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Starvation Acidosis

Metabolic Acidosis

Metabolic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>

Severe Acidosis Caused By Starvation And Stress - Sciencedirect

Severe Acidosis Caused By Starvation And Stress - Sciencedirect

Volume 42, Issue 5 , November 2003, Pages e22.1-e22.4 Get rights and content A 1-year-old boy had severe anoxic brain injury owing to a cardiorespiratory arrest. He had an initial metabolic acidosis, but this largely resolved by hospital day 2. He then had a persistent, profound metabolic acidosis. Evaluation on hospital day 6 found that the patient had ketonemia, ketonuria, and a normal serum glucose level; he had received no intravenous dextrose during his hospitalization. The dextrose-free fluids were given initially to protect his brain from the deleterious effects of hyperglycemia after brain injury. Continuation beyond 24 hours was inadvertent. The initiation of dextrose-containing intravenous fluids produced a rapid resolution of his metabolic acidosis. Starvation usually produces a mild metabolic acidosis, but when combined with physiologic stress, starvation may cause a severe metabolic acidosis. Among the few reports of severe starvation ketoacidosis, our case is unique because the patient was monitored closely in an intensive care unit, allowing us to describe the time course of the acidosis in detail. Continue reading >>

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Abstract Pregnancy is a diabetogenic state characterized by relative insulin resistance, enhanced lipolysis, elevated free fatty acids and increased ketogenesis. In this setting, short period of starvation can precipitate ketoacidosis. This sequence of events is recognized as "accelerated starvation." Metabolic acidosis during pregnancy may have adverse impact on fetal neural development including impaired intelligence and fetal demise. Short periods of starvation during pregnancy may present as severe anion gap metabolic acidosis (AGMA). We present a 41-year-old female in her 32nd week of pregnancy, admitted with severe AGMA with pH 7.16, anion gap 31, and bicarbonate of 5 mg/dL with normal lactate levels. She was intubated and accepted to medical intensive care unit. Urine and serum acetone were positive. Evaluation for all causes of AGMA was negative. The diagnosis of starvation ketoacidosis was established in absence of other causes of AGMA. Intravenous fluids, dextrose, thiamine, and folic acid were administered with resolution of acidosis, early extubation, and subsequent normal delivery of a healthy baby at full term. Rapid reversal of acidosis and favorable outcome are achieved with early administration of dextrose containing fluids. Discover the world's research 14+ million members 100+ million publications 700k+ research projects Join for free Starvation Ketoacidosis: A Cause of Severe Anion Gap Metabolic Nupur Sinha, Sindhaghatta Venkatram, and Gilda Diaz-Fuentes Division of Pulmonary and Critical Care Medicine, Bronx Lebanon Hospital Center and Albert Einstein College of Medicine, Correspondence should be addressed to Nupur Sinha; [email protected] Received  February ; Revised  May ; Accepted  May ; Published Continue reading >>

Starvation Ketoacidosis In Pregnancy

Starvation Ketoacidosis In Pregnancy

Introduction: Starvation ketosis outside pregnancy is a rare phenomenon and is unlikely to cause a severe acidosis. Pregnancy is an insulin resistant state due to placental production of hormones including glucagon and human placental lactogen. Insulin resistance increases with advancing gestation and this confers a susceptibility to ketosis, particularly in the third trimester. Starvation ketoacidosis in pregnancy has been reported and is usually precipitated by a period of severe vomiting. Ketoacidosis has been associated with intrauterine death. Case report: A 22-year-old woman in her third pregnancy presented at 32 weeks gestation with a 24 h history of severe vomiting. She had been treated for an asthma exacerbation with prednisolone and erythromycin the day prior to presentation. She was unwell, hypertensive (145/70 mmHg) with a sinus tachycardia and Kussmaul breathing. Urinalysis showed ++++ ketones, + protein and pH 5. Fingerprick glucose was 4 mmol/l and ketones were 4.0 mmol/l. Arterial blood gas showed pH 7.27, PaCO2 1.1 kPa, base excess −23, bicarbonate 8.6 mmol/l and lactate 0.6 mmol/l. The anion gap was 20. Serum ethanol, salicylates and paracetamol levels were undetectable. She was fluid resuscitated but her biochemical parameters did not improve. She was intubated and underwent emergency caesarean section. A healthy boy was delivered and her acidosis resolved over the subsequent 8 h. Discussion: We believe this case is explained by starvation ketoacidosis. There was no evidence of diabetes mellitus or other causes of a metabolic acidosis. In view of the hypertension, proteinuria and raised urate the differential diagnosis was an atypical presentation of pre-eclampsia. This case illustrates the metabolic stress imposed by the feto-placental unit. It als Continue reading >>

Starvation Acidosis

Starvation Acidosis

acidosis [as″ĭ-do´sis] 1. the accumulation of acid and hydrogen ions or depletion of the alkaline reserve (bicarbonate content) in the blood and body tissues, resulting in a decrease in pH. 2. a pathologic condition resulting from this process, characterized by increase in hydrogen ion concentration (decrease in pH). The optimal acid-base balance is maintained by chemical buffers, biologic activities of the cells, and effective functioning of the lungs and kidneys. The opposite of acidosis is alkalosis. adj., adj acidot´ic. Acidosis usually occurs secondary to some underlying disease process; the two major types, distinguished according to cause, are metabolic acidosis and respiratory acidosis (see accompanying table). In mild cases the symptoms may be overlooked; in severe cases symptoms are more obvious and may include muscle twitching, involuntary movement, cardiac arrhythmias, disorientation, and coma. In general, treatment consists of intravenous or oral administration of sodium bicarbonate or sodium lactate solutions and correction of the underlying cause of the imbalance. Many cases of severe acidosis can be prevented by careful monitoring of patients whose primary illness predisposes them to respiratory problems or metabolic derangements that can cause increased levels of acidity or decreased bicarbonate levels. Such care includes effective teaching of self-care to the diabetic so that the disease remains under control. Patients receiving intravenous therapy, especially those having a fluid deficit, and those with biliary or intestinal intubation should be watched closely for early signs of acidosis. Others predisposed to acidosis are patients with shock, hyperthyroidism, advanced circulatory failure, renal failure, respiratory disorders, or liver disease. Continue reading >>

Fasting Ketosis And Alcoholic Ketoacidosis

Fasting Ketosis And Alcoholic Ketoacidosis

INTRODUCTION Ketoacidosis is the term used for metabolic acidoses associated with an accumulation of ketone bodies. The most common cause of ketoacidosis is diabetic ketoacidosis. Two other causes are fasting ketosis and alcoholic ketoacidosis. Fasting ketosis and alcoholic ketoacidosis will be reviewed here. Issues related to diabetic ketoacidosis are discussed in detail elsewhere. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis" and "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment".) PHYSIOLOGY OF KETONE BODIES There are three major ketone bodies, with the interrelationships shown in the figure (figure 1): Acetoacetic acid is the only true ketoacid. The more dominant acid in patients with ketoacidosis is beta-hydroxybutyric acid, which results from the reduction of acetoacetic acid by NADH. Beta-hydroxybutyric acid is a hydroxyacid, not a true ketoacid. Continue reading >>

Acidosis

Acidosis

For acidosis referring to acidity of the urine, see renal tubular acidosis. "Acidemia" redirects here. It is not to be confused with Academia. Acidosis is a process causing increased acidity in the blood and other body tissues (i.e., an increased hydrogen ion concentration). If not further qualified, it usually refers to acidity of the blood plasma. The term acidemia describes the state of low blood pH, while acidosis is used to describe the processes leading to these states. Nevertheless, the terms are sometimes used interchangeably. The distinction may be relevant where a patient has factors causing both acidosis and alkalosis, wherein the relative severity of both determines whether the result is a high, low, or normal pH. Acidosis is said to occur when arterial pH falls below 7.35 (except in the fetus – see below), while its counterpart (alkalosis) occurs at a pH over 7.45. Arterial blood gas analysis and other tests are required to separate the main causes. The rate of cellular metabolic activity affects and, at the same time, is affected by the pH of the body fluids. In mammals, the normal pH of arterial blood lies between 7.35 and 7.50 depending on the species (e.g., healthy human-arterial blood pH varies between 7.35 and 7.45). Blood pH values compatible with life in mammals are limited to a pH range between 6.8 and 7.8. Changes in the pH of arterial blood (and therefore the extracellular fluid) outside this range result in irreversible cell damage.[1] Signs and symptoms[edit] General symptoms of acidosis.[2] These usually accompany symptoms of another primary defect (respiratory or metabolic). Nervous system involvement may be seen with acidosis and occurs more often with respiratory acidosis than with metabolic acidosis. Signs and symptoms that may be seen i Continue reading >>

Severe Acidosis Caused By Starvation And Stress.

Severe Acidosis Caused By Starvation And Stress.

Severe acidosis caused by starvation and stress. Department of Pediatrics, Children's Hospital of Wisconsin, Milwauke, WI, USA. A 1-year-old boy had severe anoxic brain injury owing to a cardiorespiratory arrest. He had an initial metabolic acidosis, but this largely resolved by hospital day 2. He then had a persistent, profound metabolic acidosis. Evaluation on hospital day 6 found that the patient had ketonemia, ketonuria, and a normal serum glucose level; he had received no intravenous dextrose during his hospitalization. The dextrose-free fluids were given initially to protect his brain from the deleterious effects of hyperglycemia after brain injury. Continuation beyond 24 hours was inadvertent. The initiation of dextrose-containing intravenous fluids produced a rapid resolution of his metabolic acidosis. Starvation usually produces a mild metabolic acidosis, but when combined with physiologic stress, starvation may cause a severe metabolic acidosis. Among the few reports of severe starvation ketoacidosis, our case is unique because the patient was monitored closely in an intensive care unit, allowing us to describe the time course of the acidosis in detail. Continue reading >>

Ketoacidosis

Ketoacidosis

GENERAL ketoacidosis is a high anion gap metabolic acidosis due to an excessive blood concentration of ketone bodies (keto-anions). ketone bodies (acetoacetate, beta-hydroxybutyrate, acetone) are released into the blood from the liver when hepatic lipid metabolism has changed to a state of increased ketogenesis. a relative or absolute insulin deficiency is present in all cases. CAUSES The three major types of ketosis are: (i) Starvation ketosis (ii) Alcoholic ketoacidosis (iii) Diabetic ketoacidosis STARVATION KETOSIS when hepatic glycogen stores are exhausted (eg after 12-24 hours of total fasting), the liver produces ketones to provide an energy substrate for peripheral tissues. ketoacidosis can appear after an overnight fast but it typically requires 3 to 14 days of starvation to reach maximal severity. typical keto-anion levels are only 1 to 2 mmol/l and this will usually not alter the anion gap. the acidosis even with quite prolonged fasting is only ever of mild to moderate severity with keto-anion levels up to a maximum of 3 to 5 mmol/l and plasma pH down to 7.3. ketone bodies also stimulate some insulin release from the islets. patients are usually not diabetic. ALCOHOLIC KETOSIS Presentation a chronic alcoholic who has a binge, then stops drinking and has little or no oral food intake for a few days (ethanol and fasting) volume depletion is common and this can result in increased levels of counter regulatory hormones (eg glucagon) levels of free fatty acids (FFA) can be high (eg up to 3.5mM) providing plenty of substrate for the altered hepatic lipid metabolism to produce plenty of ketoanions GI symptoms are common (eg nausea, vomiting, abdominal pain, haematemesis, melaena) acidaemia may be severe (eg pH down to 7.0) plasma glucose may be depressed or normal or Continue reading >>

Renal Fellow Network: Starvation Ketosis: A Rare Cause Of Metabolic Acidosis

Renal Fellow Network: Starvation Ketosis: A Rare Cause Of Metabolic Acidosis

Starvation Ketosis: A Rare Cause of Metabolic Acidosis Asa child growing up in India, I have seen several family members performingritual fasting. Fasting is aubiquitous religio-cultural practice that is found, in varying forms, acrossthe world. The month-long Ramadan and Buddhist Lent fasts are examples ofreligious observances practiced by followers of Islam, and Buddhism,respectively. These fasts are characterized by a documented impact on metabolic health , which can be minimized by well-known management strategies .The practice of fastingis a major part of Hinduism and can range from light restriction toextreme abstention. Mahatma Gandhi was a fervent supporter of fasting byreligious convictionand as a way of freeingoneself of theconstraints of the body. He used fasting as a means of exerting politicalpressure and engaged in several hungerstrikesto protest withnon-violence. Inthe western countries, starvation ketosis or ketoacidosis has been reported inindividuals with strict dieting (e.g. carb-restricted, ketogenic diets or Atkins diet), extreme exercise, andrarely with malnutrition. Few cases of starvation-induced ketoacidosis during pregnancy and lactation , and during the perioperative period have also been reported in literature. Isaw a young non-verbal woman with quadriplegia who was admitted from a nursinghome with a two-day history of worsening abdominal pain and leakage around herpercutaneous endoscopic gastrostomy(PEG) tube site. Her medical history was significant for severe developmentaldelay and chronic constipation. She was afebrile and the rest of the vitalswere stable. Her PEG tube feeds had been stopped one day prior to the hospitaladmission due to abdominal pain. Additionally, she received small doses of ivmorphine for pain control. Due to no oral Continue reading >>

Starvation Ketoacidosis

Starvation Ketoacidosis

Eating disorders, prolonged fasting, severely calorie-restricted diets, restricted access to food (low socioeconomic and elderly patients) may be causes of starvation ketoacidosis. When insulin levels are low and glucagon levels are high (such as in a fasting state), long chain fatty acids and glycerol from triglycerides are released from peripheral fat stores and are transported to the liver. The fatty acids undergo beta-oxidation and generate acetyl-CoA. However, with excessive amounts of acetyl-CoA, the Krebs cycle may become oversaturated, and instead the acetyl-CoA enter the ketogenic pathway resulting in production of ketone bodies. Mild ketosis (1mmol/L) results after fasting for approximately 12 to 14 hours. However, the ketoacid concentration rises with continued fasting and will peak after 20 to 30 days (8-10mmol/L). Clinical Features Nausea and vomiting Abdominal pain Dehydration Altered mental status Fatigue Kussmaul breathing Differential Diagnosis Evaluation Serum chemistry (elevated anion gap) Glucose (usually euglycemic or hypoglycemic) Urinalysis (ketonuria) Serum beta-hydroxybutyrate Lactate Salicylate level (if overdose suspected) Serum osmolality (if toxic alcohol ingestion suspected) Management Dextrose and saline solutions Dextrose Will cause increase in insulin and decrease in glucagon secretion, which will reduce ketone production and increase ketone metabolism Beta-hydroxybutyrate and acetoacetate will regenerate bicarbonate, causing partial correction of metabolic acidosis Saline or lactated ringer Will provide volume resuscitation and will in turn reduce secretion of glucagon (which promotes ketogenesis) Considerations Rate of infusion dependent on volume status If hypokalemic, need to correct before administering glucose (as glucose stimulate Continue reading >>

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

Starvation Ketoacidosis: A Cause of Severe Anion Gap Metabolic Acidosis in Pregnancy Division of Pulmonary and Critical Care Medicine, Bronx Lebanon Hospital Center and Albert Einstein College of Medicine, Bronx, NY 10457, USA Received 21 February 2014; Revised 6 May 2014; Accepted 6 May 2014; Published 20 May 2014 Copyright 2014 Nupur Sinha et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Pregnancy is a diabetogenic state characterized by relative insulin resistance, enhanced lipolysis, elevated free fatty acids and increased ketogenesis. In this setting, short period of starvation can precipitate ketoacidosis. This sequence of events is recognized as accelerated starvation. Metabolic acidosis during pregnancy may have adverse impact on fetal neural development including impaired intelligence and fetal demise. Short periods of starvation during pregnancy may present as severe anion gap metabolic acidosis (AGMA). We present a 41-year-old female in her 32nd week of pregnancy, admitted with severe AGMA with pH 7.16, anion gap 31, and bicarbonate of 5 mg/dL with normal lactate levels. She was intubated and accepted to medical intensive care unit. Urine and serum acetone were positive. Evaluation for all causes of AGMA was negative. The diagnosis of starvation ketoacidosis was established in absence of other causes of AGMA. Intravenous fluids, dextrose, thiamine, and folic acid were administered with resolution of acidosis, early extubation, and subsequent normal delivery of a healthy baby at full term. Rapid reversal of acidosis and favorable outcome are achieved with early administration of dextrose Continue reading >>

Starvation Ketoacidosis: Treatment Pitfalls

Starvation Ketoacidosis: Treatment Pitfalls

Dear Editor, Yeow et al.1 describe a case of non-diabetic euglycaemic acidosis resulting from post op dysphagia and poor intake of approximately six weeks duration. We have seen a similar case of ‘starvation ketoacidosis’ in a patient undergoing percutaneous endoscopic gastrostomy feeding tube replacement. We think that intravenous (IV) glucose should be the initial treatment, with the addition of insulin only if required. The correspondence from Frise and Mackillop2 states this strategy is effective for treating ketoacidosis in pregnancy; however, there are also some other pitfalls in treatment of starvation ketoacidosis which must be considered, and some overlap with alcoholic ketoacidosis. Unlike patients with diabetic ketoacidosis, patients with starvation ketosis release insulin when carbohydrate is administered. They are also producing high levels of glucose elevating hormones such as glucagon and have depleted glycogen stores. These hormones cause the lipolysis which helps generate ketones for fuel. The addition of exogenous insulin in this state risks hypoglycaemia. Once provided with adequate carbohydrate the insulin levels will rise and counter-regulatory hormone levels will fall, resolving the ketosis. Alcoholics are another group prone to ketosis (alcoholic ketoacidosis (AKA)) and are particularly prone to hypoglycaemia; administration of insulin to those patients would have to be with caution and literature3 on AKA reports resolution without insulin administration, although there is little evidence outside of case reports. Starved patients and alcoholics are also both at risk of thiamine deficiency. Depletion of body thiamine stores can occur within four weeks. It is important to consider this, as administration of IV glucose in thiamine deficiency can Continue reading >>

Diabetic, Alcoholic And Starvation Ketoacidosis

Diabetic, Alcoholic And Starvation Ketoacidosis

Copious amounts of ketones which are generated in insulin-deficient or insulin-unresponsive patients will give rise to a high anion gap metabolic acidosis. Ketones are anions, and they form the high anion gap. Management of DKA and HONK is discussed elsewhere. Meet the ketones Chemically speaking, a ketone is anything with a carbonyl group between a bunch of other carbon atoms. The above are your three typical ketoacidosis-associated ketone bodies. The biochemistry nerds among us will hasten to add that the beta-hydroxybutyrate is in fact not a ketone but a carboxylic acid, but - because it is associated with ketoacidosis, we will continue to refer to it as a ketone for the remainder of this chapter, in the spirit of convention. In the same spirit, we can suspend our objections to acetone being included in a discussion of ketoacidosis, which (though a true ketone) is in fact not acidic or basic, as it does not ionise at physiological pH (its pKa is 20 or so). So really, the only serious ketone acid is acetoacetate, which has a pKa of 3.77. However, beta-hydroxybutyrate is the prevalent ketone in ketoacidosis; the normal ratio of beta-hydroxybutyrate and acetoacetate is 3:1, and it can rise to 10:1 in diabetic ketoacidosis. Acetone is the least abundant. The metabolic origin of ketones The generation of ketones is a normal response to fasting, which follows the depletion of hepatic glycogen stores. Let us discuss normal physiology for a change. You, a healthy adult without serious alcohol problems, are fasting from midnight for a routine elective hernia repair. You will go to be after dinner with a few nice lumps of undigested food in your intestine, as well as about 75g of hepatic glycogen. As you sleep, you gradually digest the food and dip into the glycogen store. At Continue reading >>

Starvation Ketoacidosis As A Cause Of Unexplained Metabolic Acidosis In The Perioperative Period

Starvation Ketoacidosis As A Cause Of Unexplained Metabolic Acidosis In The Perioperative Period

Go to: Abstract Patient: Female, 24 Final Diagnosis: Starvation ketoacidosis Symptoms: None Medication: — Clinical Procedure: Lumbar laminectomy Specialty: Orthopedics and Traumatology Besides providing anesthesia for surgery, the anesthesiologist’s role is to optimize the patient for surgery and for post-surgical recovery. This involves timely identification and treatment of medical comorbidities and abnormal laboratory values that could complicate the patient’s perioperative course. There are several potential causes of anion and non-anion gap metabolic acidosis in surgical patients, most of which could profoundly affect a patient’s surgical outcome. Thus, the presence of an acute acid-base disturbance requires a thorough workup, the results of which will influence the patient’s anesthetic management. An otherwise-healthy 24-year-old female presented for elective spine surgery and was found to have metabolic acidosis, hypotension, and polyuria intraoperatively. Common causes of acute metabolic acidosis were investigated and systematically ruled out, including lactic acidosis, diabetic ketoacidosis, drug-induced ketoacidosis, ingestion of toxic alcohols (e.g., methanol, ethylene glycol), uremia, and acute renal failure. Laboratory workup was remarkable only for elevated serum and urinary ketone levels, believed to be secondary to starvation ketoacidosis. Due to the patient’s unexplained acid-base disturbance, she was kept intubated postoperatively to allow for further workup and management. Starvation ketoacidosis is not widely recognized as a perioperative entity, and it is not well described in the medical literature. Lack of anesthesiologist awareness about this disorder may complicate the differential diagnosis for acute intraoperative metabolic acidosi Continue reading >>

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