There are few field tests with proven reliability for Laboratory procedures that may serve adequately on-the-farm analysis. This is not to imply that field for clinical diagnosis may not necessarily be adequate tests are of no value but reflects a lack of information for evidence in a lawsuit. This should be recognized and data concerning their usefulness. The prior to rendering any opinion to the client concer­ diphenylamine test for nitrates will detect high con­ ning a basis for suing for damages or recovery of centration of nitrate (2%) in feed but is not sufficient­ losses. ly sensitive for nitrate concentrations (0.5%) that The future direction of clinical toxicology is depen­ dent on greater specialization of veterinary tox­ may lead to chronic nitrate intoxication. The reagent icologists and subsidized support of university and is made by adding 0.5 gm of diphenylamine to 20 ml governmental analytical laboratories to serve in a water and concentrated sulfuric acid is added q.s. to consultative capacity with the private veterinary 100 ml. This is a stock solution which is mixed with practitioner. It is impossible to speculate on the im­ equal parts of 80% sulfuric acid for use. One drop of pact of chronic intoxication on animal health because the reagent is placed on the cut surface of the plant of our limited ability for diagnosis. Since we institued and a color change from green to blue is indicative of a modest program of lead analysis in our laboratory high nitrate content (approximately 2%). Corn there has been a significant increase in the number of suspected of containing aflatoxin may be examined diagnoses of chronic lead intoxication in both pet with an ultraviolet light. If aflatoxin is present the animals and cattle. It is unlikely, however, that split corn kernel will have an area of blue fluorescence laboratory toxicologic diagnosis will ever become as around the endosperm layer. routine as the complete blood count. Practical Fluid and Electrolyte Therapy and its Pathophysiological Basis 0 "'O (D Daniel A. Gingerich, D. V.M., M .S. ~ ~ Assistant Professor (") (D Food Animal Medicine and Surgery 00 College of Veterinary Medicine 00 0........ 00 The Ohio State University ,-+- Columbus, Ohio 43210 '"i ~ ~...... 0p Introduction All of us who are involved in bovine medicine and however, is rather rare in most species but very com­ therapeutics are aware of the need for fluid therapy in mon in cattle. This is not to imply that acidosis and many disease conditions. Intimately associated with alkalosis per se are diseases of cattle which need to be dehydration, toxemia, gastro-intestinal disorders, treated. Rather, acid-base and electrolyte disorders and the need for fluid therapy are derangements of are manifestations of disease which must be taken electrolytes and acid-base balance. into account in designing a regimen of supportive Let me first acknowledge that a whole battery of therapy. laboratory tests is impractical and probably impossi­ Many excellent articles have been written on the ble in practice. The objective of this presentation is to subject of practical fluid therapy. Included in many discuss the pathophysiology of acid-base and elec­ of these papers are various formulations of fluids and trolyte disorders as they occur in bovine disease. With electrolytes for use in supportive therapy. Along such a basic understanding of pathophysiology, fluid lines I really have nothing new to add. After all, the therapy can be approached in a rational manner even standard toward which each of these formulas strives without the benefit of laboratory tests. If those of us is a standard upon which none of us can improve: who can use laboratory determinations in cattle that is plasma itself. succeed in communicating our findings to those who Instead, I would like to suggest that, as a starting don't, we will have come one stop closer toward mak­ point, two different kinds of corrective fluids are re­ ing the contribution to veterinary medicine that I feel quired: one for supportive therapy in cases of acidosis we owe. and the other for supportive therapy in alkalosis. In The bovine species is somewhat unique in that both acidosis, Eltraad L.A.,* or a formula of similar com- acidosis and alkalosis are common. Acidosis is a com­ mon c~ndition in disease in all species. Alkalosis, *Hauer-Lockhart, Shawnee, Kansas 72 position, should be used for intravenous therapy. In Table 1 the alkalotic patient, Ringer's solution or a formula of Acid-Base Disorders similar composition should be used. Oral fluids, Physio logical designed for supportive therapy of the acidotic Disturbance Meaning Examples Treatment patient and the alkalotic patient can also be used. Fluid therapy in calf scours cases is somewhat more Metabolic Gain of acid Grain overload Eltraad L.A. Acidosis (not H2co 3) Ketoacid osis Acid osis fo rmula involved. A bicarbonate-containing solution is re­ T issue anoxia "5 :4: l" solutio n quired for intravenous therapy. Oral therapy in calf Tissue catabo- scours cases may also be effective if an electrolyte li sm Asia tic fo rmula solution which contains glucose is used. Loss o f base Diarrhea Loss of sa li va Acid-Base Physiology Metabolic Gain of b ase Iatrogenic Ringe r[ s sol'n Acid-Base Balance Alkalosis Isoto ni c sa line The precise regulation of the pH or hydrogen ion Loss of acid Abomasal dis- A lkalosis formula concentration of the body fluids is one of the most (not H2co3 placement crucial physiological functions of the body. The preci­ Intestinal o b- structi o n sion of the acid-base regulatory mechanisms of the G I stasis body is well illustrated by looking at normal values (13). pH to 7.45 the absorption of acid from the rumen. Perhaps the [H+] 44. 7 X 10-6 mEq/L to 35.5 X 10-6 mEq /L best disease example of this is in grain overload lactic acidosis in which lactic acid is absorbed in large The body has various acid-base regulatory quantities from the rumen (4). mechanisms to defend against changes in body fluid Secondly, the incomplete oxidation of fat in the pH. The precise description of these delicately bovine species causes excess production of acetate, /3- balanced mechanisms is not our purpose in this dis­ hydroxy butyrate, and acetoacetate. The accumula­ cussion. We can summarize, however, by simply tion of these ketoacids results in acetonemia with stating that the pH of the body fluids is proportional which all of us are familiar. I have not had occasion to to the concentration of bicarbonate and the partial measure severe acidosis due primarily to ketosis, but 0 pressure of CO2. [HCO- ) ---- " metabolic" "'O 3 ketoacids most assuredly contribute to acidosis in (D pH oC many cases. ~ PC0 2 -- "respiratory" ~ A third cause of acid gain in disease is the in­ (") We can further simplify by saying that primary (D complete oxidation of carbohydrates. This occurs 00 alterations of the bicarbonate component of the ex­ commonly during dehydration from any cause, due to 00 0........ pression may be termed metabolic, and that primary 00 diminished tissue perfusion and oxygenation. The ,-+- alterations of the PCO2 component of the expression products of anaerobic metabolism are organic acids '"i may be termed respiratory. ~ such as lactate which may accumulate and lead to ~...... For purposes of this discussion we shall deal only acidosis. 0 with metabolic disturbances of acid-base balance. Still another reason for acid gain is the accumula­ p From the expression, we can see that any decrease in tion of tissue breakdown products such as phosphates the bicarbonate concentration would tend to cause a and sulfates. Dehydration and starvation can lead to decrease in pH, hence metabolic acidosis. Converse­ increased tissue catabolism. When renal function is ly, any increase in the bicarbonate concentration impaired at the same time, these inorganic acids may would tend to cause an increase in pH, hence accumulate in the body fluids. metabolic alkalosis. Finally, diminished kidney function can contribute Metabolic acidosis is defined as a decrease in blood to acidosis due to all of the above factors. The normal pH due to a relative decrease in the blood bicarbonate kidney is capable of excreting a large acid load. concentration. Metabolic alkalosis is an increase in Dehydration and hypovolemia imply decreased renal blood pH due to a relative increase in bicarbonate blood flow and impaired renal function. Thus, we see concentration. that dehydration, which is often the primary reason Metabolic Acidosis for initiating fluid therapy in the first place not only Metabolic acidosis is a serious acid-base distur­ causes increased organic and inorganic acid produc­ bance which is encountered commonly in bovine dis­ tion in the body, but also causes diminished ability of ease. There are many causes of acidosis in disease. the kidney to excrete the acid load. Physiologically speaking, however, there are only two Loss of Base: Metabolic acidosis due to the loss of ways that metabolic acidosis can occur: either due to base from the body frequently occurs in bovine dis­ a gain of acid by the body or due to a loss of base ease. The most obvious example of acidosis due to the (Table 1). loss of base is in diarrhea, in which large quantities of Gain of Acid: There are a number of ways that a bicarbonate are lost in the feces. The pathophysiology gain of acid can occur in bovine diseases and lead to of neonatal diarrhea has been well described before serious metabolic acidosis. First and most obvious is this convention and in numerous excellent veterinary 73 articles. I would like to point out that severe diarrhea amples of alkalosis in disease due to a gain of base.