Abstract
A 5-year-old quarter horse mare presented with unilateral, severe, chronic forelimb lameness. Radiographs revealed extensive hoof wall separation and capsular rotation of the distal phalanx. Treatment included dorsal hoof wall resection, phenylbutazone, a bar shoe, and stall rest. Whether white line disease or laminitis was the primary lesion remains unclear.
A 5-year-old quarter horse mare presented with a Grade IV/V lameness (1) in the right front leg. Lameness was of 6 weeks' duration, and the mare had been treated with stall rest and phenylbutazone (Dominion Veterinary Laboratories, Winnipeg, Manitoba), 2g/d, PO, with no appreciable improvement.
On physical examination, the mare was bright, responsive, and in excellent body condition. She was reluctant to move, had a pronounced head nod at the walk, and consistently stood “pointing” her right front foot ahead of the left. Palpation of the right front limb revealed no evidence of swelling or pain. When the mare's right fetlock and carpus were flexed manually, followed immediately by the mare being trotted, there was no change in the lameness. The mare was unresponsive when hooftesters were applied to either front hoof. The right front foot was observed to be misshapen at the toe and on the lateral quarter, and percussion of the hoof wall revealed a hollow sound over these areas. When being walked or trotted, the mare exhibited a characteristic stride pattern that consisted of marked abduction of the right front leg, followed by preferential loading of the medial portion of the right front foot. Removal of the shoe exposed an extensive hoof wall separation in the toe and lateral quarter of the right front hoof. Differential diagnoses included fracture of the proximal, intermediate, or distal phalanges; sole abscess; septic distal interphalangeal joint; white line disease; and laminitis.
A palmar digital nerve block resulted in the lameness being reduced by approximately 50%. An abaxial sesamoid block was then performed, including a dorsal ring block of the fetlock, which resulted in the lameness being reduced by 90%. Radiographs of the right front foot revealed several abnormalities, including a large gas pocket and hoof wall separation in the toe and lateral quarter, “lipping” of the distal phalanx (P3) on its dorsal parietal surface, and moderate capsular rotation of P3. Radiographs of the left front foot showed mild “lipping” of the dorsal parietal surface of P3. The final diagnosis, on the basis of physical and radiologic examination, was white line disease causing hoof wall separation and laminitis.
Treatment of the hoof included an extensive resection of the dorsal hoof wall; poulticing the foot with sugardine (granulated sugar combined with dilute povidone-iodine); application of a bar shoe; phenylbutazone (Dominion Veterinary Laboratories Ltd, Winnipeg, Manitoba), 2g, PO, q24h; and stall rest. On resection, the damaged hoof wall was observed to have a dry, crumbly quality, consistent with white line disease (1,2,3). Resected hoof material was submitted to a veterinary diagnostic laboratory (Animal Health Laboratory, Ontario Veterinary College, University of Guelph, Guelph, Ontario) for bacterial and fungal cultures, and histopathologic examination. Bacteria isolated on culture were deemed to be environmental contaminants; no fungal hyphae were observed. Histopathologic examination revealed unidentified encapsulated bodies within the tubular horn, which may have been bacteria. Final histologic diagnosis was keratin degeneration of the stratum medium of the hoof wall. Onychomycosis, therefore, could not be verified by culture or histologic examination.
White line disease in the equine foot was first described in 1990 (2). Since the initial report, a number of researchers have attempted to establish an infectious etiology (2,3,4). The majority of these investigations were directed towards isolating and identifying fungi from affected hoof tissue, thereby establishing a definitive link between onychomycosis and white line disease in horses (3,4). To date, an infectious pathogen has not been demonstrated. The extensive hoof wall separation, white crumbly appearance of the damaged hoof wall, and histologic diagnosis in this case were consistent with white line disease, but our attempt to confirm an infectious etiology by culture was unsuccessful.
There are 2 basic approaches to understanding the pathologic processes that resulted in the severe damage to this mare's foot. The first is that the primary clinical abnormality was white line disease, which caused extensive hoof wall separation and finally capsular rotation of P3 (2,3). On lateral radiographs, the capsular rotation of P3 in white line disease appears to be identical with that seen with laminitis (2,5). In this case, although the radiographic changes were similar, if not identical, to those seen with laminitis, the mare did not suffer from inflamed lamina (5,6). Displacement of P3 was due to a purely mechanical failure of the stratum medium, which therefore disrupted the normal attachment of P3 to the hoof wall (2,5).
The second is that laminitis was the primary disease, while white line disease and hoof wall separation simply represent a secondary effect of compromised hoof tissue (3). The slight “lipping” of P3 observed in radiographs of the contralateral P3 suggests that the mare may have suffered from a previous bout of laminitis (6).
This mare's presentation was unusual in that commonly accepted causes of laminitis, such as a history of steroid administration, supporting limb lameness, grain overload, or metabolic illness of any kind, were discounted (7). White line disease with hoof wall separation appeared to be the only disorder that might have precipitated rotation of P3, thereby mimicking the radiographic changes typical of laminitis. The exact pathologic relationship of white line disease and laminitis remains obscure.
A more detailed understanding of the pathogenesis of these 2 syndromes may improve treatment approaches for both laminitis and white line disease. For example, white line disease is widely regarded as a nonpainful condition (2,3). In keeping with this observation, the mare in this case was unresponsive to hooftesters. The mare's grade IV/V lameness, however, demonstrated moderate to severe pain, which we may conclude was due to capsular rotation of P3. The accuracy of prognosis for recovery may differ significantly depending on the etiology of P3 rotation. If laminitis is the primary disease present, prognosis for full recovery is guarded. However, if white line disease is the primary disorder and the lamina of the hoof are, therefore, not inflamed, the prognosis for full recovery is excellent. In either case, the treatments are very similar. In fact, some veterinarians have stated that differentiation between white line disease and chronic laminitis is irrelevant for therapeutic purposes (6), an assertion supported by this case, since extensive damage to the hoof wall appeared to have contributed to, if not caused, rotation of P3. Treatment modalities must therefore be directed towards alleviating both the pain and the mechanical disruption associated with failure of the bond between the hoof wall and P3.
Footnotes
Acknowledgments
The author thanks Drs. Antonio Cruz, Brian Hancey, and Reny Lothrop for their assistance with this case. CVJ
Dr. Oke will receive 50 free reprints of his article, courtesy of The Canadian Veterinary Journal.
Address all correspondence and reprint requests to Dr. Oke.
Dr. Oke's current address is Ontario Veterinary College, Veterinary Teaching Hospital, Large Animal Clinic, University of Guelph, Guelph, Ontario N1G 2W1.
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