Metabolic acidosis, defined as a venous pH < 7.35 is relatively common in dogs.
The opposite condition is metabolic alkalosis.
Metabolic acidosis is characterized by a decrease in plasma bicarbonate concentration < 18 mEq/L. It occurs as a result of loss of NaHCO3-rich fluids from the intestine or kidneys, increased acid production due to metabolism or reduced excretion of acids (anions).
- Diabetic ketoacidosis secondary to diabetes mellitus
- Hemorrhagic shock - global tissue hypoxia leading to anion production, endotoxemia
- Chronic renal disease, Fanconi syndrome
- Diarrhea - e.g. canine parvovirus, ulcerative colitis, pancreatic exocrine insufficiency
- Pancreatitis - usually associated with poor outcomes
- Drug toxicity - ethylene glycol, aspirin, aldicarb
- Brachycephalic syndrome - secondary to respiratory acidosis due to respiratory hypoventilation
- Peritoneal dialysis
- Acute tumor lysis syndrome
Clinical signs often relate to underlying disease but depression and compensatory tachypnea may be observed.
Treatment usually requires addressing underlying disease conditions and aggressive intravenous fluid therapy, usually with lactated Ringer's solution. Only in patients with pH < 7.2, should NaHCO3 be added to the solution.
In patients with respiratory acidosis secondary to hypoventilation, NaHCO3 therapy should be avoided because it inevitably decreases respiratory drive, thereby worsening acidosis and hypoxemia
As well, dogs with normochloremic metabolic acidosis caused by ketoacidosis are also less likely to benefit from NaHCO3 therapy. In these patients, as organic acids are metabolized they form bicarbonate anions resulting in rebound alkalosis if NaHCO3 has been administered concurrently.
- Veterinary Webinars
- Hopper K & Epstein SE (2012) Incidence, nature, and etiology of metabolic acidosis in dogs and cats. J Vet Intern Med 26(5):1107-1114
- O'Neill S et al (2012) Evaluation of cytokines and hormones in dogs before and after treatment of diabetic ketoacidosis and in uncomplicated diabetes mellitus. Vet Immunol Immunopathol 148(3-4):276-283
- Bruegger D et al (2007) Causes of metabolic acidosis in canine hemorrhagic shock: role of unmeasured ions. Crit Care 11(6):R130
- Kaplan LJ & Kellum JA (2004) Initial pH, base deficit, lactate, anion gap, strong ion difference, and strong ion gap predict outcome from major vascular injury. Crit Care Med 32:1120–1124
- Kellum JA et al (1995) Hepatic anion flux during acute endotoxemia. J Appl Physiol 78:2212–2217
- Hostutler RA et al (2004) Transient proximal renal tubular acidosis and Fanconi syndrome in a dog. J Am Vet Med Assoc 224(10):1611-1614
- Pápa K et al (2011) Occurrence, clinical features and outcome of canine pancreatitis (80 cases). Acta Vet Hung 59(1):37-52
- Anastasio JD & Sharp CR (2011) Acute aldicarb toxicity in dogs: 15 cases (2001-2009). J Vet Emerg Crit Care (San Antonio) 21(3):253-260
- Sławuta P et al (2011) Influence of the wing-of-the-nostrils correction procedure on the change of the acid-base balance parameters and oxygen concentration in the arterial blood in French bulldogs. Pol J Vet Sci 14(1):77-80
- de Morais HA et al (2008) Metabolic acid-base disorders in the critical care unit. Vet Clin North Am Small Anim Pract 38(3):559-574
- Bailey JE & Pablo LS (1998) Practical approach to acid-base disorders. Vet Clin North Am Small Anim Pract 28(3):645-662
- DiBartola SP (2000) Metabolic acid-base disorders, in DiBartola SP (ed): Fluid Therapy in Small Animal Practice, ed 2. Philadelphia, WB Saunders. pp:211-240