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What Is Dka Protocol?

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

A Preventable Crisis People who have had diabetic ketoacidosis, or DKA, will tell you it’s worse than any flu they’ve ever had, describing an overwhelming feeling of lethargy, unquenchable thirst, and unrelenting vomiting. “It’s sort of like having molasses for blood,” says George. “Everything moves so slow, the mouth can feel so dry, and there is a cloud over your head. Just before diagnosis, when I was in high school, I would get out of a class and go to the bathroom to pee for about 10–12 minutes. Then I would head to the water fountain and begin drinking water for minutes at a time, usually until well after the next class had begun.” George, generally an upbeat person, said that while he has experienced varying degrees of DKA in his 40 years or so of having diabetes, “…at its worst, there is one reprieve from its ill feeling: Unfortunately, that is a coma.” But DKA can be more than a feeling of extreme discomfort, and it can result in more than a coma. “It has the potential to kill,” says Richard Hellman, MD, past president of the American Association of Clinical Endocrinologists. “DKA is a medical emergency. It’s the biggest medical emergency related to diabetes. It’s also the most likely time for a child with diabetes to die.” DKA occurs when there is not enough insulin in the body, resulting in high blood glucose; the person is dehydrated; and too many ketones are present in the bloodstream, making it acidic. The initial insulin deficit is most often caused by the onset of diabetes, by an illness or infection, or by not taking insulin when it is needed. Ketones are your brain’s “second-best fuel,” Hellman says, with glucose being number one. If you don’t have enough glucose in your cells to supply energy to your brain, yo Continue reading >>

University Of Zagreb

University Of Zagreb

SCHOOL OF MEDICINE Mohammad Imran Khan Malik A review of the efficacy of the Milwaukee protocol in the treatment of ketoacidosis in pediatric Intensive Care Unit patients at Rebro hospital between 2009-2014. GRADUATE THESIS Zagreb, 2014 UNIVERSITY OF ZAGREB SCHOOL OF MEDICINE Mohammad Imran Khan Malik A review of the efficacy of the Milwaukee protocol in the treatment of ketoacidosis in pediatric Intensive Care Unit patients at Rebro hospital between 2009-2014. GRADUATE THESIS Zagreb, 2014 This graduation paper has been completed at the Department of Paediatrics at the University Hospital Centre Zagreb (Rebro hospital) under the supervision of Dr. sc. Mario Ćuk and was submitted for evaluation during the academic year 2013 /2014. LIST OF TABLES Table 1: DKA laboratory diagnosis criteria Table 2: Classification of DKA. Modified from Kliegman et al. Nelson Textbook of Pediatrics, 2011. Table 3: Table 3: Summary of key data of patients admitted to pediatric ICU at Rebro hospital. LIST OF FIGURES Figure 1: DKA pathogenesis. Figure 2: Ketone bodies: showing formation of negatively charged conjugate bases of the ketoacids. The conjugate bases cause the increased anion gap in DKA metabolic acidosis. Figure 3: Algorithm of key steps in DKA pathophysiology. Colour coded to highlight the two areas that treatment should target: metabolic acidosis and hyperglycemia. Figure 4: True sodium level calculations for glucose levels above 100mg/dL (5.6mmol/L). Figure 5: Goals of DKA management Figure 6: Diabetic ketoacidosis treatment: Milwaukee protocol. Modified from Kliegman et al. Nelson Textbook of Paediatrics. 2011 p.1979 Figure 7: DKA incidence between 1 st January 2009 – 30 th June 2014. LIST OF ABBREVIATIONS DKA ..............Diabetic Ketoacidosis CE...................C 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 >>

Protocols And Order Sets

Protocols And Order Sets

The order sets provided here are only a few examples from institutions involved in the management of inpatient hyperglycemia; this is not an all-inclusive list. Posting of these protocols does not constitute endorsement of any specific protocol. We believe that each institution should consult with diabetes experts to select and implement insulin protocols. Key Points Successful implementation of protocols requires: Buy-in from key stakeholders (critical care physicians, house staff, nursing, pharmacy, hospital administration, etc) Appropriate education through in-servicing of hospital staff Ongoing monitoring of results Support from endocrinologists for specific questions or when a patient does not respond to the protocol as expected It is important to keep in mind that these algorithms have not been directly compared in clinical trials. In selecting a protocol, one should look for characteristics that are compatible with the institution in which it will be implemented. Consideration should be given to the following characteristics and whether these attributes will fit within the institution: Is the protocol dynamic (ie, does it allow for variability in insulin requirements and account for rates of change in blood glucose concentrations)? What is its relative user-friendliness and complexity? To what extent does it require performance of basic calculations? Is it compatible with the local computer systems? None of the examples provided are suitable for the treatment of diabetic ketoacidosis. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

As fat is broken down, acids called ketones build up in the blood and urine. In high levels, ketones are poisonous. This condition is known as ketoacidosis. Diabetic ketoacidosis (DKA) is sometimes the first sign of type 1 diabetes in people who have not yet been diagnosed. It can also occur in someone who has already been diagnosed with type 1 diabetes. Infection, injury, a serious illness, missing doses of insulin shots, or surgery can lead to DKA in people with type 1 diabetes. People with type 2 diabetes can also develop DKA, but it is less common. It is usually triggered by uncontrolled blood sugar, missing doses of medicines, or a severe illness. 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 >>

Management Of Feline Diabetic Ketoacidosis - Wsava2013 - Vin

Management Of Feline Diabetic Ketoacidosis - Wsava2013 - Vin

Management of Feline Diabetic Ketoacidosis World Small Animal Veterinary Association World Congress Proceedings, 2013 Pru Galloway, BVSc(Distinction), MANZCVS, FANZCVS, Registered Specialist in Feline Medicine Massey University, Catmed, Lower Hutt, New Zealand 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. 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 largel 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

Diabetic Ketoacidosis

Also known as: DKA Severe diabetic ketoacidosis is a medical emergency and requires prompt treatment to correct dehydration, electrolyte disturbances and acidosis. It is a complication of insulin dependent Diabetes Mellitus. DKA is the result of marked insulin deficiency, and ketonaemia and ketoacidosis occur approximately 15 days after insulin concentrations are suppressed to fasting levels. Marked insulin suppression occurs on average 4 days after fasting glucose levels reach 30mmol/L. Many cats with DKA have other intercurrent conditions which may precipitate the condition including: infection, pancreatitis or renal insufficiency. Pathophysiology Insulin deficiency leads to increased breakdown of fat that releases fatty acids into the circulation. Free fatty acids are oxidised in the liver to ketones that are used by many tissues as an energy source instead of glucose. This occurs when intracellular levels of glucose are insufficient for energy metabolism as a result of severe insulin deficiency. In the liver, instead of being converted to triglycerides, free fatty acids are oxidised to acetoacetate, which is converted to hydroxybutyrate or acetone. Ketones are acids that cause central nervous system depression and act in the chemoreceptor trigger zone to cause nausea, vomiting and anorexia. They also accelerate osmotic water loss in the urine. Dehydration results from inadequate fluid intake in the face of accelerated water loss due to glucosuria and ketonuria. Dehydration and subsequent reduced tissue perfusion compounds the acidosis through lactic acid production. There is whole body loss of electrolytes including sodium, potassium, magnesium and phosphate and there is also intracellular redistribution of electrolytes following insulin therapy which may compound p Continue reading >>

Diagnosis And Treatment Of Diabetic Ketoacidosis

Diagnosis And Treatment Of Diabetic Ketoacidosis

85 Abstract Diabetic ketoacidosis (DKA) is the most frequent hyperglycaemic acute diabetic complication. Furthermore it carries a significant risk of death, which can be prevented by early and effective management. All physicians, irrespective of the discipline they are working in and whether in primary, secondary or tertiary care institutions, should be able to recognise DKA early and initiate management immediately. 86 Introduction Diabetic ketoacidosis (DKA) is a common complication of diabetes with an annual occurrence rate of 46 to 50 per 10 000 diabetic patients. The severity of this acute diabetic complication can be appreciated from the high death-to-case ratio of 5 to 10%.1 In Africa the mortality of DKA is unacceptably high with a reported death rate of 26 to 29% in studies from Kenya, Tanzania and Ghana.2 It is a complication of both type 1 and type 2 diabetes mellitus, although more commonly seen in type 1 diabetic patients. Of known diabetic patients presenting with DKA about one-quarter will be patients with type 2 diabetes. In patients presenting with a DKA as first manifestation of diabetes about 15% will be type 2.3 This correlates well with data from South Africa suggesting that one- quarter of patients with DKA will be type 2 with adequate C-peptide levels and the absence of anti-GAD antibodies.4 This review will focus on the principles of diagnosis, monitoring and treatment of DKA, with special mention of new developments and controversial issues. Clinical features DKA evolves over hours to days in both type 1 and type 2 diabetic patients, but the symptoms of poor control of blood glucose are usually present for several days before the onset or presentation of ketoacidosis.5 The clinical features of DKA are non-specific and patients may present with Continue reading >>

Hyperglycemia And What To Do About It

Hyperglycemia And What To Do About It

This CE activity is approved by EMS World Magazine, an organization accredited by the Continuing Education Coordinating Board for Emergency Medical Services (CECBEMS) for 1 CEU. To take the CE test that accompanies this article, go to www.rapidce.com to take the test and immediately receive your CE credit. Questions? E-mail [email protected] Both hypoglycemia and hyperglycemia are true medical emergencies. As we discussed last month, hypoglycemia often has a rapid onset and can impact any patient whose body is not provided an adequate glucose supply. While anyone can experience hypoglycemia, it is most common in patients who have been diagnosed with diabetes and whose natural insulin does not function normally. Patients with diabetes also risk developing hyperglycemia, a complex and dangerous metabolic derangement that can be fatal without proper care. The American Diabetes Association says that in 2011 there were a staggering 25 million patients with diabetes and 79 million with pre-diabetes across the United States. This month’s CE article explores the consequences of hyperglycemia on the body and the life-threatening emergencies it can cause. Diabetic Disease Progression Recall that insulin secretion is stimulated by eating. Insulin secretion is not stimulated between meals, and a decline in the body’s blood glucose levels inhibits the pancreatic islets’ insulin secretion and stimulates the secretion of glucagon, which allows glucose levels to remain in a normal range. Figure 1 demonstrates the relationship between blood glucose levels and the pancreas. With the exception of very few organs, such as the brain and the kidneys, the body’s tissues require insulin for glucose to pass through the cell walls. For patients with diabetes mellitus (DM), either thei Continue reading >>

Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Understand the management of patients with diabetic ketoacidosis and other hyperglycemic emergencies. ​ The acute onset of hyperglycemia with attendant metabolic derangements is a common presentation in all forms of diabetes mellitus. The most current data from the National Diabetes Surveillance Program of the Centers for Disease Control and Prevention estimate that during 2005-2006, at least 120,000 hospital discharges for diabetic ketoacidosis (DKA) occurred in the United States,(1) with an unknown number of discharges related to hyperosmolar hyperglycemic state (HHS). The clinical presentations of DKA and HHS can overlap, but they are usually separately characterized by the presence of ketoacidosis and the degree of hyperglycemia and hyperosmolarity, though HHS will occasionally have some mild degree of ketosis. DKA is defined by a plasma glucose level >250 mg/dL, arterial pH <7.3, the presence of serum ketones, a serum bicarbonate measure <18 mEq/L, and a high anion gap metabolic acidosis. The level of normal anion gap may vary slightly by individual institutional standards. The anion gap also needs to be corrected in the presence of hypoalbuminemia, a common condition in the critically ill. Adjusted anion gap = observed anion gap + 0.25 * ([normal albumin]-[observed albumin]), where the given albumin concentrations are in g/L; if given in g/dL, the correction factor is 2.5.(3) HHS is defined by a plasma glucose level >600 mg/dL, with an effective serum osmolality >320 mOsm/kg. HHS was originally named hyperosmolar hyperglycemic nonketotic coma; however, this name was changed because relatively few patients exhibit coma-like symptoms. Effective serum osmolality = 2*([Na] + [K]) + glucose (mg/dL)/18.(2) Urea is freely diffusible across cell membranes, thus it will Continue reading >>

Understanding And Treating Diabetic Ketoacidosis

Understanding And Treating Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab Continue reading >>

Pulmcrit- Dominating The Acidosis In Dka

Pulmcrit- Dominating The Acidosis In Dka

Management of acidosis in DKA is an ongoing source of confusion. There isn’t much high-quality evidence, nor will there ever be (1). However, a clear understanding of the physiology of DKA may help us treat this rationally and effectively. Physiology of ketoacidosis in DKA Ketoacidosis occurs due to an imbalance between insulin dose and insulin requirement: Many factors affect the insulin requirement: Individuals differ in their baseline insulin resistance and insulin requirements. Physiologic stress (e.g. hypovolemia, inflammation) increases the level of catecholamines and cortisol, which increases insulin resistance. Hyperglycemia and metabolic acidosis themselves increase insulin resistance (Souto 2011, Gosmanov 2014). DKA treatment generally consists of two phases: first, we must manage the ketoacidosis. Later, we must prepare the patient to transition back to their home insulin regimen. During both phases, success depends on balancing insulin dose and insulin requirement. Phase I (Take-off): Initial management of the DKA patient with worrisome acidosis Let’s start by considering a patient who presents in severe DKA with worrisome acidosis. This is uncommon. Features that might provoke worry include the following: bicarbonate < 7 mEq/L pH < 7 (if measured; there is generally little benefit from measuring pH) clinically ill-appearing (e.g., dyspnea, marked Kussmaul respirations) These patients generally have severe metabolic acidosis with respiratory compensation. This creates two concerns: If the metabolic acidosis worsens, they may decompensate. The patient is depending on respiratory compensation to maintain their pH. If they should fatigue and lose the ability to hyperventilate, their pH would drop. It is important to reverse the acidosis before the patient m Continue reading >>

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