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Why Do Dka Patients Need Fluids

Electrolyte And Acid–base Disturbances In A Patient With Diabetes Mellitus

Electrolyte And Acid–base Disturbances In A Patient With Diabetes Mellitus

A 28-year-old man who has had type 1 diabetes for a decade presents with diabetic ketoacidosis after an influenza-like illness. The laboratory values include plasma concentrations of sodium of 144 mmol per liter, potassium 5.7 mmol per liter, chloride 98 mmol per liter, sodium bicarbonate 13 mmol per liter, creatinine 1.5 mg per deciliter (133 μmol per liter), blood urea nitrogen 30 mg per deciliter (11 mmol per liter), and glucose 702 mg per deciliter (39 mmol per liter). The venous pH is 7.2. A dipstick urinalysis shows a specific gravity of 1.025 and a pH of 5 and no blood, albumin, white cells, or nitrites, but it does show 3+ ketones and a high glucose concentration. Although the patient is not well-oriented to time and place, he does say that he is very thirsty, and his family notes that he has been voiding frequently over the past several days. On examination, the blood pressure is 108/60 mm Hg, the pulse 100 beats per minute, and the respiratory rate 30 with deep breathing. The weight is 68 kg, and the height 168 cm. When measured at the clinic within the past month the patient’s weight was 72 kg. What strategy would provide the best support for this patient? Polling and commenting are now closed. The editor’s recommendations appear below. During diabetic ketoacidosis, there may be rapid shifts in the plasma concentration of potassium ions. Although diabetic ketoacidosis leads to a deficit in total-body stores of potassium ion, the plasma concentration is usually normal or elevated, since the acidemia leads to the exit of potassium ions from cells.1,2 The patient has a large deficit in extracellular fluid volume, which is characteristic of patients with diabetic ketoacidosis. Most such patients have an extracellular fluid-volume deficit of 5 to 10%. This pa 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 >>

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 >>

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 >>

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 >>

Fluid Management In Diabetic Ketoacidosis

Fluid Management In Diabetic Ketoacidosis

Full Text Selected References These references are in PubMed. This may not be the complete list of references from this article. Articles from Archives of Disease in Childhood are provided here courtesy of BMJ Publishing Group Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. See also the separate Childhood Ketoacidosis article. Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks). Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA). Bicarbonate below 15 mmol/L and/or venous pH less than 7.3. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] Epidemiology DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their Continue reading >>

The Management Of Diabetic Ketoacidosis In Children

The Management Of Diabetic Ketoacidosis In Children

Go to: Abstract The object of this review is to provide the definitions, frequency, risk factors, pathophysiology, diagnostic considerations, and management recommendations for diabetic ketoacidosis (DKA) in children and adolescents, and to convey current knowledge of the causes of permanent disability or mortality from complications of DKA or its management, particularly the most common complication, cerebral edema (CE). DKA frequency at the time of diagnosis of pediatric diabetes is 10%–70%, varying with the availability of healthcare and the incidence of type 1 diabetes (T1D) in the community. Recurrent DKA rates are also dependent on medical services and socioeconomic circumstances. Management should be in centers with experience and where vital signs, neurologic status, and biochemistry can be monitored with sufficient frequency to prevent complications or, in the case of CE, to intervene rapidly with mannitol or hypertonic saline infusion. Fluid infusion should precede insulin administration (0.1 U/kg/h) by 1–2 hours; an initial bolus of 10–20 mL/kg 0.9% saline is followed by 0.45% saline calculated to supply maintenance and replace 5%–10% dehydration. Potassium (K) must be replaced early and sufficiently. Bicarbonate administration is contraindicated. The prevention of DKA at onset of diabetes requires an informed community and high index of suspicion; prevention of recurrent DKA, which is almost always due to insulin omission, necessitates a committed team effort. Keywords: adolescents, cerebral edema, children, complications, diabetic ketoacidosis, fluid replacement, hypokalemia, management, prevention, recurrent DKA Go to: Introduction Definition of Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) is biochemically defined as a venous pH <7.3 or serum Continue reading >>

Diabetic Ketoacidosis – Fluid Calculator

Diabetic Ketoacidosis – Fluid Calculator

Management DKA FLUID CALCULATOR Enter Patient's Weight kg Estimate % dehydration 0 1 2 3 4 5 % (max 5) Total Fluid Bolus Given ml - if requiring >20ml/kg, seek senior advice (ED consultant/ICU) (Fluid boluses should only be given if patient is clinically shocked or under senior advice) Fluid Initial fluid should be 0.9% Normal Saline only Calculated Fluid deficit is ml (% dehydration x wt x 10) Minus fluid bolus given Rate Remaining fluid deficit To be replaced over 48 hours ml/h Plus Maintenance Fluid ml/day Rate over 24 hours ml/h Total fluid rate ml/h Add KCl to fluid if serum K<5.0 and patient has passed urine. Initially 20mmol KCl in 500ml fluid (40mmol per litre). Once blood glucose is <15, change fluid to dextrose containing solution eg. 0.9% NaCl + 5% Dextrose Occasionally 7.5% to 10 % glucose may be required. Do not change insulin infusion rate unless discussed with endocrinology. Insulin Subcutaneous insulin If pH is >7.2, subcutaneous insulin may be used. Give an initial 0.1 units/kg subcutaneously units of Actrapid or Humulin R Then 0.1 units/kg every 2 hours units of Actrapid or Humulin R until acidosis is corrected. Continue insulin according to Endocrinology advice. Insulin Infusion For pH <7.2 or if an insulin infusion is indicated: Make up 50 units of Actrapid or Humulin R in 50ml of 0.9% Normal Saline (1unit/ml) Prime line with 20ml of solution before commencing infusion. Run insulin infusion at 0.1unit/kg/hr ml/h (max 5 units/hr) DO NOT GIVE IV INSULIN BOLUSES 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 >>

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 >>

Fluid Management In Diabetic-acidosis—ringer's Lactate Versus Normal Saline: A Randomized Controlled Trial

Fluid Management In Diabetic-acidosis—ringer's Lactate Versus Normal Saline: A Randomized Controlled Trial

Objective: To determine if Ringer's lactate is superior to 0.9% sodium chloride solution for resolution of acidosis in the management of diabetic ketoacidosis (DKA). Design: Parallel double blind randomized controlled trial. Methods: Patients presenting with DKA at Kalafong and Steve Biko Academic hospitals were recruited for inclusion in this study if they were >18 years of age, had a venous pH >6.9 and ≤7.2, a blood glucose of >13 mmol/l and had urine ketones of ≥2+. All patients had to be alert enough to give informed consent and should have received <1 l of resuscitation fluid prior to enrolment. Results: Fifty-seven patients were randomly allocated, 29 were allocated to receive 0.9% sodium chloride solution and 28 to receive Ringer's lactate (of which 27 were included in the analysis in each group). An adjusted Cox proportional hazards analysis was done to compare the time to normalization of pH between the 0.9% sodium chloride solution and Ringer's lactate groups. The hazard ratio (Ringer's compared with 0.9% sodium chloride solution) for time to venous pH normalization (pH = 7.32) was 1.863 (95% CI 0.937–3.705, P = 0.076). The median time to reach a pH of 7.32 for the 0.9% sodium chloride solution group was 683 min (95% CI 378–988) (IQR: 435–1095 min) and for Ringer's lactate solution 540 min (95% CI 184–896, P = 0.251). The unadjusted time to lower blood glucose to 14 mmol/l was significantly longer in the Ringer's lactate solution group (410 min, IQR: 240–540) than the 0.9% sodium chloride solution group (300 min, IQR: 235–420, P = 0.044). No difference could be demonstrated between the Ringer's lactate and 0.9% sodium chloride solution groups in the time to resolution of DKA (based on the ADA criteria) (unadjusted: P = 0.934, adjusted: P = 0.75 Continue reading >>

Nuances In Resuscitation Part Iii: Diabetic Ketoacidosis

Nuances In Resuscitation Part Iii: Diabetic Ketoacidosis

Thus far we have discussed resuscitation in trauma and sepsis. What distinguishes those two from the resuscitation goals in DKA is timing. In trauma and sepsis, it’s all about early recognition, aggressive and quick optimization, and understanding all the possible treatment options at your disposal. In the management of DKA, it’s quite the opposite. If you remember anything from this discussion, it’s that slow and steady wins the race! In fact, overaggressive resuscitation is what leads to the most significant morbidity and mortality in DKA patients. Patients in DKA don’t die from the disease process – they die because we kill them! DKA is defined as an anion-gap metabolic acidosis, with elevated serum ketones (usually measured as beta-hydroxybutyrate), blood glucose > 250 mg/dL, pH < 7.3, and a serum HCO3 < 18 mEq/L. It is the reason for over 50% of diabetic admissions, and many DKA patients begin their inpatient hospital course in the ICU. The leading causes of DKA are medication non-compliance, underlying infection, new-onset diabetes (i.e. DKA is the first presenting illness), or underlying medical/surgical stress. In general, DKA patients will present to the ED relatively early in their disease process because the ketones produced by the body induce vomiting, prompting the patient to seek treatment. This is in contrast to hyperosmolar non-ketotic coma patients (HONK) that present much later in their illness because there are no ketones in the blood to induce vomiting and alert the patient or his/her family that something is wrong. The mainstays of DKA management are fluid replenishment, glycemic control, correction of any other metabolic anomalies, and treatment of any underlying cause for the glycemic derangement. There are definitely some differences in Continue reading >>

Diabetic Emergencies, Diabetic Ketoacidosis In Adults, Part 3

Diabetic Emergencies, Diabetic Ketoacidosis In Adults, Part 3

Clinical Management Treatment consists of rehydration with intravenous fluids, the administration of insulin, and replacement of electrolytes. General medical care and close supervision by trained medical and nursing staff is of paramount importance in the management of patients with DKA. A treatment flowchart (Table 1.3) should be used and updated meticulously. A urine catheter is necessary if the patient is in coma or if no urine is passed in the first 4 hours…. Replacement of water deficit Patients with DKA have severe dehydration. The amount of fluid needing to be administered depends on the degree of dehydration (Table 1.4). Fluid replacement aims at correction of the volume deficit and not to restore serum osmolality to normal. Isotonic solution NaCl (0.9%) (normal saline; osmolality 308 mOsm/kg) should be administered even in patients with high serum osmolality since this solution is hypotonic compared to the extracellular fluid of the patient. 10 The initial rate of fluid administration depends on the degree of volume depletion and underlying cardiac and renal function. In a young adult with normal cardiac and/or renal function 1 L of normal saline is administered intravenously within the first half- to one hour. In the second hour administer another 1 L, and between the third and the fifth hours administer 0.5–1 L per hour. Thus, the total volume in the first 5 hours should be 3.5–5 L [1]. If the patient is in shock or blood pressure does not respond to normal saline infusion, colloid solutions together with normal saline may be used.1,6 Some authors suggest replacement of normal saline with hypotonic (0.45%) saline solution after stabilization of the hemodynamic status of the patient and when corrected serum sodium levels are normal.8 However, this appro 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 >>

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