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Can Starvation Cause Metabolic Acidosis?

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 >>

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 >>

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 >>

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 >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is the most common acid–base disorder and can be life threatening. It results from excessive cellular acid production, reduced acid secretion, or loss of body alkali. The body has two buffering mechanisms to counteract an increase in acid. The initial response is to increase carbon dioxide excretion by increasing ventilation. The second response is increased renal excretion of acids and renal regeneration of bicarbonate. The adequacy of compensation can be assessed by the quick check method or the Winter formula (Table 2). Metabolic acidosis can be classified into two categories using the anion gap. Each category has a distinct differential diagnosis. Anion gap = [Sodium] – ([Chloride] + [Bicarbonate]) Normally, the anion gap is approximately 12 ± 2 meq/L (12 ± 2 mmol/L). Most unmeasured anions consist of albumin. Therefore, the presence of either a low albumin level or an unmeasured cationic light chain, which occurs in multiple myeloma, results in a low anion gap. Increased hydrogen ion concentration or decreased bicarbonate concentration will increase the gap. When the primary disturbance is a metabolic acidosis, the anion gap helps to narrow the diagnostic possibilities to an increased anion gap acidosis or a normal anion gap acidosis. Increased Anion Gap Metabolic Acidosis Common causes include ketoacidosis (diabetes mellitus, alcohol abuse, starvation), lactic acidosis, chronic kidney disease, salicylate toxicity, and ethylene glycol and methanol poisoning. Diabetic ketoacidosis is the most common cause of an increased anion gap acidosis, but a normal anion gap acidosis may be present early in the disease course when the extracellular fluid (ECF) volume is nearly normal. Ketoacidosis also may develop in patients with a histor Continue reading >>

A Rare Cause Of Severe Metabolic Acidosis: Presurgical Fasting - Sciencedirect

A Rare Cause Of Severe Metabolic Acidosis: Presurgical Fasting - Sciencedirect

Volume 42, Issue 4 , OctoberDecember 2014, Pages 312-316 A rare cause of severe metabolic acidosis: Presurgical fastingUna causa inusual de acidosis metabolica severa: ayuno prequirrgico Author links open overlay panel Carlos EduardoLaverde-Sabogala To discuss a clinical case and a non-systematic literature review on severe metabolic acidosis due to pre-surgical fasting, its incidence, etiology, and pathophysiology. Discussion of a case of a patient with fasting-induced severe metabolic acidosis during a laparoscopic cholecystectomy, its management and outcomes. The Ethics Committee of our institution approved the case discussion. The literature search included Pub Med, Scielo and Bireme. Fasting-induced metabolic acidosis is underdiagnosed and is related to the search for an alternate energy source in the absence of glucose and glycogen. Free fatty acids are these alternate source and generate ketone bodies that accumulate and lead to the development of acidosis. This is the first case of a non-diabetic patient at our institution. We found no other reports at the national level. There are some cases in the world literature associated with fasting from vomiting during the third trimester of pregnancy, psychiatric disorders, strict dieting, gastric band dysfunction and alcohol abuse. The anesthesiologist must be aware of this possibility in patients with fasting-induced metabolic acidosis with normal lactate values and hemodynamic impairment that are either too young or too old, non-diabetic and with no history of alcohol abuse. The anion gap calculation tool is a simple diagnostic approach. The incidence of the condition increases during pregnancy. Presentacin de un caso clnico y revisin no sistemtica de la literatura sobre acidosis metablica severa por ayuno prequirrg 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 >>

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 >>

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

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 >>

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 >>

Case Of Nondiabetic Ketoacidosis In Third Term Twin Pregnancy | The Journal Of Clinical Endocrinology & Metabolism | Oxford Academic

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 >>

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 >>

A Rare Cause Of Metabolic Acidosis: Ketoacidosis In A Non-diabetic Lactating Woman

A Rare Cause Of Metabolic Acidosis: Ketoacidosis In A Non-diabetic Lactating Woman

Gordon Sloan1, Amjad Ali1 and Jonathan Webster1[1] Department of Diabetes and Endocrinology, Sheffield Teaching Hospital, Sheffield, UK Summary Ketoacidosis occurring during lactation has been described infrequently. The condition is incompletely understood, but it appears to be associated with a combination of increased metabolic demands during lactation, reduction in carbohydrate intake and acute illness. We present a case of a 27-year-old woman, 8 weeks post-partum, who was exclusively breastfeeding her child whilst following a low carbohydrate diet. She developed gastroenteritis and was unable to tolerate an oral diet for several days. She presented with severe metabolic acidosis on admission with a blood 3-hydroxybutyrate of 5.4 mmol/L. She was treated with intravenous dextrose and intravenous sodium bicarbonate, and given dietary advice to increase her carbohydrate intake. She made a rapid and full recovery. We provide a summary of the common causes of ketoacidosis and compare our case with other presentations of lactation ketoacidosis. Learning points: Ketoacidosis in the lactating woman is a rare cause of raised anion gap metabolic acidosis. Low carbohydrate intake, starvation, intercurrent illness or a combination of these factors could put breastfeeding women at risk of ketoacidosis. Ketoacidosis in the lactating woman has been shown to resolve rapidly with sufficient carbohydrate intake and intravenous dextrose. Early diagnosis and prompt treatment are essential because the condition is reported to be reversible with a low chance of recurrence with appropriate dietary advice. Background Ketoacidosis is a common cause of raised anion gap metabolic acidosis. It most frequently occurs in individuals with type 1 diabetes. Starvation commonly causes ketosis but ra Continue reading >>

Acute Starvation In Pregnancy: A Cause Of Severe Metabolic Acidosis - Sciencedirect

Acute Starvation In Pregnancy: A Cause Of Severe Metabolic Acidosis - Sciencedirect

Volume 20, Issue 3 , July 2011, Pages 253-256 Acute starvation in pregnancy: a cause of severe metabolic acidosis Author links open overlay panel A.Patelab Get rights and content We report a case of starvation-induced metabolic ketoacidosis in a previously healthy 29-year-old, nulliparous woman at 32weeks of gestation. She was admitted to hospital with mild preeclampsia associated with persistent nausea and vomiting that progressed to severe preeclampsia requiring urgent control of hypertension before caesarean delivery. Prolonged and severe vomiting limited oral caloric intake and led to starvation ketoacidosis, characterised by ketonuria and a raised anion gap metabolic acidosis that required intensive care support. Despite significant metabolic derangement the patient appeared clinically well. Intravascular volume was replenished. Fluid restriction used as part of our preeclampsia treatment regimen delayed the therapeutic administration of sufficient dextrose, which rapidly corrected her metabolic derangement when commenced after delivery. Electrolyte supplementation was given to prevent re-feeding syndrome. Both mother and baby were discharged without sequelae. Continue reading >>

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