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Dka Myocardial Infarction

“pseudoinfarction” Pattern Due To Hyperkalemia

“pseudoinfarction” Pattern Due To Hyperkalemia

A 38-year-old man presented to the emergency department with nausea, vomiting, and epigastric pain. The patient had type 1 diabetes mellitus and was being treated with insulin. He was also taking lisinopril for the treatment of hypertension. The initial electrocardiogram (Panel A) revealed sinus tachycardia and ST-segment elevation in leads V1 to V3 — findings highly suggestive of acute anteroseptal myocardial infarction. Peaked T waves were noted in leads II, III, aVF, and V3 to V6. The serum glucose concentration was 839 mg per deciliter (46.6 mmol per liter), the arterial blood pH was 7.21, and the serum potassium concentration was 7.9 mmol per liter. The diagnosis of diabetic ketoacidosis was made. When the electrocardiogram was repeated several hours later, after the potassium concentration was lowered to 5.1 mmol per liter with treatment (Panel B [lead V5 is not placed]), the ST-segment elevation disappeared completely, as did the peaked T waves. This case is an example of hyperkalemia causing a “pseudoinfarction” pattern. The clue to the correct diagnosis is the T wave in V4, which is tall, narrow, and pointed, with a short QT interval. The tall T waves that are characteristic of hyperacute ischemic changes tend to be associated with a long QT interval, and the T waves are broad rather than narrow and pointed. Kyuhyun Wang, M.D. Hennepin County Medical Center, Minneapolis, MN 55415 Continue reading >>

Myocardial Injury With Biomarker Elevation In Diabetic Ketoacidosis

Myocardial Injury With Biomarker Elevation In Diabetic Ketoacidosis

Abstract We report of two patients with severe ketoacidosis, minute elevations of myocardial biomarkers (troponin T and CK-MB) and initial ECG changes compatible with myocardial infarction (MI). All successive investigations, including coronary arteriography, were normal, and the patients recovered fully without further evidence of ischemic heart disease. We suggest that acidosis and very high levels of free fatty acids could cause membrane instability and biomarker leakage. Regardless of the pathogenesis, these two case stories suggest that nonspecific myocardial injury may occur in severe diabetic ketoacidosis and that the presence of minute biomarker elevation and ECG changes does not necessarily signify MI. Continue reading >>

Distinctive Characteristics And Specific Management Of Diabetic Ketoacidosis In Patients With Acute Myocardial Infarction, Stroke And Renal Failure

Distinctive Characteristics And Specific Management Of Diabetic Ketoacidosis In Patients With Acute Myocardial Infarction, Stroke And Renal Failure

1. Introduction Diabetic ketoacidosis (DKA) is considered a predominantly acute type 1 diabetic complication, although it may occur in type 2 diabetes as well, particularly in patients who already have a decreased insulin secretion capacity. Stress –induced burst in catecholamine and ACTH secretion in acute myocardial infarction (AMI) promotes release of free fatty acids and their hepatic and muscular tissue utilization. The impairment in insulin-mediated intracellular glucose influx owing to the absent or insufficient pancreatic insulin secretion is the prerequisite for the occurrence of diabetic ketoacidosis. The results of the analysis of acid – base disturbances from our previous study [26] performed in the intensive-care unit in diabetics and non-diabetics suffering acute myocardial infarction are shown in Fig. 1. Cardiovascular accidents have a marked place among the possible causes of diabetic ketoacidosis. Cardiovascular morbidity influences the severity and duration of diabetic ketoacidosis and limits the first and most important step in its treatment- the fluid resuscitation. The resulting hyperosmolarity of body fluids precipitates a pro-thrombotic state, thus aggravating prognosis in patients with myocardial infarction. The clinical features of hyperglycemic/hyperosmolar state and diabetic ketoacidosis may overlap and are observed simultaneously (overlap cases) [44]. Acid-base disturbances in diabetics and non-diabetics suffering acute myocardial infarction: Almost one-third of diabetic patients with acute myocardial infarction had un-compensated metabolic acidosis defined as pH< 35, HCO3- < 22mmol/L. Although acidosis was mild in most of the cases at least third of these patients had criteria for true diabetic ketoacidosis (pH<30, HCO3- <15mmol/L). Addi Continue reading >>

Cardiovascular Complications Of Ketoacidosis

Cardiovascular Complications Of Ketoacidosis

US Pharm. 2016;41(2):39-42. ABSTRACT: Ketoacidosis is a serious medical emergency requiring hospitalization. It is most commonly associated with diabetes and alcoholism, but each type is treated differently. Some treatments for ketoacidosis, such as insulin and potassium, are considered high-alert medications, and others could result in electrolyte imbalances. Several cardiovascular complications are associated with ketoacidosis as a result of electrolyte imbalances, including arrhythmias, ECG changes, ventricular tachycardia, and cardiac arrest, which can be prevented with appropriate initial treatment. Acute myocardial infarction can predispose patients with diabetes to ketoacidosis and worsen their cardiovascular outcomes. Cardiopulmonary complications such as pulmonary edema and respiratory failure have also been seen with ketoacidosis. Overall, the mortality rate of ketoacidosis is low with proper and urgent medical treatment. Hospital pharmacists can help ensure standardization and improve the safety of pharmacotherapy for ketoacidosis. In the outpatient setting, pharmacists can educate patients on prevention of ketoacidosis and when to seek medical attention. Metabolic acidosis occurs as a result of increased endogenous acid production, a decrease in bicarbonate, or a buildup of endogenous acids.1 Ketoacidosis is a metabolic disorder in which regulation of ketones is disrupted, leading to excess secretion, accumulation, and ultimately a decrease in the blood pH.2 Acidosis is defined by a serum pH <7.35, while a pH <6.8 is considered incompatible with life.1,3 Ketone formation occurs by breakdown of fatty acids. Insulin inhibits beta-oxidation of fatty acids; thus, low levels of insulin accelerate ketone formation, which can be seen in patients with diabetes. Extr Continue reading >>

Case Report Issn 2450–7458

Case Report Issn 2450–7458

73 Address for correspondence: Piotr MolÄ™da, M.D., PhD. ul. Siedlecka 2, 72–010 Police Phone/fax: +48 (91) 425 38 58 e-mail: [email protected] Clinical Diabetology 2016, 5, 2, 73–76 DOI: 10.5603/DK.2016.0012 Received: 03.04.2016 Accepted: 15.04.2016 Aneta Fronczyk, Piotr MolÄ™da, Liliana Majkowska Department of Diabetology and Internal Medicine, Pomeranian Medical University in Szczecin, Poland Clinical and ECG patterns of pseudoinfarction in a young man with type 1 diabetes, diabetic ketoacidosis and normokalaemia ABSTRACT Diabetic ketoacidosis (DKA) can cause changes in the electrocardiogram (ECG) in the form of transient ST-segment depression, QT prolongation, changes in T-wave morphology and the appearance of U wave, possibly due to changes in the serum potassium level. Occasional reports indicate the possibility of transient ST-segment elevation imitating myocardial infarction in the course of hyperkalaemia accompanying DKA. In this article we present a case of a 20-year-old male patient with type 1 diabetes mellitus, DKA and normokalae- mia, who experienced severe retrosternal pain, and ECG presented ST-segment elevation imitating acute myocardial infarction of the anterior wall. On the basis of the performed cardiac tests, including laboratory testing, coronary angiography and ultrasound scan, acute coronary syndrome was ruled out. The regression of retrosternal pain and electrocardiographic changes with patient hydration and correction of metabolic disorders suggest the diagnosis of pseudopericar- ditis, i.e. non-infections irritation of the pericardial membranes due to the loss of fluid in the pericardial sac as a result of dehydration. The diagnosis of acute myocardial infarction based on ST-segment elevation in the ECG recording in a patient Continue reading >>

Diabetic Ketoacidosis Inducing Myocardial Infarction Secondary To Treatment With Dapagliflozin: A Case Report

Diabetic Ketoacidosis Inducing Myocardial Infarction Secondary To Treatment With Dapagliflozin: A Case Report

Go to: Case Report A 58‐year‐old male with dyslipidemia, an eight‐year history of T2DM, a family history, his mother, of T2DM, with no known micro‐ or macrovascular complications, was admitted to the emergency department for malaise, epigastric pain, polyuria, and progressive dyspnea which had begun 10 h ago. He had experienced a 2‐kg weight loss over the last few days. His usual medications included aspirin 100 mg q24 h, atorvastatin 40 mg q24 h, and metformin 850 mg q8 h, which had been switched to dapagliflozin 20 days before, due to poor glycemic control, with HbA1c 12% (108 mmol/mol). His vital signs included a heart rate of 122 bpm, respiratory rate 33 rpm, blood pressure 142/70 mmHg, temperature 36.1°C, and body mass index 22.5 kg/m2. On physical examination, somnolence, dry skin and mucous membranes, a Kussmaul breathing pattern, and a capillary refill of 3 sec were observed. Blood tests revealed hemoglobin 17.1 g/dL (13.5–18), leukocytes 19.5 × 103 (4–10 × 103), platelets 296 × 103 (150–450 × 103), glucose 248 mg/dL (60–100), creatinine 0.97 mg/dL (0.67–1.17), sodium 136 mmol/L (135–145), potassium 4.7 mmol/L (3.5–5.5), chloride 101 mmol/L (95–112), phosphate 4.9 mg/dL (2.5–4.5), amylase 70 U/L (10–115), lipase 28 U/L (1–67), pH 6.95 (7.35–7.45), pCO2 23 mmHg (35–45), HCO3 5 mmol/L (22–26), lactate 1.8 mmol/L (0–1.5), urine ketone bodies >150 mg/dL (0–0), CK 112 U/L (1–190), CK‐MB 7.3 ng/mL (0.1–5), and troponin I 0.07 ng/mL (0.001–0.05). The electrocardiogram (EKG) showed sinus rhythm with right bundle branch block, and nonspecific repolarization abnormalities. Because of the right bundle branch block was not previously known, a new troponin test was performed six hours later with a peak value of 4.28 ng/m Continue reading >>

Diabetes: Preventing Complications

Diabetes: Preventing Complications

Diabetes complications can be divided into two types: acute (sudden) and chronic (long-term). This article discusses these complications and strategies to prevent the complications from occurring in the first place. Acute complications Diabetic ketoacidosis (DKA) Hyperglycemic hyperosmolar non-ketotic syndrome (HHNS) Acute complications of diabetes can occur at any time in the course of the disease. Chronic complications Cardiovascular: Heart disease, peripheral vascular disease, stroke Eye: Diabetic retinopathy, cataracts, glaucoma Nerve damage: Neuropathy Kidney damage: Nephropathy Chronic complications are responsible for most illness and death associated with diabetes. Chronic complications usually appear after several years of elevated blood sugars (hyperglycemia). Since patients with Type 2 diabetes may have elevated blood sugars for several years before being diagnosed, these patients may have signs of complications at the time of diagnosis. Basic principles of prevention of diabetes complications: Take your medications (pills and/or insulin) as prescribed by your doctor. Monitor your blood sugars closely. Follow a sensible diet. Do not skip meals. Exercise regularly. See your doctor regularly to monitor for complications. Results from untreated hyperglycemia. Blood sugars typically range from 300 to 600. Occurs mostly in patients with Type 1 diabetes (uncommon in Type 2). Occurs due to a lack of insulin. Body breaks down its own fat for energy, and ketones appear in the urine and blood. Develops over several hours. Can cause coma and even death. Typically requires hospitalization. Nausea, vomiting Abdominal pain Drowsiness, lethargy (fatigue) Deep, rapid breathing Increased thirst Fruity-smelling breath Dehydration Inadequate insulin administration (not getting Continue reading >>

Misleading Electrocardiographic Results In Patient With Hyperkalaemia And Diabetic Ketoacidosis

Misleading Electrocardiographic Results In Patient With Hyperkalaemia And Diabetic Ketoacidosis

Go to: Case report A 42 year old man with diabetes presented to accident and emergency with intermittent vomiting for three days. Over the previous two days he had been feeling increasingly tired, lethargic, polyuric, and thirsty. As he was unable to keep any food or fluids down, he had omitted two insulin injections, including one on the morning of admission. He had no history of chest pain. He had had type 1 diabetes for 15 years and was injecting soluble and isophane human insulin twice daily. He had not attended the hospital clinic for several years and had no known complications of diabetes. He was known to have hypercholesterolaemia but was not taking any drugs for it. He had a strong family history of ischaemic heart disease. On initial assessment he was drowsy and dehydrated with tachypnoea, tachycardia, and a temperature of 37.1°C. There were no localising clinical signs of infection. A urine dipstick test detected ketones, bedside capillary testing with a glucometer showed “high” glucose concentrations, and arterial blood gas analysis indicated metabolic acidosis (pH 7.06, carbon dioxide partial pressure 1.8 kPa, oxygen partial pressure 15.9 kPa, bicarbonate concentration 4 mmol/l, and base excess –24 mmol/l). Blood samples were sent to the laboratory. We diagnosed diabetic ketoacidosis and started fluid replacement with 0.9% saline and intravenous soluble insulin at 6 units/hour. An electrocardiogram showed sinus tachycardia and marked ST segment elevation in the anteroseptal leads consistent with anterior myocardial infarction (fig 1). No Q waves were present. In the inferior wall leads, there was ST segment elevation and T wave inversion in leads 3 and aVF. He also had an intraventricular conduction delay similar to a right bundle branch block with d Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis is a topic covered in the Washington Manual of Medical Therapeutics. The Washington Manual of Medical Therapeutics helps you diagnose and treat hundreds of medical conditions. Consult clinical recommendations from a resource that has been trusted on the wards for 50+ years. Explore these free sample topics: -- The first section of this topic is shown below -- DKA, a potentially fatal complication of diabetes, occurs in up to 5% of patients with T1DM annually and can occur in insulin-deficient patients with T2DM. DKA is a catabolic condition that results from severe insulin deficiency, often in association with stress and activation of counter-regulatory hormones (e.g., catecholamines, glucagon). Precipitating factors for DKA include inadvertent or deliberate interruption of insulin therapy, sepsis, trauma, myocardial infarction (MI), and pregnancy. DKA may be the first presentation of T1DM and, rarely, T2DM. DKA can be prevented in many cases, and its occurrence suggests a breakdown in education, communication, and problem solving. Therefore, diabetes education should be reinforced at every opportunity, with special emphasis on (a) self-management skills during sick days; (b) the body’s need for more, rather than less, insulin during such illnesses; (c) testing of blood or urine for ketones; and (d) procedures for obtaining timely and preventive medical advice. -- To view the remaining sections of this topic, please sign in or purchase a subscription -- Continue reading >>

Steroid Induced Diabetic Ketoacidosis In Patient With Diabetes Mellitus-type 2

Steroid Induced Diabetic Ketoacidosis In Patient With Diabetes Mellitus-type 2

Objective Diabetic ketoacidosis is usually associated with type 1 diabetes; however, it is increasingly being recognized in patients with type 2 diabetes mellitus. Triggering factors usually involve infections and poor medication adherence. Other potential triggers reported are myocardial infarction, antipsychotic drug usage, malignancy and cerebrovascular accidents. No case of steroid induced diabetic ketoacidosis in a patient with type 2 diabetes mellitus has been reported in the literature. Methods Clinical and laboratory data are presented. Results We present a case of a middle age patient with a history of well-controlled type 2 diabetes on metformin, who was started on oral prednisone for lumbar disc herniation and presented with acute diabetic ketoacidosis. No other trigger for diabetic ketoacidosis but steroid initiation was found. Conclusion We concluded that patients with diabetes who receive glucocorticoids should be monitored carefully, as steroids can precipitate DKA, in the absence of any other triggering factor, even in patients with well-controlled type 2 diabetes. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Initial Evaluation Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors (Table 14–18). The most common precipitating factor is infection, followed by noncompliance with insulin therapy.3 While insulin pump therapy has been implicated as a risk factor for DKA in the past, most recent studies show that with proper education and practice using the pump, the frequency of DKA is the same for patients on pump and injection therapy.19 Common causes by frequency Other causes Selected drugs that may contribute to diabetic ketoacidosis Infection, particularly pneumonia, urinary tract infection, and sepsis4 Inadequate insulin treatment or noncompliance4 New-onset diabetes4 Cardiovascular disease, particularly myocardial infarction5 Acanthosis nigricans6 Acromegaly7 Arterial thrombosis, including mesenteric and iliac5 Cerebrovascular accident5 Hemochromatosis8 Hyperthyroidism9 Pancreatitis10 Pregnancy11 Atypical antipsychotic agents12 Corticosteroids13 FK50614 Glucagon15 Interferon16 Sympathomimetic agents including albuterol (Ventolin), dopamine (Intropin), dobutamine (Dobutrex), terbutaline (Bricanyl),17 and ritodrine (Yutopar)18 DIFFERENTIAL DIAGNOSIS Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue. Common problems that produce ketosis include alcoholism and starvation. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol. Abdominal pain may be a symptom of ketoacidosis or part of the inci Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. Continue reading >>

Ecg Review: Dka And Acute Mi?

Ecg Review: Dka And Acute Mi?

ECG Review: DKA and Acute MI? Figure. 12-lead ECG obtained from a 32-year-old man who presented in DKA. Clinical Scenario: The ECG in the Figure was obtained from a previously healthy 32-year-old African American male who presented in coma from diabetic ketoacidosis (DKA). Cardiovascular exam was unremarkable. In addition to treating this patient’s DKA, should he also be considered a potential candidate for thrombolytic therapy? Interpretation: The ECG in the Figure shows normal sinus rhythm at a rate of about 60/minute. The PR interval is at the upper range of normal (= 0.21 second). The QRS and QT intervals are normal. The mean QRS axis is +60°. In view of the patient’s age, there is no evidence of chamber enlargement. Perhaps the most remarkable finding on this tracing is the presence of diffuse ST segment elevation. This finding is present in virtually all leads except III, aVR, and V1. It is most marked in lead V5, where ST segment elevation attains at least 3 mm. Despite the presence of diffuse ST elevation, it is highly unlikely that this pattern represents acute infarction. ST segment morphology is clearly upsloping (upward concavity), with marked notching of the J point in multiple leads (especially II, V4, V5, V6). The ST segment appearance that is characteristic of acute infarction is more typically coved (downward convexity) and is usually localized to 1 or 2 specific lead areas, rather than being as generalized as it is here. Marked acute ST segment elevation indicative of acute infarction is also commonly associated with reciprocal ST segment depression, which is not seen here. Although Q waves are present in the inferolateral leads, they are quite small and narrow. This is much more consistent with normal septal q waves rather than acute evolving inf Continue reading >>

Emergency Management Of Diabetic Ketoacidosis In Adults

Emergency Management Of Diabetic Ketoacidosis In Adults

Diabetic ketoacidosis (DKA) is a potentially fatal metabolic disorder presenting most weeks in most accident and emergency (A&E) departments.1 The disorder can have significant mortality if misdiagnosed or mistreated. Numerous management strategies have been described. Our aim is to describe a regimen that is based, as far as possible, on available evidence but also on our experience in managing patients with DKA in the A&E department and on inpatient wards. A literature search was carried out on Medline and the Cochrane Databases using “diabetic ketoacidosis” as a MeSH heading and as textword. High yield journals were hand searched. Papers identified were appraised in the ways described in the Users’ guide series published in JAMA. We will not be discussing the derangements in intermediary metabolism involved, nor would we suggest extrapolating the proposed regimen to children. Although some of the issues discussed may be considered by some to be outwith the remit of A&E medicine it would seem prudent to ensure that A&E staff were aware of the probable management of such patients in the hours after they leave the A&E department. AETIOLOGY AND DEFINITION DKA may be the first presentation of diabetes. Insulin error (with or without intercurrent illness) is the most common precipitating factor, accounting for nearly two thirds of cases (excluding those where DKA was the first presentation of diabetes mellitus).2 The main features of DKA are hyperglycaemia, metabolic acidosis with a high anion gap and heavy ketonuria (box 1). This contrasts with the other hyperglycaemic diabetic emergency of hyperosmolar non-ketotic hyperglycaemia where there is no acidosis, absent or minimal ketonuria but often very high glucose levels (>33 mM) and very high serum sodium levels (>15 Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology In Continue reading >>

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