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Diabetic Ketoacidosis Treatment Iv Fluids

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 >>

Diagnosis

Diagnosis

Print If your doctor suspects diabetic ketoacidosis, he or she will do a physical exam and various blood tests. In some cases, additional tests may be needed to help determine what triggered the diabetic ketoacidosis. Blood tests Blood tests used in the diagnosis of diabetic ketoacidosis will measure: Blood sugar level. If there isn't enough insulin in your body to allow sugar to enter your cells, your blood sugar level will rise (hyperglycemia). As your body breaks down fat and protein for energy, your blood sugar level will continue to rise. Ketone level. When your body breaks down fat and protein for energy, acids known as ketones enter your bloodstream. Blood acidity. If you have excess ketones in your blood, your blood will become acidic (acidosis). This can alter the normal function of organs throughout your body. Additional tests Your doctor may order tests to identify underlying health problems that might have contributed to diabetic ketoacidosis and to check for complications. Tests might include: Blood electrolyte tests Urinalysis Chest X-ray A recording of the electrical activity of the heart (electrocardiogram) Treatment If you're diagnosed with diabetic ketoacidosis, you might be treated in the emergency room or admitted to the hospital. Treatment usually involves: Fluid replacement. You'll receive fluids — either by mouth or through a vein (intravenously) — until you're rehydrated. The fluids will replace those you've lost through excessive urination, as well as help dilute the excess sugar in your blood. Electrolyte replacement. Electrolytes are minerals in your blood that carry an electric charge, such as sodium, potassium and chloride. The absence of insulin can lower the level of several electrolytes in your blood. You'll receive electrolytes throu 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 >>

What Is The Treatments For Ketoacidosis?

What Is The Treatments For Ketoacidosis?

Management of diabetic ketoacidos Time: 0–60 mins 1. Commence 0.9% sodium chloride If systolic BP > 90 mmHg, give 1 L over 60 mins If systolic BP < 90 mmHg, give 500 mL over 10–15 mins, then re-assess. If BP remains < 90 mmHg, seek senior review 2. Commence insulin treatment 50 U human soluble insulin in 50 mL 0.9% sodium chloride infused intravenously at 0.1 U/kg body weight/hr Continue with SC basal insulin analogue if usually taken by patient 3. Perform further investigations: see text 4. Establish monitoring schedule Hourly capillary blood glucose and ketone testing Venous bicarbonate and potassium after 1 and 2 hrs, then every 2 hrs Plasma electrolytes every 4 hrs Clinical monitoring of O2 saturation, pulse, BP, respiratory rate and urine output every hour 5. Treat any precipitating cause Time: 60 mins to 12 hrs • IV infusion of 0.9% sodium chloride with potassium chloride added as indicated below 1 L over 2 hrs 1 L over 2 hrs 1 L over 4 hrs 1 L over 4 hrs 1 L over 6 hrs • Add 10% glucose 125 mL/hr IV when glucose < 14 mmol/L • Be more cautious with fluid replacement in elderly, young people, pregnant patients and those with renal or heart failure. If plasma sodium is > 155 mmol/L, 0.45% sodium chloride may be used. • Adjust potassium chloride infusion Plasma potassium (mmol/L) Potassium replacement (mmol/L of infusion) > 5.5 Nil 3.5–5.5 40 < 3.5 Senior review – additional potassium required Time: 12–24 hrs • Ketonaemia and acidosis should have resolved (blood ketones < 0.3 mmol/L, venous bicarbonate > 18 mmol/L). Request senior review if not improving • If patient is not eating and drinking Continue IV insulin infusion at lower rate of 2–3 U/kg/hr Continue IV fluid replacement and biochemical monitoring • If ketoacidosis has resolved and 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 >>

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 >>

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 Causes, Symptoms, Treatment, And Complications

Diabetic Ketoacidosis Causes, Symptoms, Treatment, And Complications

Diabetic ketoacidosis definition and facts Diabetic ketoacidosis is a life-threatening complication of type 1 diabetes (though rare, it can occur in people with type 2 diabetes) that occurs when the body produces high levels of ketones due to lack of insulin. Diabetic ketoacidosis occurs when the body cannot produce enough insulin. The signs and symptoms of diabetic ketoacidosis include Risk factors for diabetic ketoacidosis are type 1 diabetes, and missing insulin doses frequently, or being exposed to a stressor requiring higher insulin doses (infection, etc). Diabetic ketoacidosis is diagnosed by an elevated blood sugar (glucose) level, elevated blood ketones and acidity of the blood (acidosis). The treatment for diabetic ketoacidosis is insulin, fluids and electrolyte therapy. Diabetic ketoacidosis can be prevented by taking insulin as prescribed and monitoring glucose and ketone levels. The prognosis for a person with diabetic ketoacidosis depends on the severity of the disease and the other underlying medical conditions. Diabetic ketoacidosis (DKA) is a severe and life-threatening complication of diabetes. Diabetic ketoacidosis occurs when the cells in our body do not receive the sugar (glucose) they need for energy. This happens while there is plenty of glucose in the bloodstream, but not enough insulin to help convert glucose for use in the cells. The body recognizes this and starts breaking down muscle and fat for energy. This breakdown produces ketones (also called fatty acids), which cause an imbalance in our electrolyte system leading to the ketoacidosis (a metabolic acidosis). The sugar that cannot be used because of the lack of insulin stays in the bloodstream (rather than going into the cell and provide energy). The kidneys filter some of the glucose (suga Continue reading >>

68..............................................................................................................................................................................navc Clinician’s Brief / April 2011 / Diagnostic Tree

68..............................................................................................................................................................................navc Clinician’s Brief / April 2011 / Diagnostic Tree

1. IV Isotonic Crystalloid Therapy • Shock fluid therapy is warranted if cardiovascular instability is present: Full shock dose of fluids is 90 mL/kg; start with ¼ to 1/3 dose and reassess until stable • Correct dehydration, provide maintenance needs, and replace ongoing losses over 6 to 24 hours: - % dehydration × body weight (kg) × 1000 plus - 20 mL/kg/day (insensible losses) plus - 20 to 40 mL/kg/day (maintenance sensible losses) plus - Account for vomiting, diarrhea, & polyuria (ongoing sensible losses) Alice Huang, VMD, & J. Catharine Scott-Moncrieff, Vet MB, MS, MA, Diplomate ACVIM & ECVIM Purdue University Canine Diabetic Ketoacidosis D i a gno s t i c Tre e / ENDOCRINOLOGY Peer Reviewed Physical Examination • Polyuria • Weight loss • Polydipsia • Vomiting • Polyphagia • Lethargy Patient may have only 1 or more of these signs. Laboratory Results • Blood glucose (BG): Hyperglycemia (> 200 mg/dL) • Blood gas (venous or arterial): Metabolic acidosis • Urine dipstick: Glucosuria; ketonuria or ketonemia Serum ketones can be measured if urine is unavailable. Diabetic Ketoacidosis Treatment 2. Electrolyte Supplementation (see Table 1, page 70) • Monitor serum potassium Q 4–6 H until within reference interval and stable; then Q 12–24 H • Monitor serum phosphorus Q 4–6 H until > 1.5; then Q 6–24 H • When supplementing potassium and phosphorus concurrently, take into account the amount of potassium contained in the potassium phosphate • Consider magnesium supplementation in instances of refractory hypokalemia 3. Regular Insulin • Continuous rate infusion (CRI) protocol:1 - Add 2.2 U/kg of regular insulin to 250 mL of 0.9% saline - Allow 50 Continue reading >>

Pem Pearls: Treatment Of Pediatric Diabetic Ketoacidosis And The Two-bag Method

Pem Pearls: Treatment Of Pediatric Diabetic Ketoacidosis And The Two-bag Method

Insulin does MANY things in the body, but the role we care about in the Emergency Department is glucose regulation. Insulin allows cells to take up glucose from the blood stream, inhibits liver glucose production, increases glycogen storage, and increases lipid production. When insulin is not present, such as in patients with Type 1 diabetes mellitus (DM), all of the opposite effects occur. A lack of insulin causes the following downstream effects: Prevents glucose from being used as an energy source – Free fatty acids are used instead and produce ketoacids during metabolism. Causes a surge of stress hormones and induces gluconeogenesis – When blood glucose levels are elevated, the kidneys cannot absorb all of the glucose from the urine, and the extra glucose in the urine causes polyuria, even in the setting of dehydration. In addition, acidosis causes potassium to shift out of cells into the blood, and the combination of this with dehydration causes the body to preferentially retain sodium at the expense of potassium.1,2 When insulin homeostasis is disrupted and decompensates, patients are at risk for developing diabetic ketoacidosis (DKA). All of the following criteria are required for a diagnosis of DKA: Hyperglycemia (glucose >200 mg/dL) Acidosis (pH <7.3 or bicarb <15 mmol/L) Ketosis (by urine or blood test) Treatment is based on a simple principle: return the body’s glucose regulation to its normal state and replace all of the things the body consumed while insulin-deficient. While bolus insulin is common in the treatment of DKA in adults, it is relatively contraindicated in the pediatric patient. Dehydration and secondary sympathetic activation can interfere with local tissue perfusion and may cause irregular and unpredictable absorption. Step 1: Correction Continue reading >>

Management Of Feline Diabetic Ketoacidosis

Management Of Feline Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a complication of diabetes mellitus with concurrent and often severe metabolic derangements associated with hyperglycaemia, glucosuria, metabolic acidosis, ketonaemia +/- ketonuria. Patients with ketonaemia/ketosis are usually still bright, eating and maintaining their hydration. Those with ketoacidosis are dehydrated, clinically unwell (e.g., anorexia, vomiting, lethargy) and typically require hospitalisation and intensive management. DKA is distinguished from uncomplicated diabetes mellitus (DM) by a relative insulin lack and increased counter-regulatory hormones. The latter are thought to occur secondary to intercurrent disease. Concurrent disease has been documented in approximately 90% of cats with DKA, with the most common being hepatic lipidosis, chronic kidney disease, acute pancreatitis, bacterial or viral infections and neoplasia (Bruskiewicz et al. 1997). Heinz bodies, neutrophilia with a left shift, increased ALT and azotaemia is common. Most cats presenting with DKA are newly diagnosed diabetics or recently diagnosed but poorly controlled diabetics. Diagnosis Hyperglycaemia, Glucosuria, Metabolic Acidosis Plus Ketones in Plasma and/or Urine Traditionally DKA has been diagnosed using urinary ketone dipsticks, which detect acetoacetate but not beta-hydroxybutyrate. However as the latter is the principle ketone body in DKA, measuring serum beta-hydroxybutyrate is a more sensitive indicator of DKA. In humans portable meters that measure beta-hydroxybutyrate in whole blood have largely superseded urine dipsticks. These ketone meters have recently proven useful in diagnosing DKA in cats, although they tend to underestimate beta-hydroxybutyrate at higher values (Zeugswetter, Rebuzzi 2012; Weingart et al. 2012). In the absence of a ke 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 >>

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 >>

Management Of Diabetic Ketoacidosis

Management Of Diabetic Ketoacidosis

Diabetic ketoacidosis is an emergency medical condition that can be life-threatening if not treated properly. The incidence of this condition may be increasing, and a 1 to 2 percent mortality rate has stubbornly persisted since the 1970s. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus); however, its occurrence in patients with type 2 diabetes (formerly called non–insulin-dependent diabetes mellitus), particularly obese black patients, is not as rare as was once thought. The management of patients with diabetic ketoacidosis includes obtaining a thorough but rapid history and performing a physical examination in an attempt to identify possible precipitating factors. The major treatment of this condition is initial rehydration (using isotonic saline) with subsequent potassium replacement and low-dose insulin therapy. The use of bicarbonate is not recommended in most patients. Cerebral edema, one of the most dire complications of diabetic ketoacidosis, occurs more commonly in children and adolescents than in adults. Continuous follow-up of patients using treatment algorithms and flow sheets can help to minimize adverse outcomes. Preventive measures include patient education and instructions for the patient to contact the physician early during an illness. Diabetic ketoacidosis is a triad of hyperglycemia, ketonemia and acidemia, each of which may be caused by other conditions (Figure 1).1 Although diabetic ketoacidosis most often occurs in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus), more recent studies suggest that it can sometimes be the presenting condition in obese black patients with newly diagnosed type 2 diabetes (formerly called non–insulin-depe Continue reading >>

Management Of Diabetic Ketoacidosis In Children And Adolescents

Management Of Diabetic Ketoacidosis In Children And Adolescents

Objectives After completing this article, readers should be able to: Describe the typical presentation of diabetic ketoacidosis in children. Discuss the treatment of diabetic ketoacidosis. Explain the potential complications of diabetic ketoacidosis that can occur during treatment. Introduction Diabetic ketoacidosis (DKA) represents a profound insulin-deficient state characterized by hyperglycemia (>200 mg/dL [11.1 mmol/L]) and acidosis (serum pH <7.3, bicarbonate <15 mEq/L [15 mmol/L]), along with evidence of an accumulation of ketoacids in the blood (measurable serum or urine ketones, increased anion gap). Dehydration, electrolyte loss, and hyperosmolarity contribute to the presentation and potential complications. DKA is the most common cause of death in children who have type 1 diabetes. Therefore, the best treatment of DKA is prevention through early recognition and diagnosis of diabetes in a child who has polydipsia and polyuria and through careful attention to the treatment of children who have known diabetes, particularly during illnesses. Presentation Patients who have DKA generally present with nausea and vomiting. In individuals who have no previous diagnosis of diabetes mellitus, a preceding history of polyuria, polydipsia, and weight loss usually can be elicited. With significant ketosis, patients may have a fruity breath. As the DKA becomes more severe, patients develop lethargy due to the acidosis and hyperosmolarity; in severe DKA, they may present with coma. Acidosis and ketosis cause an ileus that can lead to abdominal pain severe enough to raise concern for an acutely inflamed abdomen, and the elevation of the stress hormones epinephrine and cortisol in DKA can lead to an elevation in the white blood cell count, suggesting infection. Thus, leukocytosi Continue reading >>

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