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Metabolic alkalemia is characterized by an increase in bicarbonate concentration and base excess, an increase in pH, and a compensatory increase in carbon dioxide pressure. This article outlines indications for analysis, reference ranges, causes, and clinical signs of metabolic alkalosis. Algorithms for evaluation of patients with acid-base disorders and metabolic alkalosis are included.

Hydrogen concentration is a critical determinant of many physiologic functions and is tightly regulated. Any alteration in acid-base equilibrium sets into motion a compensatory response by either the lungs or the kidneys. The compensatory response attempts to return the ratio between Pco2 and [HCO3-] to normal and thereby minimize the pH change. A primary increase or decrease in one component is associated with a predictable compensatory change in the same direction in the other component, and the expected compensation can be estimated clinically in dogs and cats.

Metabolic acidosis results from an increase in the concentration of a strong anion. Metabolic acidosis is divided into hyperchloremic metabolic acidosis and high anion gap acidosis based on the changes in the anion gap. Hyperchloremic metabolic acidosis is the result of chloride retention, excessive loss of sodium relative to chloride, or excessive gain of chloride relative to sodium. Clinical signs are related to the underlying disease that accompanies the metabolic acidosis. Treatment of hyperchloremic acidosis is based on addressing the underlying disease process.

High anion gap (AG) metabolic acidoses can be identified by a decrease in pH, decrease in HCO3- or base excess, and an increased AG. The AG represents the difference between unmeasured cations and unmeasured anions; it increases secondary to the accumulation of anions other than bicarbonate and chloride. The most common causes of high AG acidosis are renal failure, diabetic ketoacidosis, and lactic acidosis. Severe increases in concentration of phosphorus can cause hyperphosphatemic acidosis.

This article serves as a quick reference for hyponatremia. Guidelines for analysis and causes, signs, and a stepwise approach are presented.

This article serves as a quick reference for metabolic alkalosis. Guidelines for analysis and causes, signs, and a stepwise approach are presented.

This article serves as a quick reference for hypernatremia. Guidelines for analysis and causes, signs, and a stepwise approach are presented.

The recognition and management of acid-base disorders is a commonplace activity in the critical care unit, and the role of weak and strong acids in the genesis of metabolic acid-base disorders is reviewed. The clinical approach to patients with metabolic alkalosis and metabolic acidosis is discussed in this article.

Hemotrophic mycoplasmas infect a variety of mammals. Although infection in humans is rarely reported, an association with an immunocompromised state has been suggested. We report a case of a Mycoplasma haemofelis–like infection in an HIV-positive patient co-infected with Bartonella henselae.

This article serves as a quick reference for the analysis of chloride abnormalities. Guidelines for causes, signs, and stepwise approaches for corrected hypochloremia and hyperchloremia are presented.

This article serves as a quick reference for metabolic acidosis. Guidelines for analysis and causes, signs, and a stepwise approach are presented.

Canine ehrlichiosis and babesiosis have a worldwide distribution with geographic variation in prevalence and main clinical manifestations. We prospectively determined seroprevalence of canine babesiosis and ehrlichiosis, and risk factors for seropositivity. Three hundred and eighty-one dogs were randomly selected to represent the canine population at a Veterinary Teaching Hospital in south Brazil (latitude 23 degrees S). Dogs were tested with a point-of-care ELISA for Ehrlichia canis antibodies and IFA to confirm previous exposure to Babesia vogeli. Multiple logistic regression analysis was then used to estimate adjusted odds ratio (OR) and their 95% confidence intervals. One hundred and thirty-six (36%) dogs were seropositive for B. vogeli antibodies, whereas 87 (23%) dogs were seropositive to E. canis antibodies. Fifty-four (14%) dogs seroreacted to both agents. Adult dogs previously infested with ticks were more likely to seroreact to B. vogeli or E. canis. Superficial bleeding (OR = 12.4) was more common in dogs exposed to B. vogeli, whereas neurological signs (OR = 7.7) were more common in dogs seropositive to E. canis. Neurological signs (OR = 12.0) and lameness (OR = 12.8) were more prevalent in dogs that seroreacted to both organisms. Owners of dogs with ticks were more likely to have been exposed to ticks themselves (OR = 3.2). Canine babesiosis and ehrlichiosis appear to be highly prevalent in this hospital population. Clinical signs differed from the most common signs in other regions with bleeding occurring more in dogs seropositive to babesiosis, but not ehrlichiosis; neurologic signs in dogs with E. canis antibodies; and lameness in dogs that seroreacted to both organisms.