Acid-Base Disturbances in Gastrointestinal Disease

Gennari, F. John; Weise, W

doi:10.2215/cjn.02450508

Cited by 141 publications

(103 citation statements)

References 42 publications

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“…Anion gap values obtained for the control group were consistent with AG values in the literature (9,10,16,19). The calves with diarrhea presented significantly higher anion gaps than the controls.…”

Section: Discussionsupporting

confidence: 89%

“…The etiology of hypochloremia observed in our calves might be heterogeneous, i.e. resulting from many alimentary disorders, abomasal atony, vomiting, or lack of chloride reabsorption in the distal segment of the alimentary tract (19). The decrease in Cl -concentration may also represent a compensatory mechanism for prolonged acidosis associated with high concentrations of organic anions, like elevated levels of lactate (20,21).…”

Section: Discussionmentioning

confidence: 93%

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Analysis of acid–base disorders in calves with lactic acidosis using aclassic model and strong ion approach

Bednarski

Kupczyński²

2015

Turk J Vet Anim Sci

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IntroductionNeonatal calf diarrhea is a common disorder affecting calves and is an important cause of economic losses. The diarrhea of neonatal calves is usually associated with bacterial (enterotoxigenic strains of E. coli), rotaviral, and coronaviral infections and/or feeding factors (1,2). Clinical signs of diarrhea include loose watery stools, lack of appetite, and abdominal pain. This condition may result in dehydration, acid-base disorders, and electrolyte imbalances like metabolic acidosis, hyperkalemia, prolonged malnutrition, hypoglycemia, and hypothermia (3,4). The clinical status of an animal may further deteriorate due to lactic acidosis, which has been reported in diarrheic calves (5,6). Lactic acidosis is the result of elevated concentrations of L-lactate or/and D-lactate in the blood serum. L-lactate is produced by anaerobic metabolism due to tissue hypoperfusion or low oxygen supply to the tissue, while D-lactate is a byproduct of bacterial metabolism (5-7). Although levels of L-lactate or/and D-lactate can be elevated, only the nonstereospecific assay is routinely used in clinical practice.The interpretation of an acid-base balance is traditionally based on changes in pH, bicarbonate concentration (HCO 3 -), base excess (BE), and anion gap (AG) in plasma. This model characterizes four primary acid-base disturbances (i.e. respiratory acidosis and alkalosis, metabolic acidosis, and alkalosis) (8). The Stewart model (strong ion model) represents an alternative method of evaluation of acid-base status. This model is based on three independent variables to determine the acid-base balance: the strong ion difference (SID)-the difference between all completely dissociated cations and anions; the plasma partial pressure CO 2 (pCO 2 ), and the total nonvolatile weak acid concentration, mainly inorganic phosphate and albumin. The Stewart approach describes six primary acid-base disturbances (i.e. respiratory acidosis and alkalosis, strong ion acidosis and alkalosis, and nonvolatile buffer ion acidosis and alkalosis). Although the Stewart approach may give a better understanding of the mechanisms that underlie an acid-base disorder, the traditional methods are more convenient in daily practice (4,(8)(9)(10). Previous studies evaluated the use of two models for description of acid-base disturbances in cases of acute diarrhea, after intravenous fluid therapy or oral rehydration therapy (3,4,11,12).

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 93%

Analysis of acid–base disorders in calves with lactic acidosis using aclassic model and strong ion approach

Bednarski

Kupczyński²

2015

Turk J Vet Anim Sci

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“…The etiology of the hypochloremia observed in our calves might be heterogeneous. It might result from alimentary disorders, abomasal atony, vomiting or lack of chloride reabsorption in distal segment of the alimentary tract (Gennari and Weise 2008). The presence of enteropathogens in stool samples from some animals from the group III may point to infection-related impairment of chloride absorption from the gut.…”

Section: Discussionmentioning

confidence: 99%

Acid-base disorders in calves with chronic diarrhea

Bednarski¹,

Kupczyński²,

Sobiech³

2015

Polish Journal of Veterinary Sciences

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The aim of this study was to analyze disorders of acid-base balance in calves with chronic diarrhea caused by mixed, viral, bacterial and Cryptosporydium parvum infection. We compared results obtained with the classic model (Henderson-Hasselbalch) and strong ion approach (the Steward model). The study included 36 calves aged between 14 and 21 days. The calves were allocated to three groups: I -(control) non-diarrheic calves, group II -animals with compensated acid-base imbalance and group III calves with compensated acid-base disorders and hypoalbuminemia. Plasma concentrations of Na, P, albumin and lactate were measured. In the classic model, acid-base balance was determined on the basis of blood pH, pCO 2 , HCO 3 -, BE and anion gap. In the strong ion model, strong ion difference (SID), effective strong anion difference, total plasma concentration of nonvolatile buffers (A Tot ) and strong ion gap (SIG) were measured.The control calves and the animals from groups II and III did not differ significantly in terms of their blood pH. The plasma concentration of HCO 3 -, BE and partial pressure of CO2 in animals from the two groups with chronic diarrhea were significantly higher than those found in the controls. The highest BE (6.03 mmol/l) was documented in calves from group II. The animals from this group presented compensation resulted from activation of metabolic mechanisms. The calves with hypoalbuminemia (group III) showed lower plasma concentrations of albumin (15.37 g/L), Cl -(74.94 mmol/L), Mg 2+ (0.53 mmol/L), P (1.41 mmol/L) and higher value of anion gap (39.03 mmol/L). This group III presented significantly higher SID 3 (71.89 mmol/L), SID 7 (72.92 mmol/L) and SIG (43.53 mmol/L) values than animals from the remaining groups (P<0.01), whereas A Tot (6.82 mmol/L) were significantly lower. The main finding of the correlation study was the excellent relationship between the AG corr and SID 3 , SID 7 , SIG. In conclusion, chronic diarrhea leads to numerous water-electrolyte disorders. Characterization of acid-base disturbance in these cases suggests that classic model have some limitations. This model can not be recommended for use whenever serum albumin or phosphate concentrations are markedly abnormal.

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“…HCO 3 2 loss from the body via the gastrointestinal tract, as with diarrhea, can cause a nongap acidosis. Both the anion composition and the quantity of the diarrheal fluid are determinants of whether metabolic acidosis ensues (18). Thus, metabolic acidosis is more common with secretory than inflammatory diarrhea, in part because of the higher concentration of HCO 3 2 in the diarrheal fluid of the former type (18).…”

Section: Systematic Approach To Differential Diagnosis Historical Infmentioning

confidence: 99%

Differential Diagnosis of Nongap Metabolic Acidosis

Kraut

Madias

2012

Clinical Journal of the American Society of Nephrology

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SummaryNongap metabolic acidosis is a common form of both acute and chronic metabolic acidosis. Because derangements in renal acid-base regulation are a common cause of nongap metabolic acidosis, studies to evaluate renal acidification often serve as the mainstay of differential diagnosis. However, in many cases, information obtained from the history and physical examination, evaluation of the electrolyte pattern (to determine if a nongap acidosis alone or a combined nongap and high anion gap metabolic acidosis is present), and examination of the serum potassium concentration (to characterize the disorder as hyperkalemic or hypokalemic in nature) is sufficient to make a presumptive diagnosis without more sophisticated studies. If this information proves insufficient, indirect estimates or direct measurement of urinary NH 4 + concentration, measurement of urine pH, and assessment of urinary HCO 3 2 excretion can help in establishing the diagnosis. This review summarizes current information concerning the pathophysiology of this electrolyte pattern and the value and limitations of all of the diagnostic studies available. It also provides a systematic and cost-effective approach to the differential diagnosis of nongap metabolic acidosis.

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Acid-Base Disturbances in Gastrointestinal Disease

Cited by 141 publications

References 42 publications

Analysis of acid–base disorders in calves with lactic acidosis using aclassic model and strong ion approach

Analysis of acid–base disorders in calves with lactic acidosis using aclassic model and strong ion approach

Acid-base disorders in calves with chronic diarrhea

Differential Diagnosis of Nongap Metabolic Acidosis

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