The Management of Avascular Necrosis in the Carpus: Preiser’s Disease and Avascular Necrosis of the Capitate


Avascular necrosis (AVN) within the carpus is a rare occurrence. AVN is most commonly seen within the scaphoid after proximal pole fractures; however, AVN may occur throughout the carpus as a result of trauma or idiopathically. This chapter specifically addresses the surgical treatment of Preiser’s disease (AVN of the scaphoid) and AVN of the capitate.


First described by Preiser in 1910, Preiser’s disease is now defined as AVN of the scaphoid bone with no obvious antecedent fracture. This definition allows one to distinguish Preiser’s disease from AVN of the scaphoid due to fracture, which is most commonly a proximal pole fracture. Since the time of Preiser’s paper, the condition has been reported in several case reports and small series, as well as in children.

The pathophysiology of the condition is still unknown, but it is thought to be related to a disruption in the scaphoid’s blood supply. The scaphoid is almost entirely covered in hyaline cartilage, and the blood supply to the scaphoid enters through either dorsal or distal palmar attachments. The proximal pole is supplied by retrograde flow through the waist of the scaphoid. A large component of the scaphoid is supplied by a single nutrient artery, and the bone contains few intraosseous arterial anastomoses; thus, there is little collateral flow if the nutrient artery becomes injured or compromised. The mechanism of injury to this nutrient vessel is still a matter of speculation. However, it has been shown in cadaveric models that flexion of the wrist increases pressure on the dorsal aspect of the scaphoid, resulting in the potential compromise of the blood supply entering through the dorsal ridge. Disruption of this ridge may then lead to devascularization of the proximal two thirds of the scaphoid.

The small dorsal and palmar interosseous branches follow ligamentous attachments as they enter the bone. These ligamentous attachments are susceptible to repetitive microtrauma as well as inflammation, which may also lead to vascular disruption.

Clinically, patients present with complaints of radial-sided wrist pain, localized to the anatomic snuffbox and the dorsal wrist. Swelling, restricted range of motion, and decreased grip strength may also be present. Preiser’s disease affects predominantly the dominant hand and is seen more frequently in women. Reported risk factors have included systemic steroid use, smoking, heavy labor, collagen vascular disorders, vasculitis, myelodysplastic syndrome, chemotherapy, excessive alcohol use, trauma, and ipsilateral wrist surgery. Histology from removed specimens shows empty lacunae, few bone lining cells, necrotic bone marrow, and occlusion of the microvasculature.

A radiographic scale was developed by Herbert and Lanzetta in 1994 to grade the progression of AVN within the scaphoid. Stage I represents a scaphoid bone that shows no abnormalities on plain radiographs but has evidence of edema or avascularity on magnetic resonance imaging (MRI) or evidence of diffuse injury on bone scan. Stage II disease reveals increased proximal pole density with generalized osteopenia ( Fig. 56-1 ). Stage III disease shows fragmentation of the proximal pole with or without pathologic fracture ( Fig. 56-2 ). Stage IV disease has evidence of carpal collapse and osteoarthritis. Although most of the literature describes Preiser’s disease as pertaining to diffuse involvement of the scaphoid, Herbert and Lanzetta proposed that the process initiates at the proximal pole beforehand and then progresses to global involvement.


Stage II Preiser’s disease . The scaphoid on this plain radiograph exhibits increased sclerosis with minimal fragmentation.


Stage III Preiser’s disease . The proximal pole of this scaphoid has evidence of fragmentation.

More recently, Kalainov and associates have expanded on Herbert’s theory and described two patterns of Preiser’s disease, which are differentiated based on their MRI findings. Type 1 is characterized by diffuse vascular alterations involving 100% of the scaphoid, whereas type 2 is described as segmental vascular changes involving between 33% and 66% of the scaphoid. The authors found that patients with Preiser’s disease classified as type 1, compared with those with type 2, had a greater chance of progressive deterioration despite surgical intervention. In their paper, 9 of 11 type 1 patients had advanced one radiographic stage during follow-up, whereas only 2 of 8 type 2 patients advanced a full radiographic stage. In addition, there was a significant difference in outcome in both Mayo Wrist Score and grip strength between the two groups, with the type 2 patients faring better.

Treatment options range from conservative pain management to operative treatment. However, patients managed nonoperatively have been shown to progress to more severe disease, with most patients ultimately undergoing operative intervention for symptom relief. Surgical techniques have included curettage and bone grafting, partial and complete scaphoid replacement, scaphoid excision with four-corner fusion, wrist arthrodesis, total wrist arthroplasty, wrist denervation, arthroscopic drilling and debridement, closing radial wedge osteotomy, proximal row carpectomy (PRC), and vascularized bone graft (VBG). Herbert and Lanzetta reported good results with silicone replacement, whereas Vidal and associates demonstrated varied results. Unfortunately, fragmentation and particulate synovitis are now well-known long-term complications of silicone replacement. PRC has been shown to produce good results and may be useful in initial treatment of advanced disease or when other modalities have failed. Closing radial wedge osteotomy was described by Hayashi and colleagues and was noted to provide pain relief. The patient described was categorized as having Herbert stage 2 and Kalainov type 1. At 1 year postoperative, there was no radiographic disease progression, and the authors re-categorized the involvement as a Kalainov type 2, which suggests some revascularization of the scaphoid. The authors speculated that relief of pain was a result of the osteotomy decreasing the axial pressure on the radioscaphoid joint.

More recently, VBG has been shown to have promise in salvaging the devascularized scaphoid. The advantages of VBG over nonvascularized bone grafting include the preservation of osteocytes, accelerated graft consolidation, and the decreased need for creeping substitution. In addition, VBG increases bone mass with a decrease in osteopenia. Two different techniques have been recently reported. Lauder and Trumble described taking a long, narrow graft from the base of the second metacarpal, with its pedicle based on the dorsal metacarpal arcade. The scaphoid is drilled distal to proximal, and the graft is inserted in a press-fit manner into the center of the scaphoid. These patients are then splinted for 2 to 3 months or until graft incorporation is noted. The authors advocate this technique for patients with necrosis but no degenerative changes. For more advanced-stage disease, they advocate a salvage procedure. There were no follow-up results reported at the time of the publication.

Moran and associates also advocated the use of VBG in the setting of early Preiser’s disease. Their technique used a reverse-flow pedicle from the distal radius, either with the 1,2 or 2,3 intracompartmental supraretinacular artery (ICSRA) ( Fig. 56-3 ). Results were encouraging with follow-up MRI, demonstrating improvement in the T2 and/or T1 signal and normalization of marrow signal. However, incomplete revascularization of the proximal pole was noted in several patients.


Pedicled dorsal grafts available from the dorsal radial system .

Vascularized Bone Graft for Preiser’s Disease


Surgical decision making is dependent on the patient’s radiographic findings. Scaphoid preservation with vascularized bone grafting is possible when the scaphoid has an intact cartilaginous shell and there is no evidence of arthritis at the radioscaphoid articulation. Patients with evidence of osteoarthritis should be managed with scaphoid resection and four-corner fusion or PRC.

The ideal patient for VBG is one with Herbert stage I or II disease ( Box 56-1 ). There is no age limit in regard to who may undergo surgery. If the patient is skeletally immature, with open physis, then one must be sure to harvest the graft proximal to the physis. Surgery for Preiser’s disease can be performed on an elective basis but should be performed before the development of radioscaphoid arthritis.

BOX 56-1

  • Stage I : Normal radiographs with a positive bone scan or avascularity on MRI

  • Stage II : Increased density in the proximal pole on plain radiographs with generalized osteoporosis

  • Stage III : Fragmentation of the proximal pole on plain radiographs, with or without pathologic fracture

  • Stage IV : Carpal collapse with osteoarthritis



For dorsal pedicled VBGs from the distal radius, contraindications include previous dorsal wrist surgery and capsulotomy that may have disrupted the 1,2 or 4,5 intracompartmental artery. If the dorsal wrist vasculature is injured, one can opt for the use of the first dorsal metacarpal artery or a free vascularized bone flap from the medial femoral condyle or iliac crest. Patients with significant atherosclerotic disease, smokers, and females may have a higher risk for failure with this procedure according to previous reports.

Surgical Technique for Dorsal Distal Radius Vascularized Bone Graft (1,2 ICSRA Graft)

The extremity is elevated for exsanguination and a tourniquet inflated. Esmarch bandage application makes the vessel identification more difficult. A gentle curvilinear dorsal radial incision is used to expose the scaphoid and bone graft donor site ( Fig. 56-4 ). Branches of the superficial radial nerve are identified and retracted. Subcutaneous tissues are gently retracted, and the 1,2 ICSRA and venae comitantes are visualized on the surface of the retinaculum between the first and second extensor tendon compartments ( Fig. 56-5 ). The vessels are dissected toward their distal anastomosis with the radial artery (toward the anatomic snuffbox). Before elevation of the bone graft, the scaphoid must be visualized. A transverse dorsal-radial capsulotomy is made to expose the scaphoid ( Fig. 56-6 ). The scaphoid is inspected for signs of fissuring, cartilage loss, and arthritis. If arthritis is present or the scaphoid is not amenable to salvage, one may proceed to PRC or scaphoid excision and four-corner fusion. If the scaphoid’s cartilaginous shell is intact and the radioscaphoid joint is free of arthritis, it is safe to proceed with VBG.


The standard incision for use of the 1,2 ICSRA (1,2 intercompartmental supraretinacular artery) graft . R, radius; RA, radial artery; S, scaphoid.

(Copyright Mayo Foundation, all rights reserved.)


The vessel is visualized between the first and second dorsal compartments.


The scaphoid is exposed through a transverse radial capsulotomy.

At this point, the first and second dorsal extensor compartments are opened at the level of the bone graft site to create a cuff of retinaculum containing the vessels and their nutrient arteries to bone ( Fig. 56-7 ). The graft is centered approximately 1.5 cm proximal to the radiocarpal joint to include the nutrient vessels. With the blood vessels dissected, the surgeon must create the defect within the scaphoid before harvesting the bone graft. The sclerotic components of the scaphoid must be removed to maximize the chances for successful revascularization. A dorsal window is created in the scaphoid using a high-speed burr. Curets are then used to remove all remaining necrotic bone ( Fig. 56-8 A and B). A long rectangular graft is most often required ( Fig. 56-9 ). After preparation of the scaphoid, the graft is elevated. The center of the graft is placed approximately 1.5 cm from the radiocarpal joint. Graft elevation begins with ligation of the 1,2 ICSRA and accompanying veins proximal to the graft. The vessels are mobilized distal to the graft to separate them from the radius and joint capsule, but leaving them applied to the graft itself. Sharp osteotomes create the radial, ulnar, and proximal osteotomies of the graft. The distal osteotomy is performed in two stages, moving the pedicle radially then ulnarward to prevent injury to the pedicle. The graft is then gently levered out to create a distally based pedicle ( Fig. 56-10 ).


The first and second dorsal compartments are opened, and a cuff of retinaculum is left with the vessel overlying the bone.


A, The necrotic bone must be removed from the scaphoid using either a curet or a high-speed drill. B, Intraoperative imaging aids in bony resection and can prevent unwanted perforation of the subchondral bone and cartilaginous shell.


The graft is created to fill the void left by curetting.

(Copyright Mayo Foundation, all rights reserved.)

FIGURE 56-10

The graft is elevated using osteotomes taking care to protect the nutrient vessel.

(Copyright Mayo Foundation, all rights reserved.)

The graft is re-sized as needed using bone cutters and transposed beneath the radial wrist extensors. The graft is gently press-fitted into the prepared slot in the scaphoid ( Fig. 56-11 ). Additional cancellous graft can be harvested from the distal radius donor site and used as supplemental grafting material if necessary. Kirschner (K) wires may then be placed to stabilize the graft and prevent extrusion during the early postoperative period. The wrist capsule and extensor retinaculum are re-approximated loosely, taking care not to kink or compress the pedicle in any way.

Jul 10, 2019 | Posted by in ORTHOPEDIC | Comments Off on The Management of Avascular Necrosis in the Carpus: Preiser’s Disease and Avascular Necrosis of the Capitate
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