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How Does Mi Cause Dka

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 >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Tweet Diabetic ketoacidosis (DKA) is a dangerous complication faced by people with diabetes which happens when the body starts running out of insulin. DKA is most commonly associated with type 1 diabetes, however, people with type 2 diabetes that produce very little of their own insulin may also be affected. Ketoacidosis is a serious short term complication which can result in coma or even death if it is not treated quickly. Read about Diabetes and Ketones What is diabetic ketoacidosis? DKA occurs when the body has insufficient insulin to allow enough glucose to enter cells, and so the body switches to burning fatty acids and producing acidic ketone bodies. A high level of ketone bodies in the blood can cause particularly severe illness. Symptoms of DKA Diabetic ketoacidosis may itself be the symptom of undiagnosed type 1 diabetes. Typical symptoms of diabetic ketoacidosis include: Vomiting Dehydration An unusual smell on the breath –sometimes compared to the smell of pear drops Deep laboured breathing (called kussmaul breathing) or hyperventilation Rapid heartbeat Confusion and disorientation Symptoms of diabetic ketoacidosis usually evolve over a 24 hour period if blood glucose levels become and remain too high (hyperglycemia). Causes and risk factors for diabetic ketoacidosis As noted above, DKA is caused by the body having too little insulin to allow cells to take in glucose for energy. This may happen for a number of reasons including: Having blood glucose levels consistently over 15 mmol/l Missing insulin injections If a fault has developed in your insulin pen or insulin pump As a result of illness or infections High or prolonged levels of stress Excessive alcohol consumption DKA may also occur prior to a diagnosis of type 1 diabetes. Ketoacidosis can occasional Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis (DKA) is a life-threatening condition that develops when cells in the body are unable to get the sugar (glucose) they need for energy because there is not enough insulin. When the sugar cannot get into the cells, it stays in the blood. The kidneys filter some of the sugar from the blood and remove it from the body through urine. Because the cells cannot receive sugar for energy, the body begins to break down fat and muscle for energy. When this happens, ketones, or fatty acids, are produced and enter the bloodstream, causing the chemical imbalance (metabolic acidosis) called diabetic ketoacidosis. Ketoacidosis can be caused by not getting enough insulin, having a severe infection or other illness, becoming severely dehydrated, or some combination of these things. It can occur in people who have little or no insulin in their bodies (mostly people with type 1 diabetes but it can happen with type 2 diabetes, especially children) when their blood sugar levels are high. Your blood sugar may be quite high before you notice symptoms, which include: Flushed, hot, dry skin. Blurred vision. Feeling thirsty and urinating a lot. Drowsiness or difficulty waking up. Young children may lack interest in their normal activities. Rapid, deep breathing. A strong, fruity breath odor. Loss of appetite, belly pain, and vomiting. Confusion. Laboratory tests, including blood and urine tests, are used to confirm a diagnosis of diabetic ketoacidosis. Tests for ketones are available for home use. Keep some test strips nearby in case your blood sugar level becomes high. When ketoacidosis is severe, it must be treated in the hospital, often in an intensive care unit. Treatment involves giving insulin and fluids through your vein and closely watching certain chemicals in your b 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 a coma from diabetic ketoacidosis (DKA). Cardiovascular exam was unremarkable. In addition to being treated for 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, and V6). The ST segment appearance that is characteristic of acute infarction is more typically coved (downward convexity) and usually is localized to one or two specific lead areas, rather than being as generalized as it is here. Marked acute ST segment elevation indicative of acute infarction also commonly is 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 Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

OVERVIEW potentially life-threatening complication of diabetes melitus resulting from the consequences of insulin deficiency Diagnostic criteria pH < 7.3 ketosis (ketonemia or ketonuria) HCO3 <15 mmol/L due to high anion gap metabolic acidosis (HAGMA) hyperglycemia (may be mild; euglycemic DKA can occur) PATHOGENESIS increased glucagon, cortisol, catcholamines, GH decreased insulin -> hyperglycaemia -> hyperosmolality + glycosuria -> electrolyte loss -> ketone production from metabolism of TG -> acidosis HISTORY dry, abdominal pain, polyuria, weight loss, coma risk factors: non-compliance, illness, newly diagnosed ROS to rule find out possible precipitant (infection, MI, pneumonia, GI illness) normal insulin regime diabetic control previous DKA’s/admissions previous ICU admissions EXAMINATION volume assessment signs of cause e.g. (infection) GCS work of breathing INVESTIGATIONS ABG electrolytes osmolality urinalysis: ketones pregnancy test standard investigations to rule out cause: FBC, ECG, CXR MANAGEMENT Goals (1) establish precipitant and treat (2) assess severity of metabolic derangement (3) cautious fluid resuscitation with replacement of body H2O (4) provision of insulin (5) replacement of electrolytes Resuscitate intubation for airway protection if required O2 as required IV access fluid boluses (20mL/kg boluses of NS/HMN) urinary catheter Acid-base and Electrolyte abnormalities will have a severe metabolic acidosis with probable incomplete respiratory compensation K+ may be normal but patient will have a whole body K+ deficiency -> needs to be replaced once < 5mmol/L -> use KH2PO4 Na+ may be deranged acidaemia rarely requires HCO3- therapy and will respond to other treatments Specific therapy start insulin infusion (avoid bolus) 0.1u/kg/hr aim to lower glucose Continue reading >>

Diabetic Ketoacidosis - Symptoms

Diabetic Ketoacidosis - Symptoms

A A A Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) results from dehydration during a state of relative insulin deficiency, associated with high blood levels of sugar level and organic acids called ketones. Diabetic ketoacidosis is associated with significant disturbances of the body's chemistry, which resolve with proper therapy. Diabetic ketoacidosis usually occurs in people with type 1 (juvenile) diabetes mellitus (T1DM), but diabetic ketoacidosis can develop in any person with diabetes. Since type 1 diabetes typically starts before age 25 years, diabetic ketoacidosis is most common in this age group, but it may occur at any age. Males and females are equally affected. Diabetic ketoacidosis occurs when a person with diabetes becomes dehydrated. As the body produces a stress response, hormones (unopposed by insulin due to the insulin deficiency) begin to break down muscle, fat, and liver cells into glucose (sugar) and fatty acids for use as fuel. These hormones include glucagon, growth hormone, and adrenaline. These fatty acids are converted to ketones by a process called oxidation. The body consumes its own muscle, fat, and liver cells for fuel. In diabetic ketoacidosis, the body shifts from its normal fed metabolism (using carbohydrates for fuel) to a fasting state (using fat for fuel). The resulting increase in blood sugar occurs, because insulin is unavailable to transport sugar into cells for future use. As blood sugar levels rise, the kidneys cannot retain the extra sugar, which is dumped into the urine, thereby increasing urination and causing dehydration. Commonly, about 10% of total body fluids are lost as the patient slips into diabetic ketoacidosis. Significant loss of potassium and other salts in the excessive urination is also common. The most common 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 >>

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 >>

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

Diabetic Ketoacidosis

The Facts Diabetic ketoacidosis (DKA) is a condition that may occur in people who have diabetes, most often in those who have type 1 (insulin-dependent) diabetes. It involves the buildup of toxic substances called ketones that make the blood too acidic. High ketone levels can be readily managed, but if they aren't detected and treated in time, a person can eventually slip into a fatal coma. DKA can occur in people who are newly diagnosed with type 1 diabetes and have had ketones building up in their blood prior to the start of treatment. It can also occur in people already diagnosed with type 1 diabetes that have missed an insulin dose, have an infection, or have suffered a traumatic event or injury. Although much less common, DKA can occasionally occur in people with type 2 diabetes under extreme physiologic stress. Causes With type 1 diabetes, the pancreas is unable to make the hormone insulin, which the body's cells need in order to take in glucose from the blood. In the case of type 2 diabetes, the pancreas is unable to make sufficient amounts of insulin in order to take in glucose from the blood. Glucose, a simple sugar we get from the foods we eat, is necessary for making the energy our cells need to function. People with diabetes can't get glucose into their cells, so their bodies look for alternative energy sources. Meanwhile, glucose builds up in the bloodstream, and by the time DKA occurs, blood glucose levels are often greater than 22 mmol/L (400 mg/dL) while insulin levels are very low. Since glucose isn't available for cells to use, fat from fat cells is broken down for energy instead, releasing ketones. Ketones accumulate in the blood, causing it to become more acidic. As a result, many of the enzymes that control the body's metabolic processes aren't able Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. 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 >>

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 >>

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 >>

How The Treatment Of Diabetic Ketoacidosis Has Improved

How The Treatment Of Diabetic Ketoacidosis Has Improved

For patients with type 1 diabetes, one of the most serious medical emergencies is diabetic ketoacidosis (DKA). It can be life-threatening and, in most cases, is caused by a shortage of insulin. Glucose is the “fuel” which feeds human cells. Without it, these cells are forced to “burn” fatty acids in order to survive. This process leads to the production of acidic ketone bodies which can cause serious symptoms and complications such as passing out, confusion, vomiting, dehydration, coma, and, if not corrected in a timely manner, even death. High levels of ketones poison the body. DKA can be diagnosed with blood and urine tests and is distinguished from other ketoacidosis by the presence of high blood sugar levels. Typical treatment for DKA consists of using intravenous fluids to correct the dehydration, insulin dosing to suppress the production of ketones, and treatment for any underlying causes such as infections. Medical history notes that DKA was first diagnosed and described in 1886 and until insulin therapy was introduced in the 1920’s, this condition was almost universally fatal. However, with availability and advances in insulin therapy, the mortality rate is less than one percent when timely treatment is applied. A Clinical Pharmacist Examines DKA Ron Fila (RPh) is a clinical pharmacist at McLaren Northern Michigan in Petoskey, MI. He has first-hand experience in treating patients with DKA and, as one of the early adaptors of EndoTool he has seen how this algorithmically-based glucose management software can help physicians save lives and improve patient outcomes. “We started using EndoTool in 2013, for treating patients in the ICU,” he noted in a recent interview. “Later, we expanded our use of this software for DKA and pediatrics. “Since DKA i Continue reading >>

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