1. Comminuted Fracture of Tibia
Definition
A comminuted fracture of the tibia is a fracture in which the tibial shaft is broken into three or more fragments. It usually follows high-energy trauma such as road-traffic injury, fall from height, or crush injury. Because the tibia is subcutaneous along much of its anteromedial surface, such fractures have a substantial risk of soft-tissue injury, open fracture, infection, compartment syndrome, delayed union, and nonunion.
For comminuted and complex tibial-shaft fractures, intramedullary nailing is generally the preferred definitive fixation when anatomy and soft tissues permit it. Metaphyseal junction fractures may instead need plating, and circular or monolateral external fixation has an important role in severe injuries. Bailey and Love's Short Practice of Surgery, p. 459.
Relevant Anatomy
- Tibia is the major weight-bearing bone of the leg.
- It has a poor soft-tissue envelope, especially over the anteromedial surface.
- Blood supply:
- Nutrient artery supplies the inner two-thirds of cortex.
- Periosteal vessels supply the outer cortex.
- Extensive stripping of periosteum or repeated open reduction compromises healing.
- A tibial fracture can injure:
- Anterior tibial artery
- Posterior tibial artery
- Peroneal artery
- Deep peroneal nerve
- Common peroneal nerve in proximal injuries
- The leg has four compartments: anterior, lateral, superficial posterior, deep posterior. Compartment syndrome must always be excluded.
Mechanism of Injury
High-energy injury
- Road-traffic accident
- Pedestrian struck by vehicle
- Fall from height
- Industrial/crush injury
- Gunshot injury
High-energy mechanisms commonly produce comminution, displacement, soft-tissue stripping, bone loss, and open fractures.
Low-energy injury
- Twisting injury, especially in osteoporotic bone
- May produce a spiral fracture but is less likely to be severely comminuted.
Classification
1. AO/OTA classification
Tibial shaft fractures are classified as 42:
- 42-A: simple fracture
- 42-B: wedge fracture
- 42-C: complex fracture
Includes segmental and highly comminuted fractures.
A highly comminuted tibial fracture is usually a 42-C fracture.
2. Open fracture classification: Gustilo-Anderson
| Type | Description |
|---|
| I | Clean wound <1 cm, low-energy injury |
| II | Wound >1 cm without extensive soft-tissue damage |
| IIIA | High-energy injury, extensive wound but bone can be covered by local soft tissue |
| IIIB | Extensive soft-tissue loss, periosteal stripping and exposed bone, requiring flap cover |
| IIIC | Open fracture with arterial injury requiring repair |
Clinical Features
Symptoms
- Severe pain in leg
- Inability to bear weight
- Swelling and deformity
- Bleeding or wound in open fractures
- Paraesthesia or numbness
- Pain out of proportion, particularly with passive stretch, suggests compartment syndrome.
Signs
- Deformity, shortening, rotation
- Swelling, bruising, fracture blisters
- Crepitus and abnormal mobility, though repeated elicitation must be avoided
- Open wound, exposed bone, contamination
- Skin tenting or threatened skin
- Distal pulses, capillary refill and limb temperature
- Motor and sensory examination:
- Deep peroneal nerve: first dorsal web-space sensation, great-toe extension
- Superficial peroneal nerve: dorsum of foot sensation
- Tibial nerve: sole sensation, toe flexion
Important warning signs
Compartment syndrome: the 6 Ps
- Pain out of proportion
- Pain on passive stretch
- Paraesthesia
- Pallor
- Paralysis
- Pulselessness, a late sign
Do not wait for pulselessness. If the diagnosis is clinically clear, perform urgent four-compartment fasciotomy.
Investigations
1. Radiographs
Obtain:
- Anteroposterior and lateral radiographs of the entire tibia and fibula
- Include knee and ankle joints
- Assess:
- Level and pattern of fracture
- Degree of comminution
- Length and alignment
- Translation, angulation and rotation
- Segmental component
- Associated fibular fracture
- Intra-articular extension
2. CT scan
Indicated when:
- Fracture extends into knee or ankle joint
- Complex proximal or distal metaphyseal fracture
- Preoperative planning is needed
- Occult fracture pattern needs clarification
3. CT angiography
Indicated if:
- Absent or diminished pulses
- Expanding haematoma
- Active bleeding
- Ischaemic limb
- ABI <0.9, where used locally
4. Compartment-pressure measurement
Useful in an obtunded, unconscious, sedated, or uncooperative patient where compartment syndrome is suspected but uncertain.
5. Baseline laboratory tests
- CBC
- Blood group and cross-match in major trauma
- Renal function and electrolytes
- Coagulation profile
- Blood glucose
- Infection-related tests in open fractures as required
Initial Management
Follow ATLS principles.
A. Resuscitation
- Airway with cervical-spine protection
- Breathing
- Circulation: control haemorrhage, gain IV access, resuscitate appropriately
- Disability: neurological status
- Exposure: examine entire limb and patient, prevent hypothermia
B. Limb care
- Give adequate analgesia.
- Cover an open wound with a sterile saline-moistened dressing.
- Document wound size, contamination, neurovascular status, and photographs where permitted.
- Realign gross deformity gently if vascular compromise or threatened skin is present.
- Apply a well-padded long-leg splint.
- Elevate only if this does not compromise arterial perfusion.
- Repeat and document neurovascular examination after reduction and splintage.
C. Open-fracture measures
- Start IV antibiotics as soon as possible, ideally within 1 hour for open fractures, according to local protocol.
- Give tetanus prophylaxis as indicated.
- Do not repeatedly inspect or probe the wound.
- Avoid emergency-department wound washout of a major open long-bone fracture if it delays proper operative debridement.
For open long-bone fractures, current UK guidance calls for combined orthopaedic-plastic planning. Highly contaminated wounds need immediate debridement; other high-energy type IIIA/IIIB injuries should undergo debridement within 12 hours, with definitive soft-tissue cover ideally at the same sitting or within 72 hours. See the
NICE open-fracture recommendations.
Principles of Definitive Treatment
Goals
- Restore length.
- Correct axial alignment.
- Correct rotational deformity.
- Restore joint congruity if intra-articular.
- Achieve adequate stability for healing.
- Preserve fracture biology and soft-tissue blood supply.
- Permit early movement of knee and ankle.
- Prevent infection, nonunion, malunion and stiffness.
Biological fixation
In a comminuted fracture, it is often harmful to expose every fragment and attempt anatomical reconstruction of the entire shaft. The surgeon should:
- Reduce the main proximal and distal segments.
- Restore length, alignment and rotation.
- Preserve soft-tissue attachments to intermediate fragments.
- Use indirect reduction and bridge fixation where possible.
- Accept that small comminuted fragments may unite by callus formation without direct fixation.
This is the principle of relative stability and secondary bone healing.
Methods of Treatment
A. Nonoperative treatment
Indications
Usually limited to:
- Stable, minimally displaced fractures
- Patients unsuitable for anaesthesia or surgery
- Selected low-demand patients
- Temporary treatment pending definitive surgery
Method
- Above-knee plaster initially
- Conversion to patellar tendon-bearing cast or functional brace later
- Serial radiographs to monitor alignment
Limitations in comminuted fractures
Comminuted fractures are unstable and may shorten, angulate, rotate, or lose reduction. Therefore, casting is generally unsuitable for significantly displaced or high-energy comminuted shaft fractures.
Complications of prolonged casting include knee stiffness, ankle stiffness, malunion, pressure sores and loss of reduction.
B. Intramedullary nailing
Indications
- Most closed displaced and comminuted tibial-shaft fractures
- Many type I, II and selected IIIA open fractures after appropriate debridement
- Segmental fractures where the medullary canal allows nailing
Advantages
- Load-sharing fixation
- Preserves fracture haematoma and periosteal supply
- Smaller exposure than plating
- Restores length and alignment
- Enables early knee and ankle movement
- Allows earlier weight bearing when fixation and soft tissues permit
Technique principles
- Closed or minimally invasive reduction
- Reamed or unreamed nail depending on fracture, soft-tissue state and surgeon preference
- Proximal and distal locking screws
- Blocking screws may assist alignment in proximal or distal metaphyseal fractures
- Confirm length, rotation and alignment fluoroscopically
Complications
- Anterior knee pain
- Malalignment, especially in proximal or distal-third fractures
- Infection
- Delayed union/nonunion
- Broken locking screws or nail
- Fat embolism, uncommon
- Missed compartment syndrome
C. Plate fixation
Indications
- Proximal or distal metaphyseal tibial fractures not controllable with a nail
- Intra-articular extension requiring reduction of the articular surface
- Selected nonunions or malunions
- Polytrauma when a plate strategy is most appropriate
Technique
- Locking plate, usually using minimally invasive plate osteosynthesis
- Bridge plate over comminuted zone
- Fix proximal and distal main fragments while avoiding unnecessary dissection at fracture site
Disadvantages
- Wound complication and infection risk due to subcutaneous tibia
- Periosteal stripping if extensive open exposure is used
- Possible implant failure or nonunion
D. External fixation
Indications
- Severe open fracture with contamination or major soft-tissue injury
- Physiologically unstable polytrauma patient: damage-control orthopaedics
- Vascular injury requiring repair
- Compartment syndrome after fasciotomy
- Segmental bone loss
- Infected nonunion
- Need for bone transport
- When definitive fixation must be delayed
Types
- Monolateral external fixator
- Spanning external fixator
- Circular Ilizarov or hexapod frame
Advantages
- Rapid stabilisation
- Minimal disturbance of fracture zone
- Facilitates wound access, repeated debridement and flap cover
- Circular frames can correct deformity and permit bone transport
Complications
- Pin-tract infection
- Loss of reduction
- Joint stiffness
- Delayed union
- Neurovascular injury from pin placement
- Refracture after removal
E. Bone loss and reconstruction
Large comminuted injuries may have segmental bone loss.
Options
- Acute shortening and later lengthening
- Autologous cancellous bone grafting for small defects
- Masquelet induced-membrane technique
- Bone transport using circular external fixation
- Vascularised fibular graft in selected major defects
- Allograft or bone substitutes in selected settings
The sequence is: eradicate contamination/infection, obtain stable fixation, secure vascularised soft-tissue cover, then reconstruct bone defect.
Management of an Open Gustilo IIIB Comminuted Tibial Fracture
This is an orthoplastic emergency.
Definition
A type IIIB injury has:
- High-energy fracture
- Extensive soft-tissue loss
- Periosteal stripping and exposed bone
- Inadequate local soft-tissue cover
- Requirement for local or free flap reconstruction
Emergency treatment
- ATLS resuscitation.
- IV antibiotics promptly and tetanus prophylaxis.
- Sterile saline-moistened dressing.
- Photograph/document wound and neurovascular state.
- Realign and splint.
- Urgent transfer to a centre capable of combined orthopaedic and plastic surgery care.
- Assess limb viability and associated vascular injury.
Operative debridement
- Remove foreign material, clothing, soil and devitalised tissue.
- Excise nonviable skin, fat, fascia, muscle and loose avascular bone fragments.
- Preserve viable cortical fragments with soft-tissue attachments.
- Extend wounds safely using fasciotomy-type approaches when required.
- Take deep samples if infection is suspected, but do not delay antibiotics.
- Repeat debridement if viability remains doubtful.
Skeletal stabilisation
- Temporary spanning external fixation is common initially.
- Definitive fixation options:
- Intramedullary nail in selected cases
- Circular external fixator
- Plate fixation only when immediate definitive soft-tissue coverage is possible
Soft-tissue reconstruction
- Must be planned with the plastic surgeon from the first debridement.
- Options:
- Local muscle flap, for example gastrocnemius for proximal-third defects
- Soleus flap for selected middle-third defects
- Free flap, commonly for distal-third or extensive defects
- Definitive cover should not be unnecessarily delayed. Internal fixation should not be left under an uncovered wound.
The
BOA open-fracture standard recommends that the limb salvage versus amputation decision involve orthopaedics, plastic surgery, rehabilitation, the patient and family, rather than relying solely on an injury severity score.
Complications
Early
- Haemorrhagic shock in polytrauma
- Open-fracture contamination and infection
- Compartment syndrome
- Vascular injury and limb ischaemia
- Nerve injury
- Deep vein thrombosis and pulmonary embolism
- Fat embolism syndrome
- Wound necrosis
Late
- Delayed union
- Nonunion, especially at the distal tibial third
- Malunion: varus, valgus, procurvatum, recurvatum, shortening or rotational deformity
- Chronic osteomyelitis
- Implant failure
- Knee and ankle stiffness
- Chronic pain
- Complex regional pain syndrome
- Post-traumatic osteoarthritis if joint involved
Follow-up and Rehabilitation
- Serial wound and neurovascular assessment.
- Radiographs at regular intervals to assess alignment and union.
- Early active knee, ankle and toe movements.
- Weight bearing according to fracture stability, fixation method and soft-tissue condition.
- Thromboprophylaxis when indicated.
- Optimise nutrition, vitamin D status, smoking cessation and diabetic control.
- Treat pin-tract infection early in external fixation.
- Assess for union clinically and radiologically.
2. Multiple Myeloma
Definition
Multiple myeloma is a malignant clonal proliferation of plasma cells in bone marrow, usually associated with production of a monoclonal immunoglobulin or light chain, osteolytic bone disease, marrow failure, immunodeficiency and renal injury.
It is part of the spectrum:
- Monoclonal gammopathy of undetermined significance (MGUS)
- Smouldering multiple myeloma
- Symptomatic multiple myeloma
- Plasma-cell leukaemia
- Solitary plasmacytoma
Pathogenesis
- Malignant plasma cells proliferate in bone marrow.
- They secrete monoclonal immunoglobulin, called M protein, or monoclonal light chains.
- They stimulate osteoclast activity and suppress osteoblasts, causing osteolytic lesions.
- They displace normal marrow, producing anaemia, thrombocytopenia and leukopenia.
- They suppress normal immunoglobulin production, causing recurrent infection.
- Light chains cause cast nephropathy and renal impairment.
Clinical Features
A. Bone disease
- Persistent bone pain, especially back, ribs, pelvis and skull
- Pain worsened by movement
- Vertebral compression fracture
- Pathological fracture
- Spinal cord compression
- Osteoporosis and lytic lesions
The common radiographic appearance is multiple sharply defined punched-out lytic lesions without surrounding reactive sclerosis. Bone scans may be falsely negative because myeloma predominantly causes osteoclastic rather than osteoblastic activity. Campbell's Operative Orthopaedics, p. 1227.
B. Marrow failure
- Normocytic normochromic anaemia: fatigue, dyspnoea, pallor
- Leukopenia and recurrent infection
- Thrombocytopenia and bleeding tendency
C. Renal disease
- Renal impairment or acute kidney injury
- Proteinuria, often light chains
- Cast nephropathy
- Contributing factors: dehydration, hypercalcaemia, sepsis, NSAIDs and contrast exposure
D. Hypercalcaemia
- Thirst, polyuria, constipation
- Nausea and vomiting
- Confusion, drowsiness or coma
- Cardiac arrhythmia
E. Infection
- Recurrent bacterial infection, especially pneumonia and urinary infection
- Hypogammaglobulinaemia causes susceptibility to encapsulated organisms
F. Hyperviscosity, uncommon
- Headache
- Blurring of vision
- Mucosal bleeding
- Confusion
G. Neurological manifestations
- Spinal cord compression
- Radiculopathy
- Peripheral neuropathy
- Carpal tunnel syndrome in amyloidosis
The CRAB Features
The classic end-organ manifestations are:
| Letter | Finding |
|---|
| C | Hypercalcaemia |
| R | Renal impairment |
| A | Anaemia |
| B | Bone lesions |
Myeloma should be strongly suspected in an older adult with unexplained bone pain, normocytic anaemia, raised ESR, renal impairment, hypercalcaemia, recurrent infections, raised total protein or lytic bone lesions.
Diagnostic Modalities and Expected Findings
1. Complete blood count and peripheral smear
Findings
- Normocytic normochromic anaemia
- Rouleaux formation due to high serum proteins
- Leukopenia or thrombocytopenia in advanced marrow infiltration
- Raised ESR, often markedly elevated
2. Biochemistry
Essential tests
- Serum calcium, preferably corrected calcium
- Urea, creatinine and eGFR
- Electrolytes
- Albumin and total protein
- Liver function tests
- LDH
- Uric acid
- Beta-2 microglobulin
- Quantitative immunoglobulins
Findings
- Hypercalcaemia
- Renal impairment
- Raised total protein with reduced albumin-to-globulin ratio
- High beta-2 microglobulin, associated with tumour burden and prognosis
- Immunoparesis: reduction of uninvolved immunoglobulins
3. Serum protein electrophoresis
Purpose
Detect and quantify serum monoclonal protein.
Finding
- Narrow monoclonal band or M spike, usually in gamma region
- Usually IgG, then IgA
- A normal electrophoresis does not exclude light-chain myeloma or non-secretory myeloma.
4. Serum immunofixation electrophoresis
Purpose
Identifies the type of monoclonal immunoglobulin and light chain.
Example
- IgG-kappa myeloma
- IgA-lambda myeloma
It is more sensitive than electrophoresis for small quantities of M protein.
5. Serum free light-chain assay
Purpose
Measures free kappa and lambda chains and calculates the ratio.
Uses
- Diagnosing light-chain myeloma
- Assessing oligo-secretory disease
- Monitoring response
- Prognostic assessment
An involved/uninvolved free-light-chain ratio
≥100, with involved light-chain concentration
≥100 mg/L, is a myeloma-defining biomarker when other criteria are met. This is reflected in the
IMWG diagnostic criteria.
6. Urine studies
Tests
- 24-hour urine protein quantification
- Urine protein electrophoresis
- Urine immunofixation
Findings
- Monoclonal free light chains, historically called Bence Jones proteinuria
- Light-chain excretion may be present even without a major serum M spike.
7. Bone marrow aspiration and trephine biopsy
Essential diagnostic test
Findings
- Clonal plasma cells, often ≥10% of nucleated marrow cells
- Plasma cells may show eccentric nucleus, clock-face chromatin and perinuclear hof
- Marrow infiltration may suppress normal haematopoiesis.
Ancillary tests
- Flow cytometry: establishes clonality, typically aberrant CD38/CD138-positive plasma cells with light-chain restriction.
- Cytogenetics/FISH: evaluates risk.
Important high-risk abnormalities
- del(17p)
- t(4;14)
- t(14;16)
- gain or amplification of 1q
8. Imaging
A. Whole-body low-dose CT
Preferred baseline technique in many centres for detecting osteolytic lesions.
B. Whole-body MRI
Best for:
- Marrow infiltration
- Focal marrow lesions
- Spinal cord compression
- Neurological symptoms
- Occult disease before cortical bone destruction
C. FDG PET-CT
Useful for:
- Active focal bone and extramedullary disease
- Treatment response
- Suspected relapse
D. Conventional skeletal survey
May demonstrate:
- Punched-out skull lesions
- Generalised osteopenia
- Vertebral compression fractures
- Lytic lesions in long bones, ribs and pelvis
It is less sensitive than modern whole-body CT or MRI.
E. Bone scan
Not preferred. It can underestimate disease because myeloma lesions have limited osteoblastic activity.
Diagnostic Criteria: Symptomatic Multiple Myeloma
Diagnosis requires:
A. One of the following
- Clonal marrow plasma cells ≥10%, or
- Biopsy-proven bony or extramedullary plasmacytoma
And
B. At least one myeloma-defining event
CRAB end-organ injury attributable to myeloma
- Hypercalcaemia: serum calcium >1 mg/dL above the upper normal limit or >11 mg/dL
- Renal impairment: creatinine clearance <40 mL/min or serum creatinine >2 mg/dL
- Anaemia: haemoglobin >2 g/dL below normal or <10 g/dL
- Bone disease: one or more osteolytic lesions on CT, PET-CT or radiography
Biomarkers of malignancy: SLiM criteria
- S: ≥60% clonal bone-marrow plasma cells
- Li: involved/uninvolved serum free-light-chain ratio ≥100, with involved chain ≥100 mg/L
- M: >1 focal lesion on MRI, each at least 5 mm
Thus, the modern shorthand is SLiM-CRAB.
Differentiation from Related Disorders
| Disorder | Typical features |
|---|
| MGUS | M protein <3 g/dL, marrow plasma cells <10%, no CRAB/myeloma-defining event |
| Smouldering myeloma | M protein ≥3 g/dL and/or clonal marrow plasma cells 10-60%, but no CRAB or SLiM event |
| Solitary plasmacytoma | Single lesion, normal or near-normal marrow, no systemic myeloma features |
| Multiple myeloma | Clonal plasma-cell disorder plus CRAB feature or SLiM biomarker |
Staging and Prognosis
Revised International Staging System
Uses:
- Serum beta-2 microglobulin
- Serum albumin
- LDH
- High-risk FISH abnormalities
Poor prognostic factors
- High beta-2 microglobulin
- Low albumin
- Elevated LDH
- del(17p), t(4;14), t(14;16), 1q gain/amplification
- Extramedullary disease
- Renal failure
- High tumour burden
Treatment Outline
Management must be supervised by haematology.
Supportive treatment
- Hydration and prompt treatment of hypercalcaemia
- Avoid nephrotoxic drugs and unnecessary contrast
- Bisphosphonate or denosumab for myeloma bone disease when appropriate
- Analgesia
- Radiotherapy for painful focal lesions or spinal cord compression
- Orthopaedic stabilisation of impending or completed pathological fracture
- Antimicrobial treatment and selected prophylaxis
- Vaccination
- Red-cell transfusion or erythropoiesis-stimulating agent in selected patients
- Thromboprophylaxis with certain anti-myeloma regimens
Anti-myeloma therapy
Regimens vary by patient fitness, renal function, availability and transplant eligibility. Common components include:
- Proteasome inhibitor: bortezomib
- Immunomodulatory drug: lenalidomide
- Corticosteroid: dexamethasone
- Anti-CD38 monoclonal antibody: daratumumab
Transplant-eligible patients
- Induction combination therapy
- Autologous stem-cell transplantation in appropriate patients
- Maintenance therapy, often lenalidomide-based
Emergencies
- Suspected cord compression: urgent MRI, corticosteroid according to specialist protocol, haematology/radiotherapy/spinal-surgery input.
- Hypercalcaemic crisis: IV fluids, antiresorptive therapy and treatment of myeloma.
- Acute kidney injury from light chains: urgent hydration, avoid nephrotoxins and rapidly treat the plasma-cell disorder.
3. Pott’s Paraplegia
Definition
Pott’s paraplegia is weakness or paralysis of both lower limbs caused by spinal tuberculosis, usually from compression or injury of the spinal cord due to vertebral disease and its complications.
It is distinct from uncomplicated Pott’s disease, which refers to tuberculous spondylitis without neurological deficit.
Etiology and Pathogenesis
Spinal tuberculosis usually results from haematogenous spread of Mycobacterium tuberculosis to the vertebral body, commonly in the lower thoracic and thoracolumbar spine.
Infection may spread:
- From vertebral body to adjacent disc and neighbouring vertebra
- Beneath anterior or posterior longitudinal ligaments
- Into epidural space
- Into paravertebral tissues, producing a cold abscess
Mechanisms producing paraplegia
- Epidural granulation tissue compressing spinal cord
- Caseous material in epidural space
- Epidural or paravertebral abscess
- Sequestrated bone or disc fragment
- Vertebral collapse with kyphosis/gibbus
- Instability or subluxation
- Tuberculous thrombosis/vasculitis causing cord ischaemia
- Late fibrosis, adhesions, myelomalacia or bony canal stenosis
Textbook neurology describes Pott’s paraplegia as epidural cord compression due to pus or caseous granulation tissue extending from an infected vertebra. Adams and Victor's Principles of Neurology, p. 1252.
Classification
A. According to time of onset
Early-onset paraplegia
Occurs during active spinal tuberculosis.
Common causes
- Epidural abscess
- Granulation tissue
- Caseous material
- Oedema
- Sequestrum
- Mechanical instability or acute vertebral collapse
Prognosis
Usually better, because the compressive pathology is potentially reversible with prompt chemotherapy and, where required, decompression.
Late-onset paraplegia
Occurs years after apparent healing of spinal tuberculosis.
Causes
- Severe residual kyphosis
- Internal gibbus causing chronic cord stretch or compression
- Fibrosis around dura
- Spinal canal stenosis
- Reactivation of disease
Prognosis
Generally less favourable than early-onset paraplegia.
Clinical Features
A. Constitutional symptoms
May be absent, especially in chronic disease. When present:
- Low-grade fever
- Evening rise of temperature
- Night sweats
- Weight loss
- Loss of appetite
- Fatigue
B. Spinal symptoms
- Localised back pain
- Spinal tenderness
- Muscle spasm
- Restricted spinal movement
- Progressive kyphosis or angular gibbus
- Refusal to walk or sit in children
C. Cold abscess
- Paravertebral swelling
- Psoas abscess presenting as groin or thigh swelling
- Retropharyngeal abscess in cervical disease
- Chest-wall swelling in thoracic disease
D. Neurological features
Early upper motor neuron signs
- Stiffness and weakness of lower limbs
- Difficulty walking
- Spastic gait
- Hypertonia
- Exaggerated knee and ankle jerks
- Extensor plantar response
- Ankle clonus
Progression
- Spastic paraparesis
- Sensory impairment with a spinal sensory level
- Bladder urgency, retention or incontinence
- Constipation or faecal incontinence
- Complete paraplegia
Lower motor neuron pattern
May occur with cauda-equina or conus involvement:
- Flaccid weakness
- Reduced reflexes
- Saddle sensory loss
- Urinary retention
- Reduced anal tone
Neurological Examination and Documentation
A full neurological chart is essential.
Record:
- Motor power in every key muscle group
- Tone
- Deep-tendon reflexes
- Plantar responses
- Sensory level for light touch, pinprick and vibration
- Perianal sensation and anal tone if indicated
- Sacral sparing
- Gait, if patient can walk
- Bladder and bowel function
- Sexual function where relevant
- Presence of pressure sores
Serial examination is important because deterioration can be rapid.
Investigations
1. Blood tests
- CBC: may show anaemia
- ESR and CRP: often elevated but nonspecific
- Renal and liver function baseline before drug therapy
- HIV test with consent, where appropriate
- Blood cultures if pyogenic infection is a possibility
2. Tuberculosis testing
- Tuberculin skin test or interferon-gamma release assay may support TB exposure but cannot prove active spinal disease.
- Sputum examination if pulmonary symptoms or lung lesions are present.
3. Plain radiographs
Early stage
May be normal or show minor reduction in disc height.
Later findings
- Reduction of intervertebral disc space
- Destruction of adjacent vertebral end plates
- Anterior vertebral wedging
- Vertebral-body collapse
- Kyphosis or gibbus
- Paravertebral shadow from abscess
- Fusion or ankylosis in healing stage
4. MRI: investigation of choice
MRI evaluates:
- Vertebral marrow involvement
- Disc and end-plate destruction
- Epidural abscess or granulation tissue
- Cord compression
- Cord oedema or myelomalacia
- Paravertebral and psoas abscesses
- Multilevel and non-contiguous lesions
- Degree of canal compromise and neural compression
A
review of spinal tuberculosis notes that MRI is more sensitive than radiography and more specific than CT for spinal TB, and can show vertebral involvement, disc destruction, cold abscess, collapse and deformity.
5. CT scan
Useful for:
- Defining bony destruction
- Surgical planning
- Identifying sequestra
- CT-guided aspiration or biopsy
6. Tissue diagnosis
Whenever practical, obtain a specimen before or at surgery.
Methods
- CT-guided needle biopsy
- Aspiration of cold abscess
- Open biopsy during decompression
Send for
- Histopathology: granulomas with caseation may be seen
- Acid-fast bacilli smear
- Mycobacterial culture
- Nucleic-acid amplification test, for example Xpert MTB/RIF or equivalent
- Drug-susceptibility testing
Microbiological confirmation and drug sensitivity are important because drug-resistant TB changes management.
Differential Diagnosis
- Pyogenic spondylodiscitis
- Brucellar spondylitis
- Metastatic spinal tumour
- Multiple myeloma
- Lymphoma
- Vertebral osteoporotic collapse
- Fungal vertebral infection
- Ankylosing spondylitis with fracture
- Epidural tumour or abscess from another cause
Management
Principles
- Diagnose promptly and determine neurological severity.
- Confirm TB microbiologically when feasible.
- Start effective antituberculous treatment.
- Prevent or reverse cord damage.
- Decompress neural structures when indicated.
- Stabilise an unstable spine and prevent progressive deformity.
- Provide bladder, bowel, skin and rehabilitation care.
Antituberculous therapy is the foundation of management. Routine surgery for every patient is not supported, but surgery is important for selected patients with evolving neurological deficit, major abscess, severe kyphosis, instability or failure to respond medically, as summarized in the
spinal-TB review.
A. Antituberculous chemotherapy
Use national TB-programme and drug-susceptibility-guided protocols.
Usual drug-susceptible regimen
Commonly:
- Intensive phase: isoniazid, rifampicin, pyrazinamide and ethambutol
- Continuation phase: isoniazid and rifampicin
The duration for spinal TB varies among national protocols and specialist services. It is often longer than treatment for uncomplicated pulmonary TB. Do not use a fixed duration in an exam answer without stating that local/national TB guidance should determine it.
Monitoring
- Adherence and adverse effects
- Clinical improvement: pain, fever, appetite, neurology
- Liver function where indicated
- Visual assessment with ethambutol
- Serial ESR/CRP as supportive markers
- Imaging only when clinically needed, since radiological resolution lags behind clinical recovery
Drug-resistant TB
Requires specialist treatment based on molecular/culture susceptibility testing.
B. Nonoperative supportive management
Appropriate for carefully selected patients with:
- Confirmed or highly probable TB
- Mild and non-progressive neurological deficit
- No major instability
- No severe kyphosis
- No large compressive abscess
- Demonstrable response to treatment
Measures:
- Analgesia
- Nutrition and protein optimisation
- Vitamin D and bone-health assessment where appropriate
- Short-term brace or orthosis for pain control/instability when indicated
- Prevention of pressure sores
- DVT prevention in immobile patients
- Physiotherapy and safe mobilisation
- Bladder and bowel care
Prolonged absolute bed rest is generally avoided where it is not necessary, because it causes deconditioning, DVT, pressure injury, chest complications and osteoporosis.
C. Indications for Surgery
Surgical decompression and stabilisation should be considered for:
- Progressive neurological deficit despite appropriate chemotherapy
- Severe neurological deficit with significant cord compression
- Large epidural abscess or significant mass effect
- Mechanical instability
- Severe or progressive kyphosis, especially in children or junctional disease
- Vertebral collapse causing internal gibbus
- Diagnostic uncertainty, particularly concern for malignancy or pyogenic infection
- Failure of conservative treatment, persistent severe pain or worsening deformity
- Drug-resistant disease requiring debridement or diagnostic tissue
- Late-onset paraplegia from healed kyphotic deformity or canal stenosis
D. Surgical Principles and Procedures
The approach depends on site of disease, deformity, stability, location of compression and surgeon expertise.
Surgical aims
- Obtain tissue diagnosis
- Drain abscess
- Remove caseous/necrotic tissue and sequestrum
- Decompress spinal cord
- Correct deformity where safe
- Stabilise the spine
- Facilitate mobilisation
Procedures
- Anterior debridement and decompression with reconstruction
- Posterior decompression and instrumented stabilisation
- Combined anterior-posterior surgery in selected severe cases
- Drainage of paravertebral or psoas abscess, percutaneously or openly
- Deformity correction/osteotomy in selected late kyphotic paraplegia
Laminectomy alone is usually inadequate if compression is predominantly anterior from vertebral-body destruction, abscess or granulation tissue. It can also worsen instability. Decompression must address the actual site of compression.
Bladder and Bowel Care
Bladder
- Assess retention using bladder scan.
- Intermittent clean catheterisation is preferred where feasible.
- Indwelling catheter may be needed initially, but avoid unnecessary prolonged use.
- Monitor for urinary infection.
- Refer for urological/neuro-urological assessment if dysfunction persists.
Bowel
- Regular bowel programme
- Adequate fluids and fibre if appropriate
- Stool softeners or stimulant agents as needed
- Prevent constipation and faecal impaction
Rehabilitation
Begin early and individualise according to spinal stability and neurological state.
Prevent complications
- Two-hourly repositioning when immobile
- Pressure-area care
- Passive range-of-motion exercises
- Prevention of contractures
- DVT prevention
- Chest physiotherapy where needed
Restore function
- Strengthening of preserved muscle groups
- Progressive sitting, transfers and standing
- Gait training where feasible
- Orthoses, walker, crutches or wheelchair as required
- Occupational therapy for activities of daily living
- Psychological support
- Social, vocational and sexual-health rehabilitation
A recent rehabilitation review highlights management of bed-confinement complications, strengthening and mobility work, bracing where useful, and structured care for vesico-sphincter dysfunction in spinal TB with neurological complications. See the
rehabilitation review.
Prognosis
Better prognosis is associated with:
- Early diagnosis and treatment
- Early-onset neurological deficit
- Short duration of paralysis
- Incomplete deficit at presentation
- Predominantly soft compressive material, such as abscess/granulation tissue
- Prompt decompression when indicated
- Good adherence and drug-susceptible disease
Poor prognostic factors:
- Complete longstanding paraplegia
- Late-onset paraplegia
- Cord atrophy, myelomalacia or severe chronic fibrosis on MRI
- Severe rigid kyphosis
- Delayed diagnosis
- Drug-resistant TB
- Poor nutritional status or severe comorbidity
Short Exam Conclusion
Pott’s paraplegia is neurological impairment caused by spinal tuberculosis. Urgent assessment includes complete neurological examination, MRI to define cord compression, and microbiological confirmation through image-guided biopsy or surgical specimen where feasible. Effective multidrug antituberculous treatment is essential. Surgery is reserved for significant or progressive neurological deficit, mechanical instability, major abscess, deformity, uncertain diagnosis or failure of medical management. Early rehabilitation and organised bladder, bowel and skin care determine functional outcome.