34th Annual Scientific Meeting proceedings

Septic osteitis of the distal phalanx is a specific form of inflammatory osteitis caused by a puncture wound to the sole or an extension of an abscess^1,2. Sequestration of the distal phalanx may develop as the result of infection of a fragment of cortical bone, either as a consequence of a fracture occurring at the same time as the original trauma, or secondary to necrosis of the superficial layer of the bone that separates from underlying trabecular bone following loss of blood supply. In horses with laminitis, septic osteitis may also occur as a sequela to infection of the parietal or solar lamellae. If a large portion of the distal phalanx is affected, pathologic fractures may ensue. Rarely, depending on the location of the infected bone, the infection can spread to adjacent synovial or soft tissue structures.

Horses with septic osteitis of the distal phalanx usually present with lameness that varies in severity depending on how well the exudate from the affected tissues can drain; severe if drainage is poor and moderate to mild if the drainage is good. Drainage from gravel at the coronary band, a fistula or a wound, may be the primary presenting symptom. A history of trauma to the foot or other foot lameness (e.g. abscess) is common.

Standard lateromedial, dorsopalmar, and dorsoproximal-palmarodistal oblique radiographic projections may need to be supplemented with additional oblique views taken at various angles to the median plane to identify septic osteitis of the distal phalanx. The cardinal radiological sign of septic osteitis of the distal phalanx is an irregularly marginated area of lysis at the solar margin of the distal phalanx, although occasionally, radiolucent cavities can be present within the substance of the bone. Sequestra are identified as osseous radiodensities surrounded by an area of osteolysis. Osteitis and sequestra of the planum cutaneum of the distal phalanx may be difficult to detect radiographically because of its concavity. CT and MRI are very good for visualizing fragments that may not be observed on plain radiographs and MRI may identify tracts in the soft tissues of the foot that are otherwise not apparent.  MRI is useful to delineate early sequestrum formation, as dead bone produces no signal, which distinguishes it from the highly vascularized surrounding inflamed bone. MRI is very sensitive for the presence of fluid in bone and will invariable show marked bone oedema of the distal phalanx in the presence of septic osteitis. The presence of marked poly-ostotic ‘sympathetic‘ bone oedema signal in the foot (including the distal and middle phalanges and the navicular bone), may occur in the presence of an intense focus of infection. However, it is more commonly seen in horses with septic synovitis of the distal interphalangeal joint or navicular bursa, than in cases of isolated osteitis. This generalized bone oedema in multiple bones is more likely reflective of regional hyperaemia caused by inflammation, than a true sign of osteomyelitis.

MRI may also identify tracts in the soft tissues of the foot that are otherwise not apparent on other imaging modalities. A penetrating tract may be recognized on MR images by either the presence of linear fluid signal, or by the presence of haemosiderin causing susceptibility artefact along the penetrating trajectory in the soft tissues of the sole. If there is persistent drainage from a wound on the solar surface of the foot, but there is no radiographic evidence of osteitis or sequestration, and neither CR or MRI are available, then surgical exploration of the wound is appropriate.

Septic pedal osteitis can also occur in foals, usually from the spread of bloodborne bacteria to the pedal bone.³ The most common bacteria causing PO in foals include Escherichia coli, Actinobacillus, Streptococcus, Enterobacter and Salmonella.

Foals experiencing failure of passive transfer have a higher risk of septic pedal osteitis.  The distal phalanx may have a higher risk of developing infection over other bones as there are several vessels that make sharp turns within the pedal bone, encouraging bacteria to proliferate at these sites³.

Quittor is a rather specific form of septic necrosis of the distal phalanx, that affects primarily the ungular cartilage extensions at the palmar processes of the bone^1,2,4.  Quittor usually occurs following direct trauma to the ungular cartilage but may also result from ascending infection from within the foot. The infection is particularly persistent because the cartilage has a poor blood supply. The infection causes a marked unilateral inflammatory response, with lameness, swelling and draining sinuses from the integument proximal to the coronary band.

Dorsopalmar and lateromedial radiographs with a radiopaque probe inserted into a discharging sinus that reaches the ungular cartilage or the palmar process of the distal phalanx will confirm the origin of the sinus. MRI has been used in complicated cases of quittor to determine the structures involved and help guide the management and surgical approach⁵.

Management
The treatment of septic osteitis of the distal phalanx with or without sequestration is open surgical drainage and debridement under local or general anesthesia^6-10. The wound is bandaged with a topical antimicrobial dressing, and the horse treated with broad-spectrum antibiotics until all exposed surfaces are covered with granulation tissue. NSAIDs are administered as needed and tetanus prophylaxis provided. The wound heals by secondary intention.

Intravenous regional limb perfusion (IVRP) is the preferred method of delivering high antibiotic concentrations in the distal phalanx for maximum efficacy and most commonly amikacin, gentamicin, ceftiofur, ampicillin or enrofloxacin are used.

The surgery usually starts from the hoof sole, then works inward removing any diseased bone and tissue. If there is a draining tract present, it can be directly to the site of infection.  Sequestra should be removed if they are too large for spontaneous resorption. Studies show that up to 24% of the pedal bone can be removed surgically without causing long-term lameness^6-10.

Following surgical debridement, the hoof requires careful aftercare to protect the surgical site from re-infection with regular antiseptic/aseptic waterproof bandage changes. Granulation tissue typically fills in the surgical site within 7-10 days, at which time a hospital plate can be used as a more long-term method of protecting the surgical area in the sole. Once the treatment plate is in place, application of betadine to the granulation tissue every few days can help speed keratinization. Most surgical sites are completely healed by 12 weeks after debridement. Many surgeons prefer to perform debridement under general anesthesia to allow for thorough removal of affected tissue but standing surgery can be equally successful⁹.

The prognosis for returning to work in most cases of septic osteitis is guarded to favourable with 57% of horses and 50% of Thoroughbred foals returning to their previous or expected level of performance after treatment⁹.

However, extension of the infection to an adjacent structure, such as the navicular bursa, distal interphalangeal joint or deep digital flexor tendon, or pathologic fracture of the distal phalanx worsens the prognosis.

In most horses with quittor the treatment of choice is to resect the necrotic cartilage^1,2,4,11. The surgery is complicated because approximately half of the ungular cartilage resides inside the hoof capsule and only half proximal to the coronary band. Care must be taken to avoid damaging the palmar recess of the joint capsule of the distal interphalangeal joint, which lies immediately medial and is adhered to the ungual cartilage.  The surgical procedure is described elsewhere^1,2,4,11 The prognosis for elimination of the infection from an ungular cartilage is guarded to fair because recurrence is possible regardless of the surgical technique, but if successful, return to normal athletic activity can be expected^4,11.

References

1. Parks A and Schramme M. ‘The foot’ In: Equine clinical medicine, surgery and reproduction (2020)  Ed. Graham Munroe. 2nd edition. Publ. CRC Press Boca Raton, Florida. pp 61-123.
2. Fürst AE, Lischer CJ. Other Clinical Problems of the Equine Foot. Vet Clin North Am Equine Pract. 2021;37(3):695-721.
3. Neil KM, Axon JE, Todhunter PG, Adams PL, Caron JP, Adkins AR. Septic osteitis of the distal phalanx in foals: 22 cases (1995-2002). J Am Vet Med Assoc. 2007;230(11):1683-90.
4. Smith MRW. Infection of the cartilages of the foot. Equine Vet Educ. 2014;26:580–583.
5. Meehan LJ, Taylor SE, Labens R, et al. Magnetic resonance imaging assisted management in five cases of suspected quittor. Vet Comp Orthop Traumatol. 2016;29:75–82.
6. Honnas. C. M. et al., Hoof Wall Surgery in the Horse: Approaches to and Underlying Disorders. Veterinary Clinics of North America: Equine Practice. 2003. Vet Clin North Am Equine Pract. 2003;19:479–499.
7. Cauvin. E. R. J. and Munroe. G. A., Septic Osteitis of the Distal Phalanx: Findings and Surgical Treatment in 18 Cases. Cauvin ER, Munroe GA. Septic osteitis of the distal phalanx: findings and surgical treatment in 18 cases. Equine Vet J. 1998;30(6):512-9.
8. O’Brien. T. and Hunt. R. J., Recent Advances in Standing Equine Orthopedic Surgery. Vet Clin North Am Equine Pract. 2014;30(1):221-37.
9. Cillán-Garcia. E. et al., Comparison of Long-Term Outcome Following Surgical Treatment of Septic Pedal Osteitis in Horses under Standing Sedation and General Anaesthesia. Equine Vet J 50, Suppl. 52 (2018) 5–35.
10. Gaughan EM, Rendano VT, Ducharme NG. Surgical treatment of septic pedal osteitis in horses: nine cases (1980-1987). J Am Vet Med Assoc. 1989;195(8):1131-4.
11. Honnas CM, Ragle CA, Meagher DM. Necrosis of the collateral cartilage of the distal phalanx in horses: 16 cases (1970-1985). J Am Vet Med Assoc. 1988;193:1303–1307.