Acidosis. Clinical Aspects and Treatment with Isotonic Sodium Bicarbonate Solution

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It is likely that the stress involved with admission in the hospital also played a significant role here. In general, it has to be assumed that the first branch of the decision tree plays a minor role in practice since a practitioner is unlikely to be called to treat a diarrheic calf that is clinically unaffected. Overdosed calves were significantly younger and had significantly lower D-lactate concentrations than successfully treated patients. Naylor [ 33 ] has shown that diarrheic calves during their first week of life are less acidemic than older calves with similar clinical signs.

This finding was included in several protocols for determining bicarbonate requirements for diarrheic calves under field conditions [ 11 , 12 , 13 ]. Nevertheless, patients that suffered from diarrhea within their first week of life had significantly higher base excess values and significantly lower D-lactate concentrations than older calves [ 17 ]. Even though patients with incurable diseases were disregarded, calves with further health problems were not explicitly excluded in our study. Thus it cannot be completely ruled out that clinical signs in some calves were more pronounced due to concurrent problems e.

Therefore, some calves may have received higher amounts of sodium bicarbonate than necessary. The treatment protocol used in this study is based on 5 liter bags of isotonic saline and 8. It has been shown previously that slightly hypertonic sodium bicarbonate solutions can be used safely to achieve a faster correction of acidosis than with isotonic solutions [ 25 , 34 ]. We used 4. The reason for the latter was to insure that correction of acidosis is achieved even in situations under field conditions where the entire determined infusion volume is not administered because of technical problems.

It is obvious that the undiluted use of the commercially available 8. However, a recent review paper discussed the risks of the direct use of 8. To our knowledge the use of 8. Koch and Kaske [ 35 ] compared the clinical efficacy of hypertonic saline and sodium bicarbonate solutions combined with the administration of an oral electrolyte solution. They reported good results and no major adverse reactions in 12 calves receiving an 8. Coskun et al. The use of 8. However, the accumulation of more clinical data would be desirable before a recommendation on the safe and successful use can be given.

For means of rehydration we used a volume of 5 liters of isotonic saline per calf, irrespective of the degree of dehydration to test the hypothesis that taking into account the oral fluid intake, all calves would be successfully rehydrated using this volume. However, our results indicate that the provided infusion volumes of 5.

Even though the oral route for further fluid therapy would be preferable, this may not always be possible, especially in weak calves with a low milk intake and high intestinal losses of fluids and buffer substances. A clinical study on the dynamics of D-lactate concentration during the course of therapy has also shown that calves with a marked D-lactic acidosis may need a repeated treatment with buffer substances for correction of acidosis and D-lactatemia and the associated clinical signs [ 25 ]. In 13 calves of the present study, metabolic acidosis was not corrected in a satisfactory manner.

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Nine of these calves showed the same clinical picture on initial examination. Several reasons were found in the remaining four isolated cases, which may explain undercorrection of metabolic acidosis. One calf that received ORS as sole treatment suffered from profound diarrhea watery consistency of feces and had a low intake of milk and ORS. In two other calves, development of ruminal acidosis due to ruminal drinking was recognized during the study period.

Ruminal drinking is a frequently observed complication of neonatal diarrhea [ 37 ] and bacterial fermentation of substrates in the rumen and subsequent absorption of D-lactate can contribute to systemic metabolic acidosis in this situation [ 38 ]. A previous clinical study reported that the risk of failure to correct acidosis increases with D-lactate concentrations [ 25 ]. Adequate assessment and categorization of clinical parameters, especially attempts to lift the calves to their feet, may have contributed to the latter point.

In addition, it may explain the lack of a significant difference in the base excess values between treatment groups III and IV, on the one hand, and the treatment group V, on the other hand. In the light of the finding that moderate alkalosis does not seem to have any detrimental effect it can be speculated that less accurate clinical examinations, without lifting of the calf when it was unable or unwilling to stand up, might have resulted in a smaller number of underdosed calves. However, since a clinical impact of higher degrees of alkalosis cannot be excluded on the basis of this study, and higher amounts of bicarbonate provided will also increase the costs of treatment it is still reasonable to avoid severe overdosing, as it would have occurred without the attempt to lift the calves e.

Even though an attempt to lift the calf to its feet may not always be feasible in ambulatory practice, it allows the veterinarian to perform a more detailed clinical examination and consequently more accurate estimation of the degree of acidosis, especially in calves where an inability to stand is expected.

Recommended version of the decision tree for treating metabolic acidosis in calves with neonatal diarrhea in bovine field practice. The term enophthalmos is defined as a visible gap between the eyeball and caruncula lacrimalis, which corresponds to a measured eyeball recession of at least 3—4 millimeters. Theoretical outcome of therapy of metabolic acidosis in diarrheic calves based on previously published recommendations for the dosage of sodium bicarbonate [ 12 ].

Retrospective studies usually lack standardization of clinical examination techniques and recording of clinical signs, which is not the case in this prospective study. This study evaluated the success and feasibility of a protocol for the treatment of diarrheic calves with emphasis on the required minimal amounts of sodium bicarbonate for sufficient correction of metabolic acidosis. However, calves that stand insecurely and are not able to correct their position if pushed require higher doses of sodium bicarbonate than previously suggested, if there is clinical evidence of a marked D-lactic acidosis.

Determining the degree of loss of the palpebral reflex, which had been reported to be a reliable clinical tool for diagnosing elevations of D-lactate concentrations [ 7 , 8 ], was identified as a useful decision criterion to provide an additional amount of sodium bicarbonate in those calves. This work shows the clinical relevance of the discovery that D-lactate is responsible for most of the clinical signs exhibited by neonatal diarrheic calves suffering from metabolic acidosis.

We gratefully thank Wolfgang Klee and Gabriela Knubben-Schweizer for critically revising the manuscript. This article is published under license to BioMed Central Ltd.

Skip to main content Skip to sections. Advertisement Hide. Download PDF. Construction and validation of a decision tree for treating metabolic acidosis in calves with neonatal diarrhea. Open Access. First Online: 06 December Part of the following topical collections: Neurology and neuroscience. Background The aim of the present prospective study was to investigate whether a decision tree based on basic clinical signs could be used to determine the treatment of metabolic acidosis in calves successfully without expensive laboratory equipment.

Background Metabolic acidosis is a frequently observed complication of neonatal diarrhea in calves. Animals For the purpose of this prospective study, calves with a diagnosis of neonatal diarrhea admitted for treatment to the Clinic for Ruminants, LMU Munich, between September, , and April, , were examined. Blood samples were collected from the jugular vein for laboratory analysis at given times.

Attempts to lift the calves to their feet were carried out by two persons. The hydration status of each calf was assessed by estimating the degree of enophthalmos and the duration of skin tenting on the upper eyelid. Blood biochemistry analysis included determination of D-lactate, L-lactate and glucose from heparinized blood samples containing sodium fluoride as glycostatic agent and determination of total protein, urea, creatinine and activity of y-glutamyltransferase from serum samples Automatic Analyzer Hitachi , Roche Diagnostics, Indianapolis, USA.

Determination of D-lactate was carried out by using D-lactate dehydrogenase as described by Lorenz et al. Calves that were neither dehydrated nor assumed to be acidemic received an oral rehydration solution ORS as sole therapy. In order to prevent any deterioration of the general condition in such calves, the intake of ORS was tested immediately after the initial examination.

Short-term infusions by rapidly infusing 1 or 1. If impairment of ability to stand was evident in such calves, part of the total amount of sodium bicarbonate was rapidly infused beforehand in 1 liter of a 2. Open image in new window. Figure 1 Assessed decision tree on the basis of recommendations for the dosage of sodium bicarbonate by Lorenz and Lorch [ 9 ]. Considering recommendations for the use of antimicrobials [ 21 , 22 ] as well as potentially useful clinical predictors of septicemia in diarrheic calves [ 23 , 24 ], the following criteria were defined for initiation of antimicrobial therapy: presence of a local infection e.

Improvement of clinical and laboratory parameters was evaluated.

Management of Diabetic Ketoacidosis

A computer-assisted model was created in order to determine, and especially improve, the theoretical success of the assessed treatment regime. This approach was additionally used to analyze and compare the theoretical outcome of another previously published protocol [ 12 ]. Antimicrobial therapy was deemed necessary in 66 calves Dextrose was added to infusion fluids in 20 cases.

Due to severe ruminal acidosis milk and ORS were withheld in two of these calves. Five calves of treatment group IV had to be treated alternatively for reasons of expected treatment failure. All calves had to be helped to rise and were not able to correct position if pushed. They had an impaired palpebral reflex delayed or absent and responded only to painful stimuli e. Figure 2 Marked D-lactic acidosis in a diarrheic calf with expected treatment failure. No significant difference in base excess values on admission could be detected between calves of groups III and IV on the one hand and calves of group V on the other hand.

D-lactate concentrations were most massively increased in calves of group III impairment of ability to stand, no enophthalmos. Figure 3 Base excess values and D-lactate concentrations of calves at times of examination. Table 4 Blood concentrations of selected laboratory parameters in different treatment groups on admission and at the end of the study period. These calves were identified as the five expected treatment failures mentioned above. As mentioned above, five calves had to be treated alternatively for reasons of expected treatment failure.

Thus metabolic acidosis could not be treated adequately in 13 calves Figure 4 Theoretical outcome of therapy of metabolic acidosis in diarrheic calves using a computer-assisted analysis. As indicated by the presence of persistent enophthalmos visible gap between the eyeball and caruncula lacrimalis dehydration was not corrected in 17 calves.

Table 5 Number of still dehydrated calves at the end of the study period depending on the severity of enophthalmos mm on admission. However, 24 of these overdosed calves had already positive base excess values on admission. This was attributed to pretreatment in 11 patients, which had initial base excess values ranging from 1. Calves with metabolic alkalosis were younger and exhibited significantly higher base excess values, higher L-lactate and lower D-lactate concentrations before treatment. Body masses of calves did not differ significantly between groups.

Table 6 Age, body mass and selected laboratory parameters in relation to the outcome of therapy. Table 7 Clinical parameters and the suckling behavior at the end of the study period in relation to the outcome of therapy. Nine of the 13 underdosed calves fell into that category on admission including the five calves with expected treatment failure. The rightsholder did not grant rights to reproduce this item in electronic media. For the missing item, see the original print version of this publication. The commonly used diagnostic criteria for diabetic ketoacidosis and average deficits of water and electrolytes are given in Table 1.

Diabetic ketoacidosis. Ellenberg and Rifkin's Diabetes mellitus. Stamford, Conn. Major components of the pathogenesis of diabetic ketoacidosis are reductions in effective concentrations of circulating insulin and concomitant elevations of counterregulatory hormones catecholamines, glucagon, growth hormone and cortisol. Hyperglycemia initially causes the movement of water out of cells, with subsequent intracellular dehydration, extra-cellular fluid expansion and hyponatremia.

It also leads to a diuresis in which water losses exceed sodium chloride losses. Urinary losses then lead to progressive dehydration and volume depletion, which causes diminished urine flow and greater retention of glucose in plasma. The net result of all these alterations is hyperglycemia with metabolic acidosis and an increased plasma anion gap.

Acidosis - 1st Edition

The history and physical examination continue to be important aspects of management. Even in comatose patients, information documenting a history of diabetes or insulin therapy may be available. The physical examination can provide supportive evidence for the diagnosis of diabetic ketoacidosis and can point to precipitating factors Table 2. Hyperglycemic crises in urban blacks. Although usually straightforward, the diagnosis of diabetic ketoacidosis is occasionally missed in unusual situations, such as when it is the initial presentation of diabetes in infants or elderly patients or when patients present with sepsis or infarction of the brain, bowel or myocardium.

These presentations can distract the physician from the underlying diagnosis of diabetic ketoacidosis. The laboratory tests needed to confirm the presence of diabetic ketoacidosis and to screen for precipitating events are summarized in Table 1 4 and Figure 2. The essential data can be obtained promptly in the emergency department.


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Protocol for the management of patients with diabetic ketoacidosis. The therapeutic goals for diabetic ketoacidosis consist of improving circulatory volume and tissue perfusion, reducing blood glucose and serum osmolality toward normal levels, clearing ketones from serum and urine at a steady rate, correcting electrolyte imbalances and identifying precipitating factors. A suggested flow sheet for monitoring therapeutic response is provided in Figure 3.

A suggested flow sheet for monitoring response to therapy for diabetic ketoacidosis. Diabetic ketoacidosis and the hyperglycemic hyperosmolar nonketotic state. Joslin's Diabetes mellitus. The severity of fluid and sodium deficits Table 1 4 is determined primarily by the duration of hyperglycemia, the level of renal function and the patient's fluid intake. Dehydration can be estimated by clinical examination and by calculating total serum osmolality and the corrected serum sodium concentration. Total serum osmolality is calculated using the following equation:. The measured serum sodium concentration can be corrected for the changes related to hyperglycemia by adding 1.

The initial priority in the treatment of diabetic ketoacidosis is the restoration of extra-cellular fluid volume through the intravenous administration of a normal saline 0. This step will restore intravascular volume, decrease counterregulatory hormones and lower the blood glucose level.

In patients with mild to moderate volume depletion, infusion rates of 7 mL per kg per hour have been as efficacious as infusion rates of 14 mL per kg per hour. When the blood glucose concentration is approximately mg per dL This allows continued insulin administration until ketonemia is controlled and also helps to avoid iatrogenic hypoglycemia. Another important aspect of rehydration therapy in patients with diabetic ketoacidosis is the replacement of ongoing urinary losses. Modern management of diabetic ketoacidosis has emphasized the use of lower doses of insulin.

This has been shown to be the most efficacious treatment in both children and adults with diabetic ketoacidosis. It is prudent to withhold insulin therapy until the serum potassium concentration has been determined. In the rare patient who presents with hypokalemia, insulin therapy may worsen the hypokalemia and precipitate life-threatening cardiac arrhythmias.

Standard low-dose insulin therapy consists of an initial intravenous bolus of 0. In clinical situations in which continuous intravenous insulin cannot be administered, the recommended initial insulin dose is 0. Subsequently, regular insulin should be given in a dosage of 0. If the blood glucose concentration does not fall by 50 to 70 mg per dL 2. Either of these treatments should be continued until the blood glucose level falls by 50 to 70 mg per dL.

Normal intestinal fluid balance

Low-dose insulin therapy typically produces a linear fall in the glucose concentration of 50 to 70 mg per dL per hour. More rapid correction of hyperglycemia should be avoided because it may increase the risk of cerebral edema. This dreaded treatment complication occurs in approximately 1 percent of children with diabetic ketoacidosis. Cerebral edema is associated with a mortality rate of up to 70 percent. When a blood glucose concentration of mg per dL has been achieved, the continuous or hourly insulin dosage can be reduced to 0.

The insulin and fluid regimens are continued until ketoacidosis is controlled. This requires the achievement of at least two of these acid-base parameters: a serum bicarbonate concentration of greater than 18 mEq per L, a venous pH of 7. Although the typical potassium deficit in diabetic ketoacidosis is to mEq to mmol , most patients are hyperkalemic at the time of diagnosis because of the effects of insulinopenia, hyperosmolality and acidemia.

One protocol entails using insulin and intravenous fluids until the serum potassium concentration is less than 5. At this time, potassium chloride is added to intravenous fluids in the amount of 20 to 40 mEq per L. The exact amount of potassium that is administered depends on the serum potassium concentration. When the serum potassium level is less than 3. If the serum potassium is greater than 3. The goal is to maintain the serum potassium concentration in the range of 4 to 5 mEq per L 4 to 5 mmol per L. In general, supplemental bicarbonate therapy is no longer recommended for patients with diabetic ketoacidosis, because the plasma bicarbonate concentration increases with insulin therapy.

Retrospective reviews and prospective randomized studies have failed to identify changes in morbidity or mortality with sodium bicarbonate therapy in patients who presented with a pH of 6. Therefore, the use of bicarbonate in a patient with a pH greater than 7. Furthermore, bicarbonate therapy carries some risks, including hypokalemia with overly rapid administration, paradoxic cerebrospinal fluid acidosis and hypoxia.

Some authorities, however, recommend bicarbonate administration when the pH is less than 7. If bicarbonate is used, it should be given as a nearly isotonic solution, which can be approximated by the addition of one ampule of sodium bicarbonate in mL of sterile water. The bicarbonate solution is administered over a one-hour period. A small percentage of patients who have diabetic ketoacidosis present with metabolic acidosis and a normal anion gap. Therefore, they have fewer ketones available for the regeneration of bicarbonate during insulin administration.

Osmotic diuresis leads to increased urinary phosphate losses. During insulin therapy, phosphate reenters the intracellular compartment, leading to mild to moderate reductions in the serum phosphate concentration. Loss of bile. Excessive urinary loss. Impaired renal function.

Urinary diversion operations. Excessive loss of sweat. Drug-induced electrolyte disturbances. Electrolyte disturbances associated with intravenous therapy. Physical examination of the patient. Mucous membranes. Jugular venous pressure. Blood pressure. Cardiac assessment. Tendon reflexes. Restless patient. Fontanelle in infancy. Fluid balance records and their interpretation. Fluid balance chart. Fluid intake. Fluid output. Prescription for intravenous fluids.

Laboratory data and useful investigations. Chemical substances in body fluids. Base excess and buffer base. Actual and standard bicarbonate. Plasma total CO2, plasma bicarbonate. Chemical substances in urine. Enzymes and hormones in urine. Renal function tests. Haematological tests. Central venous pressure. Haemodynamic monitoring using the Swan Ganz catheter. Radiological investigations. Solutions for intravenous therapy and their uses. Sodium chloride solutions. Sodium bicarbonate. One-sixth molar sodium lactate. Potassium chloride. Potassium acetate.

Magnesium sulphate. Isotonic mixed electrolyte solutions. Colloidal solutions. Nutritive solutions. Ammonium chloride. Forced dieresis. Water loss syndrome. Pure deprivation of water. Increased water loss. Physical signs of water loss. Laboratory findings of water loss. Treatment of water loss syndrome. Amount of water required.

panel.hipwee.com/40432-phone-number.php Water excess syndrome. Water excess caused by intravenous infusion. Water excess caused by irrigation. Symptoms and signs of water excess. Laboratory findings. Treatment of water excess. Sodium loss syndrome. Causes of sodium loss syndrome. Diarrhoeal causes. Treatment of diarrhoeal loss. Gastrointestinal and biliary fistulae.

Treatment of loss via fistulae. Loss through intact skin. Treatment of heat exhaustion. Loss through damaged skin. Treatment of loss through skin. Sequestration of extracellular fluid. Treatment of sequestration of extracellular fluid. Intrinsic renal disease. Treatment of renal loss of sodium. Adrenocortical insufficiency. Treatment of acute adrenal insufficiency.

Diabetic keto-acidosis. Treatment of diabetic keto-acidosis. Paracentesis or acupuncture. Drug-induced sodium loss. Bartter's syndrome. Hyponatraemia without sodium loss. Dilutional hyponatraemia.