The metabolic activities of the cat’s body must be carried out in body fluids with suitable pH. The relative constant pH of body fluids is an important component in maintaining homeostasis of the internal environment. Various enzymes, hormones, electrolytes, etc. in the body can only function normally when the internal environment is stable. Under pathological conditions, body fluids may experience acid-base overload or regulatory mechanism disorders, leading to the destruction of acid-base homeostasis in the body fluid environment and causing acid-base balance disorders. This will inevitably have an impact on the normal physiological functions of body tissues, organs, etc., especially when the body's self-regulatory ability is reduced under disease conditions, so timely detection and correct treatment of these acid-base disorders often become the key to the success or failure of disease treatment.

Cats will develop acidosis and alkalosis if there is an acid-base imbalance in their bodies. Cat metabolic acidosis is also the most common clinical acid-base disorder in cats. Because it has a greater impact on various systems, treatment must be given when severe metabolic acidosis exists.

1. Causes of metabolic acidosis

Based on the triggering factors, the causes of metabolic acidosis can be divided into: ① increased intake of fixed acids by the body (for example, ethylene glycol, salicylates, ammonium chloride); ② increased metabolic production of fixed acids (for example, lactic acid Acidosis, diabetic ketoacidosis); ③ Reduced ability of the kidneys to secrete fixed acid (e.g., renal failure, adrenocortical insufficiency, distal renal tubular acidosis); ④ The body loses HCO3--rich fluid: gastrointestinal tract (eg, small bowel diarrhea) or kidney (eg, carbonic anhydrase inhibitors, proximal renal tubular acidosis).

According to the ion gap, the causes of metabolic acidosis can be divided into: ① Increased ion gap, also known as positive chlorine metabolic acidosis, such as ethylene glycol poisoning, salicylate poisoning, and diabetic ketoacidosis , uremic acidosis, lactic acidosis, etc.; ② Normal ion gap, also known as hyperchloremic metabolic acidosis, such as diarrhea, renal tubular acidosis, metabolic acidosis after hypocapnia, dilution acidosis (e.g., rapid infusion of 0.9% NaCl), hypoadrenocorticism, cationic amino acid (e.g., lysine, arginine, histidine) treatment, etc.

2. Impact on the body system

Metabolic acidosis can cause abnormalities in multiple systems due to the imbalance of acid and base in the body and may be accompanied by other electrolyte abnormalities. The most important aspects can be seen in the following three aspects: ① Impact on the respiratory system: increased hydrogen ion concentration stimulates peripheral and central chemoreceptors to increase alveolar ventilation, and high ventilation reduces P CO2, which can counteract the impact of HCO3- concentration on pH; ② Effects on the kidneys/urinary system: In metabolic acidosis, the kidneys secrete net acid, mainly increase the excretion of NH4+, and increase the reabsorption of HCO3- to compensate for the change in pH; ③ Effects on the cardiovascular system: When the pH is lower than 7.2, myocardial contractility decreases and the heartPredisposed to ventricular arrhythmias and ventricular fibrillation.

3. Clinical characteristics

Metabolic acidosis can cause a variety of clinical symptoms, the common ones are: ① Cardiovascular system: decreased cardiac output, prone to ventricular arrhythmia or ventricular fibrillation; when venous vasoconstriction, blood volume increases, It can induce pulmonary congestion; the blood oxygen curve shifts to the right; ② During severe acidosis, the liver can change from a lactic acid scavenger to a lactic acid producer; ③ Severe acidosis can damage the brain's regulation of its own volume, leading to dullness and coma; ④ Acute inorganic acid Poisoning can lead to hyperkalemia, but organic acidosis does not have this effect; ⑤ An acute drop in pH can convert protein-bound calcium into ionized calcium, causing hyperionic calcium; ⑥ Chronic metabolic acidosis can cause bone buffer (mainly calcium carbonate) is released, producing osteodystrophy and hypercalciuria. ​​​​​​

4. Case Analysis

1. Basic information: Norwegian forest cat, female, 8 years old, 2.7kg, never vaccinated, not dewormed, usually feeds on cat food.

2. Medical history: Past health.

3. Chief Complaint: I fed food from the refrigerator a few days ago. I vomited a few hours later and now I have no appetite.

4. Clinical symptoms: loss of appetite and vomiting.

5. Physical examination: moderate dehydration (about 8%), the surface of the kidneys is not smooth when palpated, and only the right kidney is palpable.

6. Clinical pathological examination: Routine blood tests, biochemical tests and blood gas ion analysis will be performed according to symptoms.

7. X-ray examination: The kidney image is not clear, and there is a high-density image inside it.

8. B-ultrasound examination: The left kidney has completely atrophied and there are stones in the right kidney.

Analysis: All blood routine indicators were within the reference value range, with no obvious abnormalities. Blood biochemical tests showed that urea nitrogen, creatinine, and phosphorus were all much higher than the upper limit of the reference values, indicating the presence of renal failure. Blood gas ion analysis: pH decreases, severe acidemia exists. Since PCO2 is normal, HCO3- concentration is lower than the lower limit of the reference value, and AnGap is higher than the upper limit of the reference value, indicating the existence of metabolic acidosis. Blood glucose concentrations above the upper limit of the reference value may be caused by stress during the blood draw and insulin resistance in renal failure. Low sodium, high potassium and low chloride may be caused by renal failure, adrenal insufficiency, etc. A comprehensive analysis should be due to a combination of anuria caused by severe renal failure and hyperkalemia caused by severe acidosis. X-ray and B-ultrasound examination confirmed renal failure.

Diagnosis: Acute onset of chronic renal failure, accompanied by severe metabolic acidosis and hyperkalemia.

Treatment measures: First treat hyperkalemia. Since severe metabolic acidosis also exists, consider infusing 5% sodium bicarbonate solution first. The advantage of using sodium bicarbonate is that it can correct acidosis at the same time.can lower blood potassium concentration. Then give 5% glucose solution and short-acting insulin to continue lowering the serum potassium concentration. The dosage of short-acting insulin is 0.5IU/kg, and the dosage of glucose is 2g glucose/IU insulin, which should be infused within 1 hour. Then replenish the amount of dehydration. After correcting dehydration, recheck the blood gas ion concentration about 8 hours later.