Why Do Dka Patients Need Fluids

Management Of Pediatric Diabetic Ketoacidosis: Does Aggressive Fluid Resuscitation Actually Result In Cerebral Edema? The Case Of A 6-year-old With Aggressive Fluid Resuscitation

Our patient was a 6-year-old female presenting to the emergency room of a regional hospital partially obtunded and severely dehydrated following a short illness. She had been taken in by her mother, who reported that the patient had experienced a 6-day history of fatigue and progressive thirst, 4 days of left earache, and a 2-day history of vomiting. This patient was the middle of 5 siblings and had been previously well, although the family was known to social services for some child care issues, and there was no personal or family history of significance. The patient weighed 22 kg and was severely dehydrated on assessment with an impaired level of consciousness (Glasgow Coma Score [GCS] of 9/15 [E 2, V 3, M4]). She was hyperventilating and maintaining her airway with 30 respirations per minute. Her oxygen saturation was maintained between 96 and 100% with 5 L of oxygen via a rebreathing mask. She was afebrile with a temperature of 36.6°C, displayed tachycardia with a pulse of 145 beats per minute, and her blood pressure was 113/81 mm Hg. Additional findings on examination included dry mucus membranes, impaired capillary refill time, decreased skin turgidity, and sunken eyes. Her initial random glucose was 31.8 mmol/L. She was acidotic with a pH of 6.8, had an incalculable base excess, and bicarbonate of 3 mmol/L. The patient was managed with aggressive fluid resuscitation in consultation with the pediatric intensivist from the pediatric intensive care unit (PICU) of a tertiary center because of the assessed degree of dehydration. She received an initial bolus of 20 mL/kg of normal saline (NS) given rapidly as a push. Following the administration of saline, unusual behavior was observed with concerns that this could be the result of a seizure and, therefore, she was gi Continue reading >>

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 >>

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 >>

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 >>

Hyperglycemic Crises In Patients With Diabetes Mellitus

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. 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 inadequate to f Continue reading >>

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 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 >>

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 >>

Episode 63 – Pediatric Dka

Pediatric DKA was identified as one of key diagnoses that we need to get better at managing in a massive national needs assessment conducted by the fine folks at TREKK – Translating Emergency Knowledge for Kids – one of EM Cases’ partners who’s mission is to improve the care of children in non-pediatric emergency departments across the country. You might be wondering – why was DKA singled out in this needs assessment? It turns out that kids who present to the ED in DKA without a known history of diabetes, can sometimes be tricky to diagnose, as they often present with vague symptoms. When a child does have a known history of diabetes, and the diagnosis of DKA is obvious, the challenge turns to managing severe, life-threatening DKA, so that we avoid the many potential complications of the DKA itself as well as the complications of treatment – cerebral edema being the big bad one. The approach to these patients has evolved over the years, even since I started practicing, from bolusing insulin and super aggressive fluid resuscitation to more gentle fluid management and delayed insulin drips, as examples. There are subtleties and controversies in the management of DKA when it comes to fluid management, correcting serum potassium and acidosis, preventing cerebral edema, as well as airway management for the really sick kids. In this episode we‘ll be asking our guest pediatric emergency medicine experts Dr. Sarah Reid, who you may remember from her powerhouse performance on our recent episodes on pediatric fever and sepsis, and Dr. Sarah Curtis, not only a pediatric emergency physician, but a prominent pediatric emergency researcher in Canada, about the key historical and examination pearls to help pick up this sometimes elusive diagnosis, what the value of serum Continue reading >>

Original Contributions Effect Of Volume Of Fluid Resuscitation On Metabolic Normalization In Children Presenting In Diabetic Ketoacidosis: A Randomized Controlled Trial

Abstract Our aim was to determine whether the volume of fluid administration in children with DKA influences the rate of metabolic normalization. We performed a randomized controlled trial conducted in a tertiary pediatric emergency department from December 2007 until June 2010. The primary outcome was time to metabolic normalization; secondary outcomes were time to bicarbonate normalization, pH normalization, overall length of hospital treatment, and adverse outcomes. Children between 0 and 18 years of age were eligible if they had type 1 diabetes mellitus and DKA. Patients were randomized to receive intravenous (IV) fluid at low volume (10 mL/kg bolus + 1.25 × maintenance rate) or high volume (20 mL/kg bolus + 1.5 × maintenance rate) (n = 25 in each). After adjusting for initial differences in bicarbonate levels, time to metabolic normalization was significantly faster in the higher-volume infusion group compared to the low-volume infusion group (hazard ratio [HR] = 2.0; 95% confidence interval [CI] 1.0–3.9; p = 0.04). Higher-volume IV fluid infusion appeared to hasten, to a greater extent, normalization of pH (HR = 2.5; 95% CI 1.2–5.0; p = 0.01) than normalization of serum bicarbonate (HR = 1.2; 95% CI 0.6–2.3; p = 0.6). The length of hospital treatment HR (0.8; 95% CI 0.4–1.5; p = 0.5) and time to discharge HR (0.8; 95% CI 0.4–1.5; p = 0.5) did not differ between treatment groups. Higher-volume fluid infusion in the treatment of pediatric DKA patients significantly shortened metabolic normalization time, but did not change overall length of hospital treatment. ClinicalTrials.gov ID NCT01701557. Continue reading >>

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 >>

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 >>

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 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-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 >>