Category: Topics

Simple bone cyst (Unicameral bone cyst)

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  • 3% of primary bone tumors. 
  • Nearly always in first 2 decades.
  • Most often between 4-10years.
  • 2:1 male female ratio.

Pathology

  • Common sites are proximal humerus – 50%, proximal femur- 18-27% and proximal tibia, distal tibia and calcaneum.
  • Cyst cavity may become multiloculated after fracture healing.
  • Categorized as latent and active.
    • Lesions <0.5cm from physis are considered active.
    • Epiphyseal involvement rare but seen in aggressive lesions.
    • Latent cysts also have growth potential.
  • Recurrence and worsening rare after skeletal maturity.
  • >75% detected in childhood.
  • >95% involve metaphysis.
  • Cyst is filled with fluid rich in protein content. Shown to have elevated levels of IL-1, IL-6, prostaglandins, lysosomal enzymes, IL1B, TNF-A, Nitric oxide production thought to be important.
  • Oxygen free radicals thought to be important.
  • Fluid shows increased intraosseous pressure of >30cm H2O.
  • Fluid may be straw coloured or serosanguinous.
  • Most characteristic histopathologic finding is thin membrane like lining of epithelium like cells.
  • Osteoclasts, cholesterol cells and fat cells also seen.
  • Genetic analysis shows single and multifocal cytogenetic rearrangements.

Theories about causation

Mirra- Intraosseous entrapment of synovium.

Jaffe and Lichtenstein- Localized failure of ossification during periods of rapid growth.

Cohen- Blockage of venous drainage.

Current evidence supports blockage of intraosseous venous circulation. 

Clinical features

Fractures occur in up to 90%.

Physeal closure occur after fracture in 10%.

Fracture readily heals but cyst does not.

Spontaneous healing of cyst after fracture occurs in <5%.

Radiological features

Symmetrically expansive, radiolucent with a thin shell of cortical bone.

Fallen fragment sign seen in less than 10%.

MRI shows complex appearance with heterogenous fluid signals with nodular and thick peripheral enhancements.

Double density fluid levels, septation and low signal on T1 with high signal on T2 suggest ABC.

Differential diagnosis

ABC

Fibrous dysplasia

Atypical eosinophilia

Treatment

Treatment if necessary should be undertaken immediately after the fracture ha healed.

Treatment more aggressive in younger children and in older individuals with lesions in weight bearing bones.

Treatment options

Corticosteroid injection

Injection of autologous marrow.

Multiple drilling and drainage

Curretage and bone grafting

Corticosteoid injection

Reported by Scaglietti in 1979.

Healing occurs in 90%.

Thickening of cortex, increasing opacity, remodelling and bone scar are signs of healing.

Cysts with rapid venous flow shown by radiografin instillation show higher rates of failure.

Look for loculation.

Each locule must be injected.

40-120mg of methylprednisolone injected.

Repeated every 2 months for 2-5 dosestill complete healing occurs.

Follow-up xrays taken every 2-3 months.

Temporary Cushing syndrome may be seen.

Other materials injected

Autologous bone marrow- Single injection recurrence rate of 12%

Demineralized bone matrix

Bioabsorbable calcium phosphate paste

Multiple drilling

Percutaneous drilling of multiple holes.

Lavage with saline

Multiple K wires, flexible nails or cannulated screws fixation

Displaced pathological fractures of femur needs curettage, bone  grafting and internal fixation.

Paediatric Monteggia Fractures

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  • Monteggia fracture first described by Giovanni Monteggia in 1814.
  • 16-50% of paediatric Monteggia fractures are missed initially at presentation.

Anatomy

  • Annular ligament and quadrate ligament are primary static stabilizers of proximal radioulnar joint.
  • Weitbrecht ligament or oblique cord which extend from just distal to radial notch on the ulna to the bicipital tuberosity and the interosseous ligament are the other stabilizers.
  • These ligaments are most taut in supination because of radial bow and elliptical shape of radial head, and the longer axis of the elliptical radial head is perpendicular to radial notch of ulna in supination.
  • 80% of load from carpus is carried by radius.
  • 33% of valgus stability of elbow provided by radial head.

Classification

Letts Classification

  1. Anterior dislocation with apex anterior plastic bowing of ulna
  2. Anterior dislocation with apex anterior green stick fracture of ulna.
  3. Anterior dislocation with apex anterior complete fracture
  4. Posterior dislocation with apex-posterior fracture of ulna
  5. Lateral dislocation with apex-lateral fracture of ulna

75% of acute paeditric Monteggia injuries and 85% of missed paediatric Monteggia fractures are anterior dislocation types.

Bado classification

  1. Anterior dislocation with apex-anterior fracture of ulna. Due to hyperextension (hyperextension theory of Tompkins)
  2. Posterior dislocation with apex-posterior fracture of ulna. Due to fall with elbow flexed to 60 degrees.
  3. Lateral dislocation with apex-lateral fracture of ulna. Due to varus stress.
  4. Radial head dislocation with fracture of radius and ulna. Due to hyper-pronation.

Natural history

  • Ulnar fracture unites.
  • The annular ligament and anterior capsular structures fall into radiocapitellar joint producing block to reduction.
  • Dysplastic changes develop in the radial head, capitellum and the radial notch of ulna.
  • Valgus instability of elbow develops.
  • Cubitus valgus develops.
  • Secondary osteoarthritis of elbow develops.
  • Late paralysis of ulnar nerve can develop due to cubitus valgus.
  • Late median nerve and posterior interosseous nerve palsy can develop due to tenting by the anteriorly dislocated radial head.

Diagnosis

  • Storen line – The axis of radius passes through the centre of the capitellum.
  • Head neck ratio- Ratio between widest part of head and narrowest part of neck. Normal is less than 1.5.
  • Lincoln and Mubarak method- The line drawn along the subcutaneous border of ulna is within <2-3mm of the ulnar shaft. if more, the ulna is deformed.

Treatment

  • In acute setting, treatment is by closed reduction and long arm casting in supination.
  • Closed reduction can be attempted up to 4 weeks.
  • Contraindications for surgery are duration more than 3 years and age > 12 years.
  • Generally reduction is successful if done within one year of injury irrespective of age.
  • Depending on the chronicity and the severity of changes, adjunct procedures are required to maintain the reduction.
  • Treatment needs 3 strategies
    • Reduction of radial head
    • Reconstruction of ligamentous stabilizers
    • Correction of ulnar deformity
  • Bell Tawse procedure
    • Described in 1968.
    • Posterolateral approach
    • Excision of interposed tissue
    • Reduction of radial head
    • Reconstruction of annular ligament by passing the central slip of triceps circumferentially around the neck of radius.
    • According to Seel and Peterson, the reconstructed ligament produces a posterolateral pull and hence is useful for anteromedial dislocations, but not for other types of dislocations.
  • Seel and Peterson developed a 2-drill hole technique that produces a centrally directed force.
  • Lloyd Roberts and Bucknill added radio-capitellar pinning to Bell Tawse procedure to protect the reconstructed ligament for 6 weeks.
  • To avoid intra-articular pin breakage, Letts described radioulnar pinning instead of radio-capitellar pinning.
  • Kalamchi procedure
    • Osteotomy of ulna using multiple passes of K wire and open reduction of radial head.
  • Ladermann procedure
    • Closed reduction of radial head after ulnar osteotomy and lengthening of ulna.
  • Bor technique
    • Using Ilizarov technique to lengthen the ulna, angulate the ulna and reduce the radial head.
  • According to Delpont (2014) annular ligament reconstruction is not beneficial in conjunction with ulnar osteotomy.  (Delpont M, Jouve JL, Sales de Gauzy J, Louahem D, Vialle R, Bollini G, Accadbled F, Cottalorda J. Proximal ulnar osteotomy in the treatment of neglected childhood Monteggia lesion. Orthop Traumatol Surg Res. 2014 Nov; 100(7):803-7. Epub 2014 Oct 7.)
  • Osteotomy is useful in Bado 1 lesions but less effective in Bado 3 lesions.
  • Ulnar osteotomy can be corrective (Straightens the posterior cortical line), over-corrective (reverses original deformity) or stabilizing (reduces the radial head).
  • Overcorrection has been shown to produce significantly better outcomes. (Inoue G, Shionoya K. Corrective ulnar osteotomy for malunited anterior Monteggia lesions in children. 12 patients followed for 1-12 years. Acta Orthop Scand. 1998 Feb;69(1):73-6.)
  • Osteotomy can be at the CORA or at the proximal metaphyseal area. Osteotomy at the proximal metaphyseal area have better healing and can be performed through the same incision.

Notes on Robotic Total Knee Replacement

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  • Term ‘robot’ originates from the Czech word ‘robota’, which means forced labour or activity.
  • Karel Capek first used the term ‘Robot’ in his 1921 play called Rossum’s Universal Robots.
  • Robots are defined as an array of computer controlled machines that perform preprogrammed, precise, and repetitive procedures.
  • Robotic technology allow to sustain levels of precision, productivity, and efficiency that were not possible with humans alone.
  • First robotic surgical procedure was performed by Kwoh  in 1988 using the PUMA 560 robotic system (Westinghouse Electric, Pittsburgh, Pennsylvania) to undertake neurosurgical biopsies with improved precision.
  • Advantages of robotic surgery
    • Smaller skin incisions
    • Improved precision of soft-tissue dissection
    • Better visualisation of the surgical field
    • Comprehensive data capture for surgical training
    • Early recovery
    • Shorter hospital stay
  • Disadvantages
    • Expensive to install
    • Needs separate applications for total hip arthroplasty, TKA, and unicompartmental knee arthroplasty.
    • Compatible with a limited number of implants from the manufacturer of the robotic device
    • Additional costs are incurred for preoperative imaging
    • Radiation exposure for CT
    • Increased operating times during the learning phase
    • Needs training the surgical team
    • Updating of computer software needed
    • Needs servicing contracts and consumables.
    • Additional time needed for planning and modelling
    • Product specialists needed in the OT
    • Technical issues with robot arm may need intra-operative conversion to conventional jigs
    • Maintenance costs
    • Paucity of long-term data showing any functional benefit

Why consider robots for TKR?

  • Up to 20% of patients remaining dissatisfied following TKA.
  • Surgeon controlled variables affecting outcome in TKR
    • Accurate implant positioning
    • Balanced flexion-extension gaps
    • Proper ligament tensioning
    • Preservation of periarticular soft-tissue envelope
  • Conventional jig-based TKA uses preoperative radiographic films, intra-operative anatomical landmarks, and manually positioned alignment jigs to guide bone resection and implant positioning.
  • Conventional jig-based TKA is associated with poor reproducibility of alignment-guide positioning, inadvertent saw blade injury to the periarticular soft-tissue envelope, and limited intra-operative data on gap measurements or ligamentous tensioning to fine tune the implant positioning.
  • Suboptimal implant positioning may lead to
    • Poor functional recovery
    • Reduced clinical outcomes
    • Increased instability
    • Reduced implant survivorship
  • In navigated TKR, computer software converts anatomical information obtained from preoperative CT or intra-operative osseous mapping into a virtual patient-specific 3D model of the knee joint.
  • Virtual model is used to plan optimal bone resection, implant positioning, bone coverage, and limb alignment based on the patient’s unique anatomy.
  • Computer navigated TKA provides patient-specific anatomical data with recommendations for bone resection and optimal component positioning.
  • In robotic TKR, a robotic device helps to execute this preoperative patient-specific plan with a high level of accuracy.
  • Robotic TKR uses optical motion capture technology to assess intra-operative alignment, component positioning, range of movement, flexion-extension gaps, and soft tissue balancing.
  • RTKR actively controls and/or restrains the surgeon’s motor function to improve the accuracy of achieving the planned bone resection and implant positioning.
  • Real-time intra-operative data can then be used to fine-tune bone resection and guide implant positioning, in order to achieve the desired knee kinematics and limit the need for additional soft-tissue releases.
  • First robotic TKA was performed in 1988 using the ACROBOT robotic system (Imperial College, London, United Kingdom).

Classification

  • Classified into
    • Imageless or Image guided
    • Fully-active or semi-active
  • Fully active is actively involved in all steps of bone resection and soft tissue balancing.
  • Semi-active provides the surgeon with visual, tactile, and audio feedback that provides stereotactic boundaries that confines the saw blade to pre-planned haptic femoral and tibial windows to achieve accurate bone resection and soft tissue balancing.
  • RTKR associated with improved accuracy of achieving the planned femoral and tibial implant positioning, joint line restoration, limb alignment, and posterior tibial slope compared with conventional jig-based TKA.
  • Results in improved accuracy in implant positioning in all three planes and reduces outliers.
  • RTKR associated with learning curve of six to 20 cases for operative times, but there is no learning curve for achieving the planned femoral or tibial implant positioning. This allows even low volume surgeons to improve accuracy.
  • Improved accuracy of implant positioning and enhanced postoperative rehabilitation in robotic TKA have not translated to any differences in middle- to long-term functional outcomes compared with conventional TKA.
  • There is a paucity of prospective randomized controlled trials reporting on longer-term outcomes.

Based on the Open access article published in Bone and Joint Research

Robotic total knee arthroplasty clinical outcomes and directions for future research by Babar Kayani & Fares S Haddad.

https://online.boneandjoint.org.uk/doi/full/10.1302/2046-3758.810.BJR-2019-0175

Examination of Spine

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The purpose of clinical examination are many.  First and foremost, the identification of patients who need emergent or urgent care and treatment, and then, identify the cause of patient’s symptoms, its impact on the patient and the needs and expectations of the patient. Any associated medical conditions that have an impact on the treatment of the primary condition should also be identified. Proper physical examination achieves these objectives and allows the clinician to develop a healthy rapport with the patient as well.

The information generated from the history and examination must differentiate normal from abnormal, provide a reliable measure of the abnormality, and permit a valid interpretation. It should fulfil the criteria of normality, reliability, validity, utility, compliance and cost effectiveness. (Waddell 1982)

Examination of spine involves 2 steps: history taking and physical examination. A detailed and chronological history and a structured clinical examination is essential for diagnosis. History taking provides information about the past and the present health status of the patient, his symptoms and the disease. It helps in the assessment of disability caused by the disease. History provides the foundation for making decisions regarding the working diagnosis,  investigations needed for work-up, treatment options, follow-up, outcome analysis, prognostication and prevention.

History taking

History taking is an art. The clinician should learn to talk less and listen more. It should be detailed and chronological. History taking is divided into various components such as presenting complaint, history of presenting complaint, treatment history, past history, personal history, family history, occupational history, nutritional history etc. Depending on the setting of the patient interview, either some or all these components may have to be gone into.

History taking starts with simple, open ended questions  that allows the patient to communicate her perception of the problem and to let the surgeon understand the treatment goals. Later more focussed questions should be asked to get specific details about various aspects of the symptoms. The questions should be simple, clear, unambiguous and phrased in patient’s own everyday language. It should avoid medical terminology and inappropriate cultural assumptions (Waddell 1982). The information sought should be within patient’s knowledge. 

History taking helps in localisation of the symptoms to the diseased part, discern the evolution of symptoms, identify the underlying pathology and elucidate the effect of the disease on the patient. It helps in identifying the associations and co-morbidities. The root cause of symptoms in spine patients may be vertebral, paravertebral or referred. It may be musculoskeletal, neurological or combined. Vertebral causes may present with pain, deformity, limitation of movement, swelling or functional limitation. Neurological causes may present with upper motor or lower motor neurone  symptoms. Neurological symptoms may be sensory, motor or sphincter related. 

Most common presenting complaint is pain. Pain may be somatic, visceral, neurogenic or psychosomatic. Somatic pain is due to local causes which can be mechanical or non-mechanical. Mechanical pain may be discogenic, capsuloligamentous or stenotic in origin. Discogenic pain may be disco-dural or disco-radicular. Disco-dural pain presents with acute lumbago, chronic backache or sciatica. Disco-radicular symptoms pain that radiating pain or neurological deficit in body area supplied by the roots affected and occur when the neuronal cell bodies in the dorsal root ganglion situated within the intervertebral foramen are chemically or mechanically irritated by various causes; most commonly by a prolapsed disc. Mechanical causes of pain may be herniated nucleus pulposus, osteoarthritis, spinal canal stenosis, spondylolisthesis or compression fracture. Non-mechanical causes may be inflammatory spondylarthritis, infective spondylitis, tumours, osteoporotic fractures or visceral causes.

Pain due to spinal canal stenosis presents with unilateral or bilateral neurogenic claudication. Neurogenic claudication is worsened by standing or walking and is relieved by sitting, squatting or stooping forwards. It is often associated with neurological symptoms such as weakness, numbness or sphincter disturbance. Dural and root symptoms and signs are generally absent. 

The cause of pain may be identified from patient history based on the site of pain, onset, duration, radiation, relation to activity and posture. Somatic pain is sharp, localised and worsened by activity. Visceral pain is poorly localised and not affected by activity or rest. Neurogenic pain is burning or pricking type of pain felt along the involved dermatomes. Psychosomatic pain is due to underlying psychological diseases and is a diagnosis by exclusion of other causes by detailed evaluation.

Site of pain is described as per the anatomic borders delineated by International Society for Study of Pain (IASP). Low back pain as the site may be lumbar, sacral, coccygeal, loin or gluteal pain. 

According to the duration of symptoms, pain of duration less than 5 weeks is considered as acute, 5 weeks to 3 months as subacute and more than 3 months as chronic pain. Radiculopathy is defined by IASP as “Pain perceived as arising in a limb or the trunk wall caused by ectopic activation of nociceptive afferent fibres in a spinal nerve or its roots or other neuropathic mechanisms.”

Pain history

  1. Duration – How long the pain is present?
  2. Onset- How did it start?
  3. Progress – What happened afterwards?
  4. Site- Where do you feel the pain, point it out with a single finger?
  5. Character- What is the nature of pain? Is it throbbing, pricking or burning type of pain?
  6. Intensity of pain – What is the severity of pain at present, at rest and during activity? How severe was the worst pain you experienced?
  7. Temporal factors – Continuous or intermittent, diurnal variation.
    1. Is the pain continuous or intermittent?
    2. If intermittent, how long does each episode last?
    3. If intermittent, is it  colicky in nature?
    4. Is there any relation between the severity of pain and the time of day?
    5. Is there any sleep disturbance due to pain?
  8. Aggravating factors.
    1. Is it aggravated by activity? Suggestive of mechanical pain.
    2. Is it aggravated when getting up in the morning? If yes, how long does the increased pain last? Morning stiffness is present if the pain lasts for more than one hour. Morning stiffness is suggestive of inflammatory spondylarthropathy.
    3. Is it aggravated by walking? Suggestive of vascular or neurogenic claudication.
    4. Is it aggravated by standing? Suggestive of neurogenic claudication.
  9. Relieving factors.
    1. Is it relieved by activity? Suggestive of inflammatory spondylarthropathy.
    2. Is it relieved by rest? Suggestive of mechanical pain.
    3. If aggravated by walking, is it relieved by standing? Suggestive of vascular claudication.
    4. If aggravated by standing and walking, is it relieved by sitting down or stooping forwards? Suggestive of neurogenic claudication.
  10. Associated symptoms.

History taking in spinal deformity

  1. When was the deformity noticed?
  2. How was the deformity noticed?
  3. What happened to the severity of deformity after it was noticed?
  4. Is it painful?
  5. Is there any difficulty in walking?
  6. Is there any weakness or numbness in the upper or lower limbs?
  7. Is there any urinary retention or urinary incontinence?
  8. Is there any bowel complaints?
  9. Is there any exercise intolerance or exertional dyspnoea?
  10. Is there any associated symptoms?
  11. In girls presenting with spinal deformity, ask about age of menarche.

In the history, red flag and yellow flag signs which suggest serious underlying disease should be specifically looked for.  

Red flag symptoms

Age > 50 years

Duration of symptoms > 1month

Rest pain

Night pain

Bilateral sciatica

Significant neurological deficit

Progressive neurological deficit

Bowel or bladder disturbance

Unexplained weight loss 

Fever

History of significant trauma 

History of malignancy

History of steroid intake

Yellow flag symptoms

Denotes negative psychosocial factors that are associated with chronicity and long term disability. It may be related to work, beliefs, behaviour or affective disorders.

General Examination

Development of secondary sexual characteristics using  Tanner stages should be done in children with spinal deformity. 

Tanner stages.

  • Used to assess sexual age by assessing the onset and progression of pubertal changes.
  • Boys and girls assessed on a 5-point scale.
  • Boys are assessed by genital development and pubic hair growth, and girls by breast development and pubic hair growth.
  • Girls
    • Pubertal hair development
      • Stage I (Preadolescent) – Vellos hair develops over mons pubis similar to that over the anterior abdominal wall. There is no sexual hair.
      • Stage II – Appearance of sparse, long, pigmented, downy, straight or only slightly curled hair mainly along the labia.
      • Stage III – Appearance of darker, coarser, and curlier sexual hair appears sparsely over the junction of the pubes.
      • Stage IV – The hair distribution similar to adult but decreased in total quantity. No spread to the medial surface of the thigh.
      • Stage V – Pubic hair similar to adults in quantity and appearance.  Distribution have an inverse triangle and extends to the medial surface of the thighs. No extension above the base of the inverse triangle.
    • Breast development
      • Stage I (Preadolescent) – Only the papilla is elevated above the level of the chest wall.
      • Stage II – (Breast Budding) – Elevation of the breasts and papillae above the level of chest wall may as small mounds along with increase in the diameter of the areolae.
      • Stage III – The breasts and areolae continue to enlarge, and show no difference in contour.
      • Stage IV – The areolae and papillae form secondary mounds above the level of breast.
      • Stage V – Mature female breasts have developed. The papillae project due to recession of the areolae.
  • Boys
    • Pubertal hair development
      • Stage I (Preadolescent) – Only vellos hair over the pubes similar to that over the abdominal wall is present. 
      • Stage II – Sparse long pigmented, slightly curled or straight, downy hair begins to appear.
      • Stage III –  Darker, coarser, and curlier pubic hair with its distribution spread over the junction of the pubes. 
      • Stage IV – Adult type hair distribution but quantity less. No spread to the medial surface of the thighs.
      • Stage V – Adult type hair distribution in an inverse triangle shape with extension to medial thigh. Quantity and type similar to adult.
    • Male genitalia development
      • Stage I (Preadolescent)- The testes, scrotal sac, and penis similar to early childhood in size and proportion.
      • Stage II – Enlargement of the scrotum and testes with changes in the texture of the scrotal skin. 
      • Stage III – Along with increased growth of the testes and scrotum, there is growth of the penis mainly in length, with some increase in diameter. 
      • Stage IV – Penis and glans penis significantly enlarged in length and diameter. Testes and scrotum enlarge further with darkening of the scrotal skin. 
      • Stage V – Similar to adult in size and shape.

Facial hair

Voice change

Signs of generalised ligamentous laxity

Neurocutaneous markers should be looked for in patients with scoliosis to rule out neurofibromatosis 1. 

Height

Sitting height

Upper segment : lower segment ratio

Arm span

Inspection

Inspection starts with assessment of the patient as a whole with observation of his posture, demeanour,  and gait. Next inspect the entire vertebral column from the front, sides and back. Inspection should be done with the patient standing, sitting, supine and prone. First assess the surface anatomy of the spine.

Surface markings

  • First palpable spinous process – C2
  • Hyoid – C3
  • Adam’s apple – C4/5
  • Cricoid cartilage – C6
  • Carotid tubercles (Chassaignac tubercle) – C6
  • Most prominent spinous process- C7
  • Longest spinous process – T1
  • Sternal notch – T3/4
  • Spine of scapula – T3
  • Inferior angle of scapula – T7
  • Highest point of iliac crest – L4/5
  • Posterior superior iliac spine – S2

Assessment of posture

Spinal deformity is defined as a deviation from normal spinal alignment. Deformity should be defined in relation to the ‘neutral upright spinal alignment’ in asymptomatic individuals. Neutral upright spinal alignment (NUSA) position in asymptomatic individuals is determined with the patient standing with the knees and hips comfortably extended, the shoulders neutral or flexed, the neck neutral, and the gaze horizontal. If there is a limb length discrepancy of >2cm, it should be corrected by using blocks. 

Assess the posture first and then look for deformities and how it is compensated. Deformity is assessed by asking the patient to stand in the NUSA position and in the forward bend position. Look for any deviation from normal and for asymmetry. In addition to deformity, look for how it is compensated either fully or partially. If alignment changes in one region, then the region above and below will develop compensatory changes to maintain global spinal alignment. Alterations and compensations can happen in the sagittal and coronal planes. Compensatory movements can occur at the hip also. 

Stand on the side of the patient at a distance to get a lateral view of the patient. Drop an imaginary plumb line from the ear of the patient; the following is the normal alignment in the sagittal plane on the lateral view with regard to the plumb line.

  • Head- Through the ear lobes
  • Shoulders- Through the acromion.
  • Thorax- Bisects the chest anteroposteriorly.
  • Lumbar area- Midway between the lumbar spine and abdomen and slightly anterior to the sacroiliac joint.
  • Hips- Posterior to the hip, through the greater trochanter.
  • Knee- Slightly anterior to the centre of knee.
  • Ankle- Just in front of lateral malleolus through the tuberosity of 5th metatarsal.

Stand behind the patient to have a posterior view. On the posterior view, the plumb line passes normally as follows.

  • Head- Bisects the head through the external occipital protuberance 
  • Shoulders- Midway between the shoulders.
  • Trunk- Bisects the trunk
  • Pelvis- Through the gluteal cleft.
  • Knee- Equidistant from both knees.
  • Ankle- Equidistant from both malleoli. 

  To assess the posture and symmetry of spine ask the following questions.

            From the front

  1. Are the eyes at the same level?
  2. Are the ears at the same level?
  3. Is the nose in the midline?
  4. Is there tilting of the head?
  5. Is the head turned to one side?
  6. Is the prominence of both sternocleidomastoids identical?
  7. Is the concavity of both supraclavicular and infraclavicular fossa comparable?
  8. Are the shoulders level?
  9. Are the nipples at the same level?
  10. Is the shape of thorax comparable on both sides?
  11. Is there abnormal prominence or concavity of sternum?
  12. Is the distance between the arms and trunk on both sides identical?
  13. Is the anterior superior iliac spines at the same level?

From the sides

  1. Is the head tilted anteriorly or posteriorly?
  2. Is the head held anteriorly or posteriorly?
  3. Is the neck curvature normal in the sagittal plane?
  4. Does the ear lobes and acromion lie in the same line?
  5. Is there anteroposterior widening or narrowing of the thorax?
  6. Is the normal kyphosis of thoracic spine maintained?
  7. Is the normal lumbar lordosis present?
  8. Is there anterior or posterior tilting of the pelvis?
  9. How does the plumb line dropped from ear pass in relation to the shoulder, trunk and lower limb joints?

From the back

  1. Is there tilting of the head?
  2. Is the head turned to one side?
  3. Is the prominence of paravertebral muscles identical?
  4. Is there periscapular wasting?
  5. Are the scapulae level?
  6. Are the iliac crests at the same level?
  7. Is there a rib hump?
  8. Is there abnormal prominence of spinous processes?
  9. Is the distance between the arms and trunk on both sides identical?
  10. Is the normal curvature of the spine maintained?
  11. How does the plumb line dropped from the external occipital protuberance pass in relation to the shoulders, trunk and gluteal cleft?

Florence Peterson Kendall author of ‘Muscles: Testing and Function with Posture and Pain” described the Kendall’s postural types. 

Kyphosis-lordosis posture– Head held forwards, neck hyperextended, thoracic spine in long kyphosis, lumbar spine lordotic, pelvis tilted anteriorly, hips flexed and knees hyperextended.

Swayback posture– Head held forwards, neck hyperextended, thoracic spine in long kyphosis, lumbar spine flattened or slightly flexed, pelvis tilted posteriorly, hips hyperextended, knees hyperextended and ankle in neutral.

Military type posture– Head neutral, neck straight, thoracic spine neutral or flattened, lumbar spine hyperextended, pelvis tilted anteriorly, knees hyperextended and ankles slightly plantarflexed.

Flatback posture– Head held forwards, neck slightly extended, upper thoracic spine flexed, lower thoracic spine and lumbar spine flattened, pelvis tilted posteriorly, hips extended, knees hyperextended with plantarflexed ankles or knee flexed with  ankle in dorsiflexion.

Swelling

Muscle wasting

Cutaneous abnormalities

Spinal dysraphism is classified into occult (occulta) and open (operta). In the open type, there is a defect in the skin and posterior elements that exposes the neural elements. It includes myelomeningocoele, myelocoele, hemimyelomeningocoele and hemimyelocoele. Closed spinal dysraphism with subcutaneous mass are lipomas with subcutaneous mass such as lipomeningocoele, lipomyelomeningocoele etc. Most common site is lumbosacral. 

A combination of 2 or more congenital midline cutaneous lesions is taken as strong sign of spinal dysraphism. Cutaneous lesions can be subcutaneous lipomas, dermal sinuses, tails and local hypertrichosis. Most common cutaneous sign is a sacral dimple. Sacral dimple can be simple or atypical. Simple dimple is <0.5mm in diameter and <2.5cm closer to the anus. Atypical dimple is >5mm in size and >2.5cm from the anus. A flame shaped hairy patch may be seen which is called faun tail. 

Palpation

Palpation helps to narrow down the cause of pain. Tenderness on palpation of specific structures help in identification of pain generators. Palpation starts with feeling for local rise of temperature with the dorsal aspect of fingers. Palpate the superficial structures first and then the deeper structures. Identify the bony landmarks. During palpation, look for tenderness, bony abnormalities or bone defects.

Deformities

Note the following points

Kyphosis

  • Location of apex
  • Extent
  • Compensatory lordosis above and below
  • Knuckle type – Prominence of a single spinous process due to collapse of a single vertebra.
  • Angular type- Collapse of 2-3 vertebra.
  • Rounded type- Collapse of several vertebra.

Scoliosis

  • Location of apex
  • Side of convexity
  • Extent
  • Largest curve
  • Symmetry
    • Shoulder level
    • Adams forward bending test
  • Rib hump
  • Loin hump
  • Waist asymmetry
  • Pelvic obliquity
    • Decompensation
      • Head- Plumb line dropped from C7
      • Trunk- Plumb line dropped from apex of the curve
  • Flexibility of curve
    • Push-prone test
    • Side bending
    • Traction

Tenderness

 Skin

Range of movements

Movements

Assess the range of movements in the whole of spine. Aggravation of pain in the lower limbs during extension and relief with flexion indicates spinal stenosis. Aggravation of pain during flexion and relief with extension indicates disc disease.

Measurements

Inter-pupillary angle– Angle between the inter-pupillary line drawn between the pupils and the horizontal reference line. Measures tilting of the head due to coronal malalignment.

Shoulder tilt angle – Angle between the line drawn between the right and left corocoid processes and the horizontal line. Measures the tilting of the shoulder due to coronal malalignment.

Angle of trunk inclination– Measured with the patient in forward bent position using an inclinometer. It is the angle between the horizontal reference line and the plane of greatest rib or lumbar hump. Measures the trunk asymmetry due to axial malrotation of vertebra.

Chin-Brow vertical angle– Measures the angle between a line connecting the chin to the forehead with the vertical line when the patient is viewed from the side. it assesses the coronal malalignment. Normally the lines are parallel.

Pelvic Obliquity– The angle subtended between the horizontal reference line and the line connecting the top of iliac crests or the ASIS on boot sides.

Lumbar Lordosis– Keep a tape-measure tensed between thoracic and sacral prominences when the patient is standing erect. If the maximum distance between the tape measure and the concavity of lumbar spine is less than 2cm then the lumbar lordosis is reduced. (Waddell 1982)

Sciatic list– Drop a plumb line from the lower thoracic convexity and measure the offset from the gluteal cleft. (Waddell 1982)

Lateral flexion– Mark the point in the midaxillary line at the level of dimple of Venus. Mark the second pint in the midaxillary line 10cm above the first mark. Ask the patient to lateral flex to the opposite side. Normal range is at least 3 cm increase in the distance between the 2 lines. (Waddell 1982)

Modified Schober test (Moll 1971)

Schober described the test in 1937. It was modified by Moll and Wright of Arthritis research unit of Leeds in 1971 as follows. 

Patient position- Standing.

Examiner position- On the back of the patient.

Instruments required- Measuring tap, skin marking pen.

Procedure- 3 marks are made. First, at the lumbosacral junction represented by a line connecting the dimple of Venus on either side. Second, 5 cm below the first line and third, 10 cm above the first line. Keep the measuring tape at the uppermost mark. Make sure that the distance between the uppermost and lowermost markings is 15cm. Ask the patient to touch the toes without bending the knee. Measure the distance between the upper most and lowermost lines. 

Interpretation- Normal excursion should be more than 5 cm.

Rib-pelvis distance test

Patient position- Standing with the upper limbs raised in front to the horizontal position.

Examiner position- Standing behind the patient with his hands insinuated between the inferior margin of ribs and superior edge of iliac crest in the midaxillary line.

Instruments required- None.

Procedure- Measure the distance between the inferior margin of ribs and superior edge of iliac crest in fingerbreadths.

Interpretation- Distance of two fingerbreadths or less is considered positive for kyphosis due to osteoporotic vertebral compression fractures.  Distance less than one finger breadth is 88% sensitive and 46% specific for osteoporotic vertebral compression fractures.

Wall-occiput distance test

Patient position- Standing with the back to the wall and the heels touching the wall .

Examiner position- Standing on the side.

Instruments required- Measuring tape.

Procedure- Ask the patient to put the back of head against the wall, strigntening up as much as possible with the eyes level. Measure the distance between external occipital protuberance and the wall.

Interpretation- Inability to touch the wall is positive for kyphosis due to osteoporotic vertebral compression fractures. WO-Distance increases by 1.3cm for every osteoporotic vertebral compression fracture. WOD of 4cm had specificity of 92% and sensitivity of 41% for osteoporotic vertebral compression fracture. WOD of more than 6 cm had an odds ratio of 17.8 for osteoporotic vertebral compression fracture.

Kyphotic index

Patient position- Standing in the best upright position.

Examiner position- Standing behind the patient.

Instruments required- Skin marking pen, flexible ruler, graph paper.

Procedure- Mark C7 and the lumbosacral junction. Mold the flexible ruler to the spine. Place the ruler on the graph paper and trace the outline. Measure the length and width of thorax.

Interpretation- Kyphotic index is equal to thoracic width divided by thoracic length multiplied by 100. Clinical kyphosis is present if KI is > 13.  

Special Tests

Straight leg raising test

Straight leg raising test was described by JJ First in his doctoral thesis in 1881. He attributed the test to his teacher Charles Lasègue, hence called Lasègue sign. He attributed the sign to be due to compression of sciatic nerve by the hamstrings. In 1884, de Beurmann in a cadaveric study identified the stretching of the sciatic nerve by straight leg raising and attributed the pain to the stretching of sciatic nerve.

Done with the patient supine. Raise the affected side with knee in extension. Positive if patient complains of pain in the back of thigh radiating into the calf. 

True positive SLR is exacerbation or reproduction of pain radiating along the back of thigh into the calf in the symptomatic side at 0-700 of limb elevation. It is a test of nerve root irritation. If patient complains of pain in the back or gluteal region, then the test is false positive.

It is highly sensitivity for lower lumbosacral root compressions (0.80-0.97) but low specificity (0.40). Hence a negative SLR is more important clinically than a positive SLR.

Verification of SLR 

Verification of SLR done to differentiate between pain due to hamstring tightness and sciatica.

Verification manoeuvre – Do SLR. Flex the knee slightly when pain is produced, pain disappears the limb can be raised further. Pain persists if false positive.

Variants of SLR test

Crossed SLR – Described by Fajersztan.  Raising of straightened contralateral limb produced symptoms on the symptomatic side. Has a high specificity of 0.90.

Bragaard’s test– Described by Fajersztan. Do SLR. Lower the limb slightly when pain is produced, dorsiflex the ankle. Pain reproduced if positive.

Bowstring test– Do SLR. Lower the limb slightly when pain is produced, Pain disappears. Press on the popliteal fossa. Pain reproduced if positive.

Cross-over sign– Do SLR. pain radiates into the affected limb and the opposite limb. Indicates a midline lesion, severe enough to compress nerve roots on both sides.

Slump test

Position of patient- Seated upright.

Position of examiner- Standing on the side of the patient

Procedure- Ask the patient to slump first. If pain is not produced then ask the patient to bring his head on to the chest, extend his knee and dorsiflex his ankle one step at a time.

Interpretation- Provocative sciatica is taken as a sign of neuromenigeal irritation.

Use- Used as an alternative for SLR test.

Quadrant test

Position of patient- Standing

Position of examiner- Standing behind the patient

Procedure- Keep one hand over the patient’s contralateral shoulder and apply axial pressure. Ask the patient to hyperextend, rotate and laterally flex to the contralateral side.

Interpretation- Provocative pain is taken as a sign of lumbar instability.

Use- Used if pain cannot be produced by forward flexion, lateral flexion etc.

Adams forward bending test

Position of patient- Standing with feet together, knee extended.

Position of examiner- Standing behind the patient first then in front of the patient.

Procedure- Rule out limb length discrepancy. Ask the patient to bend forwards at the waist till the back is in the horizontal plane. Palms should be held together.

Interpretation- If there is a rib or loin hump present, then there is structural scoliosis with rotation.

Use- To differentiate between structural and non-structural scoliosis.

Validity of test-  For a patient with 400 structural scoliosis, the test has a sensitivity of 0.83 and a specificity of 0.99.

Background- Described by William Adams in the 10th lecture of 12 lectures delivered in the Grosvenor Place School of Medicine in 1860-61 called “Lectures on the pathology and treatment of lateral and other forms of curvature of the spine”. His attention was first drawn into the rotation of vertebral bodies in scoliosis in the post mortem he conducted in 1852 on Gideon Algernon Mentell: a surgeon, geologist and palaeontologist who was one of the first to describe the dinosaur fossils.

Waddell’s nonorganic signs

Described by Prof Gordon Waddell in 1980 to identify nonorganic or psychological component of chronic back pain. Consist of 5 categories and 8 signs

Category 1- Tenderness

Sign 1- Superficial tenderness: Skin over a wide area is tender to touch.

Sign 2- Non-anatomical tenderness: Deep tenderness over a large area that is not localised to one anatomical structure and crossing into non-anatomical areas. 

Category 2- Simulation tests

Sign 3- Back pain on simulated tests for axial loading: Downward pressure over the top of head elicits lumbar pain

Sign 4- Back pain on simulated rotation of the hips: The shoulder and hip passively rotated together in the same plane with the patient standing. Considered positive if pain appears within 300 of rotation.

Category 3- Distraction 

Sign 5- Straight leg raise improves when patient is distracted: Straight leg raising painful when in supine, but not positive when the knee is extended in the seated position when the patient is distracted.

Category 4- Regional disturbances

Sign 6- Non-dermatomal sensory changes: Sensory loss over an area that is not in the dermatomal pattern.

Sign 7- Non-anatomical distribution of weakness: Weakness that cannot be explained on a neuroanatomical basis. 

Category 5- Overreaction

Sign 8- Disproportionate and exaggerated painful response that cannot be reproduced when done later. 

If three or more categories are positive then the finding is considered clinically significant. It suggests only symptom magnification or pain behaviour, but doesn’t rule out organic causes. Positive Waddell signs should not be considered as malingering or for secondary gain. It just indicates that in addition to treatment, the psychosocial and behavioural aspects of the illness also should be addressed. Waddell signs are associated with poorer treatment outcomes.

Neurological Assessment

Complete neurological assessment should be done to identify any associated neurological deficit.

References

  1. Schober, P (1937) The lumbar vertebral column and backache. Munch. Med. Wschr. , 84,336.
  2. Moll JPH, Wright V. (1971) Normal range of spinal mobility: An objective clinical study. Ann. Rheum. Dis. 30, 381.
  3. Gordon Waddell, Chris J Main, Emyr W Morris, Robert M Venner, Peter S Rae, Samir H Sharmy & Helen Galloway.(1982) Normality and reliability of clinical assessment of backache. BMJ. 284. 1519-1523. 

Charcot Osteoarthropathy

Dr Rajesh PLeave a comment
  • Charcot neuropathic osteoarthropathy (CNO) is a noninfective, inflammatory condition affecting periarticular soft tissue and bone in patients with peripheral neuropathy which if not properly treated may lead to progressive resorption of bone, disruption of soft tissues and disorganization of joints resulting in permanent deformity, altered biomechanics, predisposition to skin ulceration, infection and osteomyelitis.
  • It most commonly affects the foot and ankle region.
  • In the early stages there are local inflammatory changes followed by progressive bone loss, tissue disruption, joint dislocation and development of deformities.
  • The deformities lead to abnormal loading patterns, skin break down, infection and ultimately result in osteomyelitis.
  • Most common cause is diabetic peripheral neuropathy.
  • Lifetime prevalence of CNO in diabetic patients is 0.1-10% which increases to 29-35% if there is peripheral neuropathy.
  • The prevalence in diabetics, depend upon the diagnostic method, with MRI showing positive findings in up to 75% and x-ray findings in 30%. 
  • 28% mortality rate has been reported within 5 years of diagnosis (Sohn 2009).
  • In the early phase, differentiation from acute osteomyelitis is difficult.
  • Natural history (Saltzman 2005)
    • Risk of amputation increased 15-40 fold.
    • 2.7% annual amputation rate.
    • 40% chance of ulceration.
    • 28% mortality within 5 years of diagnosis (Sohn 2009).

History

1703 – Musgrave described CNO as an arthralgia caused by venereal disease.

1831 – JK Mitchell described the relationship with spinal lesion.

1868 – Jean Martin Charcot described the neuropathic aspect.

1881 – JM Charcot at the 7th International Medical Congress described the association with tabes dorsalis.

1936 – WR Jordan described CNO in association with diabetes mellitus.

Pathogenesis

  • Development of CNO is due to interplay between several pathways leading to dysregulation of  bone formation and resorption, persistent inflammatory response, increased glycation of collagen and accumulation of advanced glycation end products (AGLEPs) in the tissues. 
  • In genetically predisposed individuals with peripheral neuropathy, decreased neuropeptides such as nitrous oxide and calcitonin gene related peptide leads to increased levels of receptor activator nuclear factor kappa beta ligand (RANKL). Increased RANKL potentiates osteoclastogenesis resulting in uncoupling of bone formation and resorption. 
  • 3 theories – 
    • Neuro-traumatic theory – Damage to sensory feedback results in repeated trauma. Repeated trauma leads to increased proinflammatory cytokines such as interleukin-1β, interleukin-6, tumour necrosis factor α which causes bone resorption.
    • Neurovascular theory – Due to changes in vascularity caused by dysregulation of vasomotor and trophic nerve supply. 
    • Neuro-inflammatory theory – Abnormal persistence of inflammatory response and inability to terminate the inflammatory response are thought to be important in the pathogenesis. Unregulated inflammatory process triggers increased expression of receptor activator of nuclear kappa ligand (RANKL) in susceptible individuals. RANKL increases production of nuclear factor kappa beta (NF-κβ) which stimulates maturation of osteoclast precursor cells to osteoclasts. RANKL also stimulates synthesis of osteoprotogerin (OPG) by the osteoblasts. The decreased secretion of calcitonin gene related peptide (CGRP) which is an antagonist of RANKL by the damaged nerve endings is also theorized as a cause. Dysfunction of Wnt/βcatenin pathway  which regulate bone and vascular metabolism is also proposed as a cause. Increased RANKL expression is thought to be mediated by advanced glycation end products (AGEs), reactive oxygen species and oxidized lipids. Increased AGEs in diabetes is due to hyperglycemia as well as increased oxidative stress. Increased blood glucose and decreased circulating receptor for AGEs leads to nonenzymatic glycation of collagen and accumulation of AGEs in the tissues. AGEs induce apoptosis in the mesenchymal cells and hence may affect the mechanical parameters of type I collagen.
  • Causes of CNO
    • Diabetes mellitus
    • Leprosy
    • Peripheral neuropathy
    • Syringomyelia
    • Poliomyelitis
    • Multiple sclerosis
    • Tabes dorsalis
    • Toxins
    • Rheumatoid arthritis

Clinical features

  • Physical findings may be neurological, musculoskeletal and vascular abnormalities.
  • The onset may be following a triggering event, which may be trauma, surgery or infection.
  • Clinical findings depend on the stage of disease.
  • There are 3 stages clinico-radiologically.
    • Dissolution stage
    • Coalescence stage
    • Resolution stage
  • Patients present with acute onset unilateral swelling of foot and ankle which may extend up to the knee.
  • Pain is absent in 50% of patients. (Brodsky 1993) 
  • Some patients may complain of mild pain or discomfort.
  • Initial stages show marked inflammation evidenced by erythema, edema, warmth and more than 20C temperature difference when compared to opposite side.
  • Skin temperature measurement using surface temperature sensing devices such as infrared thermometer is useful in assessing severity of inflammation due to neuropathy.
  • Erythema due to CNO will dissipate if the limb is elevated above the level of heart for 10-15 minutes, while erythema due to infection will not.
  • During the coalescence stage, swelling and inflammation begins to dissipate but deformities start developing.
  • During the resolution stage, the signs of inflammation resolves completely and deformities persist.
  • Deformities lead to marked alteration of load bearing pattern of the sole of foot predisposing the high pressure areas to ulceration. 
  • Ulceration lead to infection which may progress to deep infection and osteomyelitis.
  • Deformities affect the forefoot, midfoot, hindfoot or the ankle.
  • Forefoot deformity may involve the first metatarsophalangeal joint in the form of dorsal or plantar dislocation.
  • Mid foot is affected in more than 60% of patients. Patients may develop abduction or adduction deformity at the Lisfranc joint or plantar dislocation of the tarsometatarsal joint leading to classical rocker bottum foot.
  • In the ankle, equinus or calcaneus deformity may develop. 
  • Sagittal instability of foot assessed by Assal and Stern method. The ankle is locked by dorsiflexion, pressure on the forefoot demonstrates instability leading to collapse of longitudinal arch.
  • Contracture of the tendoachilles leads to plantar flexion of the calcaneus and midfoot collapse leads to rocker bottom foot with dorsiflexion of forefoot.  
  • In severe cases the joints may be dislocated and unstable.

Diagnosis

  • Diagnosis needs establishment of the presence of peripheral sensory neuropathy with reduced pain perception and establishment of arthropathy by clinical findings and imaging studies,
  • Peripheral neuropathy diagnosed by
    • Decreased reflexes, reduced vibration sense and weakness
    • Decreased sensation on Semmes-Weinstein monofilament examination of sensation.
    • Pinprick sensation
    • Neurometer test
    • Electrophysiological studies
  • Diagnosis of osteomyelitis done by
    • Presence of ulceration or history of ulceration or previous amputation.
    • Ulcerations bigger than 2cm2and deeper than 3mm.
    • Probe-to-bone test – Thin probe can be inserted to the level of bone.
    • Leukocytosis, raised ESR, CRP and procalcitonin
    • X-ray showing lytic lesions and periosteal elevation.
    • Scintigraphy
    • MRI
    • Bone biopsy
    • Culture of tissue specimens
  • Diagnosis of vascular occlusion
    • History of claudication
    • Absent or low volume pulse
    • Trophic changes
    • Doppler study
    • Transcutaneous oxygen tension assessment
    • Angiography
  • Diabetic neuropathy starts as small fiber predominant neuropathy which progresses to bilateral distal symmetrical polyneuropathy.
  • Bone biopsy shows increased Howship’s lacunae, increased woven bone and inflammatory infiltrate in the marrow spaces consisting of lymphocytes and eosinophils.
  • Later stages show development of deformities especially rigid flat foot, rocker bottom foot with skin changes and ulcerations.

Differential diagnosis

  • Cellulitis
  • Abscess
  • Osteomyelitis
  • Acute gout
  • Fractures
  • Complex regional pain syndrome
  • Deep vein thrombosis

Imaging

  • Basic work up needs weight bearing dorsoplantar view of foot, weight bearing lateral view of foot and ankle and the AP view of ankle.
  • Early stages show soft tissue edema, patchy osteoporosis, small flecks of bone, minor joint incongruence and bone infractions.
  • Bone destruction takes 6-12 months to be visible on the x-rays.
  • Later stage x-rays show fractures, subluxations and dislocations. Typical findings include gross disorganization of joints with osseous debris.
  • More than 60% of patients have involvement of the midfoot.
  • In the rocker bottom foot, plantar flexion of calcaneus, midfoot collapse with plantar subluxation of cuboid and navicular is seen on the weight bearing lateral view.
  • Talo-first metatarsal angle shows negative angle due to dorsal collapse of the forefoot.
  • Dorsoplantar view shows abduction or adduction deformity due to midtarsal malalignment and deformed metatarsals.
  • MRI imaging is very valuable in the early stages when the x-rays are normal as the condition is reversible if treated at this stage.
  • In the early stages, MRI shows periarticular bone marrow edema in 2 or more bones, adjacent soft tissue edema, fluid in multiple tarsal joints and microtrabecular fractures or stress fractures. 
  • 99mTc-MDP three or four phase scintigraphy is highly sensitive but has low specificity.
  • Scintigraphy with 99mTc-WBC nebo 111In-WBC labelled leukocytes is highly sensitive and specific but cannot differentiate between cellulitis and osteomyelitis.
  • PET-CT with fluorine 18 fluorodeoxyglucose (18F-FDG) is 100% sensitive and 93.8% sensitive in differentiating CNO from osteomyelitis. 
  • Patients with CNO show low-intensity diffuse uptake.

Classifications

Eichenholz classification

Classifies the stage of disease depending on clinical features and radiological findings

Sanders and Frykberg Classification

Classifies according to area of involvement of foot and ankle region.

Brodsky and Rouse Classification

Schon classification 

Classifies the area of involvement in the midfoot into four types I to IV. Severity of involvement is classified into three types A to C.

Sella and Barrette 5 stage classification

Classifies the midfoot involvement.

Rogers and Bevilacqua 2 Axis Classification

X-axis marks anatomic location. Y-axis describes degree of complication.

MRI Classification

Treatment

  • When a patient with diabetes presents with an acute fracture, the sensation should be carefully assessed using Semmes -Weinstein monofilaments to rule out neuropathy. If neuropathy is present, look for early signs of CNO. Rule out peripheral vascular disease. If signs of inflammation are present, rule out infection.
  • Goal of treatment are the following;
    • Structural stability of foot and ankle.
    • Prevention of skin ulceration.
    • Plantigrade foot that can be fitted into prescription foot wear.
  • Treatment is mostly conservative.
  • Mainstay of treatment is immobilization in a total contact cast and offloading of weight till edema and warmth subside and the x-ray shows consolidation of bone.
  • Offloading is the most important aspect of management during the acute active stage.
  • In the active phase, immobilize and advise complete cessation of weight bearing.
  • Immobilization is by total contact cast which is changed after 3 days after first application and then every week.
  • During the dissolution stage, the patient advised to use wheel chair than crutches to prevent overloading and injury to normal limb.
  • Immobilize till the edema subsides and the skin temperature comes to be below 20C of the normal limb.
  • May take 6-12 weeks of immobilization.
  • Then use removable brace or Charcot Restraint Orthotic Walker (CROW) for 4-6 months.
  • In the resolution stage, custom total contact inserts and braces are needed to prevent ulcerations.
  • Bisphosphonates and intranasal calcitonin may be useful in the active stage.
  • Bisphosphonates efficacy has been shown to be not significant.
  • One randomized study showed intranasal calcitonin to be useful.
  • Foot reconstruction indications
    • Stable but nonplantigrade foot
    • Unstable foot
    • Recurrent ulcerations
    • To avoid amputation
  • Contraindications for surgery
    • Infection of bone or soft tissue
    • Eichenholz stage I disease
    • Uncontrolled diabetes or malnutrition
    • Peripheral vascular disease
    • Insufficient bone stock
    • Noncompliant or unreliable patient
  • Goals of surgery
    • Alignment of foot on the leg to provide a plantigrade foot that is stable, braceable and walkable
    • Restoration of stability
    • Clearance of infection
    • Relief of pressure points
    • Contouring of foot to allow fitting of orthosis
  • Surgical options
    • Foot reconstruction
    • Excision of bony prominences
    • Major amputations
  • Resection of bony prominences indications
    • Stable foot with isolated bone prominences causing skin problems
    • Stable foot with inability to fit an orthosis due to bony prominences
    • Resection of infected bone in patients being planned for foot reconstruction.
  • Exostosectomy is useful only in the midfoot.
  • Prerequisites for successful arthrodesis
    • Careful removal of all cartilage and debris
    • Debridement to bleeding bone
    • Reshaping to ensure maximum contact
    • Complete removal of soft tissues
    • Stable fixation
    • Immobilization and bracing till consolidation
  • Major amputation indications
    • Severe peripheral vascular disease
    • Severe bone destruction including osteomyelitis
    • Failed previous surgery
  • Transcutaneous oxygen tension of more than 35mm is successful healing after below knee amputation.
  • If an ulcer is present, first step is to get the ulcer heal by debridement, antibiotics and total contact casting.
  • Super-construction principles for foot reconstruction (Sammarco 2009)
    • Arthrodesis should be extended beyond affected area into neighboring joints.
    • Resection of bone to produce mild shortening to enable foot repositioning without overstretching of soft tissues to avoid tissue hypoperfusion.
    • Use strongest possible implant.
    • Place the implant in a manner that provides maximum mechanical stability.
  • External fixation using circular fixators have the advantage of three dimensional stability, gradual correction of deformity and avoidance of internal fixation that may increase the chance of infection.
  • Indications for external fixation
    • Poor soft tissue envelope
    • Active infection
    • Severe deformity that preclude acute correction
    • Poor bone quality
  • For internal fixation, axial screws are preferable as they provide long working length, better stability and least amount of surgical exposure.
  • Surgery is preferably done in the resolution stage.
  • Indications for surgery in the inflammatory stage. 
    • Severe instability
    • Progression of deformity
    • Prevention of dislocation
    • Failure of conservative treatment
  • Surgery in the acute inflammatory phase may worsen the inflammation and may increase the chance of infection.
  • Foot reconstruction depends on the localization of deformities as per the Sanders and Frykberg classification.
  • Sanders I is usually treated conservatively. If there is first metatarsophalangeal dislocation, arthrodesis using 2 screws or a plantar plate is done.
  • Sanders II is often associated with Sanders III deformity. Sanders II is corrected by resection arthrodesis to correct the abduction or adduction deformity of the forefoot and the dorsal dislocation of the Lisfranc joint.
  • Correction of Sanders III deformity proceeds in a stepwise manner. 
    • First step is correction of hindfoot.
    • Second step is correction of Lisfranc joint.
    • Third phase is correction of Chopart’s joint
    • Last step is insertion of  medial and lateral midfoot bolts
      • Medial bolt inserted from the first metatarsal head into the talus.
      • Lateral bolt inserted through the cuboid in the region of fourth metatarsal into the calcaneum. 
  • Operative treatment by medial or lateral column arthrodesis using large intramedullary bolts is called beaming.
  • Correction of equinus is done by either tendoachilles lengthening or gastrocnemius recession.
  • Gastrocnemius recession – 5 options
    • Silfverskiold -Proximal gastrocnemius recession
    • Baumann- Deep gastrocnemius recession
    • Strayer – Distal gastrocnemius recession
    • Endoscopic gastrocnemius recession
    • Baker – Superficial gastrocnemius recession
  • Sanders IV is treated by ankle and subtalar arthrodesis using external fixator. Severe cases may need talectomy and tibiocalcaneal fusion. Some very severe cases with infection and skin ulceration may need below knee amputation.
  • Sanders V with involvement of calcaneum is the least common. Majority are treated conservatively and some may need subtalar fusion.

References

  1. M.-W. Sohn, T. A. Lee, R. M. Stuck, R. G. Frykberg, and E. Budiman-Mak, “Mortality risk of charcot arthropathy compared with that of diabetic foot ulcer and diabetes alone,” Diabetes Care, vol. 32, no. 5, pp. 816–821, 2009.
  2. R. Gupta, “A short history of neuropathic arthropathy,” Clinical Orthopaedics and Related Research, no. 296, pp. 43–49, 1993.
  3. J. K. Mitchell, “On a new practice in acute and chronic rheumatism,”The American Journal of theMedical Sciences, vol.8, pp. 55–64, 1831.
  4. J. M. Charcot, “Sur quelques arthropathies qui paraissent dependre d’une lesion du cerveau ou de la moelle epimere,” Archives de Physiologie Normale et Pathologique, vol. 1, article 161, 1868. 
  5. W. R. Jordan, “Neuritic manifestations in diabetes mellitus,” Archives of Internal Medicine, vol. 57, no. 2, pp. 307–366, 1936.
  6. M. Assal and R. Stern, “Realignment and extended fusion with use of a medial column screw for midfoot deformities secondary to diabetic neuropathy,” The Journal of Bone & Joint Surgery—American Volume, vol. 91, no. 4, pp. 812–820, 2009.
  7. S. N. Eichenholtz, Charcot Joints, Charles C. Thomas, Springfield, Ill, USA, 1st edition, 1966.
  8. E. A. Chantelau and G. Grutzner, “Is the Eichenholtz classification still valid for the diabetic Charcot foot?” Swiss Medical Weekly, vol. 144, Article IDw13948, 2014.
  9. C. L. Saltzman, M. L. Hagy, B. Zimmerman, M. Estin, and R. Cooper, “How effective is intensive nonoperative initial treatment of patients with diabetes and Charcot arthropathy of the feet?” Clinical Orthopaedics and Related Research, no. 435, pp. 185–190, 2005.
  10. V. J. Sammarco, “Superconstructs in the treatment of charcot foot deformity: plantar plating, locked plating, and axial screw fixation,” Foot and Ankle Clinics, vol. 14,no. 3, pp. 393–407, 2009.
  11. Tomas Kucera,1,2 Haroun Hassan Shaikh,1 and Pavel Sponer1,2. . Charcot Neuropathic Arthropathy of the Foot: A Literature Review and Single-Center Experience. Journal of Diabetes Research Volume 2016, Article ID 3207043, 10 pages http://dx.doi.org/10.1155/2016/3207043
  12. R. G. Frykberg and R. Belczyk, “Epidemiology of the Charcot foot,” Clinics in Podiatric Medicine and Surgery, vol. 25, no. 1, pp. 17–28, 2008.
  13. A. Folestad, M. ˚ Alund, S. Asteberg et al., “Role of Wnt/𝛽- catenin and RANKL/OPG in bone healing of diabetic Charcot arthropathy patients,” Acta Orthopaedica, vol. 86,no. 4, pp. 415– 425, 2015.
  14. A.Nather,W.K. Lin, Z. Aziz, C. H. J.Ong, B. Feng, and C. B. Lin, “Assessment of sensory neuropathy in patients with diabetic foot problems,” Diabetic Foot & Ankle, vol. 2, article 6367, 2011.
  15. B. C. Callaghan, H. T. Cheng, C. L. Stables, A. L. Smith, and E. L. Feldman, “Diabetic neuropathy: clinical manifestations and current treatments,”The Lancet Neurology, vol. 11,no. 6, pp. 521– 534, 2012.
  16. D. G. Armstrong, W. F. Tood, L. A. Lavery et al., “The natural history of acute Charcot’s arthropathy in a diabetic foot speciality clinic,” Diabetic Medicine, vol. 14, no. 5, pp. 357–363, 1997.
  17. K. T. A. Low andW. C. G. Peh, “Magnetic resonance imaging of diabetic foot complications,” SingaporeMedical Journal, vol. 56, no. 1, pp. 23–34, 2015.
  18. S. E. Sanverdi, F. B. Ergen, and A. Oznur, “Current challenge in imaging of the diabetic foot,” Diabetic Foot and Ankle, vol. 3, 2012.
  19. B. M. Ertugrul, B. A. Lipsky, and O. Savk, “Osteomyelitis or charcot neuroosteoarthropathy? Differentiating these disorders in diabetic patients with a foot problem,” Diabetic Foot and Ankle, vol. 4, Article ID21855, 2013. 
  20. C. L. Ramanujam and Z. Facaros, “An overview of conservative treatment options for diabetic Charcot foot neuroarthropathy,” Diabetic Foot & Ankle, vol. 2, article 6418, 2011.
  21. A. Koller, R. Springfield, G. Engels et al., “German-Austrian consensus on operative treatment ofCharcot neuroarthropathy: a perspective by the Charcot task force of the German association for foot surgery,” Diabetic Foot & Ankle, vol. 2, 2011.
  22. T. E.Milne, J. R. Rogers, E. M. Kinnear et al., “Developing an evidence-based clinical pathway for the assessment, diagnosis and management of acute Charcot Neuro-Arthropathy: a systematic review,” Journal of Foot and Ankle Research, vol. 6, no. 1, article 30, 2013.
  23. Johnson JT. Neuropathic fractures and joint injuries. Pathogenesis and rationale of prevention and treatment. J Bone Joint Surg Am 1967; 49:1–30.
  24. Sanders LJ, Frykberg RG . The Charcot Foot (Pied de Charcot). In: Bowker JH, Pfeifer MA, editors. Levin and O’Neal’s The Diabetic Foot. 7th ed. Philadelphia, PA: Mosby Elsevier; 2008:257–283.
  25. Brodsky JW. Outpatient diagnosis and care of the diabetic foot. Instr Course Lect. 1993;42:121-139. 
  26. Moura-Neto A, Fernandes TD, Zantut-Wittmann DE, et al. Charcot foot: skin temperature as a good clinical parameter for predicting disease outcome. Diabetes Res Clin Pract. 2012;96(2):e11-e14. 
  27. Richard JL, Almasri M, Schuldiner S. Treatment of acute Charcot foot with bisphosphonates: a systematic review of the literature. Diabetologia.2012;55(5):1258-1264. 
  28. Bem R, Jirkovská A, Fejfarová V, Skibová J, Jude EB. Intranasal calcitonin in the treatment of acute Charcot neuroosteoarthropathy: a randomized controlled trial. Diabetes Care. 2006;29(6):1392-1394.
  29. Hoche G, Sanders LJ. On some arthropathies apparently related to a lesion of the brain or spinal cord, by Dr JM Charcot, January 1868. J Hist Neurosci 1992;1:75–87.
  30. Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation. Basis for prevention. Diabetes Care 1990;13:513–21.
  31. Reiber GE, Vileikyte L, Boyko EJ, et al. Causal pathways for incident lower extremity ulcers in patients with diabetes from two settings. Diabetes Care 1999;22:157–62.
  32. S. E. Johnson-Lynn, A. W. McCaskie, A. P. Coll, A. H. N. Robinson. Neuroarthropathy in diabetes: pathogenesis of Charcot arthropathy. Bone Joint Res 2018;7:373–378.