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Metabolic Acidosis & Metabolic Alkalosis

Metabolic Acidosis & Metabolic Alkalosis

Published by Lambert Morgan Modified over 2 years ago Presentation on theme: "Metabolic acidosis & Metabolic alkalosis" Presentation transcript: 1 Metabolic acidosis & Metabolic alkalosis 3 Primary Change Secondary change Net effect Hco3 Pco2 pH ( H+) Pco2 should by 1.2 mmHg for each mEq plasma Hco3 Inability to excrete dietary acid load Renal failure Renal tubular acidosis type 1 &4 Increased H+ load Lactic acidosis Ketoacidosis Toxin ingestions Increased HCO3 loss diarrhoea 5 Normal anion gap or hyper chloremic acidosis AG = Na+ (Hco3 + Cl ) Normal = 12 4 ( 8 16 ) Measure of unmeasured anion (protiens) Normal anion gap or hyper chloremic acidosis High anion gap 6 Metabolic acidosis Lactic acidosis Ketoacidosis Diarrhoea High anion gap Normal anion gap Lactic acidosis Ketoacidosis Renal failure Toxin ingestions Salicylate Methanol Ethylene glycol Diarrhoea Renal tubular acidosis 7 Clinical features Kussmals respiration (increased depth than rate) Neurologic symptoms: lethargy to coma In severe acidosis (pH< 7.1): Cardiac arrhythmia Reduced cardiac contractility Decreased inotropic response to catecholamines. Chronic acidosis Impaired growth in children Osteomalacia/osteopenia 8 Treatment Treat the underlying cause NaHCO3 therapy: Severe metabolic acidosis (pH<7.1) Chronic acidosis (sodium or potassium citrate) To alkalanise urine in salicylate poisoning 9 NaHCO3 therapy in severe acidosis: pH <7.1 Always treat the pH and not the HCO3 Only one half of bicarbonate deficit to be corrected in initial 12 hrs NaHCO3 dose= desired HCO3 observed HCO3 * 50%of body wt desired HCO3 =12 meq/L in HAG acidosis and meq/L in NAG 10 Example A 24 yr old type 1 diabetic male, weighing aroud 50 Kg presenting with fever, tachypnoea and abd pain to the EMU pH HCO pCo Urine ketones + BP 100 Continue reading >>

Chapter 47. Acidosis And Alkalosis

Chapter 47. Acidosis And Alkalosis

DuBose TD, Jr.. DuBose T.D., Jr. DuBose, Thomas D., Jr.Chapter 47. Acidosis and Alkalosis. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J Eds. Dan L. Longo, et al.eds. Harrison's Principles of Internal Medicine, 18e New York, NY: McGraw-Hill; 2012. Accessed April 24, 2018. DuBose TD, Jr.. DuBose T.D., Jr. DuBose, Thomas D., Jr.. "Chapter 47. Acidosis and Alkalosis." Harrison's Principles of Internal Medicine, 18e Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson J, Loscalzo J. Longo D.L., Fauci A.S., Kasper D.L., Hauser S.L., Jameson J, Loscalzo J Eds. Dan L. Longo, et al. New York, NY: McGraw-Hill, 2012, Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms. The control of arterial CO2 tension (Paco2) by the central nervous system (CNS) and respiratory systems and the control of the plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali. The metabolic and respiratory components that regulate systemic pH are described by the Henderson-Hasselbalch equation: Under most circumstances, CO2 production and excretion are matched, and the usual steady-state Paco2 is maintained at 40 mmHg. Underexcretion of CO2 produces hypercapnia, and overexcretion causes hypocapnia. Nevertheless, production and excretion are again matched at a new steady-state Paco2. Therefore, the Paco2 is regulated primarily by neural respiratory factors and is not subject to regulation by the rate of CO2 production. Hypercapnia is usually the result of hypoventilation rather than of increased CO2 production. Increases or decreases in Paco2 represent de Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Professor of Pediatric Endocrinology University of Khartoum, Sudan Introduction DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. Epidemiology DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa. DKA at the time of first diagnosis of diabetes mellitus is reported in only 2-3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries . Consequences The latter observation is annoying because it implies the following: The late diagnosis of type 1 diabetes in many developing countries particularly in Africa. The late presentation of DKA, which is associated with risk of morbidity & mortality Death of young children with DKA undiagnosed or wrongly diagnosed as malaria or meningitis. Pathophysiology Secondary to insulin deficiency, and the action of counter-regulatory hormones, blood glucose increases leading to hyperglycemia and glucosuria. Glucosuria causes an osmotic diuresis, leading to water & Na loss. In the absence of insulin activity the body fails to utilize glucose as fuel and uses fats instead. This leads to ketosis. Pathophysiology/2 The excess of ketone bodies will cause metabolic acidosis, the later is also aggravated by Lactic acidosis caused by dehydration & poor tissue perfusion. Vomiting due to an ileus, plus increased insensible water losses due to tachypnea will worsen the state of dehydr Continue reading >>

Risk Factors For Developing Metabolic Acidosis After Radical Cystectomy And Ileal Neobladder

Risk Factors For Developing Metabolic Acidosis After Radical Cystectomy And Ileal Neobladder

Risk Factors for Developing Metabolic Acidosis after Radical Cystectomy and Ileal Neobladder Affiliation Department of Urology, Ewha Womans University School of Medicine, Seoul, Korea Affiliation Department of Urology, Ewha Womans University School of Medicine, Seoul, Korea Affiliation Department of Urology, Ewha Womans University School of Medicine, Seoul, Korea Affiliation Department of Urology, Ewha Womans University School of Medicine, Seoul, Korea Affiliation Department of Urology, Ewha Womans University School of Medicine, Seoul, Korea Affiliation Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, Korea Affiliation Department of Urology, Ewha Womans University School of Medicine, Seoul, Korea Risk Factors for Developing Metabolic Acidosis after Radical Cystectomy and Ileal Neobladder To investigate the serial changes of metabolic acidosis and identify associated risk factors in patients who underwent radical cystectomy and ileal neobladder. From January 2010 to August 2014, 123 patients who underwent radical cystectomy and ileal neobladder reconstruction for bladder cancer were included in this study. Metabolic acidosis was defined as a serum bicarbonate level less than 22 mEq/L and impaired renal function was defined as a GFR <50ml/min. The presence of metabolic acidosis was evaluated at 1 month, 1 year, and 2 years after surgery. Multivariate logistic regression analysis was conducted to identify risk factors associated with development of metabolic acidosis. Metabolic acidosis was observed in 52%, 19.5%, and 7.3% of patients at 1 month, 1 year, and 2 years after surgery, respectively. At 1 month after surgery, impaired renal function was the only independent risk factor associated with metabolic acidosis (OR 3.87, P = 0.046). At Continue reading >>

Late Metabolic Acidosis: A Reassessment Of The Definition.

Late Metabolic Acidosis: A Reassessment Of The Definition.

Late metabolic acidosis: a reassessment of the definition. Schwartz GJ, Haycock GB, Edelmann CM Jr, Spitzer A. The term "late metabolic acidosis" is generally used to define a population ofapparently healthy LBW infants who fail to grow and have a base deficit in excessof 5 mEq/l (CO2TOT less than 21 mM). A relationship between hypobasemia and thelack of appropriate growth was postulated. This conclusion was reached, however, in the absence of adequate information regarding the distribution of acid-basevariables in healthy LBW infants. The results of this study demonstrate that the CO2TOT of LBW infants (n = 114) rises between birth and three weeks of life from a mean of 18.6 to 20.3 mM. The frequency distribution of CO2TOT values did notshow any significant deviations from normality, and 2 SD included values as lowas 14.5 mM. No difference in the rate of growth was detected between"hypobasemic" infants given a solution of bicarbonate calculated to bring theirblood CO2TOT to greater than 21 mM and those given similar amounts of isotonicsaline solution. The ability of the LBW infants to excrete an ammonium chlorideload was not related to their acid-base status and was comparable to that of terminfants. It is apparent that the definition of late metabolic acidosis needs tobe reconsidered. Continue reading >>

Renal Tubular Acidosis | American Academy Of Pediatrics Textbook Of Pediatric Care, 2nd Edition | Pediatric Care Online | Aap Point-of-care-solutions

Renal Tubular Acidosis | American Academy Of Pediatrics Textbook Of Pediatric Care, 2nd Edition | Pediatric Care Online | Aap Point-of-care-solutions

This is the touchback warning message modal. The following terms and conditions are an agreement (the Agreement) governing your access and use of the [Pediatric Care Online (PCO)] website(the Website) and its content (collectively, the Materials). Please read these terms carefully. If you agree to all of the terms ofthis Agreement please click the I Agree button below to indicate your acceptance and you will automatically be taken to the Website. If you do notwish to be bound by these terms, you may not access or use the Materials - in such event you should click the I Do Not Agree button below and followthe instructions to obtain a refund of any subscription fees paid by you. 1. Materials. The American Academy of Pediatrics (AAP) hosts the Website and related Materials on its servers and makesthem available via the Internet to subscribers for non-commercial research and education purposes and for use in providing healthcare services. Inconsideration of payment of the applicable subscription fee, the AAP is willing to provide access to the Materials to you and, if applicable, your Users(as defined below), subject to all of the following terms. You acknowledge that certain portions or content of the Website or Materials may containinformation, materials or content provided by a third party provider or licensor (a Provider) and that the liability and obligations of suchProviders is limited as provided herein. (a) Subject to the terms of this Agreement, the AAP grants to you a non-exclusive, non-assignable and non-transferable right to access and use theMaterials for the purpose of providing healthcare services to your patients (the License). (b) User means you and your authorized users for whom a subscription has been activated. For individual enrollment use of the Mater Continue reading >>

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic AcidosisTreatment & Management Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN more... Treatment of acute metabolic acidosis by alkali therapy is usually indicated to raise and maintain the plasma pH to greater than 7.20. In the following two circumstances this is particularly important. When the serum pH is below 7.20, a continued fall in the serum HCO3- level may result in a significant drop in pH. This is especially true when the PCO2 is close to the lower limit of compensation, which in an otherwise healthy young individual is approximately 15 mm Hg. With increasing age and other complicating illnesses, the limit of compensation is likely to be less. A further small drop in HCO3- at this point thus is not matched by a corresponding fall in PaCO2, and rapid decompensation can occur. For example, in a patient with metabolic acidosis with a serum HCO3- level of 9 mEq/L and a maximally compensated PCO2 of 20 mm Hg, a drop in the serum HCO3- level to 7 mEq/L results in a change in pH from 7.28 to 7.16. A second situation in which HCO3- correction should be considered is in well-compensated metabolic acidosis with impending respiratory failure. As metabolic acidosis continues in some patients, the increased ventilatory drive to lower the PaCO2 may not be sustainable because of respiratory muscle fatigue. In this situation, a PaCO2 that starts to rise may change the plasma pH dramatically even without a significant further fall in HCO3-. For example, in a patient with metabolic acidosis with a serum HCO3- level of 15 and a compensated PaCO2 of 27 mm Hg, a rise in PaCO2 to 37 mm Hg results in a change in pH from 7.33 to 7.20. A further rise of the PaCO2 to 43 mm Hg drops the pH to 7.14. All of this would have occurred whi Continue reading >>

Rapid Saline Infusion Produces Hyperchloremic Acidosis In Patients Undergoing Gynecologic Surgery | Anesthesiology | Asa Publications

Rapid Saline Infusion Produces Hyperchloremic Acidosis In Patients Undergoing Gynecologic Surgery | Anesthesiology | Asa Publications

Rapid Saline Infusion Produces Hyperchloremic Acidosis in Patients Undergoing Gynecologic Surgery Received from the Clinic of Anesthesiology, Ludwig-Maximilians-University, Klinikum Grosshadern, Munich, Germany. Submitted for publication April 3, 1998. Accepted for publication November 30, 1998. Supported by the research budget of Ludwig-Maximilians-University, Munich, Germany. Address reprint requests to: Professor Dr. Finsterer: Clinic of Anesthesiology, Ludwig-Maximilians-University, Marchioninistr. 15, D-81377 Munich, Germany. Address electronic mail to: Rapid Saline Infusion Produces Hyperchloremic Acidosis in Patients Undergoing Gynecologic Surgery Anesthesiology 5 1999, Vol.90, 1265-1270. doi: Anesthesiology 5 1999, Vol.90, 1265-1270. doi: Stefan Scheingraber, Markus Rehm, Christiane Sehmisch, Udilo Finsterer; Rapid Saline Infusion Produces Hyperchloremic Acidosis in Patients Undergoing Gynecologic Surgery . Anesthesiology 1999;90(5):1265-1270. 2018 American Society of Anesthesiologists Rapid Saline Infusion Produces Hyperchloremic Acidosis in Patients Undergoing Gynecologic Surgery You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account This article is accompanied by an Editorial View. Please see Prough DS, Bidani A: Hyperchloremic metabolic acidosis is a predictable consequence of intraoperative infusion of 0.9% saline. Anesthesiology 1999; 90:12479. DESPITE the common practice of crystalloid infusion during surgery, few data have been published that describe acid-base changes associated with infusion of 0.9% saline. The recognition that 0.9% saline contains chloride in a nonphysiologic concentration led to the introduction of lactated Ringer's solution. [ 1 ] Onl Continue reading >>

Rumen Acidosis - The Cattle Site

Rumen Acidosis - The Cattle Site

Managing disease can be a frustrating proposition. This Guide can help you identify which disease is damaging your cattle. Rumen acidosis is a metabolic disease of cattle. Like most metabolic diseases it is important to remember that for every cow that shows clinical signs, there will be several more which are affected sub-clinically. Acidosis is said to occur when the pH of the rumen falls to less than 5.5 (normal is 6.5 to 7.0). In many cases the pH can fall even lower. The fall in pH has two effects. Firstly, the rumen stops moving, becoming atonic. This depresses appetite and production. Secondly, the change in acidity changes the rumen flora, with acid-producing bacteria taking over. They produce more acid, making the acidosis worse. The increased acid is then absorbed through the rumen wall, causing metabolic acidosis, which in severe cases can lead to shock and death. The primary cause of acidosis is feeding a high level of rapidly digestible carbohydrate, such as barley and other cereals. Acute acidosis, often resulting in death, is most commonly seen in ‘barley beef’ animals where cattle have obtained access to excess feed. In dairy cattle, a milder form, sub-acute acidosis, is seen as a result of feeding increased concentrates compared to forage. Acute acidosis often results in death, although illness and liver abscesses may be seen before hand. Cattle may become depressed, go off feed, have an elevated heart rate or diarrhea. Because subacute ruminal acidosis is not detected at the time of depressed ruminal pH, there is no specific treatment for it. Secondary conditions may be treated as needed. The key to prevention is reducing the amount of readily fermentable carbohydrate consumed at each meal. This requires both good diet formulation (proper balance Continue reading >>

Acid-base (anesthesia Text)

Acid-base (anesthesia Text)

There are four native buffer systems – bicarbonate, hemoglobin, protein, and phosphate systems. Bicarbonate has a pKa of 6.1, which is not ideal. Hemoglobin has histidine residues with a pKa of 6.8. Chemoreceptors in the carotid bodies, aortic arch, and ventral medulla respond to changes in pH/pCO2 in a matter of minutes. The renal response takes much longer. Arterial vs. Venous Gases Venous blood from the dorsum of the hand is moderately arterialized by general anesthesia, and can be used as a substitute for an ABG. pCO2 will only be off by ~ 5 mm Hg, and pH by 0.03 or 0.04 units [Williamson et. al. Anesth Analg 61: 950, 1982]. Confounding variables include air bubbles, heparin (which is acidic), and leukocytes (aka “leukocyte larceny”). VGB/ABG samples should be cooled to minimize leukocyte activity, however when blood is cooled, CO2 solubility increases (less volatile), and thus pCO2 drops. As an example – a sample taken at 37°C and at 7.4 will actually read as a pH of 7.6 if measured at 25°C. Most VBG/ABGs are actually measured at 37°C. A-aDO2 increases with age, as well as with increased FiO2 and vasodilators (which impair hypoxic pulmonary vasoconstriction). In the setting of a shunt, pulse oximetry can be misleading, thus the A-aDO2 should be calculated. If PaO2 is > 150 mm Hg (i.e., Hg saturation is essentially 100%), every 20 mm Hg of A-aDO2 represents 1% shunting of cardiac output. A/a is even better than A-aDO2 because it is independent of FiO2. PaO2/FiO2 is a reasonable alternative, with hypoxia defined as PaO2/FiO2 < 300 (a PaO2/FiO2 < 200 suggests a shunt fraction of 20% or more). Mixed venous blood should have a pO2 of ~ 40 mm Hg. Values < 30 mm Hg suggest hypoxemia, although one must always keep in mind that peripheral shunting and cyanide tox Continue reading >>

Respiratory Acidosis And Alkalosis

Respiratory Acidosis And Alkalosis

Automatically changes to Flash or non-Flash embed The presentation is successfully added In Your Favorites . This Presentation is Public Favorites: feed backs are mostly welcomed.. for further details u can feel free to contact me at [email protected] Respiratory Acidosis And Alkalosis Dr. Aalekh Raj DahalMBBS Respiratory Acidosis Defination: Respiratory acidosis is a condition in which a build-up of carbon dioxide in the blood produces a shift in the body's pH balance and causes the body's system to become more acidic. This condition is brought about by a problem either involving the lungs and respiratory system or signals from the brain that control breathing. There is primary increase in Pco2 with compensatory increase in HCO3 ; pH usually low but may be near normal. (Ventilatory failure; Respiratory failure; Acidosis respiratory) Carbon dioxide is produced constantly as the body burns energy, and this CO2 will accumulate rapidly if the lungs do not adequately dispel it through alveolar ventilation. Alveolar hypoventilation thus leads to an increased PaCO2 (called hypercapnia). The increase in PaCO2 in turn decreases the HCO3/PaCO2 ratio and decreases pH resulting respiratory acidosis. Etiology: HypoventilationDiseases of the airways (such as asthma and chronic obstructive lung disease), which send air into and out of the lungsDiseases of the chest (such as scoliosis), which make the lungs less efficient at filling and emptyingDiseases affecting the nerves and muscles that "signal" the lungs to inflate or deflateDrugs that suppress breathing (including powerful pain medicines, such as narcotics, and "downers," such as benzodiazepines), especially when combined with alcoholSevere obesity, which restricts how much the lungs can expand Signs and symptoms: Symptoms an Continue reading >>

Respiratory Acidosis-alkalosis

Respiratory Acidosis-alkalosis

To view this video please enable JavaScript, and consider upgrading to a web browser that supports HTML5 video Published by Claud Lamb Modified over 3 years ago -Respiratory acidosis occurs when the lungs cant remove enough carbon dioxide (CO2). Excess CO2 makes the blood more acidic. This is because the body must balance the ions that control pH.- Normal PH: Normal Pco2 : mm Hg Normal Hco3: 22 24 mEq/L 7 Causes :- Causes of respiratory acidosis include: Diseases of the airways (such as asthma and chronic obstructive lung disease.PE. pneumonia) Diseases of the chest (such as scoliosis) Diseases affecting the nerves and muscles that "signal" the lungs to inflate or deflate(multiple sclerosis.kyphoscoliosis.MG) Drugs that suppress breathing (including powerful pain medicines, such as narcotics, and "downers," such as benzodiazepines), especially when combined with alcohol Hypoventilation 8 Clinical features Initial signs of acute respiratory acidosis include: headache anxiety blurred vision restlessness Without treatment, other symptoms may occur. These include: sleepiness tremors delirium 9 Diagnosis :- Several tools can help doctors diagnose respiratory acidosis. Blood Gas Measurement (ABC) This test measures oxygen and CO2 in the blood. High levels of CO2 can indicate acidosis. Lung Function Tests Many people with this condition have reduced lung function .especially airflow obstruction Chest X-Ray X-rays can help doctors see injuries or other problems likely to cause acidosis like pneumothorax and pneumonia Respiratory alkalosis occurs when carbon dioxide levels drop too low. This causes the pH of the blood to rise and become too alkaline Hco3 Pco2 PH 13 2.2 in Hco3 for each 10 inPco2 ((Acute)) Pco2 Alkalosis 14 Causes :- Hyperventilation Anxiety Early asthma Sepsis Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

What is respiratory acidosis? Respiratory acidosis is a condition that occurs when the lungs can’t remove enough of the carbon dioxide (CO2) produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic. Normally, the body is able to balance the ions that control acidity. This balance is measured on a pH scale from 0 to 14. Acidosis occurs when the pH of the blood falls below 7.35 (normal blood pH is between 7.35 and 7.45). Respiratory acidosis is typically caused by an underlying disease or condition. This is also called respiratory failure or ventilatory failure. Normally, the lungs take in oxygen and exhale CO2. Oxygen passes from the lungs into the blood. CO2 passes from the blood into the lungs. However, sometimes the lungs can’t remove enough CO2. This may be due to a decrease in respiratory rate or decrease in air movement due to an underlying condition such as: There are two forms of respiratory acidosis: acute and chronic. Acute respiratory acidosis occurs quickly. It’s a medical emergency. Left untreated, symptoms will get progressively worse. It can become life-threatening. Chronic respiratory acidosis develops over time. It doesn’t cause symptoms. Instead, the body adapts to the increased acidity. For example, the kidneys produce more bicarbonate to help maintain balance. Chronic respiratory acidosis may not cause symptoms. Developing another illness may cause chronic respiratory acidosis to worsen and become acute respiratory acidosis. Initial signs of acute respiratory acidosis include: headache anxiety blurred vision restlessness confusion Without treatment, other symptoms may occur. These include: sleepiness or fatigue lethargy delirium or confusion shortness of breath coma The chronic form of Continue reading >>

Drug-induced Metabolic Acidosis

Drug-induced Metabolic Acidosis

SummaryDrug causes of metabolic acidosis are numerous and their mechanisms are diverse. Broadly, they can cause metabolic acidosis with either a normal anion gap (e.g. drug-induced renal tubular acidosis) or an elevated anion gap (e.g. drug-induced lactic acidosis or pyroglutamic acidosis). This review describes the drugs that can cause or contribute to metabolic acidosis during therapeutic use, the mechanisms by which this occurs, and how they may be identified in practice. aNeurointensive Care Unit, St George's University Hospitals NHS Foundation Trust bClinical Pharmacology, St George's University of London, London, UK Correspondence to Andrew W. Hitchings, Senior Lecturer in Clinical Pharmacology and Consultant in Neurointensive Care, St George's University Hospitals NHS Foundation Trust and St George's University of London, Cranmer Terrace, London SW17 0RE, UK. Tel: +44 20 8725 5380; e-mail: [email protected] Editor: R E Ferner, MSc, MD, FRCP, Director of the WestMidlands Centre for Adverse Drug Reaction Reporting and Consultant Physician at City Hospital, Birmingham, UK. Assistant Editor: Mr C Anton, MA, MEng. Editorial Board: Australia: Dr M Kennedy, Professor G M Shenfield, Denmark: Professor J S Schou; England: Dr J K Aronson,Dr A Hitchings; India: Professor N Gogtay; Netherlands: Professor C J van Boxtel, Dr B H Ch Stricker; New Zealand: Dr T Maling; Scotland: Dr D N Bateman; Wales: Professor P A Routledge. Copyright 2017 Wolters Kluwer Health, Inc. All rights reserved. Thought you might appreciate this item(s) I saw at Adverse Drug Reaction Bulletin. Your message has been successfully sent to your colleague. Some error has occurred while processing your request. Please try after some time. Continue reading >>

Acidosis - Extension

Acidosis - Extension

Acidosis is also known as toxic indigestion. It occurs when a high proportion of concentrate (carbohydrates)is fed in the ration, either acutely or chronically. Signs: Signs may include depression, lack of appetite, bloat, lack of rumination, staggering, diarrhea or lack of manure, muscle twitching,and teeth grinding. Severerumen acidosis can be accompanied by systemic and often fatal acidosis. Respiratory distress, shock, cardiovascular collapse, coma, seizures and death occur in severe cases. Treatment: Administer 2 to 3 ounces of sodium bicarbonate by mouth,which will help neutralize acid in the rumen. Magnesium hydroxide or magnesium oxide can also be used to neutralize rumen acid. Encourage consumption of long-stemmed grass hay andwater. Many animals with acidosis will require IV fluids to survive.Antibiotics will help prevent secondary bacterial overgrowth with undesirable organisms. Thiamintreatment is recommended becausepolioencephalomalacia is a potential sequela. Anti-inflammatories will help prevent toxicity and founder. Probiotics should be administered to replace the beneficial rumen organisms that have been killed due to low rumen pH. If a goat is showing clinical signs of this disease, a veterinarian should be called to administer proper treatment due to the seriousness of the illness, complicated treatmentand number of possible severe complications. Control/Prevention: Control consists of gradual introduction of goats to grain. If goats are being fed a high-concentrate diet, distribute grain over three or more meals per day, at 2 to 3 pounds per meal. Feed wholegrains instead of finely-ground grains and dry grain instead of wet. Feed roughage before grain, first thing in the morning. Supplement with bicarbonate of soda or calcium carbonate and magnesium Continue reading >>

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