Diagnosing fatal sinker syndrome and implementing treatment Plan A - DVM
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Diagnosing fatal sinker syndrome and implementing treatment Plan A
Part 4 in a series on understanding the disease progression of abnormal hoof anatomy.


DVM360 MAGAZINE


If there is an area in the study of laminitis that requires dedicated research, fatal sinker syndrome is at the top of my list. This syndrome can strike without warning in hours or weeks. It might give you clues of its onset or it might not. It can be slow and insidious or a horse can suddenly walk out of its hooves.

Fatal sinker syndrome is an uncommon form of Grade IV laminitis. Usually it is a few weeks in the making and occurs after rotational laminitis. However, fatal sinker syndrome does not have to follow the rules and can occur within 24 hours of the acute phase of a laminitic bout. The syndrome can occur in one or all four feet.

Clients must be alerted to the grave prognosis of fatal sinker syndrome and the extensive rehabilitation and cost of correction. Pain management will not help or halt progression if it is used as the sole therapy. Casting with or without transcortical pinning and hoof wall ablation is the most common technique applied.

Pathogenesis of fatal sinker syndrome

We do not know what catastrophic mechanism causes fatal sinker syndrome, but we do know that the end result is entire circulatory collapse with subsequent laminar necrosis and loss of the hoof capsule. Severe systemic illness such as pleuropneumonia, metritis, enteritis, colitis or any endotoxemic event is the cause of most cases of fatal sinker syndrome. The worst cases I have seen involved mares with retained placenta that developed metritis.

I have also seen fatal sinker syndrome as a sequela to supporting limb laminitis. These cases do not have the terrible endotoxin challenge but are instead an overloading and circulatory compression problem—usually affecting one foot—and have a better prognosis if treated immediately.

Fatal sinker syndrome can also be caused by excessive concussion after exertion (e.g., galloping on hard surfaces), infections of the distal interphalangeal joint, excessive grain consumption with subsequent renal failure, and compromised immune systems after exogenous challenge, such as in the use of high-dose corticosteroid treatment.


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Source: DVM360 MAGAZINE,
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