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 also Continue reading >>
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 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 >>
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 >>
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 >>
- Practical Approach to Using Trend Arrows on the Dexcom G5 CGM System for the Management of Adults With Diabetes | Journal of the Endocrine Society | Oxford Academic
- Drinking wine can fight diabetes: Regular glass can cut risk by a third say experts
- One third of Americans are headed for diabetes, and they don't even know it
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 >>
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 >>
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 >>
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 >>
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 >>
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 Treatment & Management
Approach Considerations 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 while the serum HCO3- level remained at 15 mEq/L. In lactic acidosis and diabetic ketoacidosis, the organic anion can r Continue reading >>
- Diabetes management 3: the pathogenesis and management of diabetic foot ulcers
- Mastery in Diabetes Management: Doxycycline Treatment for Insulin Resistance
- Relative effectiveness of insulin pump treatment over multiple daily injections and structured education during flexible intensive insulin treatment for type 1 diabetes: cluster randomised trial (REPOSE)
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 >>
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 >>
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 >>
