Pott Disease

Pott disease is tuberculous spondylitis, spinal involvement by Mycobacterium tuberculosis, most commonly reaching the spine via hematogenous spread from a primary (often pulmonary) focus, though the primary site is frequently no longer clinically active by the time spinal disease presents.

It remains an important cause of spinal infection globally, particularly in TB-endemic regions, and is a leading infectious cause of potentially preventable paraplegia if diagnosis is delayed.

The thoracolumbar spine is most commonly affected, with infection typically starting in the anterior vertebral body (adjacent to the richly vascularized subchondral region) and spreading beneath the anterior longitudinal ligament to involve adjacent vertebrae and the intervening disc, a pattern distinguishing it from pyogenic spondylodiscitis.

Onset is typically insidious, over weeks to months, with back pain (often the earliest and most persistent symptom), low grade fever, night sweats, and weight loss.

As vertebral body destruction progresses, a gibbus deformity (an angular kyphosis) may develop.

Neurological complications ("Pott's paraplegia") result from spinal cord compression by an epidural abscess, granulation tissue, or direct bony collapse and instability, presenting with progressive limb weakness, sensory loss, and bladder/bowel dysfunction, and represent a genuine spinal emergency requiring urgent recognition.

A cold abscess (paravertebral or psoas abscess, so termed given the relative absence of the acute inflammatory signs seen with pyogenic infection) may track along fascial planes and present as a soft tissue mass at a site distant from the spine itself, classically in the groin along the psoas sheath.

MRI with contrast is the imaging investigation of choice, showing vertebral body destruction, disc space narrowing, paraspinal or epidural collection, and the degree of any cord compression, with substantially higher sensitivity than plain radiography, particularly for early disease
Plain radiographs may show vertebral body collapse and disc space narrowing but are typically only positive once substantial bone destruction (often 30 to 50%) has occurred
Microbiological confirmation via CT-guided or open biopsy of the affected vertebra or paraspinal collection, sent for Ziehl-Neelsen or auramine staining, mycobacterial culture (though slow, taking weeks), and, where available, GeneXpert MTB/RIF for rapid molecular confirmation and detection of rifampicin resistance
Assessment for a primary or concurrent TB focus (CXR, sputum studies where relevant), and HIV testing given the strong association and mutual influence on presentation and management
Inflammatory markers (ESR, CRP) are typically elevated but non-specific

Standard antituberculous therapy as detailed in the Tuberculosis entry: intensive phase with isoniazid, rifampicin, pyrazinamide, and ethambutol for 2 months, followed by a continuation phase of isoniazid and rifampicin, with spinal TB total treatment duration generally extended to 9 to 12 months given the poorer drug penetration into avascular, necrotic bone and disc tissue and the higher relapse risk compared with pulmonary disease
Pyridoxine (vitamin B6) 10 to 25 mg PO od co-administered with isoniazid to reduce peripheral neuropathy risk
Bracing or immobilization may be used adjunctively for spinal stability and pain relief in selected cases, per orthopedic or spinal surgery input
Surgical intervention (decompression, debridement, and, where instability results, spinal stabilization/fusion) is indicated for significant or progressive neurological deficit, spinal instability, failure to respond to medical therapy alone, or a large abscess requiring drainage; surgery does not replace the need for the full antituberculous drug course
Close neurological monitoring throughout treatment given the risk of neurological deterioration even after treatment initiation, particularly in the first weeks

Referral: spinal surgery for any neurological deficit, instability, or significant abscess; infectious disease or respiratory medicine for antituberculous therapy coordination and monitoring; HIV testing and, where positive, coordinated HIV and TB management per the principles in the Tuberculosis and HIV entries.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Subtrochanteric Fracture

A subtrochanteric fracture occurs in the proximal femoral region extending from the inferior border of the lesser trochanter to approximately 5 cm distally.

These fractures experience very high mechanical stresses and powerful deforming muscle forces.

The typical deformity is:

Proximal fragment

Flexed by iliopsoas
Abducted by gluteus medius and minimus
Externally rotated by short external rotators

Distal fragment

Adducted by adductor muscles
Shortened proximally

This explains why subtrochanteric reduction is often more difficult than passage of the nail itself.

Seinsheimer classification

Type I

Nondisplaced
Less than 2 mm displacement

Type II

Two part fracture.

IIA

Transverse two part fracture

IIB

Spiral fracture
Lesser trochanter remains with proximal fragment

IIC

Spiral fracture
Lesser trochanter remains with distal fragment

Type III

Three part fracture.

IIIA

Lesser trochanter is a separate third fragment

IIIB

Third fragment is a butterfly fragment

Type IV

Four or more major fragments
Comminuted fracture

Type V

Subtrochanteric fracture extending proximally into the intertrochanteric region.

Russell Taylor classification

This system describes involvement of the piriformis fossa and lesser trochanter.

Type IA

Piriformis fossa intact
Lesser trochanter intact

Type IB

Piriformis fossa intact
Lesser trochanter involved

Type IIA

Piriformis fossa involved
Lesser trochanter intact

Type IIB

Both piriformis fossa and lesser trochanter involved.

Modern cephalomedullary implants have reduced the treatment relevance of the Russell Taylor system because trochanteric entry nails can be used despite many proximal fracture extensions.

Older patients commonly sustain low energy osteoporotic fractures.

Younger patients generally require high energy trauma.

Findings include:

Severe proximal thigh pain
Inability to bear weight
Shortened externally rotated limb
Significant swelling

A transverse lateral cortical fracture after minimal trauma should raise concern for an atypical femoral fracture, particularly with prolonged antiresorptive therapy.

Prodromal thigh pain may precede an atypical fracture for weeks or months.

Most subtrochanteric fractures require surgery.

Definitive fixation

A cephalomedullary intramedullary nail is the preferred fixation for most fractures.

The implant should generally span the fracture adequately, with long nails commonly used for true subtrochanteric and more distal extension.

The fracture must be reduced before and during nail passage. Do not expect the nail to correct a displaced subtrochanteric fracture automatically.

Reduction principles

Restore:

Length
Rotation
Neck shaft angle
Medial cortical alignment

Avoid varus.

Persistent varus or flexion of the proximal fragment may require:

Percutaneous Schanz pin joystick
Ball spike pusher
Percutaneous clamp
Cerclage cable in carefully selected long spiral patterns
Limited open reduction

A small controlled open reduction is preferable to accepting major malalignment.

Avoid extensive periosteal stripping.

Plate fixation

Fixed angle plating has a more limited role but can be useful when:

Femoral canal anatomy prevents nailing
Previous implants block the canal
Severe proximal deformity exists
Associated femoral neck fracture requires another strategy
Nail entry cannot be safely achieved

Atypical subtrochanteric fracture

A complete atypical fracture generally requires intramedullary fixation.

An incomplete tension side fracture with persistent pain or a clear lateral cortical fracture line should be strongly considered for prophylactic intramedullary fixation because progression to complete fracture is common.

Assess the opposite femur.

Review long term bisphosphonate or other antiresorptive therapy and optimise calcium and vitamin D status.

Postoperative management

Permit weight bearing according to reduction quality, fixation stability and bone quality.

Stable geriatric constructs should support early mobilisation whenever possible.

Monitor closely for:

Varus malunion
Delayed union
Nonunion
Implant fatigue failure

Subtrochanteric fractures commonly heal more slowly than routine intertrochanteric fractures because of the high mechanical environment and predominantly cortical bone.

Pott Disease

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management