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 >>
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 >>
Four Case Studies Of Severe Metabolic Acidosis In Pregnancy
Summarized from Frise C, Mackillop L, Joash K et al. Starvation ketoacidosis in pregnancy. Eur J Obstet Gynecol 2012. Available online ahead of publication at: Arterial blood gas analysis in cases of metabolic acidosis reveals primary decrease in pH and bicarbonate, and secondary (compensatory) reduction in pCO2. The most common cause of metabolic acidosis is increased production of endogenous metabolic acids, either lactic acid, in which case the condition is called lactic acidosis, or keto-acids, in which case the condition is called ketoacidosis. Ketoacidosis most commonly occurs as an acute and life-threatening complication of type I diabetes, due to severe insulin deficiency and resulting reduced glucose availability for energy production within cells (insulin is required for glucose to enter cells). Keto-acids accumulate in blood as a result of metabolism of fats mobilized to fill the energy gap created by reduced availability of glucose within cells. Starvation is also associated with reduced availability of (dietary) glucose and potential for ketoacidosis, although compared with diabetic ketoacidosis, starvation ketoacidosis is rare, usually mild and not life-threatening. Except, that is, when it occurs during pregnancy. In a recently published paper the authors outline four cases of severe starvation ketoacidosis, all occurring in the third trimester of pregnancy, following prolonged vomiting over a period of days. All four women presented for emergency admission in a very poorly state and still vomiting with severe partially compensated metabolic acidosis (bicarbonate in the range of 8-13 mmol/L and base deficit in the range of 14-22 mmol/L). All four required transfer to intensive care and premature delivery of their babies by emergency Cesarean section. Fort Continue reading >>
Metabolic Acidosis
Practice Essentials Metabolic acidosis is a clinical disturbance characterized by an increase in plasma acidity. Metabolic acidosis should be considered a sign of an underlying disease process. Identification of this underlying condition is essential to initiate appropriate therapy. (See Etiology, DDx, Workup, and Treatment.) Understanding the regulation of acid-base balance requires appreciation of the fundamental definitions and principles underlying this complex physiologic process. Go to Pediatric Metabolic Acidosis and Emergent Management of Metabolic Acidosis for complete information on those topics. Continue reading >>
Metabolic Acidosis Clinical Presentation
Changes in insulin strength, manufacturer, type, or method of administration may affect glycemic control and predispose to hypoglycemia or hyperglycemia. These changes should be made cautiously under close medical supervision and the frequency of blood glucose monitoring should be increased. Hypoglycemia is the most common adverse reaction of insulin, including Fiasp®, and may be life-threatening. Increase glucose monitoring with changes to: insulin dosage, co-administered glucose lowering medications, meal pattern, physical activity; and in patients with renal impairment or hepatic impairment or hypoglycemia unawareness. As with all insulins, Fiasp® use can lead to life-threatening hypokalemia, which then may cause respiratory paralysis, ventricular arrhythmia, and death. Monitor potassium levels in patients at risk for hypokalemia and treat if indicated. Fluid retention and heart failure can occur with concomitant use of thiazolidinediones (TZDs), which are PPAR-gamma agonists, and insulin, including Fiasp®. Patients should be observed for signs and symptoms of heart failure. If heart failure occurs, dosage reduction or discontinuation of the TZD must be considered. Continue reading >>
Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy
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 containing fluids. 1. Introduction A relative insulin deficient state has been well described in pregnancy. This is due to placentally derived hormones including glucagon, cortisol, and human placental lactogen which are increased in periods of stress [1]. The insulin resistance increases with gestational age Continue reading >>
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 >>
Ketosis: Symptoms, Signs & More
Every cell in your body needs energy to survive. Most of the time, you create energy from the sugar (glucose) in your bloodstream. Insulin helps regulate glucose levels in the blood and stimulate the absorption of glucose by the cells in your body. If you don’t have enough glucose or insufficient insulin to get the job done, your body will break down fat instead for energy. This supply of fat is an alternative energy source that keeps you from starvation. When you break down fat, you produce a compound called a ketone body. This process is called ketosis. Insulin is required by your cells in order to use the glucose in your blood, but ketones do not require insulin. The ketones that don’t get used for energy pass through your kidneys and out through your urine. Ketosis is most likely to occur in people who have diabetes, a condition in which the body produces little or no insulin. Ketosis and Ketoacidosis: What You Need To Know Ketosis simply means that your body is producing ketone bodies. You’re burning fat instead of glucose. Ketosis isn’t necessarily harmful to your health. If you don’t have diabetes and you maintain a healthy diet, it’s unlikely to be a problem. While ketosis itself isn’t particularly dangerous, it’s definitely something to keep an eye on, especially if you have diabetes. Ketosis can be a precursor to ketoacidosis, also known as diabetic ketoacidosis. Ketoacidosis is a condition in which you have both high glucose and high ketone levels. Having ketoacidosis results in your blood becoming too acidic. It’s more common for those with type 1 diabetes rather than type 2. Once symptoms of ketoacidosis begin, they can escalate very quickly. Symptoms include: breath that smells fruity or like nail polish or nail polish remover rapid breat Continue reading >>
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 >>
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 >>
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 >>
Case Of Nondiabetic Ketoacidosis In Third Term Twin Pregnancy | The Journal Of Clinical Endocrinology & Metabolism | Oxford Academic
We provided appropriate management with fluid infusion after cesarean delivery. The patient and her two daughters survived, and no disabilities were foreseen. Alcohol, methanol, and lactic acid levels were normal. No signs of renal disease or diabetes were present. Pathological examination revealed no abnormalities of the placentae. Toxicological tests revealed a salicylate level of less than 5 mg/liter, an acetaminophen level of less than 1 mg/liter, and an acetone level of 300 mg/liter (reference, 520 mg/liter). We present a case of third term twin pregnancy with high anion gap metabolic acidosis due to (mild) starvation. Starvation, obesity, third term twin pregnancy, and perhaps a gastroenteritis were the ultimate provoking factors. In the light of the erroneous suspicion of sepsis and initial fluid therapy lacking glucose, one wonders whether, under a different fluid regime, cesarean section could have been avoided. Severe ketoacidosis in the pregnant woman is associated with impaired neurodevelopment. It therefore demands early recognition and immediate intervention. A 26-yr-old patient was admitted to our hospital complaining of rapid progressive dyspnea and abdominal discomfort. She was pregnant with dichorial, diamniotic twins for 35 wk and 4 d. Medical history showed that she was heterozygous for hemochromatosis. Two years before, she had given birth to a healthy girl of 3925 g by cesarean section, and 1 yr before, she had had a spontaneous abortion. Her preadmission outpatient surveillance revealed slightly elevated blood pressure varying from 132158 mm Hg systolic and 7995 mm Hg diastolic. Glucose and glycosylated hemoglobin were tested at 24 wk and were normal at 4.6 mmol/liter and 5.4% (36 mmol/mol), respectively. Urine analysis at the outpatient obstetri Continue reading >>
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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 >>
Alcoholic Ketoacidosis
Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Treatment is IV saline solution and dextrose infusion. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis. Counter-regulatory hormones are increased and may further inhibit insulin secretion. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs. Diagnosis requires a high index of suspicion; similar symptoms in an alcoholic patient may result from acute pancreatitis, methanol or ethylene glycol poisoning, or diabetic ketoacidosis (DKA). In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), BUN and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement. The absence of hyperglycemia makes DKA improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated Hb (HbA1c). Typical laboratory findings include a high anion gap metabolic acidosis, ketonemia, and low levels of potassium, magnesium, and phosphorus. Detection of acidosis may be com Continue reading >>
Ketoacidosis
Kamel S. Kamel MD, FRCPC, Mitchell L. Halperin MD, FRCPC, in Fluid, Electrolyte and Acid-Base Physiology (Fifth Edition), 2017 Introduction Although ketoacidosis is a form of metabolic acidosis because of the addition of acids, it is discussed separately in this chapter to emphasize the metabolic and biochemical issues required to understand the clinical aspects of this disorder (see margin note). We discuss the metabolic setting that is required to allow for the formation of ketoacids in the liver at a high rate and what sets the limit on the rate of production. Removal of ketoacids occurs mainly in the brain and kidneys. We examine what sets the limit on the rate of removal of ketoacids by these organs. We believe that understanding the biochemical and metabolic aspects of ketoacidsis provides the clinician with a better understanding of this disorder and allows for a better design of therapy in the individual patient with ketoacidosis. Relevant to the pathophysiology of this case, the soft drinks the patient consumed contained a large quantity of glucose, fructose, and caffeine. Ketoacids • A ketone is an organic compound that has a keto group (C=O) on an internal carbon atom. • Acetone is a ketone but not an acid. • Only acetoacetic acid is a ketoacid. β-Hydroxybutyric acid has a hydroxyl group (C–OH) on its internal carbon, so it is a hydroxy acid and not a ketoacid. Abbreviations β-HB, beta hydroxybutyrate anion AcAc, acetoacetate anion ADP, adenosine diphosphate ATP, adenosine triphosphate NAD+, nicotinamide adenine dinucleotide NADH,H+, reduced form of NAD+ FAD, flavin adenine dinucleotide FADH2, hydroxyquinone form of FAD EABV, effective arterial blood volume PAnion gap, plasma anion gap PGlucose, concentration of glucose in plasma POsmolal gap, plasm Continue reading >>
