Kienbock's Disease
Published on Nov 19, 2015
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PRESENTATION OUTLINE
KIENBOCKS DISEASE
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Avascular necrosis of the lunate bone, thought to be caused by repetitive micro trauma. May or may not be associated with a fall on an outstretched hand.
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Named after the Austrian radiologist Robert Kienbock, who in 1910 noted collapse and sclerosis of the lunate bone on radiographs, which he attributed to progressive vascular compromise resulting from repetitive wrist sprains and contusions. Also called lunate malacia, idiopathic, avascular or traumatic lunate necrosis.
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Kienbock presented clinical and radiographic evidence of 16 patients with osteomalacia of the lunate in 1910. He described a stepwise progression of disease from isolated proximal lunate involvement, to fragmentation and collapse of the lunate, evolving to radiocarpal involvement with degenerative changes. He believed the osteomalacia to be a result of “a disturbance in the nutrition of the lunate caused by rupture of the ligaments and blood vessels during contusions, sprains, or subluxations."
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EPIDEMIOLOGY AND RISK FACTORS
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Kienbock's Disease most commonly affects people aged 20-40, with a male to female ratio of 2:1. It is classified as a rare disease, meaning there are less than 200,000 reported cases among the US population. There are occasional cases seen in children, with the youngest age of diagnosis to date being 8 years old. The disease most commonly affects the dominant wrist. Cases of bilateral KD are rare or nonexistent.
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Risk Factors:
Repeated wrist injury, long radius compared to ulna (called negative ulnar variation), prolonged use of corticosteroids, and poor lunate vascularity. The blood supply to the lunate bone varies widely between people...
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In most people, extraosseous blood supply to the lunate consists of contributions from the radial, ulnar, anterior interosseous and deep palmar arch arteries, which coalesce to form a rich vascular plexus on the dorsal and palmar lunate surfaces. Most people also have a complex interosseous network of anastamoses between the dorsal and palmar vessels.
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Some lunate bones, however, have only a single palmar vessel with minimal internal branches, especially to the proximal surface. These bones may develop AVN after traumatic arterial disruption. It has also been demonstrated that in KD the interosseous pressure in the lunate is higher than in the radial styloid, capitate, and normal lunate bones. This may imply that venous congestion rather than primary arterial insufficiency is the precipitating event.
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The exact aetiology of KD remains unclear. The most popular hypothesis to date is that negative ulnar variance is a predisposing factor to KD as it results in greater transmission of force across the wrist to the lunate. Forces are translated across the lunate particularly in dorso flexion and ulnar deviation. Ulnar variance, as defined by Hulten:
Negative variance = Neutral variance = -1 to +1mm
Positive variance = > +1mm
Ulnar variance is though.
Positive variance = > +1mm
Ulnar variance is though.
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Negative ulnar variance has long been associated with KD, both as a causal link and as a basis for therapeutic recommendations. This causal relationship was first hypothesised in 1920. Many surgical interventions for KD have been targeted at reducing ulnar variance.
In 2013 the Journal of Plastics and Reconstructive Surgery published an extensive article based on case control studies, meta analysis, and application of Bradford Hill Criteria, which concluded that there is currently "insufficient information to sustain the hypothesis of negative ulnar variance causing KD".
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CLINICAL PRESENTATION
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Wrist pain and tenderness.
Stiffness and loss of motion at the wrist.
Tenderness and swelling.
Loss of grip strength.
Insidious onset of pain, initially localised to lunate region. Later patients report stiffness, clicking or grinding, and increasing pain. Late stage symptoms are consistent clinically with carpal degenerative arthritis.
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Examination reveals swelling at the dorsum of the wrist, dorsal tenderness near the lunate, decreased grip strength and range of motion, grinding and crepitus.
Differential diagnoses include: Rheumatoid arthritis, post-traumatic arthritis, synovial inflammatory diseases, fracture, carpal instability, and ulnar abutment syndromes.
Clinical diagnosis may be confirmed by radiographic examination, contrast MRI, and CT.
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DIAGNOSIS AND STAGING
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Early radiographs may appear normal. Later they typically demonstrate increased density of the lunate, accompanied by fracture lines, fragmentation, and progressive collapse. Advanced collapse is associated with proximal migration of the capitate, increased inter carpal widening of the proximal row, and permanent flexion of the scaphoid.
On MRI, hallmark findings of AVN are uniformly decreased signal intensity on both T1 and T2 weighted images.
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Staging of KD is based upon the Lichtman classification system.
Stage I:
Normal X-ray. Bone scans are characteristically 'hot'. MRI demonstrates diffuse decreased signals on T1 and T2 weighted images. Physical findings indistinguishable from wrist sprain.
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Stage II:
Density changes in the lunate may be observed. Lunate may show fracture lines or minimal collapse on the radial border. Overall size, shape, and relationship to the carpal bones are not significantly altered. Clinically there is recurrent pain, swelling, and wrist tenderness.
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Stage III:
Collapse of the lunate. AP views show a shortened lunate with elongation in the saggital plane, accompanied by proximal migration of the capitate. Clicking and clunking of the joint may also be noted.
Stage IIIA:
No fixed carpal derangement a or instability.
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Stage IIIB:
Fixed rotation of the scaphoid, decreased carpal height, and ulnar migration of the triquetrium. Progressive weakness, stiffness and pain. Defined as a radio-scaphoid angle of greater than 60 degrees.
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Stage IV:
In addition to the radio graphic findings in Stage IIIB, this stage is associated with generalised degenerative changes in the carpal region. Clinically, this stage is indistinguishable from generalised arthritis of the wrist.
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TREATMENT
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Treatment of initial injury:
Rest, ice, compressive elastic bandaging, and immobilisation in a cast or splint. After immobilisation, stretching and strengthening of the joint is recommended (physiotherapy or OT). NSAIDS eg aspirin or ibuprofen.
Heat packs should be used before stretching. Cold packs may be used to relieve pain and reduce inflammation in both acute and chronic cases.
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Surgical shortening of the radius or lengthening of the ulna is often performed to reduce pressure on the lunate, however it has not been demonstrated that establishing equal length of the distal articular surfaces of the radius and ulna is superior to placebo treatment or improves on the natural history of the disease. These operations may also introduce incongruency into the distal radio ulnar joint and induce degeneration of the cartilage. Radial shortening osteotomy remains a well known treatment for KD.
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Surgical options for treatment include resection arthroplasty of the lunate, denervation surgery, prosthetic replacement, revascularisation and fusion. The success rates for these interventions range from 55% to 88% after follow up (3-11 years). These results are not conclusively better than the natural history of the disease. Many patients report mild or absent pain on follow up without intervention. One study found 77% of patients were free of pain without surgery, after a follow up of 18 years.
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Treatment by stage
Stage I: immobilisation in a well-fitted short cast for up to 3 months. May allow the lunate to heal via re vascularisation.
Stage II - IIIA: a Direct revascularisation techniques, eg vascular bundle transfer of the second dorsal intermetacarpal artery and vein. Or Pronator quadratus pedicled bone grafts, or pedunculated pisiform transfers. All have demonstrated restoration of the lunate viability.
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Stage IIIB: Intercarpal arthrodesis. Either 'triscaphe' (scaphotrapeziotrapezoid) or 'scaphocapitate' fusion.
Stage IV: Proximal row carpectomy (ie. remove three carpal bones), or total wrist fusion.
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COMPLICATIONS
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Prolonged healing if usual activities are resumed too soon.
Frequent recurrence of symptoms, sometimes causing prolonged disability. Wrist stiffness or weakness. Arthritis of the wrist.
Post operative infection. Exacerbation of joint degeneration. Spontaneous wrist fusion. Closed tendon rupture.
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RESOURCES
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'Critical Analysis of Causality between Negative Ulnar Variance and Kienbocks Disease' Stahl, Meisner et al, Plastic and Reconstructive Surgery, Issue 132, October 2013, pp. 899-909
'Kienbocks Disease' Jeffrey Weinzweig 2010, Plastic Surgery Secrets Plus, 2nd Ed, Chapter 150, pp. 972-978
'Kienbocks Disease', Cross and Matullo, Orthopedic Clinics of North America, Vol. 45, Issue 1 2014, pp.141-152
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'Kienbocks Disease', Schwind, Eslami et al, Journal of Bone and Joint Surgery, Issue 90, pp. 133-9
'Instructions for Sports Medicine Patients', Safron, Zachazewski and Stone, 2nd Ed. Saunders 2012
'Outcome of KD 22 Years after Distal Radius Shortening Osteotomy', Raven et al, Journal of Clinical Orthopedics Issue 1, 2007
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