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Ruminal alkalosis
The rumen is a fermentation tank whose chemical balance is fragile. When its contents become too acidic, we speak of ruminal acidosis; when it becomes too alkaline, that is to say the opposite, we speak of Ruminal alkalosis. Alkalosis is th...
What is it?
The rumen is a fermentation tank whose chemical balance is fragile. When its contents become too acidic, we speak of ruminal acidosis; when it becomes too alkaline, that is to say the opposite, we speak of Ruminal alkalosis. Alkalosis is the exact mirror of acidosis. Acidosis comes from excess grains, sugars and starch. Alkalosis comes from an excess of nitrogenous materials that are too quickly degraded: dietary urea, cakes distributed without measure, poorly mixed commercial nitrogenous foods, very rich young grass, or moldy and rotten fodder. Rumen micro-organisms transform this nitrogen into ammonia. When too much happens at once, ammonia builds up, digestion stops and the excess passes into the blood, where it becomes toxic to the nervous system. The most brutal form is urea poisoning: an animal that accesses a bag of urea, a nitrogen fertilizer or a lick block can die within a day. From a distance, acidosis and alkalosis look similar: a slaughtered animal that no longer chews the cud. Only examination of the contents of the rumen makes it possible to decide, and the two are corrected in opposite directions. This is exactly why you should never deal at random.
Key point
An animal that accesses urea, nitrogen fertilizer or concentrated feed can die within a day. Remove the food from the entire batch and call the veterinarian immediately, even if only one animal is affected.
Commonly observed signs
These signs are neither exhaustive nor specific. Only a veterinarian can establish a diagnosis.
Related signs — each one links to its page:
The animal stops ruminating and refuses to eat: this is almost always the first visible sign.
Despondency, lowered head, animal that stays away from the crowd and no longer reacts to distribution.
The left side is full, pasty, sometimes bloated, and the hand placed in the hollow of the side hardly feels any contractions.
Salivation, sometimes foamy around the mouth.
Watery diarrhea, often dark and with a very bad smell.
Dehydration and weakness when the situation persists.
In forms linked to urea, everything happens very quickly and the signs are violent: muscle tremors, stiffness, staggering gait, rapid breathing, bloating, groaning, then falling, convulsions and death within a few hours.
A detail that the veterinarian looks for: the contents of the rumen give off a strong smell of ammonia, the one that stings the nose, very different from the sour and acidic smell of acidosis.
When to consult without delay
This list does not replace veterinary advice. It gathers situations that justify a prompt consultation.
Causes and risk factors
Distribution of poorly dosed or poorly mixed dietary urea in the ration: this is the most dangerous cause, because it can affect an entire batch at the same time.
Accidental access to a bag of urea, a nitrogen fertilizer, a concentrated feed or a licking block left within reach: a poorly closed door is enough.
Sudden intake of cakes or foods very rich in nitrogen, without transition and without associated energy: the micro-organisms in the rumen cannot use all this nitrogen and ammonia accumulates.
Grazing very young, very green and very nitrogenous grass, particularly after rain or fertilization, without additional long fiber.
Moldy, wet, fermented or rotten forage or feed, which results in putrefaction of the rumen contents.
Ration low in fermentable energy: without sugars or starch, micro-organisms do not have the means to transform nitrogen into usable proteins.
Prolonged shutdown of the rumen for another reason, which leaves the contents to putrefy in place.
Rations supplemented with urea or based on commercial nitrogenous feeds, especially when the mixture is prepared on the farm without suitable equipment.
Storage of urea, fertilizers and concentrates in a room accessible to animals.
Hungry animals, at the end of a drought or coming out of a scarcity, which throw themselves on the feeder and swallow in a few minutes what was supposed to last the day.
Sudden change of ration, purchase of a new batch of food without transition.
Put out to grass on young and nitrogenous regrowth in spring, without distribution of hay before going out.
Fodder stored in poor conditions, wet wheels, moldy food.
Animals already weakened, at the end of gestation or at the beginning of lactation, in which the slightest indigestion degenerates more quickly.
Diagnosis and care
Diagnosis is the veterinarian's responsibility, based on clinical examination and laboratory tests. Care is decided case by case.
The veterinarian begins with a general examination and listening to the rumen: contractions are absent or very slow, the left flank is full.
He takes rumen juice with a probe and examines it. The smell of ammonia, the color and measuring the acidity, with a test paper or a device, can distinguish alkalosis from acidosis. These two conditions result in the same slaughtered animal which no longer chews the cud, but they are corrected in the opposite direction: making a mistake makes the animal worse instead of saving it.
If possible, he observes the flora of the rumen under a microscope: in established alkalosis, the micro-organisms which ensure digestion are dead or immobile.
He questions the breeder in detail about the ration: what was distributed, when, in what quantity, who prepared the mixture, if a bag was spilled or a door left open. It is very often this questioning which gives the diagnosis, more than the examination of the animal.
In the event of suspicious death, an autopsy and examination of the contents of the rumen confirm the origin and protect the rest of the herd.
Treatment
Alkalosis is an emergency, especially in its urea-related form: call the veterinarian immediately and immediately remove the suspect food from the entire flock, not just the sick animal.
The principle of the treatment is simple but its application is not: it involves returning the contents of the rumen to normal acidity and stopping the production of ammonia. The veterinarian has acid solutions administered by probe and, in severe cases, rumen washing.
Do not attempt to do it yourself. The quantity, concentration and speed of administration are as important as the product, and liquid forced into the mouth of a weakened animal travels into the lungs.
Infusion, liver support and anti-inflammatories may be necessary depending on the animal's condition.
When the rumen has been stopped for a long time, the veterinarian can suggest re-seeding it with rumen juice taken from a healthy animal: this is a very effective gesture to restart digestion, which is carried out under veterinary supervision.
The recovery is done with good quality hay, clean water as desired, and a gradual return of concentrates once rumination returns.
In all cases, correcting the ration and storage of food is part of the treatment: without it, cases repeat themselves.
Treatment depends on the cause and the animal's condition: it must be determined by a veterinarian. No self-medication.
Prevention
Never leave urea, nitrogen fertilizers and concentrated feed within reach of animals: a locked room is not a luxury, it is the most profitable measure on the farm.
If the ration includes urea or a nitrogenous food, have the mixture established and checked by the veterinarian or a technician. A mixture made with a shovel in a wheelbarrow is never homogeneous: the first served receive everything.
Always associate nitrogen with a source of energy and long fiber: this is what allows the microorganisms in the rumen to use the nitrogen instead of letting it accumulate.
Respect progressive transitions with each change of ration, food or plot.
Never present a full feeder to hungry animals: distribute roughage first.
Remove moldy, wet or fermented forage, and protect stocks from rain and rodents.
On young and very green shoots in spring, distribute hay before going out and limit the duration of grazing in the first days.
Monitor the herd's rumination: when resting, a large proportion of lying animals must ruminate. A lot that no longer ruminates is a warning signal even before the first signs appear.
Possible complications
Rapid death in urea poisoning, often before the arrival of the veterinarian.
Damage to the liver and kidneys from ammonia passed into the blood.
Associated meteorization, which adds respiratory distress to the intoxication.
Long-lasting destruction of the rumen flora: the animal remains without appetite and loses weight for several weeks after the crisis.
False swallowing pneumonia when liquids have been forcibly administered by mouth.
Abortion, or shift to pregnancy toxemia in ewes at the end of gestation.
Batch-wide recurrences until feed ration and storage is corrected.
When to see a veterinarian
An animal has had access to urea, nitrogen fertilizer or a bag of concentrated feed: call immediately, even if it still appears normal.
An animal no longer chews the cud, refuses to eat and stays away.
He trembles, staggers or stiffens his limbs.
His left side is full or swollen and he is breathing quickly.
Watery and very smelly diarrhea appears.
Several animals from the same batch are slaughtered after a change in ration or distribution of nitrogenous feed.
An animal is found dead after a distribution: have it examined before the rest of the batch follows.
Prognosis
Moderate alkalosis, caught early and corrected by the veterinarian, progresses well: rumination returns within one to a few days.
Urea poisoning has a poor prognosis because it progresses within a few hours and many animals die before any treatment. Survivors generally recover well.
Trailing forms, with destroyed rumen flora, require several weeks of convalescence and the animal does not always recover.
At the herd level, the prognosis depends solely on the correction of the ration and the storage of nitrogen products: it is a disease that we suppress, not an illness that we suffer.
Frequently asked questions
What is the difference with ruminal acidosis?
Both are rumen imbalances, but in opposite directions. Acidosis comes from an excess of cereals and sugars, alkalosis from an excess of nitrogen, often urea or oilcake. From a distance, the animal looks the same: dejected, it no longer chews the cud. The veterinarian decides by examining the contents of the rumen, and this is essential, because treating one would aggravate the other.
My sheep licked a bag of fertilizer, what should I do?
Call the veterinarian right away, even if the animals appear normal: nitrogen poisoning sets in within a few hours. Remove the bag and remove the entire batch from the area. Don't wait for the first tremors to react.
Can I give urea in the ration as I was advised?
Urea is used in breeding, but it requires a homogeneous mixture, a gradual transition and a ration providing enough energy and fiber. Prepared by hand in a wheelbarrow, it becomes dangerous: the first animals served receive a lethal dose. Have the ration established by the veterinarian or a technician.
My sheep hasn't chewed the cud since yesterday, is this serious?
A rumen stopped for more than twenty-four hours is never trivial. This can be simple indigestion, but also acidosis, alkalosis, esophageal obstruction or a more serious illness. Remove the suspect food, leave hay and water, and have the animal examined.
References
FAO — Organisation des Nations unies pour l'alimentation et l'agriculture
EFSA — Autorité européenne de sécurité des aliments
Content reviewed by the TunisieVet editorial team · Updated 11 August 2026
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