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Ketoacidosis When Pregnant

Ketoacidosis

Ketoacidosis

High blood glucose levels can put you at risk of a serious condition called ketoacidosis. If there is not enough insulin for your body cells to use glucose for energy, your blood glucose levels will rise and your body will break down fats instead (as another energy source). However, fat breakdown leads to your body forming ketones which you can detect in your blood or urine. High blood glucose levels and ketones can result in diabetic ketoacidosis (DKA), requiring hospitalisation. Ketoacidosis may occur when you are unwell, forget to take your insulin or don’t take enough insulin. To check for ketones you can: Test your blood (using a monitor which can test for both glucose and ketones in your blood) OR Test your urine (using urine test strips available where you buy your blood testing strips) The risk of ketoacidosis increases during pregnancy and is very dangerous, especially for the baby. It is important to go to hospital immediately if your blood glucose levels are high and there is any sign of ketoacidosis (blood ketones more than 0.6 or urine ketones more than 1+). Continue reading >>

Four Case Studies Of Severe Metabolic Acidosis In Pregnancy

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 >>

Eating Disorders And Diabetic Ketoacidosis In A Pregnant Woman With Type 1 Diabetes: A Case Report

Eating Disorders And Diabetic Ketoacidosis In A Pregnant Woman With Type 1 Diabetes: A Case Report

Abstract OBJECTIVE: To describe a case of diabetic ketoacidosis (DKA) in a pregnant woman with type 1 diabetes (T1DM) and disordered eating behaviour treated with a continuous subcutaneous insulin infusion, and to discuss some aspects of the monitoring and management of DKA in pregnancy and whether a pump is the safest therapeutic choice in the presence of some eating disorders. CASE REPORT: This 26-year-old Caucasian woman affected by T1DM was hospitalised during the last weeks of her fourth pregnancy because of DKA due to disordered eating. She was treated with a fluid infusion, intravenous insulin, and her electrolyte imbalance was carefully corrected. An elective cesarean section was performed after the correction of DKA in the 34th week (+6 days) of gestation. CONCLUSIONS: We suggest that pregnancy in T1DM women with eating disorders may not be rare. The prevention, early recognition and aggressive management of DKA can minimise the possible complications, and is mandatory for the safety of the fetus and mother. 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 >>

Life-threatening Ketoacidosis In A Pregnant Woman With Psychotic Disorder

Life-threatening Ketoacidosis In A Pregnant Woman With Psychotic Disorder

Pregnancy is an insulin resistant state. Hyperglycaemia and gestational diabetes mellitus are well-recognised complications even in women without existing metabolic syndrome or obesity. Pregnant women also appear to be more vulnerable to ketoacidosis, particularly after short periods of reduced oral intake in the third trimester, and may present with very severe starvation ketoacidosis, prompting emergent delivery. We present a case of a woman with a background of depression and psychotic episodes. Olanzapine had been commenced after a psychotic episode at 20 weeks’ gestation. Gestational diabetes mellitus was diagnosed at 28 weeks, and she was then admitted at 31 weeks with severe euglycaemic ketoacidosis following a short period of vomiting. She underwent caesarean section when the metabolic disturbances did not resolve with medical treatment. We believe atypical antipsychotic therapy contributed to the profound insulin resistance seen here, and that obstetricians, physicians and psychiatrists must be aware of the risks conferred by these agents in pregnancy. 1. Knight M, Tuffnell D, Kenyon S, et al. (eds) on behalf of MBRRACE-UK. Saving Lives, Improving Mothers' Care – Surveillance of maternal deaths in the UK 2011–13 and lessons learned to inform maternity care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2009–13. Oxford: National Perinatal Epidemiology Unit, University of Oxford, 2015. Google Scholar 2. Jin, H, Meyer, JM, Jeste, DV. Phenomenology of and risk factors for new-onset diabetes mellitus and diabetic ketoacidosis associated with atypical antipsychotics: an analysis of 45 published cases. Ann Clin Psychiatry 2002; 14: 59–64. Google Scholar, Crossref, Medline 3. Leslie, DL, Rosenheck, RA. Incidence of newly dia Continue reading >>

Diabetic Ketoacidosis In Pregnancy.

Diabetic Ketoacidosis In Pregnancy.

Abstract Pregnancies complicated by diabetic ketoacidosis are associated with increased rates of perinatal morbidity and mortality. A high index of suspicion is required, because diabetic ketoacidosis onset in pregnancy can be insidious, usually at lower glucose levels, and often progresses more rapidly as compared with nonpregnancy. Morbidity and mortality can be reduced with early detection of precipitating factors (ie, infection, intractable vomiting, inadequate insulin management or inappropriate insulin cessation, β-sympathomimetic use, steroid administration for fetal lung maturation), prompt hospitalization, and targeted therapy with intensive monitoring. A multidisciplinary approach including a maternal-fetal medicine physician, medical endocrinology specialists familiar with the physiologic changes in pregnancy, an obstetric anesthesiologist, and skilled nursing is paramount. Management principles include aggressive volume replacement, initiation of intravenous insulin therapy, correction of acidosis, correction of electrolyte abnormalities and management of precipitating factors, as well as monitoring of maternal-fetal response to treatment. When diabetic ketoacidosis occurs after 24 weeks of gestation, fetal status should be continuously monitored given associated fetal hypoxemia and acidosis. The decision for delivery can be challenging and must be based on gestational age as well as maternal-fetal responses to therapy. The natural inclination is to proceed with emergent delivery for nonreassuring fetal status that is frequently present during the acute episode, but it is imperative to correct the maternal metabolic abnormalities first, because both maternal and fetal conditions will likewise improve. Prevention strategies should include education of diabet Continue reading >>

Diabetic Ketoacidosis In Pregnancy

Diabetic Ketoacidosis In Pregnancy

Diabetic ketoacidosis is a serious metabolic complication of diabetes with high mortality if undetected. Its occurrence in pregnancy compromises both the fetus and the mother profoundly. Although predictably more common in patients with type 1 diabetes, it has been recognised in those with type 2 diabetes as well as gestational diabetes, especially with the use of corticosteroids for fetal lung maturity and β2-agonists for tocolysis.1–3 Diabetic ketoacidosis usually occurs in the second and third trimesters because of increased insulin resistance, and is also seen in newly presenting type 1 diabetes patients. With increasing practice of antepartum diabetes screening and the availability of early and frequent prenatal care/surveillance, the incidence and outcomes of diabetic ketoacidosis in pregnancy have vastly improved. However, it still remains a major clinical problem in pregnancy since it tends to occur at lower blood glucose levels and more rapidly than in non-pregnant patients often causing delay in the diagnosis. The purpose of this article is to illustrate a typical patient who may present with diabetic ketoacidosis in pregnancy and review the literature on this relatively uncommon condition and provide an insight into the pathophysiology and management. MAGNITUDE OF THE PROBLEM In non-pregnant patients with type 1 diabetes, the incidence of diabetic ketoacidosis is about 1–5 episodes per 100 per year with mortality averaging 5%–10%.4 The incidence rates of diabetic ketoacidosis in pregnancy and the corresponding fetal mortality rates from different retrospective studies5–8 are summarised in the table 1. As is evident from the table, both the incidence and rates of fetal loss in pregnancies have fallen in recent times compared with those before. In 1963 Continue reading >>

Euglycemic Diabetic Ketoacidosis In Pregnancy

Euglycemic Diabetic Ketoacidosis In Pregnancy

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Fetal Effects Of Diabetic Ketoacidosis

Fetal Effects Of Diabetic Ketoacidosis

The greatest hazard facing the pregnant diabetic patient with DKA is fetal loss. The exact fetal loss rate is difficult to assess because of the small reported series in the literature. Historically, the reported fetal mortality ranged between 30 and 90%7 but remarkable progress has been made both in fetal assessment techniques and in the treatment of DKA, and mortality rates in more recent reviews are 10%.20 Needless to say, fetal loss is primarily related to the severity of the maternal illness and the degree of metabolic decompensation. Most fetal losses occur prior to diagnosis and therefore to the onset of efficient treatment. As ketone bodies freely cross the placenta, maternal acidosis is assumed to cause fetal acidosis; however, the exact mechanism by which maternal DKA affects the fetus remains unclear. Suggestions include a decrease in uterine blood flow and fetal hypoxemia, maternal hyperke-tonemia inducing fetal hypoxemia, and fetal hyperglycemia causing an increased fetal oxidative mechanism and a decreased fetal myocardial contractility. Indeed, fetal potassium deficit has been found to lead to fetal cardiac arrest.7 Fetal hypoxia may also be attributed to a DKA-associated phosphate deficit which leads to depletion of red cell 2,3-diphosphoglycerate and consequent impairment of oxygen delivery. The risk of fetal distress, and even death, during the maternal DKA state makes it mandatory to continuously monitor the fetal heart and to assess the biophysical score, and to evaluate the fetal acid-base balance by cordocentesis if necessary. In the few case reports of fetal monitoring during maternal DKA, a nonreassuring pattern with tachycardia, reduced variability and late decelerations was reported.21,22 LoBue and Goodlin23 found that the administration of jus Continue reading >>

A Case Of A Woman With Late-pregnancy-onset Dka Who Had Normal Glucose Tolerance In The First Trimester

A Case Of A Woman With Late-pregnancy-onset Dka Who Had Normal Glucose Tolerance In The First Trimester

Hiromi Himuro, Takashi Sugiyama, Hidekazu Nishigori, Masatoshi Saito, Satoru Nagase, Junichi Sugawara and Nobuo Yaegashi Department of Obstetrics and Gynecology Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi 980-8574, Japan Summary Diabetic ketoacidosis (DKA) during pregnancy is a serious complication in both mother and fetus. Most incidences occur during late pregnancy in women with type 1 diabetes mellitus. We report the rare case of a woman with type 1 diabetes mellitus who had normal glucose tolerance during the first trimester but developed DKA during late pregnancy. Although she had initially tested positive for screening of gestational diabetes mellitus during the first trimester, subsequent diagnostic 75-g oral glucose tolerance tests showed normal glucose tolerance. She developed DKA with severe general fatigue in late pregnancy. The patient's general condition improved after treatment for ketoacidosis, and she vaginally delivered a healthy infant at term. The presence of DKA caused by the onset of diabetes should be considered, even if the patient shows normal glucose tolerance during the first trimester. The presence of DKA caused by the onset of diabetes should be considered, even if the patient shows normal glucose tolerance during the first trimester. Symptoms including severe general fatigue, nausea, and weight loss are important signs to suspect DKA. Findings such as Kussmaul breathing with ketotic odor are also typical. Urinary test, atrial gas analysis, and anion gap are important. If pH shows normal value, calculation of anion gap is important. If the value of anion gap is more than 12, a practitioner should consider the presence of metabolic acidosis. Background Diabetic ketoacidosis (DKA) is an acute metabol Continue reading >>

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>

Diabetic Ketoacidosis In Pregnancy

Diabetic Ketoacidosis In Pregnancy

Diabetic ketoacidosis affects only 1% to 3% of pregnancies complicated by diabetes; nonetheless it is an acute medical emergency with a potential for dire consequences for both mother and fetus.9,19,31 The maternal mortality rate secondary to diabetes has fallen remarkably from a preinsulin era high of 50% to less than 1% today.18 The rate of maternal loss owing to diabetic ketoacidosis in pregnancy is unknown but most likely ranges from 4% to 15%.18,24,46 The majority of reports on ketoacidosis in pregnancy contain data on 20 or fewer patients, thus maternal mortality rates once ketoacidosis ensues must be extrapolated from nonpregnant data. In the series reported by Gabbe and co-workers,18 7 of 24 deaths in pregnant diabetic women resulted from metabolic complications, with 4 caused by ketoacidosis. Clements and Vourganti11 and Hollingsworth28 have suggested that many of these deaths could have been prevented by appropriate management. Diabetic ketoacidosis more commonly occurs in the second and third trimesters when increased insulin resistance is present.18,41 Fetal mortality has also decreased markedly since the introduction of insulin; however, it is still excessively high. Historically, fetal loss rates have ranged from 30% to 90%.16,32,33 Recently, Montoro and co-workers39 studied 20 type I diabetic pregnant women with ketoacidosis. On admission, seven women (35%) were diagnosed with a fetal demise. None of the remaining 13 women sustained fetal loss once therapy was begun. Kilvert and colleagues31 reported a fetal loss rate of 22% (including spontaneous abortions), with only one (14%) loss among seven cases occurring after the first trimester. Kent and co-workers30 compared fetal mortality among 21 pregnant women with brittle diabetes (those with recurrent keto Continue reading >>

Diabetes Ketoacidosis In Pregnancy

Diabetes Ketoacidosis In Pregnancy

Abstract Diabetic ketoacidosis (DKA) is a serious medical and obstetrical emergency usually occurring in patients with type 1 (insulin-dependent) diabetes mellitus. Although modern management of the patient with diabetes should prevent the occurrence of DKA during pregnancy, this complication still occurs and can result in significant morbidity and mortality for mother and/or fetus. Metabolic changes occurring during pregnancy can predispose a pregnant diabetic to DKA. The diagnosis of DKA can be more challenging during pregnancy as it does not always manifest with the classic presenting symptoms or laboratory findings. In fact, although uncommon, during pregnancy, DKA may develop even in the setting of relative normoglycemia. Prompt diagnosis and management is essential in order to optimize maternal and fetal outcomes. This article will provide the reader with information regarding the pathophysiology underlying DKA complicating pregnancy and will provide practical management guidelines for the diagnosis and management of this condition. Continue reading >>

What Is Diabetes?

What Is Diabetes?

My current understanding compels me to formulate the following brief answer: If both type 1 (an autoimmune) and type 2 (a lifestyle) diabetes are pulled together, I’d describe them with the unifying name ‘fuel partitioning disease of insulin’. Now, that’s not to say that type 1 diabetes does not have a strong lifestyle component as well… You may rightfully ask what I mean by ‘fuel partitioning disease’? Understanding the physiological role of insulin in the body leads you to this conclusion. The general role of insulin was perfectly described by George Cahill in his Banting Memorial Lecture way back in 1971: “Insulin serves as the body's signal for the fed or fasted state. High insulin levels, the “fed” signal, initiate tissue uptake and storage of fuels. Low insulin levels, the “fasted” signal, initiate mobilization of stored fuels from tissue stores, the rate being proportional to the lowness of the insulin. Certain metabolic states such as obesity or trauma alter the concentration of insulin at which no net transfer of fuel occurs, resulting in insulin resistance or hyper-sensitivity.” Our understanding has been refined to some extent since then, but the basics are well described. In fact, where our knowledge has improved the most is the mechanisms underlying the impaired action of insulin. As it seems now, as soon as (especially superficial, below the waistline) subcutaneous fat depots fail to take up and store lipids (fat) in an appropriate (insulin sensitive) way, these lipids get deposited in less appropriate places. First, in deeper subcutaneous, then visceral, epicardial, etc. adipose depots, and if those become full as well, fat starts flooding all insulin sensitive organs, such as the liver, the pancreas, and the endothelium (the inn Continue reading >>

Life-threatening Ketoacidosis In A Pregnant Woman With Psychotic Disorder

Life-threatening Ketoacidosis In A Pregnant Woman With Psychotic Disorder

Go to: Case A 27-year-old female in her fourth pregnancy presented at 31 weeks’ gestation to the delivery suite with reduced fetal movements on a background of a week-long history of vomiting, poor oral intake and intermittent upper abdominal pain radiating to her back. Her past medical history was notable for depression and a psychotic episode 2 years prior to this pregnancy. Her previous pregnancies were not complicated by GDM. She had stopped her antipsychotic medication prior to her booking appointment, but was admitted to a psychiatric hospital at 20 weeks of gestation with a further episode. At that time olanzapine 20mg daily was commenced in addition to the 40mg fluoxetine that she had been taking regularly prior to and throughout pregnancy. At 23 and 27 weeks of gestation, glycosuria was identified on urine dipstick testing. Metformin was commenced after an abnormal oral glucose tolerance test (fasting glucose 8.1mmol/L, 2h glucose 12.7mmol/L) at 28 weeks. Metformin resulted in some improvement in glycaemic control. She had taken no other medications during pregnancy and denied any substance misuse. Booking body mass index was 37kg/m2. On examination she looked unwell. She was tachypnoeic, tachycardic and hypertensive (heart rate 130 beats per minute, blood pressure 162/103mm Hg). On abdominal palpation there was tenderness in the epigastric region without peritonism. The gravid uterus was an appropriate size for gestational age. Cardiotocography was reassuring. Blood tests were notable for anaemia (haemoglobin 10.4g/dL) and neutrophilia (20.1×109/L). Urinalysis was positive for protein (trace) and ketones (4+). Arterial blood gas analysis showed a profound metabolic acidosis with partial respiratory compensation (pH 7.24, PaCO2 1.4kPa, PaO2 15.5kPa, base exc Continue reading >>

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