2 Ruminal Lactic Acidosis

Transcript

Dear vets,

Greetings to all!

Last lesson- lesson one we have discussed the Introduction of Rumen omasal impaction and dysfunction in cattle, a List of disorders related to the Rumen omasum in cattle, and Simple indigestion and Ruminal impaction, in which we have discussed Etiopathogenesis, Clinical findings, Diagnosis, and Treatment of Simple indigestion and Ruminal impaction. In this second lesson, we are going to discuss a very important disease in the field condition, it is having a lot of influence and diagnosis skills at the field level. So, it is mainly because of the man-made problem because of the management aspect, excessive feeding that is called acute carbohydrate engorgement or Rumen lactic acidosis. This is a main problem in the field conditions, if you have diagnosed the condition, it is very easy to treat. For that, we need to learn something regarding Etiopathogenesis, Clinical signs, Diagnosis skills, and Treatment.

Let us enter into the topic of proper Etiopathogenesis; excessive carbohydrate ingestion will lead to the production of lactic acid, the lactic acid is responsible for so many pathophysiological changes in the rumen. So let us take one by one it is also increasing the carbon dioxide production in the cellular respiration, by this way it is leading to Kussmaul’s respiration that is called commentary hyperventilation, so increased elimination of carbon dioxide, that’s the first animal is brought with the symptoms of some respiratory distress, in case of lactic acidosis and another thing is the Gram-positive bacteria will be dominating like a Gram-negative bacteria is decreasing, Gram-positive bacteria are dominating. So, it leads to the lactic acid’s corrosive nature. Sometimes it is going to leads to some damage in the ventral half of the rumen and there is a chance of getting perforation, which is leading to acute peritonitis and it will also lead to toxemia.

The next thing is that lactic acid is going to cause Chemical rumenitis and Mycotic rumenitis, there is a chance of three to four days after the lactic acid accumulation in the rumen it will favor the multiplication of absidia, mucor, rhizopus this fungus will be more predominant. So that is leading to Fungal ruminant. Sometimes the lactic acid is absorbed in the system and it will go for systemic academia low pH and lactic acidemia are there in the system circulation, which is leading to further anaerobic metabolism, the production of further lactic acid in the system. That is again reducing the blood pressure, which is leading to hypotension. The ruminal vessels will be damaged through the rumen vessels, the fusobacterium necrophorum will enter and go to the liver, and there it is causing liver abscess, small nodular liver abscess, that is called sawdust liver.

Then histamine is released because of the acute carbohydrate enrichment in the rumen and that is leading to laminitis, it is going to accumulate in the current region and animals will be finding difficulty in walking. Then the growth of the rumen papilla, will be more and it will be altered so that will be leading to ruminal parakeratosis, thus all the clinical-pathological changes are going to occur because of the lactic acid in the rumen.

Let us discuss Clinical signs: In mild cases suppose ingestion of carbohydrates source in the morning, rice, or whatever memorize crude oil in the morning. So, the animal will be showing the symptoms of anorexia, dullness, depression and sometimes it is a mild dose of carbohydrate engorgement, the animal may recover spontaneously within 3-4 days, so the initial period of indigestion only is going to happen.

Next severe cases- suppose if it is a severe case, the animal may go for recumbents also sometimes, in acute cases there may be a severe production of or heavy production of lactic acid is going to happen. Here the lactic acid is hygroscopic in nature, so that’s why drawing the water from the systemic circulation leads to severe dehydration and if you are seeing the left paralumbar fossa, it will have a fluid splashing sound and rumen motility will be reduced, suspended rumination is there and the animal will be going to develop a drunken gait, so incoordination, ataxia will be there due to this dehydration and lactic acidemia and the animal is having diarrhea, it is initially it will be somewhat semi-solid nature and it is voluminous it is small waters due to that, the dietary diarrhea is prognostic in the phosphate prognostic indicator it should be there, so the purified materials should come out, then only the animal is going to recover. So diarrhea animals may recover, the animal which does not have diarrhea in acidosis is going to suffer, in severe cases, and the animal is going to have laminitis. In the picture you could able to see the sunken eyeball, you have to see that there is a gap between the eyeball under the eyelids, and another test is to be there to assess the dehydration by skin tenting test, you have to pinch the grass the neck skin and leave it for a second it is 1-2 second within that you have to it should have normalcy. If it is persisting as a tent that is indicating dehydration more than 8% or 10% like that. You have to do the succussion, so to identify whether the animal is having any fluid splashing sound or not you have to do the succussion on the left paralumbar fossa, which will have a fluid splashing sound over the left paralumbar fossa. You can also occult it or you can also hear the normal with the distance also. You have to collect the rumen liquor and you have to go for a physical examination. The color of the rumen liquor in case of acidosis is milky green and it is sour-smelling and watery in nature. Then if you are seeing the pH and protozoa, protozoan won’t be available. The protozoan is nil almost all protozoans would have been dead and the low pH is not conducive for the survival of the protozoan then pH will be below the normal range of 6.2 -7.2 is a normal range it is below that 5-6 is the normal range. you can see the rumen fluid with a pH of around 5-6.

In the picture, the Diagnosis of rumen lactic acidosis or carbohydrate engorgement is mainly of history. History of excessive intake of carbohydrates. Sometimes the normally, routinely is having a lot of carbohydrates but a little bit more excess will also lead to carbohydrate engorgement.

Then Clinical signs: Sunken eyeball, fluid splashing sound, abdominal distension, laminitis all together is going to give some idea. Then rumen fluid examination is going to confirm the ruminal lactic acidosis disease. This disease is going to be differentially diagnosed with simple indigestion, Toxemia- some animals going for recumbency. In case of severe acidosis also, animals are going to be recumbents. So, you have to go to examine the udder and any peritonitis is there, you have to go for peritonitis synthesis. So, the peritonitis or the coliform mastitis will lead to toxemia and subsequent recumbency in animals will also simulate acute carbohydrate engorgement and you have to differentiate diagnosis with the subacute rumen acidosis, here subacute rumen acidosis – the animal is fed with a continuous carbohydrate source, the animal would have been adopted for that but even then the animal is having diarrhea and suddenly sometimes we may have indigestion problems. So, we have to look for subacute rumen acidosis by history, it is a herd problem.

Parturient paresis- that means milk fever, in case of milk fever the animal will be going for recumbency, the lateral kink of the neck will be there. So, to differentiate milk fever from acute carbohydrate engorgement, we need to take the rumen liquor and you have to examine and you have to do the succussion on the left paralumbar fossa, if the fluid splashing sound is there that is a major clinical sign related to the acute carbohydrate engorgement or ruminal lactic acidosis.

Treatment in Parturient paresis: emergency treatments to be there. The first thing is we need to lavage the rumen as much as possible to remove the lactic acid present which is there in the rumen to be evacuated as much as possible, bypassing the stomach tube and sodium bicarbonate administration. Sodium bicarbonate administration, you can do it with the millie equivalent of sodium bicarbonate requirement is equal to 0.3 multiplied with a base deficit that will be measured based on the clinical signs and laboratory examination, and body weight. so that will give a milliequivalent of sodium bicarbonates to be administered to the animal.

mEq of NaHCO3 = 0.3 * base deficit * BWT(kg)

So, if it is not done we can go for 5% – five liters of sodium bicarbonate intravenously over 30 minutes and 1.3% of this isotonic sodium bicarbonate solution that can be administered 6-12 hours like a 150 ml per kg body weight. But at the field level, you will calculate the sodium bicarbonate requirement and you can administer it, while giving the sodium bicarbonate it is very simple you are having a 7.5%, 8.4% sodium bicarbonate solution available in the market. We are going to dilute with the distilled water to administer the sodium bicarbonate at the rate of 5% only we are going to administer to the animals. That too you have to mix it with the normal saline, so in mild cases, Ringer’s lactate can also be given, when the circulation is proper. The lactate is going to be liver and it will be converted into bicarbonate that will take care of the rumen acidosis, but in case of severe dehydration you have to try to avoid Ringer’s lactate, so because the circulation is Ringer’s lactate, we are giving the periphery it is not going to the liver and it is not going to convert. Again, the lactate is going to deteriorate the condition. Here two things are there: L lactic acid, D lactic acid. The D lactic acid is actually persisting, lactic acid is metabolized.

And another treatment is Oral: so, our aim is first to evacuate the content and give bicarbonate to systemic acidosis and we are going to give some oral antacids like a Magnesium hydroxide or Magnesium oxide at the dose rate of 500 grams per animal, you have to mix it with the 10 liters of water and so that will help neutralize the pH in the rumen. other Ancillary treatments like Antihistamine because of histamine release there will be laminitis, you have to give Antihistamines, Chlorpheniramine we can give and because of inflammatory changes is going to happen in the rumen ventral wall, we need to give Non-steroidal anti-inflammatory drugs (NSAIDs), but that would also be judicially used and Thiamine, the rumen is only in ruminants the rumen is responsible for the synthesis of B complex, vitamins we need to submit the B complex, vitamins especially Thiamine, which is responsible for the so many biochemical reactions in the body and you can also move that content by giving Laxatives[1]Parasympathomimetics and Calcium borogluconate. Calcium will also be low in some cases of Lactic acidosis, we need to supplement calcium borogluconate and Oral antibiotics as we know that there is a Gram-positive bacteria domination usually there should be Gram-negative bacteria. So, we need to just kill the Gram-positive bacteria by giving oral antibiotics, especially Sulfonamides and oxidative cycling. Then one of the important things the next day, first today you have to treat this, then probiotics you want to give probiotics that will help for the regeneration of the microflora and it will also help for the metabolism of the lactic acid. The Cut transplantation; as we discussed in this simple indigestion we need to collect from the healthy animal or from the slaughterhouse, which should be administered 2-3 liters within half an hour to one hour of collection. Should not be stored for a long time. During the transit, it should be closely, tightly capped, and should not be having exposure to the environment. The other important management advice to the farmer is to restrict the water intake, in case of ruminant lactic acidosis the animal is willing to take more water it is willing to take but it is going to engorge, and it will develop some aspects here it will engorge the rumen and it will compress the diaphragm, it is leading to some motility in animals. So, you have to give water but in a restricted manner. So, half bucket, two hours after that you are given another bucket. Another thing is we have to go for giving the palatable hay, so that will help rumen motility by irritating the rumen mucosa, so the animal regains its normal appetite.

In lesson two we have discussed Etiopathogenesis, Clinical signs and Diagnostic Aspects, and Treatment of ruminal lactic acidosis in cattle.

In lesson three we are going to discuss three topics: Subacute ruminal acidosis, Ruminal drinkers, Ruminal alkalosis.

Thank you!