Many people are familiar with the condition of founder in the horse; a condition that can cause devastating pain and permanent damage to the foot. What is unfamiliar to many novice cattle owners is that the cow can suffer the same damage as a horse with a similar aftermath.
Founder or laminitis is an inflammation of the lamina surrounding the hoof bone. This lamina is the soft tissue that separates the hoof wall from the boney structures of the foot. It is rich in intricate blood vessels that feed the hoof and encompasses the foot bone in a lacey network. This network interacts with the bone itself in the interlocking boney lamina underneath. The health of the sensitive lamina is of utmost importance to the overall well being and longevity of the animal.
The tiny vessels that supply the horn producing areas are very vulnerable to the affects of toxins or poisons produced in the body (or sometimes from outside the body). These toxins cause the vessels to dilate and loose blood or serum through the vessel walls. This leads to increased pressure inside the foot and pain. The damage to the vessels causes clots to form, which then reduces the blood supply to the horn-producing areas. These clots later turn into scar tissue and undoubtedly predispose the foot to further damage by the same process. Laminitis can be caused by a number of things, such as traumatic injury to a single foot, or those toxins produced from severe infections or inflammation such as metritis (uterine infection, usually after calving) mastitis (infection in the udder, usually after calving, but can occur prior to calving) and footrot.
However the most common cause of laminitis in the cow is associated with feeding of highly fermentable starches or sugars (heavy grain consumption) and the subsequent overproduction of organic acids that may occur in the rumen. These acids cause a die off of normal rumen microorganisms and poisons (endotoxins) are released and absorbed into the bloodstream. These endotoxins attack the vessels of the foot, causing inflammation and release of histamine from the inflamed tissues. Histamine contributes to the ongoing vascular damage occurring in the foot.
Laminitis can be acute, chronic, or subclinical.
Acute laminitis is an extremely painful condition. The animal may arch its back and keep its legs under the body; occasionally the front legs will be crossed and the hind legs wide apart. The animal will shift its weight from one foot to another and obviously doesn’t want to move. Because walking is evidently so painful, the animal may spend an abnormally long time lying down. Acute laminitis is frequently associated with grain overload.
If you measure heart rate and respiration, they will be increased from normal, and appetite will be diminished or completely absent. There may be a bounding pulse to the foot and the area just above the hoof may appear puffy and swollen. The hooves themselves appear normal, but may feel warm and sensitive to the touch. The lateral hind claws are generally the most severely affected. In very severe cases, there may be hemorrhage and serum that ooze out of the bottom of the foot. As the acute incident passes, the damage it caused may become evident weeks or months later.
Subclinical laminitis is characterized by the absence of obvious lameness during the initial period of vascular disturbance, and can be ongoing as a result of subclinical rumen acidosis. Feet must be carefully examined to find evidence of the condition. Even then, lesions in the hoof horn are not seen until several weeks or even months after the inflammatory insult to the lamina. Chronic laminitis refers to the changes in the hoof that develop later on as a result of either acute or subclinical forms of the disease. Hooves typically become longer, flattened and widened, with grooves along the dorsal hoof wall. The hoof wall is produced in the coronary segment (that is, the ridge of tissue just above and encircling the hoof) at a rate of about 5 mm per month, varying a little based on the season of the year, the individual claw and the nutritional status of the cow. As the wall grows, it “slides” over the lamina covering the distal ½ of the hoof. Any interruption in growth of the hoof, as might occur with systemic illness or a sudden change in diet, may result in a ridge or groove (called a “hardship grove”) on the hoof wall. By measuring the distance in millimeters from the “hardship groove” and the coronary band the time of the actual insult to the hoof can be estimated. The sole of the hoof normally is about 8-10 mm thick and thus it takes hemorrhages about 2-3 months after the initial insult to show up at the weight bearing surface.
Chronic changes to the foot as a result of laminitis include yellow discoloration of the sole, hemorrhages of the sole, separation of the white line, erosion of the heel, abscesses of the sole, sole ulceration, sole overgrowth, inflamed coronary band, horizontal grooves in the hoof wall, sunken or rotated distal phalanx (the bone of the hoof), overgrowth of the claw and double sole. Separation of the white line can lead to impaction with foreign material, such as gravel or manure, and lead to the formation of abscesses also.
Although with resolution of the acute phase of the disease, the hoof may appear to be normal, there may be permanent damage inside the hoof itself that predisposes these animals to further episodes of laminitis.
Treatment of acute laminitis truly should be considered an emergency, just as it is in the horse. Direct treatment for the feet may include antihistamines, corticosteroids or pain-reducing drugs which inhibit prostaglandin synthesis (phenylbutazone or flunixin). Just like in the horse, standing in cold water can reduce pain and keep the animal on its feet. Standing in warm water may help to increase the circulation to the damaged capillary bed, and there is some debate over which is more helpful. Certainly providing soft, deep bedding to keep the animal as comfortable as possible is mandatory. During the acute phase, it is wise to prevent any unnecessary activity. It is also important to treat the underlying cause of the insult.
Treatment of subclinical laminitis is by its very definition, impossible, because the animal is showing no signs of disease and controlling it requires steps aimed at prevention.
Prevention of laminitis in the cow requires steps taken to prevent rumen acidosis. Feeding of grain, or grain products, fruit, etc will alter the environment of the rumen. Feeding hay or haylage will provide fiber to stimulate saliva and buffer the acid produced. Dry hay requires adequate saliva to moisten it to allow swallowing. Haylage already is moist, and will not require as much saliva to permit swallowing. Both will encourage saliva production as the cud is chewed. Poorly ensiled haylage may actually contribute to acid levels in the rumen. Feeding grain should never be seen as an innocuous process. Animals should be slowly acclimated to the level of grain they are to receive. The more frequently they are fed grain or similar products; the better will be the adjustment period. Animals fed grain twice per day are less likely to suffer the effects of acidosis than those fed grain just once a day. (I.e. split the daily ration in two.) Use every available means to prevent gorging on grain products. This can mean locking up the grain bin so escaped animals cannot gain access, or it can mean making sure every animal in the pen comes up to eat grain when it is fed. Aggressive feeders may very well get more than their fair share of feed, and may not show evidence of problems until lesions of chronic laminitis show up in their feet. Remember that easily digested carbohydrates include such things as day old bread, various types of fruit, or grazing on high fiber corn stalks if there is a large volume of corn to be found.
Other than preventing further episodes of laminitis, keeping a diligent schedule of hoof trimming is the only available option for the chronically affected feet. Most cases of chronic laminitis can be kept comfortable and functional if further damage is prevented.