → TB spine |
| Serology for HIV | Immunosuppression risk | Positive HIV → higher TB/abscess risk |
| Tumour markers / CT chest‑abdomen‑pelvis | Metastatic disease work‑up | Elevated markers or lesions on CT suggest primary tumour |
| Urinalysis & post‑void residual | Neurogenic bladder assessment | High residual → cord involvement |
Diagnosis and severity
- Confirmatory diagnosis – Correlate a compatible clinical picture (pain, motor/sensory/autonomic deficits, sensory level) with imaging that demonstrates compression of the cord or cauda equina. MRI is the gold standard; CT or X‑ray may supplement when MRI unavailable.
- Severity grading (based on neurological status)
| Grade | Clinical picture | Management urgency |
|---|---|---|
| Grade 0 – No neurological deficit | Pain only, normal exam | Urgent imaging; treat underlying cause promptly |
| Grade 1 – Mild deficit | Slight weakness, hyperreflexia, no sphincter involvement | Imaging within 24 h; consider steroids and early decompression if progressive |
| Grade 2 – Moderate deficit | Motor strength ≤ 3/5, sensory level, early bladder change | Imaging ASAP; high‑dose steroids (e.g., methylprednisolone) while arranging surgical/medical decompression |
| Grade 3 – Severe deficit | Motor ≤ 2/5, complete sensory loss below level, urinary retention | Immediate MRI and emergency decompression (surgical or percutaneous) within hours |
| Grade 4 – Complete cord transection | No motor or sensory function below level, flaccid paralysis, absent reflexes (spinal shock) | Urgent decompression if any residual cord; otherwise focus on rehabilitation and complication prevention |
- Prognostic indicators – Rapid onset, severe motor loss, and delayed decompression (> 24 h) predict poorer functional recovery. Presence of infection (TB, abscess) or malignancy also influences long‑term outcome.
Management
1. Immediate stabilisation
| Step | Rationale |
|---|---|
| Immobilise spine (log‑roll, rigid cervical collar, thoracolumbar board) | Prevent further mechanical insult while the cord is vulnerable |
| Maintain MAP ≥ 85 mmHg (fluid bolus, vasopressor if needed) | Improves spinal cord perfusion; ischemia worsens neurological loss |
| High‑flow oxygen (if hypoxic) | Optimises oxygen delivery to injured cord |
| Analgesia & anti‑spasm (e.g., benzodiazepine, baclofen) | Reduces pain‑induced hypertension and muscle spasm that can increase cord compression |
| Urgent neuro‑imaging (MRI spine, preferably within 24 h) | Confirms level, extent and aetiology; guides definitive therapy |
| Steroid therapy (short‑course dexamethasone) only if tumour or inflammatory lesion suspected and no contraindication | Diminishes vasogenic oedema; not indicated for TB or pyogenic abscesses |
2. Definitive treatment – tailored to aetiology
| Aetiology | First‑line definitive measure | Adjuncts |
|---|---|---|
| Metastatic tumour | Urgent decompressive laminectomy ± instrumented fusion + radiotherapy (post‑op) | Steroids peri‑operatively, oncologic systemic therapy |
| Epidural abscess (TB, pyogenic) | Surgical drainage + targeted antimicrobial therapy (anti‑TB regimen or broad‑spectrum antibiotics) | Immobilisation for 4–6 weeks, physiotherapy |
| Vertebral fracture (trauma, osteoporotic) | Posterior instrumentation ± vertebroplasty; early mobilisation | Analgesia, calcium/vit D, bisphosphonates if appropriate |
| Disc herniation with acute cord compromise | Anterior cervical discectomy & fusion (or posterior approach depending on level) | Post‑op steroids for 24 h, early rehab |
| Haematological (sickle cell vaso‑occlusive) | Exchange transfusion to reduce HbS, analgesia, hydration | Consider surgical decompression if infarction confirmed |
3. Monitoring & follow‑up
- Neurological exam (motor, sensory, sphincter) every 2 h for first 24 h, then q4‑6 h.
- MAP and urine output (target > 0.5 ml/kg/h).
- MRI repeat if deterioration or if initial study limited.
- Post‑op wound inspection, drain output, infection markers.
- Early physiotherapy and occupational therapy to prevent contractures.
4. Contra‑indications & safety
- Steroids contraindicated in uncontrolled diabetes, active infection, peptic ulcer disease.
- Early mobilisation contraindicated until spinal stability confirmed radiologically.
- Anticoagulation must be held before any surgical decompression to avoid epidural haematoma.
Complications and prognosis
| Complication | Clinical impact |
|---|---|
| Permanent motor deficit (paraplegia/quadriplegia) | Loss of ambulation, dependence on assistive devices |
| Neurogenic bladder/bowel | Recurrent UTIs, renal impairment, social disability |
| Spinal instability / deformity | Chronic pain, need for further surgery |
| Post‑operative wound infection / epidural abscess | May require repeat drainage, prolonged antibiotics |
| Thrombo‑embolism (DVT/PE) | Immobilisation risk; prophylaxis with compression devices |
| Respiratory compromise (high cervical lesions) | Need for ventilatory support, risk of pneumonia |
Prognosis hinges on time to decompression: neurological recovery is greatest when surgery occurs within 24 h of onset. Early presentation, preserved sensation, and non‑malignant aetiology (e.g., disc herniation) carry a better outlook. Late presentation, complete motor loss, or malignant infiltration portend poorer functional recovery.
High‑yield exam points
- Look‑alike conditions: transverse myelitis, acute demyelinating disease, peripheral neuropathy, Guillain‑Barré syndrome.
- Commonest wrong first step: proceeding to MRI without spinal immobilisation; examiners expect collar/board first.
- Bedside exam question: “Explain why the patient has a sensory level at T8 and what this tells you about the lesion location.”
- Key examiner probe: “What manoeuvre would you avoid in a patient with suspected cervical cord compression and why?” (Answer: neck flexion/extension without protection – risk of worsening compression).
- Management hierarchy: stabilise → maintain perfusion → obtain MRI → definitive decompression.
Clinical case
Case: A 38‑year‑old HIV‑positive male (CD4 = 180 cells/µL) presents with a 3‑day history of worsening mid‑back pain, bilateral lower‑limb weakness (grade 3/5), numbness below the umbilicus, and urinary retention. No trauma. Examination: sensory level at T10, brisk knee reflexes, positive Babinski bilaterally. MRI shows a posterior epidural collection from T8–T11 compressing the cord, with rim enhancement.
Questions
- What is the most urgent next step?
Answer: Arrange emergent surgical decompression (laminectomy and drainage) after stabilising the spine and ensuring MAP ≥ 85 mmHg.
- Which antimicrobial regimen should be started empirically?
Answer: Initiate anti‑TB therapy (isoniazid, rifampicin, ethambutol, pyrazinamide) plus broad‑spectrum coverage for pyogenic organisms until cultures return, because TB is common in this setting and HIV increases risk of atypical infections.
- What prognostic factor in this patient is most favourable?
Answer: Presence of incomplete motor loss (grade 3/5) and a short interval (< 48 h) between symptom onset and decompression.
Practice questions
Question 1
A 45‑year‑old woman with known breast cancer presents with new‑onset neck pain and progressive weakness of both arms. MRI shows an anterior cervical epidural mass compressing the cord at C4‑C5. What is the next best step?
A. High‑dose steroids only
B. Immediate posterior cervical laminectomy
C. Anterior cervical corpectomy and fusion
D. Observation for 48 h
Answer: C. Anterior cervical corpectomy and fusion – provides direct decompression of an anterior lesion and stabilises the spine.
Question 2
A 22‑year‑old male with sickle cell disease presents with back pain, lower‑limb weakness and a sensory level at L2 after a vaso‑occlusive crisis. Which feature most helps differentiate spinal infarction from an epidural abscess?
A. Fever > 38 °C
B. Rapid progression over minutes
C. Positive blood cultures
D. Elevated ESR
Answer: B. Rapid progression over minutes – spinal infarction typically evolves abruptly, whereas abscesses develop over days.
Question 3
A patient with tuberculous meningitis develops new thoracic back pain and leg weakness. MRI shows vertebral collapse with a paravertebral collection. Which intervention is contraindicated at this stage?
A. Anti‑TB chemotherapy
B. Surgical debridement and instrumentation
C. High‑dose steroids for edema
D. Bed rest with TLSO brace
Answer: C. High‑dose steroids for edema – steroids can worsen infection in TB and are not indicated for vertebral TB.
Question 4
A 60‑year‑old man after a fall is found to have a burst fracture of L1 with retropulsion compressing the cord. He is neurologically intact. What is the safest immediate management?
A. Immediate posterior instrumentation
B. Rigid lumbar brace and observation
C. High‑dose methylprednisolone
D. Cervical collar
Answer: B. Rigid lumbar brace and observation – with intact neurology, non‑operative immobilisation is appropriate while planning definitive fixation.
Question 5
During a bedside exam, a student attempts to assess the Hoffmann sign in a patient with suspected cervical cord compression by rapidly flicking the distal phalanx of the middle finger. Why is this manoeuvre discouraged?
A. It may cause a fracture
B. It can exacerbate cord compression
C. It is not a reliable test for upper‑motor‑neuron signs
D. It interferes with MRI imaging
Answer: B. It can exacerbate cord compression – vigorous finger‑flicking can produce neck movement that worsens an unstable cervical lesion.
Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.