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Dka Management Guidelines

My Site - Chapter 15: Hyperglycemic Emergencies In Adults

My Site - Chapter 15: Hyperglycemic Emergencies In Adults

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) should be suspected in ill patients with diabetes. If either DKA or HHS is diagnosed, precipitating factors must be sought and treated. DKA and HHS are medical emergencies that require treatment and monitoring for multiple metabolic abnormalities and vigilance for complications. A normal blood glucose does not rule out DKA in pregnancy. Ketoacidosis requires insulin administration (0.1 U/kg/h) for resolution; bicarbonate therapy should be considered only for extreme acidosis (pH7.0). Note to readers: Although the diagnosis and treatment of diabetic ketoacidosis (DKA) in adults and in children share general principles, there are significant differences in their application, largely related to the increased risk of life-threatening cerebral edema with DKA in children and adolescents. The specific issues related to treatment of DKA in children and adolescents are addressed in the Type 1 Diabetes in Children and Adolescents chapter, p. S153. Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are diabetes emergencies with overlapping features. With insulin deficiency, hyperglycemia causes urinary losses of water and electrolytes (sodium, potassium, chloride) and the resultant extracellular fluid volume (ECFV) depletion. Potassium is shifted out of cells, and ketoacidosis occurs as a result of elevated glucagon levels and absolute insulin deficiency (in the case of type 1 diabetes) or high catecholamine levels suppressing insulin release (in the case of type 2 diabetes). In DKA, ketoacidosis is prominent, while in HHS, the main features are ECFV depletion and hyperosmolarity. Risk factors for DKA include new diagnosis of diabetes mellitus, insulin omission, infection, myocardial infarc Continue reading >>

Hyperglycemic Crises In Adult Patients With Diabetes

Hyperglycemic Crises In Adult Patients With Diabetes

Diabetic ketoacidosis (DKA) and the hyperosmolar hyperglycemic state (HHS) are the two most serious acute metabolic complications of diabetes. DKA is responsible for more than 500,000 hospital days per year (1,2) at an estimated annual direct medical expense and indirect cost of 2.4 billion USD (2,3). Table 1 outlines the diagnostic criteria for DKA and HHS. The triad of uncontrolled hyperglycemia, metabolic acidosis, and increased total body ketone concentration characterizes DKA. HHS is characterized by severe hyperglycemia, hyperosmolality, and dehydration in the absence of significant ketoacidosis. These metabolic derangements result from the combination of absolute or relative insulin deficiency and an increase in counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). Most patients with DKA have autoimmune type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness such as trauma, surgery, or infections. This consensus statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS in adult subjects. It is based on a previous technical review (4) and more recently published peer-reviewed articles since 2001, which should be consulted for further information. Recent epidemiological studies indicate that hospitalizations for DKA in the U.S. are increasing. In the decade from 1996 to 2006, there was a 35% increase in the number of cases, with a total of 136,510 cases with a primary diagnosis of DKA in 2006—a rate of increase perhaps more rapid than the overall increase in the diagnosis of diabetes (1). Most patients with DKA were between the ages of 18 and 44 years (56%) and 45 and 65 years (24%), with only 18% of patie Continue reading >>

The Management Of Diabetic Ketoacidosis In Adults

The Management Of Diabetic Ketoacidosis In Adults

Action 1: Commence 0.9% sodium chloride solution (use large bore cannula) via infusion pump. See Box 2 for rate of fluid replacement Action 2: Commence a fixed rate intravenous insulin infusion (IVII). (0.1unit/kg/hr based on estimate of weight) 50 units human soluble insulin (Actrapid® or Humulin S®) made up to 50ml with 0.9% sodium chloride solution. If patient normally takes long acting insulin analogue (Lantus®, Levemir®) continue at usual dose and time Action 3: Assess patient o Respiratory rate; temperature; blood pressure; pulse; oxygen saturation o Glasgow Coma Scale o Full clinical examination Action 4: Further investigations • Capillary and laboratory glucose • Venous BG • U & E • FBC • Blood cultures • ECG • CXR • MSU Action 5: Establish monitoring regimen • Hourly capillary blood glucose • Hourly capillary ketone measurement if available • Venous bicarbonate and potassium at 60 minutes, 2 hours and 2 hourly thereafter • 4 hourly plasma electrolytes • Continuous cardiac monitoring if required • Continuous pulse oximetry if required Action 6: Consider and precipitating causes and treat appropriately BOX 1: Immediate management: time 0 to 60 minutes (T=0 at time intravenous fluids are commenced) If intravenous access cannot be obtained request critical care support immediately Systolic BP (SBP) below 90mmHg Likely to be due to low circulating volume, but consider other causes such as heart failure, sepsis, etc. • Give 500ml of 0.9% sodium chloride solution over 10-15 minutes. If SBP remains below 90mmHg repeat whilst requesting senior input. Most patients require between 500 to 1000ml given rapidly. • Consider involving the ITU/critical care team. • Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

Hyperglycemic Crises In Diabetes

Hyperglycemic Crises In Diabetes

Ketoacidosis and hyperosmolar hyperglycemia are the two most serious acute metabolic complications of diabetes, even if managed properly. These disorders can occur in both type 1 and type 2 diabetes. The mortality rate in patients with diabetic ketoacidosis (DKA) is <5% in experienced centers, whereas the mortality rate of patients with hyperosmolar hyperglycemic state (HHS) still remains high at ∼15%. The prognosis of both conditions is substantially worsened at the extremes of age and in the presence of coma and hypotension (1–10). This position statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS. It is based on a previous technical review (11), which should be consulted for further information. PATHOGENESIS Although the pathogenesis of DKA is better understood than that of HHS, the basic underlying mechanism for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones, such as glucagon, catecholamines, cortisol, and growth hormone. These hormonal alterations in DKA and HHS lead to increased hepatic and renal glucose production and impaired glucose utilization in peripheral tissues, which result in hyperglycemia and parallel changes in osmolality of the extracellular space (12,13). The combination of insulin deficiency and increased counterregulatory hormones in DKA also leads to the release of free fatty acids into the circulation from adipose tissue (lipolysis) and to unrestrained hepatic fatty acid oxidation to ketone bodies (β-hydroxybutyrate [β-OHB] and acetoacetate), with resulting ketonemia and metabolic acidosis. On the other hand, HHS may be caused by plasma insulin concentrations that are in Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis (DKA) is a metabolic emergency occurring in Type 1 diabetes. It is characterised by the following: Acidosis: Blood pH below 7.3 or plasma bicarbonate below 18mmol/litre Ketonaemia: Blood ketones (beta-hydroxybutyrate) above 3mmol/litre Hyperglycaemia: Blood glucose levels are generally high (above 11mmol/litre), although children with known Type 1 diabetes can less commonly develop DKA with normal blood glucose levels DKA can be life threatening. The three complications which account for the majority of deaths in these children are cerebral oedema, hypokalaemia and aspiration pneumonia. An understanding of the principles discussed in the ‘Approach to the Seriously Unwell Child’ article and an awareness of the British Society of Paediatric Endocrinology and Diabetes (BSPED) guideline for DKA management (1) will help you manage these children appropriately. 31,500 children and young people under the age of 19 in the UK have diabetes. The vast majority of them (over 95%), have Type 1 Diabetes Mellitus (T1DM.) The peak age for diagnosis is between 9 and 14 years (2). In established T1DM, the risk of DKA is 1–10% per patient per year (3). Reported mortality rates from DKA in children in the UK are around 0.3%, the majority of which are attributable to cerebral oedema, which has a mortality rate of 25 % (4). T1DM can be seen as ‘starvation in the midst of plenty,’ where blood glucose levels are raised as it cannot be used for metabolism or stored due to an absolute deficiency of insulin. This leads to a rise in counter-regulatory hormones including glucagon, cortisol, catecholamines and growth hormone. The increase in these gluconeogenic hormones not only raises the blood glucose concentration further, but also leads to accelerated break down o Continue reading >>

Management Of Diabetic Ketoacidosis (dka)

Management Of Diabetic Ketoacidosis (dka)

Management of Acute Diabetic Ketoacidosis (DKA) Below is the link to the care pathway for the management of diabetic ketoacidosis in adults. Specific guidelines exist for the management of DKA in children. In patients aged 13-16 years presenting with DKA, the management of DKA should be discussed with relevant paediatric staff. Diagnosis Severe uncontrolled diabetes with: Hyperglycaemia (blood glucose >14mmol/L, usually but not exclusively) Metabolic acidosis (H+ >45mEq/L or HCO3- <18mmol/L or pH <7.3 on venous gases) Ketonaemia (>3mmol/L) / ketonuria (>++) Severity criteria One or more of the following may indicate severe DKA and should be considered for level 2 care (MHDU if available). It may also be necessary to consider a surgical cause for the deterioration. Blood ketones >6mmol/L Bicarbonate level <5mmol/L Venous / artierial pH <7.1 Hypokalaemia on admission (<3.5mmol/L) GCS <12 or abnormal AVPU scale Oxygen saturation <92% on air (assuming normal baseline respiratory function) Systolic BP <90mmHg, pulse >100bpm or <60bpm Anion gap >16 [anion gap = (Na+ + K+) – (Cl- + HCO3-)] Cerebral oedema The care pathways for the emergency management of DKA should be used for all eligible patients. Complete pathways for 0–4 hours and 4 hours–discharge for each DKA episode. These provide instruction on fluid balance, insulin and potassium replacement. Please note there are DKA order sets on TrakCare (DKA baseline and DKA continuing care). The care pathways are available within relevant departments or online at NHSGGC Managed Clinical Networks / Diabetes MCN / Clinical Guidelines and Protocols / DKA Care Pathway. Supplementary notes as per care pathway 0–4 hours Continue background SC insulin (glargine, levemir, degludec, isophane insulin) while on fixed rate intravenou Continue reading >>

Ebm Diabetic Ketoacidosis

Ebm Diabetic Ketoacidosis

Epidemiology New diagnosis of diabetes 10-27%. Infection ~ 35%, inadequate insulin ~ 30%, surgery, trauma, alcohol, cocaine and drugs such as steroids, thiazides, sympathomimetics, pentamidine. No cause in 19-38%, but poor compliance / economic reasons frequent. Mortality 1% in adults, but 5% if over 65 years. Also high 15% in patients with hyperglycaemic, hyperosmolar non-ketotic syndrome (HHNS), when BSL usually > 50 mmol/L, more dehydrated with osmolality is > 320 mosm/L – can calculate latter by (2[NA + K] + glucose). Diagnostic Criteria Raised glucose >11.1 mmol/L Acidosis with arterial / venous pH < 7.3, or venous bicarb < 15 mmol/L Ketonaemia or ketonuria (urinalysis may miss 3-beta hydroxybutyrate early). Management / Complications Hypoperfusion Rapid initial crystalloid, especially for significant circulatory insufficiency, at 15-20 mL/kg in first hour ie. 1-1.5 L. Possible role for bicarbonate is in patients with impending cardiovascular collapse, if pH < 6.9. Dilute 100 mmol 8.4% bicarbonate in 250-1000 mL 0.45% NS, and give over 30-60 minutes with 20 mmol K via infusion pump. (Note there are no prospective data concerning bicarbonate use below pH 6.9, and from 6.9-7.1 morbidity and mortality outcomes are equivocal ie. not proven). Fluid replacement Total body water deficit 100 mL/kg, and sodium deficit 7-10 mmol/kg. Restore normal hydration with 0.9% NS at 4-14 mL/kg/hr, to correct estimated fluid deficit over first 24 hours, without exceeding change in osmolality greater than 3 mOsm/kg per hour. One regime is NS 1000 mL in first hour, 500 mL/hr next 4 hours, then 250 mL/hr next 4 hours ie. around 4 L in first 9 hours. Aim to restore fluid deficits over 24 hours in adults, or up to 48 hours in children. Insulin infusion Insulin infusion at 0.1 units/kg/hr 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 >>

Diabetes Mellitus

Diabetes Mellitus

See also: Background: Diabetic ketoacidosis (DKA) is the combination of hyperglycemia, metabolic acidosis, and ketonaemia. It may be the first presentation for a child with previously undiagnosed diabetes. It can also be precipitated by illness, or poor compliance with taking insulin. All patients presenting with a blood glucose level (BGL) ≥ 11.1mmol/l should have blood ketones tested on a capillary sample using a bedside OptiumTM meter. If this test is positive (>0.6 mmol/l), assess for acidosis to determine further management. Urinalysis can be used for initial assessment if blood ketone testing is not available. The biochemical criteria for DKA are: 1. Venous pH < 7.3 or bicarbonate <15 mmol/l 2. Presence of blood or urinary ketones If ketones are negative, or the pH is normal in the presence of ketones, patients can be managed with subcutaneous (s.c.) insulin (see ' new presentation, mildly ill' below). Assessment of children and adolescents with DKA 1. Degree Of Dehydration (often over-estimated) None/Mild ( < 4%): no clinical signs Moderate (4-7%): easily detectable dehydration eg. reduced skin turgor, poor capillary return Severe(>7%): poor perfusion, rapid pulse, reduced blood pressure i.e. shock 3. Investigations Venous blood sample (place an i.v. line if possible as this will be needed if DKA is confirmed) for the following: FBE Blood glucose, urea, electrolytes (sodium, potassium, calcium, magnesium, phosphate) Blood ketones (bedside test) Venous blood gas (including bicarbonate) Investigations for precipitating cause: if clinical signs of infection consider septic work up including blood culture For all newly diagnosed patients: Insulin antibodies, GAD antibodies, coeliac screen (total IgA, anti-gliadin Ab, tissue transglutaminase Ab) and thyroid function Continue reading >>

Fluid Replacement Give Sodium Chloride 0.9% Intravenously As Follows:

Fluid Replacement Give Sodium Chloride 0.9% Intravenously As Follows:

Diabetic emergencies: guidelines for the management of diabetic ketoacidosis and management of hyperosmolar non-ketotic diabetic coma The following guideline is approved only for use at University College London Hospitals NHS Foundation Trust. It is provided as supporting information for the UCLH Injectable Medicines Administration Guide. Neither UCLH nor Wiley accept liability for errors or omissions within the guideline. Wherever possible, users of the Guide should refer to locally produced practice guidelines. UCLH’s guidelines represent the expert opinion of the clinicians within the hospital and may not be applicable to patients outside the Trust. Adapted from UCLH Guidelines for the management of common medical emergencies and for the use of antimicrobial drugs Reviewed by: Dr Stephanie Baldeweg, Consultant Endocrinologist, UCLH and Mrs Sejal Rabone, Pharmacist, MES Directorate, UCLH January 2006 Management of diabetic ketoacidosis and management of hyperosmolar The principal problems are dehydration and acidosis. Diabetic ketoacidosis is a medical emergency. Aim of treatment: Correct acidosis with IV fluids and insulin, and restore electrolyte balance. Criteria for diagnosis: • Blood glucose > 10 mmol/L and • Positive urine ketones test and • Acidosis (pH ≤ 7.3 or bicarbonate ≤ 15 mmol/L) Also look for thirst and polyuria, hyperventilation (Kussmaul), abdominal pain, vomiting. Immediate admission to critical care must take priority over all except lifesaving interventions. Refer the patient to the DMR immediately whilst continuing management in A&E. Contact a member of the diabetic team (registrar bleep MX109); it is better to seek advice early than late. Urgent Investigations • Blood glucose. This is accurate up to abou Continue reading >>

Diabetic Ketoacidosis Treatment & Management

Diabetic Ketoacidosis Treatment & Management

Approach Considerations Managing diabetic ketoacidosis (DKA) in an intensive care unit during the first 24-48 hours always is advisable. When treating patients with DKA, the following points must be considered and closely monitored: It is essential to maintain extreme vigilance for any concomitant process, such as infection, cerebrovascular accident, myocardial infarction, sepsis, or deep venous thrombosis. It is important to pay close attention to the correction of fluid and electrolyte loss during the first hour of treatment. This always should be followed by gradual correction of hyperglycemia and acidosis. Correction of fluid loss makes the clinical picture clearer and may be sufficient to correct acidosis. The presence of even mild signs of dehydration indicates that at least 3 L of fluid has already been lost. Patients usually are not discharged from the hospital unless they have been able to switch back to their daily insulin regimen without a recurrence of ketosis. When the condition is stable, pH exceeds 7.3, and bicarbonate is greater than 18 mEq/L, the patient is allowed to eat a meal preceded by a subcutaneous (SC) dose of regular insulin. Insulin infusion can be discontinued 30 minutes later. If the patient is still nauseated and cannot eat, dextrose infusion should be continued and regular or ultra–short-acting insulin should be administered SC every 4 hours, according to blood glucose level, while trying to maintain blood glucose values at 100-180 mg/dL. The 2011 JBDS guideline recommends the intravenous infusion of insulin at a weight-based fixed rate until ketosis has subsided. Should blood glucose fall below 14 mmol/L (250 mg/dL), 10% glucose should be added to allow for the continuation of fixed-rate insulin infusion. [19, 20] In established patient Continue reading >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemic State In Adults: Treatment

INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS, also known as hyperosmotic hyperglycemic nonketotic state [HHNK]) are two of the most serious acute complications of diabetes. They are part of the spectrum of hyperglycemia, and each represents an extreme in the spectrum. The treatment of DKA and HHS in adults will be reviewed here. The epidemiology, pathogenesis, clinical features, evaluation, and diagnosis of these disorders are discussed separately. DKA in children is also reviewed separately. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Epidemiology and pathogenesis".) (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Clinical features, evaluation, and diagnosis".) Continue reading >>

The Evolution Of Dka Management | Dhatariya | British Journal Of Diabetes

The Evolution Of Dka Management | Dhatariya | British Journal Of Diabetes

Address for correspondence: Dr Ketan Dhatariya Norfolk and Norwich University Hospital NHS Foundation Trust, Colney Lane, Norwich, Norfolk, NR4 7UY, UK. The Joint British Diabetes Societies (JBDS) looked in detail at the evidence based management for diabetic ketoacidosis (DKA) and generated a set of guidelines to support the management of this complex condition. Because of the nature of research into DKA there are some areas which have less of an evidence base, so expert commentary and experience support several of the recommendations. This article describes the historical basis of the development of the management of this condition, how we came to arrive at the present situation and why the ongoing national DKA audit is so important in elucidating what is currently happening across the UK in clinical practice. Key words: diabetic ketoacidosis, guideline development, diabetic coma, insulin, evidence based medicine. In 2010 the JBDS produced a national guideline for the management of DKA.1 By 2013 data presented at the Diabetes UK Annual Professional Conference showed that over 85% of all UK hospitals who responded to an online questionnaire said that they had either adopted or adapted the guideline. In 2013 the guideline was then updated to reflect new evidence and to incorporate some of the suggestions, criticisms and comments made about the first edition.2 However, there remain some concerns about the document; most frequently aired are those surrounding the lack of evidence for many of the recommendations. For this reason the current national audit on the management of DKA is taking place to try to gather information about what is currently being done, and whether the current guideline helps or hinders management, or if there are areas that need to change to improv Continue reading >>

Management Of Adult Diabetic Ketoacidosis

Management Of Adult Diabetic Ketoacidosis

Go to: Abstract Diabetic ketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management. Keywords: DKA treatment, insulin, prevention, ESKD Go to: Introduction In 2009, there were 140,000 hospitalizations for diabetic ketoacidosis (DKA) with an average length of stay of 3.4 days.1 The direct and indirect annual cost of DKA hospitalizations is 2.4 billion US dollars. Omission of insulin is the most common precipitant of DKA.2,3 Infections, acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke) and gastrointestinal tract (bleeding, pancreatitis), diseases of the endocrine axis (acromegaly, Cushing’s syndrome), and stress of recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hor Continue reading >>

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