1 This condition which is also called ''acute carbohydrate
engorgement'' or ''lactic acidosis'', is life threatening and must be
handled as an emergency. Treatment must begin as soon as it is realized
that the goat has eaten a more than normal amount (as little as half
again as much) of grain or other sources of readily fermentable starch.
The longer treatment is delayed, the more difficult it is to reverse
the progressive chain of events that will end in death in 2 to 4 days.
The underlying problem is the rapid fermentation of starch in the rumen
with the resultant production of lactic acid. This acid is picked up by
the blood stream in dangerously high amounts that disrupt the normal
2 Clinical Signs
The severity of the signs depends largely upon the amount eaten. In
the first few hours, a full rumen, restlessness and crying in pain may
be all that is seen. There are mild forms which do not progress beyond
simple indigestion. However, in severe forms there may be evidence of
extreme pain (crying and getting up and down) which will become
intermittent and then be predominated by depression. They will often
stagger and even appear blind. The appetite will disappear during the
first day as will rumen contractions. The fecus may become soft.
3 The temperature will become sub-normal unless the animal is exposed
to hot sun. As the acidosis (lactic acid level in the blood and body
fluids) increases, circulatory collapse (shock) will begin; this will
increase the heart rate. In cattle, animals with a heart rate of less
than 100 will much more likely respond to treatment than one with a
heart rate of 120-140. It seems likely that a similar prognostic aid
would be valid in goats. Respiratory rate becomes fast and breathing is
shallow. Diarrhea usually develops and is profuse.
4 The excess lactic acid in the rumen causes a large amount of body
fluid to be transported into the rumen. This is a dehydration process
which is detectable by an increase in the hematocrit (the percentage
of red blood cells in whole blood). This decrease in the amount of
fluid in the blood and the acidosis cause circulatory collapse. The
shock is best detected clinically by a paling of the mucous membranes,
a fast heart but barely perceptible pulse. As long as the hematocrit
stays normal (30-40) the prognosis (outlook) is favorable. A
hematocrit above 45aids in the diagnosis of grain overload and
indicates a less favorable prognosis.
5 The rumen may feel full and doughy; if less grain was consumed, it
may feel resilient because of increased fluid and gas. The rumen will
have no contractions but one may hear a lot of gas rising through
6 Usually after two days the animal will lie down and not voluntarily
get up. They will be extremely depressed.
7 Tissue Changes
In animals dying within two days; the cornified rumenal epithelium
is soft and easily removed; there is hemorrhage of the underlying
surface. There may be abomasitis and enteritis. There is an odor
suggestive of fermentation and, if the necropsy is conducted within an
hour of death, the pH of rumen contents will be 4 to 5.
8 In cases lasting 2-3 days, the rumen and reticulum walls may be
greatly edematous and hemorrhagic resulting in marked thickening.
When there is a known exposure to grain, the signs may be easy to
interpret. When grain is offered to a group of animals, especially for
the first time, a predominant fast-eating bully animal may be able to
overfeed on the grain meant for the other animals. However, if one does
not expect or can't find evidence of overload, the symptoms are quite
similar to any other acute septicemic disease such as peracute mastitis
or metritis or diffuse peritonitis. Careful clinical examination by the
veterinarian will be very useful and the most revealing tool will be
the collection and finding of rumen fluid with a pH of 4 to 4.8 and no
Under most management systems, grain overload in goats results from
escape of animals from their pens and finding an open or otherwise
unsecured source of grain. The first step of prevention is having good
pens. Even then escape occasionally occurs; therefore the most important
step is to store grain inside a room or shed that is absolutely
goat-proof. To avoid human error, the door should be self-closing and
Because grain overload is life threatening, your veterinarian
should be consulted immediately. Two different clinical possibilities
exist which require different courses of action. In the first the
animals are ''caught in the act'' or you find them out of their pens
with evidence that they have eaten grain. They are not yet ill. The
second situation should be less common if the goats and facilities are
observed frequently. Here engorgement took place 12-48 hours previously
and they now show signs of lactic acidosis.
12 When the animals are found eating illicit grain, call your
veterinarian. In the event a veterinarian is not immediately available
the following course of action is recommended.
13 First, remove all sources of feed and water for 12-24 hours except
good quality hay equal to a one-half days ration per animal. Exercise
them 5-10 minutes every hour. The author prefers to give 1 tablespoon
(15cc) of Milk of Magnesia orally followed by 1 ounce (30cc) of water
(no more than 2 ounces) to an adult goat. This should be repeated
later if the animal starts to show signs of restlessness or discomfort.
14 The second situation involves animals that have engorged themselves
12-48 hours previously and have progressively worsened. They may be
discovered this way or are worsening despite early treatment. These
goats should be isolated and observed closely.
15 The color of the mucous membrane of the eyes (or vulva or sheath of
the penis) should be observed early and regularly for evidence that the
healthy pink is changing to pale pink to white. The heart rate can be
counted by pulling a front leg forward and placing ones ear over the
chest where the goat's elbow was. If the heart rate of the resting,
unexcited goat is as high as 90-100 beats per minute range, they must
be watched closely.
16 If the mucous membranes are becoming pale and the heart rate is
above 100-110, if the animal is becoming depressed or if it staggers
slightly or is showing evidence of pain, the veterinarian should
personally evaluate and treat the animals.
17 In moderate cases drenching or dosing 50 grams of magnesium
hydroxide or magnesium oxide in a liter of warm water to a 70 kg (155
pound) goat, followed by kneading the rumen to obtain mixing may be
sufficient treatment. In more severe cases that are still standing and
the rumen pH is 5 to 6, a large stomach tube may be passed and the
rumen washed with 10-15 irrigations. Tepid water is pumped in until
obvious rumen distension occurs; then the rumen is allowed to empty by
gravity flow. It is not enough to retrieve the water pumped in; grain
must be washed out.
18 Systemic acidosis is combated with oral or intravenous fluid
administration. Five percent sodium bicarbonate is given intravenously
for severe acidosis at the rate of 500 ml per 100 lbs of body weight
over a period of 30 minutes. This is followed by 1.3odium
bicarbonate at the rate of 65 ml per lb of body weight over the next
19 In severe cases, where the animal is down, in shock (as judged by
pale mucous membranes and a heart rate of 120-140 or faster), severely
depressed and rumen pH below 5, the only life saving procedure may be
surgical removal of the grain from the rumen by rumenotomy. This is a
high risk procedure because of the already extremely bad condition of
the animal. In cases that progress this far, there is also a rather
high possibility of severe fungal rumenitis developing in 3 to 5 days.
The owner should realize that surgery is much more apt to be
successful earlier in the course of the disease at a time when
conservative treatment still has a chance to work. The owner, with the
advice of the veterinarian must decide the degree of acceptable risk.
20 Goats that respond favorably to rumen washings or rumenotomy and
fluid therapy will show greater muscle strength and urinate within one
hour and attempt to stand in 6-12 hours.
21 All goats that have not been vaccinated for Cl perfringens type C
and type D must be given the antitoxin because of the greatly increased
risk of enterotoxemia under these conditions.