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Acidosis or Acute Carbohydrate Engorgement

Acidosis or Acute Carbohydrate Engorgement is a type of indigestion in ruminants caused by the ingestion of a carbohydrate (CHO) rich diet, which could cause severe toxaemia and a change in ruminal pH towards acidic, which in turn complicates metabolic acidosis, dehydration, complete ruminal stasis, and recumbency fallowed suddenly by death.

Synonyms of Acidosis or Acute Carbohydrate Engorgement are:

Acidosis
Acute Carbohydrate Engorgement
Grain Engorgement
Acid Indigestion
Lactic Acidosis
Ruminal Lacto-acidosis
Grain Overload in Ruminants

Etiology

Sudden accidental ingestion of a highly fermentable carbohydrate diet.

The most common sources are rich wheat floors, crushed grains, bakery dough, and rotten fruits.

Pathogenesis

Accessing crushed grains appears to have a more pronounced pathogenic impact compared to whole grains. Symptoms typically manifest within a relatively short window of 2 to 6 hours following ingestion. During this period, there is a notable reduction in pH levels, which creates a favourable environment for the proliferation of Streptococcus bovis, leading to heightened production of lactic acid and subsequently lowering the pH to below 5.5. This acidic pH condition then triggers the activation of Lactobacillus species, further driving down the pH to approximately 4.5. Consequently, there is an increased osmolarity of the ruminal fluid, which, in turn, leads to the withdrawal of fluids from the systemic circulation, ultimately resulting in an enlargement of the rumen.

The withdrawal of fluid from the blood causes dehydration and hemoconcentration.

The reduction in pH diminishes cellulolytic microbes and the release of endotoxins and histamine, which cause ruminal stasis. There is increased absorption of lactate, resulting in metabolic acidosis and toxaemia, an irreversible change in the buffer system.

Clinical Signs

Usually, symptoms are visible 6 to 12 hours after ingestion. The animal is dull, showing signs of abdominal pain (kicking at the belly), increased situps, restlessness, and distention of the rumen, leading to distention of the paralumbar fossa initially and, in later stages, bilateral distention of the abdomen. Absence of ruminal contractions, complete anorexia, grinding of teeth, elevated HR and RR, subnormal temperature Upon palpation of rumen bellotment, a fluid flashing sound could be auscultated.

In some cases, there is regurgitation of ruminal contents, usually diarrhoea, and the outcome is about 24 hours. The faeces are semisolid, grey-coloured, and have a foul smell. Advanced cases show CNS signs like apparent blindness, staggering gait, head pressing, and even laminitis.

Acidosis or Acute Carbohydrate Engorgement is categorised into:

Peracute Acidosis
Acute Acidosis
Subacute Acidosis

Clinical signs in Peracute Acidosis are:

Recumbency
More than 10% dehydration
Atonic rumen pH is 5.0 (4.5-5.0)
Heart rate more then 120 per minute
Pupils are dilated
Typical fluid splashing sound from atonic rumen
Congested mucus membrane

Clinical signs in Acute Acidosis are:

Recumbency or standing
Dehydration between 6-8%
Atonic rumen pH is 5.5 (5.0-6.0)
Heart rate is 90-100 per minute
Pupils dilated but response to light
Fluid splashing sound from rumen
Atonic rumen
Shows ataxia

Clinical signs in Subacute Acidosis are:

Standing position
No much signs of dehydration
Rumen pH between 6-6.8
Heart rate is less than 90 per minute
Respiratory rate is 22-25 per minute
Doughy rumen
Decreased ruminal contractions
No specific treatment is required (Liver extracts also advised) (However NaHCO₃ can be administered as precautionary measure)

Diagnosis

History should be collected, like animals that ate any carbohydrate-rich diet in large amounts, which could have caused acidosis.

Based on clinical signs: Acute, subacute, or peracute and advanced cases show diarrhoea; faeces may contain partially digested food grains with an offensive smell; in some of the acute cases, there is regurgitation of ruminal contents through the nose; and some animals show signs of laminitis due to vitamin deficiency (Thiamin).

Examination of the ruminal fluid reveals: pH of 4.5 to 6.0, Absence of protozoa, less microflora but motility is sluggish in Subacute type, In acute cases microflora are totally absent and even traces of microflora are not seen, Color is milky grey, Smell is sour and acidic pungent.

MBRT: Elevated to 10-15 minutes (normal value is 3-5 min).

SAT: It is higher than normal of 7-9 min or absent.

Biochemical tests in acidosis:

Blood lactate estimation > 25 mg / dL
HCO₃ is decreased because lactic acid is proton donor. The level falls to 20- 22m moles per liter as against the normal value of 24/30 mmoles/ltr
Hypocalcaemia is seen (sub clinical < 6.5 mg/dl)
Blood glucose is increased in initial stages followed by slight decreased or normal glucose level
Enzymes like SGOT, LDH, serum arginase, gamma glutanyl transferase (GGT) are elevated due to hepatic insufficiency.

Differential diagnosis

Acidosis or Acute Carbohydrate Engorgement should be differential diagnosed from Diffused peritonitis, Coliform mastitis and Simple indigestion.

Diffused peritonitis

Increased peritoneal fluid
Pyrexia is seen which is not seen in lactic acidosis
No specific change in ruminal fluid but change in peritoneal fluid whiah is turbid with flakes and tends to clot

Coliform mastitis

Septicemia is very severe
Animal is recumbent
No change in ruminal parameters

Simple indigestion

Decreased motility
Dull animal
Microflora + to ++
Ruminal pH is 6.6 – 7.4

Treatment

Treatment of Acidosis or Acute Carbohydrate Engorgement is divided in First Aid, Actual Treatment and Supportive Treatment.

First Aid

Delaying access to water for 8 to 12 hours, even when the animal is thirsty and dehydrated.
If the animal shows signs of appetite, which is typically reduced (anorectic), offer high-quality hay. This can stimulate cellulolytic organisms and help control Streptococcus bovis.
If the animal can support its weight, consider providing gentle exercise. If diarrhea is observed, it can be viewed as a positive sign because it aids in eliminating toxic contents from the gastrointestinal tract.

Actual Treatment

Correction of pH and prevention of further production of lactic acid by using alkalising agent like NaHCO₃ and MgOH (Dose rate: 1gm/kg body weight as 8-12 hours interval for 2-3 days).

Further production of lactic acid is stopped by administering oral or parenteral or intra-ruminal antibiotics to prevent lactic acid producing bacterial over growth (Amoxicillin, Chloramphenicol, OTC etc.).

Restoration of fluid and electrolyte balance: Sodium Bicarbonate (NaHCO₃) parentally to restore metabolic acidosis. Alternatively, Ringers Lactate (RL) can be administered as per the fluid requirement of the animal. Lactate is converted into bicarbonate in the liver and helps in reducing metabolic acidosis.

Rejuvenation of ruminal microflora and creating a positive ruminal ecosystem.

If, despite the aforementioned treatment, the animal exhibits a lack of interest in eating for approximately 10 days, it becomes necessary to restore the balance of the ruminal ecosystem. In this situation, oral administration of Herbostrong is recommended, while caution should be exercised when considering motility-inducing drugs such as potassium antimony tartarate, especially when the ruminal mucosa is already compromised, as it may lead to exfoliation. However, the most effective treatment option is cud inoculation at a rate of 5-10 ml per kilogram of body weight.

Supportive Treatment

Antihistamines like Chlorpheniramine Maleate: 10 ml in large animls and 3 ml in small animals.
Corticosteroids (0.5mg/kg b.wt) in peracute cases to prevent shock.
Thiamine supplementation at the rate of 10 mg / kg b.wt gives encouraging results.
Parasympathomimetics like Neostigmine, calcium to attempt restoration of ruminal motility.

Prevention

Education of formers to not offer festival waste products
Increased roughage feeding of animals
Avoiding grain rich feed