• Open Access

Incidence, Nature, and Etiology of Metabolic Alkalosis in Dogs and Cats

Authors


Corresponding author: K. Hopper, Department of Veterinary Surgical and Radiological Sciences, University of California, Davis, Room 2112 Tupper Hall, Davis CA 95616; e-mail: khopper@ucdavis.edu.

Abstract

Background

The incidence and causes of metabolic alkalosis in dogs and cats have not been fully investigated.

Objectives

To describe the incidence, nature, and etiology of metabolic alkalosis in dogs and cats undergoing blood gas analysis at a veterinary teaching hospital.

Animals

Dogs and cats at a veterinary medical teaching hospital.

Methods

Acid–base and electrolyte results for dogs and cats measured during a 13-month period were retrospectively collected from a computer database. Only the first measured (venous or arterial) blood gas analyzed in a single hospitalization period was included. Animals with a base excess above the reference range for the species were included.

Results

A total of 1,805 dogs and cats were included. Of these, 349 (19%) were identified as having an increased standardized base excess, 319 dogs and 30 cats. The mixed acid–base disorder of metabolic alkalosis with respiratory acidosis was the most common abnormality identified in both dogs and cats. Hypokalemia and hypochloremia were more common in animals with metabolic alkalosis compared to animals without metabolic alkalosis. The 4 most commonly identified underlying diseases were respiratory disease, gastrointestinal tract obstruction, furosemide administration, and renal disease.

Conclusions and Clinical Importance

Metabolic alkalosis was less common than metabolic acidosis in the same population of animals. Evidence of contraction alkalosis was present in many patients in this study. Hypokalemia and hypochloremia were more frequent in patients with metabolic alkalosis and suggest the importance of evaluation of acid–base status in conjunction with serum electrolyte concentrations.

Abbreviations
GI

gastrointestinal

SBE

standardized base excess

Metabolic alkalosis has been reported to be the most common acid–base disorder in several studies of hospitalized human patients.[1-4] Despite this, there has been more research focused on metabolic acidosis compared to metabolic alkalosis. A PubMed® search for metabolic acidosis identified more citations than did a search for metabolic alkalosis. Similarly, there have been relatively few investigations into metabolic alkalosis in dogs and cats.

According to the Henderson–Hasselbalch approach, metabolic alkalosis is characterized by an increase in serum bicarbonate concentration or an increase in base excess. Base excess is calculated by blood gas machines and often is reported as standardized base excess (SBE). An increase in base excess can be attributable to a primary metabolic alkalosis in which pH will be higher than normal or it may reflect a compensatory response to a respiratory acidosis (increased PCO2) in which the pH will be lower than normal. Metabolic alkalosis also can occur simultaneously with a primary respiratory acid–base abnormality creating a mixed disorder. The SBE provides specific evaluation of the metabolic system, being minimally affected by respiratory system abnormalities, and makes it a suitable screening tool for identifying metabolic acid–base disorders.

Clinical studies in humans have identified several common causes for metabolic alkalosis. These include overzealous bicarbonate administration, diuretic treatment, nasogastric suctioning, and high doses of citrate via blood product administration or during therapeutic plasma exchange.[5] The few reports of metabolic alkalosis in small animal patients have been associated with bicarbonate treatment, diuretic treatment, gastrointestinal (GI) tract obstruction, gastric fluid removal, and parathyroid hormone administration.[6-10] Gastrointestinal tract obstruction causes metabolic alkalosis, commonly in conjunction with hypochloremia and hypokalemia. Metabolic alkalosis traditionally has been associated with more proximal anatomic locations of obstruction within the GI tract, although the authors of a report of another retrospective case series did not find an association between acid–base diagnosis and the location of the obstruction.[8]

The clinical relevance of metabolic alkalosis remains unknown. Studies in human medicine from the 1970s and 1980s found a strong correlation between alkalemia and morbidity and mortality in hospitalized patients.[11, 12] A recent study performed in an intensive care unit found the incidence of metabolic acidosis and acidemia was significantly decreased when the use of IV fluids containing high chloride concentration was restricted.[13] Concurrently, there was an increase in the incidence of metabolic alkalosis and alkalemia. Whether this alteration in incidence of metabolic alkalosis translates to a difference in outcome is uncertain, but is under current investigation in humans. As acid–base analysis becomes more common in veterinary medicine, an understanding of the nature of acid–base disorders that occur in small animal patients and their relevance to clinical management, fluid treatment decisions, and outcome is important. The aim of this study was to describe the incidence, nature, and etiology of metabolic alkalosis in small animal patients in a veterinary teaching facility undergoing blood gas analysis for any reason.

Materials and Methods

Acid–base and electrolyte results for dogs and cats measured during a 13-month period (January 1, 2009–January 31, 2010) at the University of California, Davis, William R. Pritchard, Veterinary Medical Teaching Hospital were retrospectively collected from a computer database. Only the first measured (venous or arterial) blood gas analyzed in a single hospital period was included. The incidence of metabolic acidosis in this group of patients has been reported previously.[14]

The normal reference range of venous results used for comparison in this study was previously determined from 10 normal dogs and 8 normal cats (Table 1) using the mean ± 2SD. These animals were considered healthy on the basis of history and physical examination. Packed cell volume and total protein concentration were determined at the time of blood gas analysis and all were in the reference range. Previously published normal values for canine arterial blood gas parameters were used for comparison of arterial samples.[15]

Table 1. Venous acid–base results and electrolyte concentrations of healthy dogs and cats used as a comparison group
VariableDogsCats
  1. SBE, standardized base excess.

Sodium (mmol/L)144–152148–156
Potassium (mmol/L)3.6–4.73.4–4.7
Ionized calcium (mmol/L)1.2–1.51.1–1.4
Chloride (mmol/L)111–121115–126
Venous blood gas results
pH7.32–7.437.34–7.43
PvCO2 (mmHg)37–4534–39
Bicarbonate (mmol/L)18–2620–23
SBE (mmol/L)−4 to −1−5 to 0
Arterial blood gas results[14]
pH7.367–7.423N/A
PaCO2 (mmHg)34–40N/A
Bicarbonate (mmol/L)20–23N/A
SBE (mmol/L)−3 to 0N/A

Inclusion criterion for metabolic alkalosis in dogs was defined as a venous SBE of >−1 mmol/L or an arterial SBE of >0 mmol/L. For cats, it was defined as an SBE of >0 mmol/L. The medical records of all patients enrolled in the study were searched to determine the major underlying disease processes at the time of blood gas analysis. For animals with a GI foreign body obstruction, the most proximal location of the obstruction, as determined at the time of removal, was recorded. Medical records were reviewed and patients on potassium bromide treatment were identified. The chloride results for these patients were removed from statistical analysis.

Measurements

Heparinized blood samples for acid–base analysis and electrolyte concentrations were measured within 5 minutes after sample collection on a point-of-care machine.1 The majority of samples were collected as whole blood and immediately transferred to 125 μL glass heparinized clinitubes, purpose-made for the blood gas machine. Some of the samples were collected in commercial heparinized glass tubes containing 50 units of heparin with a minimum sample volume of 1 mL of blood. The 3rd technique involved manual heparinization of a 1 mL polypropylene syringe with 1,000 unit/mL heparin. After coating the barrel of the syringe with heparin, the excess heparin was forcibly expelled multiple times and the syringe was filled with a minimum of 0.8 mL of whole blood.

Calculated Variables

Bicarbonate and SBE were calculated by the analyzer using the Henderson–Hasselbalch and Van Slyke equations, respectively.[16] The SBE equation used, was recommended by the Clinical Laboratory Standards Institute (C46-A2). The value for CO2 solubility (SCO2) in plasma used by the blood gas machine1 was 0.03 mmol/L/mmHg. The following equation was used for the determination of bicarbonate:

display math

where pK′1 used was derived from the formula: pK′1 = 6.125 − log[1 + 10(pH−8.7)]

Acid–base disorders were classified using the following criteria:

Dogs

  1. Simple metabolic alkalosis
    • Venous: pH > 7.43, SBE > −1.0 mmol/L, with compensatory changes in PvCO2 within the range predicted by the formula: PCO2 = 41 + (0.7 × ΔHCO3) ± 3 mmol/L.
    • Arterial: pH > 7.42, SBE > 0 mmol/L, with compensatory changes in PaCO2 within the range predicted by the formula: PCO2 = 37 + (0.7 × ΔHCO3) ± 3 mmol/L.
    • Note: ΔHCO3 = Mid-normal HCO3 [22 mmol/L] − Measured HCO3.
  2. Simple respiratory acidosis
    • Venous: pH < 7.33, PvCO2 > 45 mmHg, with compensatory changes in HCO3 within the range predicted by the formula: HCO3 = 22 + (0.15 − 0.35 × ΔPCO2) ± 3 mmol/L
    • Arterial: pH < 7.37, PvCO2 > 40 mmHg, with compensatory changes in HCO3 within the range predicted by the formula: HCO3 = 21.5 + (0.15 − 0.35 × ΔPCO2) ± 3 mmol/L
    • Note: ΔPCO2 = Mid-normal PCO2 [41 mmHg] − Measured PCO2.
  3. Mixed disturbances
    • Compensatory calculations listed above were based on previously published guidelines for dogs.[17] A mixed disorder was diagnosed when changes in the secondary system (change in PCO2 for a primary metabolic alkalosis and change in bicarbonate for a primary respiratory acidosis) were not within the range predicted from the calculations provided above.
  4. Concurrent respiratory acidosis was identified when the measured PCO2 was higher than that predicted by the compensation calculation.
  5. Hypochloremia in dogs was defined as a chloride concentration <111 mmol/L. The evaluation of hypochloremia was based on both the measured chloride concentration and the corrected chloride concentration for comparison.
  6. The chloride concentration was corrected for changes in water balance using the following formula: corrected chloride = measured chloride × [normal sodium (mmol/L)/measured sodium (mmol/L)].[18] The mid-normal sodium concentration in this study was 148 mmol/L for dogs.

Cats (all venous values)

  1. Metabolic alkalosis
    • pH > 7.43, SBE > 0
  2. Respiratory acidosis
    • pH < 7.34 and PvCO2 > 39 mmHg
  3. Mixed disturbances
    • Compensation was not calculated for cats, if abnormalities were present in both PvCO2 and SBE they were reported as 2 coexisting abnormalities.
    • (a) Concurrent respiratory acidosis was identified when PCO2 was >39 mmHg.
    • (b) Concurrent respiratory alkalosis was identified when PCO2 was <34 mmHg.
  4. Hypochloremia in cats was defined as chloride concentration <115 mmol/L.
  5. Chloride concentration was corrected for changes in water balance as described for dogs. The mid-normal sodium concentration in this study was 152 mmol/L for cats.

Statistics

Data sets were analyzed and found not to be normally distributed. Spearman correlation coefficients were calculated for SBE, potassium, chloride, corrected chloride, and ionized calcium concentrations.2 In the subset of patients with GI obstruction, the Spearman correlation coefficient was calculated for SBE, potassium, chloride, corrected chloride, and ionized calcium concentrations. The proportion of patients with electrolyte abnormalities was compared between patients with metabolic alkalosis versus all other patients with a Fisher's exact test. A P < .05 was considered significant.

Results

Over the 13-month period of this study, a total of 1,805 dogs and cats were identified in which ≥1 blood gas sample was analyzed. Of these, 349 (19%) were identified as having an increased SBE, including 319 dogs and 30 cats. All the feline samples in this study were venous. Of the 319 canine samples, 260 were venous and 59 were arterial. Hyponatremia occurred more frequently in dogs with metabolic alkalosis, but there was no difference in the occurrence of hyponatremia in cats with metabolic alkalosis compared to the rest of the population (Table 2). Hypokalemia occurred more frequently in dogs (43%) and cats with (67%) metabolic alkalosis. Nine of the canine samples were excluded because of potassium bromide administration. Of the remaining 310 samples, hypochloremia was evident in 27% of dogs and 41% of cats, and the incidence of hypochloremia in animals with metabolic alkalosis was greater than that of the rest of the population. When corrected chloride concentrations were analyzed, 7% of dogs and 87% of cats were classified as hypochloremic. Ionized hypocalcemia occurred more frequently in dogs (30%) with metabolic alkalosis compared to the rest of the population.

Table 2. Electrolyte abnormalities in dogs and cats grouped by the presence or absence of an increased standardized base excess on blood gas analysis
AbnormalityPatients with Metabolic AlkalosisPatients without Metabolic Alkalosis
Dogs (%)Cats (%)Dogs (%)Cats (%)
  1. a

    Significant difference compared to the value for the same species with metabolic alkalosis (P < .05).

Hyponatremia232317a21
Hypokalemia436733a34a
Hypochloremia (measured)27419a17a
Hypochloremia (corrected)7872.5a10a
Hypocalcemia (ionized)30324a21

In dogs, there was a weak correlation of SBE with potassium (r = −0.23; P < .001), poor correlation with chloride (r = −0.12; P = .03), poor correlation with corrected chloride (r = 0.19; P < .001), and a mild correlation with ionized calcium (r = −0.37; P < .001). In cats, SBE showed no correlation with potassium (P = .83), chloride (P = .23), or ionized calcium (P = .66), but a moderate correlation with corrected chloride (r = −0.49; P = .004). In dogs and cats with GI obstruction, SBE showed moderate correlation with potassium (r = −0.53; P = .002), strong correlation with chloride (r = −0.71; P < .001), strong correlation with corrected chloride (r = −0.73; P < .001), and no correlation with ionized calcium (P = .06).

The magnitude of the change in acid–base parameters varied with the nature of the acid–base disorder present as shown in Tables 3, 4, and 5. A simple metabolic alkalosis was present in 15% of the 260 venous canine samples and none of the arterial canine samples. The incidence of a simple metabolic alkalosis in cats was difficult to determine as the role of respiratory compensation in cats is not clear. The mixed acid–base disorder of metabolic alkalosis with concomitant respiratory acidosis was the most common acid–base abnormality identified both dogs and cats. A compensatory response to a respiratory acidosis occurred in 25% of dogs and 17% of cats.

Table 3. Venous acid–base results for dogs with increased standardized base excess on blood gas analysis (median and range)
Dogsn (%)pHPCO2 (mmHg)HCO3 (mmol/L)SBE (mmol/L)
Metabolic alkalosis—all causes2607.389 (7.12–7.697)44.6 (22.6–103)26 (24–50.7)1.3 (−0.9 to 25.2)
Primary metabolic alkalosis38 (15)7.428 (7.415–7.535)40 (37.7–60.7)26 (24.2–50.7)2 (0.2–25.2)
Mixed disorder: metabolic alkalosis & respiratory alkalosis38 (15)7.510 (7.438–7.697)34 (23–39)26 (24–32)3.3 (0.7–10)
Mixed disorder: metabolic alkalosis & respiratory acidosis3 (1)7.373 (7.322–7.469)51 (38–61)28 (26–31)3.3 (0.9–5.2)
Mixed disorder: metabolic alkalosis & respiratory acidosis (pH normal)128 (49)7.376 (7.322–7.419)45.5 (39.5–55)26 (24–34)1.3 (−0.9–9)
Primary respiratory acidosis (metabolic compensation)53 (20)7.304 (7.12–7.437)56 (39.5–103)26 (24.2–31.7)0.3 (−0.9 to 3.9)
Table 4. Arterial acid–base results for dogs with increased standardized base excess on blood gas analysis (median and range)
Dogsn (%)pHPCO2 (mmHg)HCO3 (mmol/L)SBE (mmol/L)
Metabolic alkalosis—all causes597.385 (7.184–7.504)44 (32.6–80.5)26 (24.2–33.5)1.3 (0–8.9)
Mixed disorder: metabolic alkalosis & respiratory alkalosis 17 (29)7.428 (7.385–7.504)39 (32.6–52.1)26 (24.2–33.5)1.9 (0.3–8.9)
Mixed disorder: metabolic alkalosis & respiratory acidosis (normal pH)15 (25)7.4 (7.373–7.444)42 (38.1–49.6)26 (24.4–29.2)1.3 (0–4.6)
Primary respiratory acidosis (metabolic compensation)27 (46)7.33 (7.184–7.37)56 (44.1–80.5)27 (24.9–31.5)0.8 (0–6.6)
Table 5. Venous acid–base results for cats with an increased standardized base excess on blood gas analysis. (median and range)
Catsn (%)pHPCO2 (mmHg)HCO3 (mmol/L)SBE (mmol/L)
  1. Compensation was not determined for cats.

Metabolic alkalosis—all causes307.382 (7.14–7.521)47 (31.8–105)27 (24.2–33.7)2.3 (0–7.9)
Metabolic alkalosis & normal PCO22 (7)7.459 (7.451–7.467)35 (34.8–35.7)24 (24.3–24.6)1.2 (0.9–1.4)
Mixed disorder: metabolic alkalosis & respiratory acidosis (normal pH)22 (73)7.388 (7.334–7.492)46 (39.6–58.9)26 (24.2–31.5)2.2 (0–7.9)
Mixed disorder: metabolic alkalosis & respiratory alkalosis 1 (3)7.52131.825.73
Primary respiratory acidosis5 (17)7.251 (7.14–7.311)68 (57.8–105)29 (26.6–33.7)2.6 (0.8–5.2)

Patients identified with increased SBE in this study had a broad range of diseases. The major underlying disease processes are shown in Table 6. The majority of animals had multiple coexisting diseases. The 4 most commonly identified underlying diseases were respiratory disease (including both pulmonary parenchymal disease and airway disease), GI tract obstruction, furosemide administration, and renal disease (Table 6). All of the diabetic animals included in the study were considered stable, nonketotic patients at the time of blood gas analysis except for 1 cat that was positive for ketones in its urine at the time an increased SBE was detected. Of the 32 patients with GI foreign bodies, the most proximal location of the obstruction was esophageal in 1 dog, gastric in 18 dogs, duodenum in 1 dog, jejunum in 10 dogs, ileum in 1 dog, and colon in 1 dog. The single cat in the study with a GI foreign body had a gastric location for its foreign body.

Table 6. Underlying disease mechanisms identified in 319 dogs and 30 cats with an increased standardized base excess on blood gas analysis. Animals can be represented in more than 1 category
Underlying DiseasesDogs n (%)Cats n (%)
  1. CHF, congestive heart failure.

Respiratory disease (not including CHF)41 (13)8 (27)
Pulmonary parenchymal disease21 (7)3 (10)
Airway disease (upper and lower)20 (6)5 (7)
Gastrointestinal obstruction31 (10)1 (3)
Gastrointestinal disease (not including obstruction)19 (6)1 (3)
Renal15 (5)8 (27)
Diabetes13 (4)3 (10)
CHF and furosemide12 (4)5 (17)
Furosemide10 (3)1 (3)
Renal disease1 (0.3)1 (3)
Lung disease not CHF8 (2.5)0
Other1 (0.3)0
Multiple disorders230 (72)10 (33)

Discussion

An increased SBE occurred in 19% of the small animal patients at a veterinary teaching hospital that had blood gas evaluation in this study. In contrast, metabolic acidosis (defined as decreased SBE) was far more common in the same patient group, occurring in 49% of animals.[14] In a previous retrospective study of 962 dogs that had blood gas evaluation performed, metabolic alkalosis was only identified in 13 animals (1.4%) whereas a report of 220 dogs found metabolic alkalosis in 4% of animals.[7, 19] In contrast, several studies from the human literature report metabolic alkalosis occurred in 32–51% of patients evaluated.[1, 3, 4, 20] The discrepancies in these results may reflect differences in the populations studied. They also may reflect differences in the criteria used to diagnose metabolic alkalosis. The previous veterinary studies used a relatively high pH (>7.5) to identify alkalemia as part of the diagnostic criteria for metabolic alkalosis. This approach prevents identification of many mixed disorders and limits diagnosis to only the more severe primary metabolic alkaloses (or a mixed respiratory and metabolic alkalosis). In this study, only 3.9% of the animals with metabolic alkalosis had a pH > 7.5, which is similar to previous veterinary reports.

Both arterial and venous canine blood samples were analyzed in this study and the incidence of acid–base disorders varied between the 2 sample types. In our institution, arterial blood samples are most commonly collected by our anesthesia service. As anesthetized patients commonly have changes in PCO2 that are not attributable to underlying disease, the interpretation of acid–base disorders in this group of patients may not be applicable to a more general population. There was a far greater proportion of simple respiratory acidosis in the arterial blood gas group, which probably is the result of the respiratory depressant effects of sedative and anesthetic drugs.

A mixed acid–base disorder of metabolic alkalosis with a concurrent respiratory acidosis and a normal pH was the most common disorder found in both dogs and cats. This may suggest that metabolic alkalosis tends to occur in patients with complex disease processes. An alternative possibility is that the formulas used to calculate compensatory responses in normal dogs are not accurate for animals with disease. It also could reflect the population enrolled in this study, it is probable that animals with severe or prolonged disease processes would be more likely to have blood gas analysis performed. This finding highlights the importance of thorough acid–base analysis because a normal pH does not necessarily indicate normal acid–base balance.

A mixed disorder of metabolic alkalosis with respiratory acidosis (in the absence of furosemide administration) was evident in 50% of dogs and 1 cat in this study. Metabolic alkalosis (defined as a bicarbonate concentration higher than that predicted for compensation) also has been reported in human patients with chronic respiratory disease.[21, 22] The most likely initiating cause in these cases is metabolic alkalosis as compensation for hypercapnia. If rapid improvement in PCO2 occurs (as may occur on initiation of treatment) the patient will have a serum bicarbonate value that remains increased for a period of time, because renal excretion of bicarbonate is not immediate. This process can be further delayed if the patient has a decreased effective circulating volume.[19, 23]

Gastric acid loss has been well recognized as a cause of metabolic alkalosis in both human and veterinary patients.[22-24] Gastrointestinal foreign body obstruction was the second most common underlying disease associated with metabolic alkalosis in dogs in this study, and the majority of the dogs in this study had gastric foreign bodies. Given the design of this study, the incidence of metabolic alkalosis in all dogs with GI obstruction cannot be determined. When Boag et al correlated acid–base status with the location of GI foreign bodies in dogs, they found metabolic alkalosis was the most common acid–base disorder evident, regardless of the location of the foreign body.[8] Similarly, only 20/32 (63%) animals with intestinal obstruction and increased SBE in this study had a proximal (duodenal or orad) foreign body. From this information, it would appear that the presence of a metabolic alkalosis in dogs with signs of GI obstruction is suggestive of a proximal obstruction, but it is not specific. Hypochloremia occurred more frequently in animals with metabolic alkalosis in this study and, in the subset of dogs with GI foreign bodies, there was a strong correlation with both chloride and corrected chloride concentrations. The presence of metabolic alkalosis and hypochloremia should prompt the clinician to consider GI foreign body as a potential cause.

Hypochloremia was present in fewer dogs when the corrected chloride concentration was considered compared to the measured chloride concentration. In contrast, hypochloremia was far more common in cats when corrected chloride was considered. Furthermore, the correlation of the corrected chloride concentration with the SBE in cats was improved compared to the correlation of the measured chloride concentration and SBE. This suggests that a free water deficit occurred in the group of cats from this study more frequently than it did in the dogs. With a free water deficit, sodium, chloride, and bicarbonate concentrations are all expected to increase.[25] This may indicate that a contraction alkalosis occurs more commonly in cats than in dogs. In the animals with metabolic acidosis identified from the same population of dogs and cats as this study, free water excess was found to be far more common in dogs than cats.[14] These findings suggest that abnormalities in water balance are relevant to acid–base analysis in small animal patients, and a quantitative acid–base analytical approach could provide valuable insight. Quantitative acid–base analysis would require the measurement of albumin (or at least total protein) and phosphorus, results that were not available in this study.

Furosemide administration was one of the most common etiologies of metabolic alkalosis identified in dogs and cats in this study. Furosemide causes metabolic alkalosis both by decreased effective circulating volume and increased renal acid excretion.[23] It can lead to development of metabolic alkalosis despite other coexisting disease processes. In this study, furosemide treatment was primarily identified in animals with lung disease, both of cardiac and noncardiac origin. When metabolic alkalosis is recognized in small animal patients, furosemide administration should be considered as a potential cause.

When effective circulating volume is adequate, hypokalemia can cause persistent metabolic alkalosis. Hypokalemia promotes renal acid excretion and bicarbonate reabsorption via several mechanisms, including transcellular hydrogen ion shifts and stimulus of the hydrogen-potassium ATPase and hydrogen ion ATPase pumps in the distal nephron.[26-29] Hypokalemia was more common in animals with metabolic alkalosis compared to the rest of the population in this study, suggesting a possible association. Although there was minimal correlation between SBE and potassium concentration, additional studies to establish a true cause and effect relationship are required.

It is very difficult to separate the clinical signs associated with metabolic alkalosis and those attributable to the underlying disease. In general, metabolic alkalosis is considered asymptomatic in human patients although signs such as confusion, stupor, cardiac dysrhythmias, and seizures have been reported in patients with severe metabolic alkalosis.[22, 30] Decreased ionized calcium concentration is a well-recognized consequence of alkalemia and may be responsible for many of the clinical signs reported.[31] In this study, hypocalcemia was present in 30% of dogs with increased SBE, although there was only a mild correlation between SBE and ionized calcium concentration. The lack of a strong correlation is likely to be because ionized calcium concentration is impacted by pH, not SBE. Human studies have associated alkalemia with increased mortality although these findings were not specific for metabolic alkalosis.[11, 12] The clinical relevance of metabolic alkalosis in veterinary patients cannot be determined in this study.

This study has numerous limitations. As a retrospective study, the exact timing between blood gas evaluation and presence of specific disease states can be difficult to determine. In addition, not all potential causes of metabolic alkalosis could be evaluated in the patients included in this study, in particular the role of decreased effective circulating volume was difficult to identify. Metabolic alkalosis can be divided into that associated with volume depletion and that not associated with volume depletion.[28, 32] This classification of metabolic alkalosis was not possible in this study and would be an interesting aspect for a future prospective study. We generated a reference range of venous acid–base values for our blood gas machine for both dogs and cats using a small group of animals and would be strengthened if a larger sample of animals had been included. As we did not have a reference range for arterial samples on our blood gas machine, we used a previously published reference range. As this range was developed on a different machine in a relatively small group of dogs, it provides another source of error for our acid–base diagnosis. As we only evaluated the first blood gas sample measured in a hospital visit, metabolic alkalosis that developed during hospitalization may not have been identified in this study.

Metabolic alkalosis was not uncommon in small animal patients at a veterinary teaching hospital in which blood gas evaluation is performed, although it was far less common than metabolic acidosis in the same population of animals. Hypochloremia and hypokalemia occurred more frequently in the dogs and cats with metabolic alkalosis in this study, compared to the rest of the population suggesting the importance of routine evaluation of these electrolytes in patients with metabolic alkalosis. Evidence of contraction alkalosis was present in many patients in this study. Quantitative acid–base analysis that can assess the contribution of factors such as water imbalance and abnormalities of albumin concentration could provide valuable insight in the assessment of metabolic alkalosis in small animal patients.

Acknowledgments

The study was performed at the University of California Davis, Veterinary Medical Teaching Hospital. This study was not supported by a grant. This study has not been presented at a meeting.

Conflict of Interest Declaration: Authors disclose no conflict of interest.

Footnotes

  1. 1

    ABL 705; Radiometer Medical A/S, Copenhagen, Denmark

  2. 2

    Prism 6.0; Graph Pad Software, La Jolla, CA

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