Diabetic Ketoacidosis
4 Evaluation 5 Management Defining features include hyperglycemia (glucose > 250mg/dl), acidosis (pH < 7.3), and ketonemia/ketonuria Leads to osmotic diuresis and depletion of electrolytes including sodium, magnesium, calcium and phosphorous. Further dehydration impairs glomerular filtration rate (GFR) and contributes to acute renal failure Due to lipolysis / accumulation of of ketoacids (represented by increased anion gap) Compensatory respiratory alkalosis (i.e. tachypnea and hyperpnea - Kussmaul breathing) Breakdown of adipose creates first acetoacetate leading to conversion to beta-hydroxybutyrate Causes activation of RAAS in addition to the osmotic diuresis Cation loss (in exchange for chloride) worsens metabolic acidosis May be the initial presenting of an unrecognized T1DM patient Presenting signs/symptoms include altered mental status, tachypnea, abdominal pain, hypotension, decreased urine output. Perform a thorough neurologic exam (cerebral edema increases mortality significantly, especially in children) Assess for possible inciting cause (especially for ongoing infection; see Differential Diagnosis section) Ill appearance. Acetone breath. Drowsiness with decreased reflexes Tachypnea (Kussmaul's breathing) Signs of dehydration with dry mouth and dry mucosa. Perform a thorough neurologic exam as cerebral edema increases mortality significantly, especially in children There may be signs from underlying cause (eg pneumonia) Differential Diagnosis Insulin or oral hypoglycemic medication non-compliance Infection Intra-abdominal infections Steroid use Drug abuse Pregnancy Diabetic ketoacidosis (DKA) Diagnosis is made based on the presence of acidosis and ketonemia in the setting of diabetes. Bicarb may be normal due to compensatory and contraction alcoholosis so the Continue reading >>
Does Fluid Choice Make Any Difference In Dka?
Your patient is a 21 year-old female with a history of type 1 diabetes mellitus who was brought to the ED by her boyfriend for diminished responsiveness. In a stupor, she is unable to give any history. Her vitals are: BP 102/66, pulse 120, respiratory rate 24, temperature 98.9 oral, and O2 saturation 98% on room air. Her finger stick glucose is >500 mg/dl. She looks dry and is somnolent (GCS 9). Pupils are equal, round, and reactive. Neck is supple. She is protecting her airway well, her lungs are clear, and you hear no murmurs. Her belly is soft, and you see no signs of trauma or exanthema. Her skin tents when you pinch it. She is moving all extremities in response to noxious stimulus. As the rest of her labs (including serum osmolality and cultures, of course!) are sent off, her boyfriend tells you that she has not been taking her medications over the past 2 weeks and has had symptoms consistent with polydipsia and polyuria most noticeably over the past few days. A rapid shock panel returns with a glucose level of >500 mg/dl, pH 7.2, bicarbonate 10, and a urine dipstick shows large ketones. These confirm your suspicion of diabetic ketoacidosis (DKA). You wait for further results to decide whether a full sepsis work-up and antibiotics are necessary. In the meantime, you look at the bag of normal saline (0.9% saline solution) that is already hanging and you wonder, “Am I sure this is really the best solution to resuscitate a patient with DKA?” Consensus for Resuscitation in DKA Diabetic ketoacidosis is one of the diseases for which emergency physicians are expected to have a plan to quickly put into action. The basics should be familiar: Manage the patient’s ABCs, place an IV, put the patient on a monitor to check vitals frequently, and start with an intravenous f Continue reading >>
Dka And Thrombosis
Josephine Ho and associates1 report an unfortunate case of a 6-year-old girl with diabetic ketoacidosis (DKA) and thromboembolic stroke. Although the authors do a credible job of describing the diverse causes of pediatric stroke and the controversies surrounding treatment of children, there was little emphasis on the danger of extreme hyperosmolar states and risks of thrombosis. More information about the initial presentation of the patient, with specific reference to the concentration of serum sodium and serum osmolarity, would have been helpful in determining her risks of thrombosis. Diabetes is associated with a prothrombotic state through a number of mechanisms.2 The mostly adult entity of hyperosmolar nonketotic coma has had various degrees of association with thrombosis,2,3 as has extreme hypernatremia in breast-feeding neonates.4 Recent evidence has also demonstrated that among children with DKA, there is a higher incidence of deep venous thrombosis with femoral central venous lines.5,6 Serum glucose and sodium concentrations and hence effective plasma osmolarity were significantly higher in those patients with blood clots.5 Although there is no direct evidence for its efficacy, our practice has been to use prophylactic anticoagulation in patients with DKA who are in a significant hyperosmolar state, as well as to eliminate the use of femoral catheters in patients with these risk factors. There is significant controversy surrounding the dose of anticoagulant therapy, specifically whether the efficacy of dosages for prophylaxis of deep venous thrombosis outweighs the risks associated with full systemic anticoagulation.7 As with most clinical issues, particularly in pediatric critical illness, this controversy lends itself well to a clinical trial in patients with Continue reading >>
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Severe Hypercalcemia In Diabetic Ketoacidosis: A Case Report
A 12-year-old boy presented to a district hospital with diabetic ketoacidosis (DKA): pH, 6.97; base excess, −27.5 mmol/L; bicarbonate, 2.5 mmol/L; glucose 29 mmol/L. A urinalysis showed 4+ ketones (≥160 mg/dL). Standard DKA management according to U.K. guidelines was instituted (1). Fluid was replaced at maintenance plus 7.5% dehydration, with correction over 48 h. Within 2 h, the boy developed signs and symptoms of cerebral edema and was treated with intravenous mannitol (5 mL/kg × 2), and fluids were decreased by one-third. A further fall in his Glasgow Coma Score was managed with hypertonic (2.7%) saline (5 mL/kg), intubation and ventilation, and transfer to the regional pediatric intensive care unit (PICU). At the PICU, a decision was made to give maintenance fluid plus 5% dehydration correction over 72 h as a neuroprotective strategy. Within an hour of the boy’s admission to the PICU, an elevated, corrected calcium of 2.96 mmol/L was noted (normal range [NR]: 2.10–2.56 mmol/L). Retrospective analysis of the district hospital’s sample taken 4 h earlier showed a corrected calcium of 2.57 mmol/L. Over the next 24 h, the boy gradually developed acute, severe hypercalcemia with corrected calcium levels reaching a maximum of 3.75 mmol/L 33 h after the initial presentation. Parathyroid hormone was 8.3 ng/L (NR: 11–35), urine calcium/creatinine ratio, 0.17 (NR: 0–0.7), and maximum alkaline phosphatase 423 units/L (NR: 76–308). He had significant hyperglycemia, requiring up to 0.2 units/kg/h of intravenous insulin. Severe metabolic acidosis persisted for 4 days. This was attributed to a combination of severe dehydration, combined ketoacidosis and lacticacidosis, and hyperchloremia (maximum chloride levels, 145 mmol/L). Other electrolyte imbalances included Continue reading >>
Hyponatremia In Diabetes Mellitus: Clues To Diagnosis And Treatment
Department of Internal Medicine, School of Medicine, University of Ioannina, Ioannina, Greece Citation: Liamis G, Tsimihodimos V, Elisaf M (2015) Hyponatremia in Diabetes Mellitus: Clues to Diagnosis and Treatment. J Diabetes Metab 6: 560. doi: 10.4172/2155-6156.1000560 Copyright: © 2015 Liamis G, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Diabetes & Metabolism Hyponatremia is the most common electrolyte abnormality in clinical practice and is associated with increased morbidity and mortality [1,2]. Even small decreases of serum sodium are associated with increased probability for adverse outcomes (cognitive impairment, falls, osteoporosis and fractures) [3]. Decreased serum sodium levels are occasionally observed in patients with diabetes mellitus and can be attributed to numerous underlying pathogenetic mechanisms (Table 1) [4,5]. A) Non hypotonic hyponatremia With increased Posm: Hyperglycemia - induced (dilutional) With normal Posm: Pseudohyponatremia (marked hypertriglyceridemia and hyperproteinemia) B) Hypotonic hyponatremia • Hypovolemia-induced • Drug –induced hyponatremia (mainly with thiazides and first generation sulphonylureas) • Diabetes mellitus - associated hyponatremia • Syndrome of inappropriate antidiuresis associated with coexisting disorders or administered drugs • Chronic renal failure (diabetic nephropathy) or associated with the syndrome of hyporeninemichypoaldosteronism Table 1: Causes of hyponatremia in diabetic patients. The direct measurement of serum osmolality (Posm) can differentiate be Continue reading >>
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 >>
Restoring Electrolyte Balance
Looking for news and information on electrolyte balance? Here are a few more articles on the topic: Management of chronic kidney disease: An emphasis on delaying disease progression and treatment options Improving quality of life for patients with kidney failure Defenses gone awry: Inflammatory bowel disease Restoring electrolyte balance CE credit is no longer available for this article. (Expired May 2007) Originally posted May 2005 By Sonia M. Astle, RN, MS, CCRN Sonia Astle is a critical care clinical specialist at Inova Fairfax Hospital in Falls Church, VA, and a member of the RN editorial board. The author has no financial relationships to disclose. A shift up. A shift down. Either way, an imbalance in electrolytes spells trouble for your patients. Averting a crisis hinges on your clinical skills. This review will help you sharpen them. Electrolytes, or ions, are the charged particles in body fluids that help transmit electrical impulses for proper nerve, heart, and muscle function.1,2 The number of positive ions, called cations, and negative ions, called anions, is supposed to be equal. Anything that upsets this balance can have life-threatening consequences. There's a long list of conditions that lead to electrolyte imbalances, including dehydration, diabetic ketoacidosis, cancer, and even head injury. But renal disease is at the top of the list.1-3 It's the kidneys' job to control fluid, electrolyte, and acid-base balance. Because too much or too little of any one of the electrolytes quickly becomes a major problem of its own, doing everything possible to maintain the proper balance is a vital component of patient care. Therefore, monitoring electrolytes and checking for signs of an imbalance should be an integral part of your nursing assessment. Here, then, is a Continue reading >>
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 >>
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 >>
Diabetic Ketoacidosis
Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>
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 >>
Management Of The Complicated Diabetic
Proceeding of the NAVC North American Veterinary Conference Reprinted in the IVIS website with the permission of the NAVC Close window to return to IVIS Small Animal - Endocrinology Debra L. Zoran, DVM, PhD, Diplomate ACVIM Texas A&M University College Station, TX INTRODUCTION Diabetes mellitus is a common endocrinopathy in dogs and cats, and in most animals presents as a problem that is readily recognized and managed with routine diagnostic and therapeutic approaches. However, there are always exceptions to every rule, and this true for diabetes as well. This manuscript will review the recognition and management of insulin resistance, diabetic ketoacidosis, and the very uncommon, but challenging problem of nonketotic, hyperosmolar diabetes. The Complicated Diabetic – Insulin Ineffectiveness or Insulin Resistance? There are a number of factors that must be assessed in a dog or cat with diabetes that does not have adequate glycemic control. The first step is to determine whether the patient is an uncontrolled diabetic because of ineffective insulin or because of insulin resistance. There are many recognized causes of insulin ineffectiveness, and these include: • inactive insulin • diluted insulin • improper administration technique • inadequate dose • somogyi effect • inadequate frequency of insulin administration • impaired insulin absorption (especially long acting insulins) • anti-insulin antibody Insulin effectiveness should be assessed first, as it is the simplest group of problems to recognize and treat. Insulin ineffectiveness can be caused by inactive insulin, which is most often due to improper handling (e.g. insulin was damaged by heat or being dropped, shaken, etc). This problem is easily assessed by re-ev Continue reading >>
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 Management In Diabetic Ketoacidosis
Young people with insulin dependent diabetes mellitus are three times more likely to die in childhood than the general population.1 Despite advances in management over the past 20 years, the incidence of mortality associated with diabetic ketoacidosis (DKA) remains unchanged. Cerebral oedema is the predominant cause of this mortality; young children are particularly at risk, with an incidence of 0.7–1% of episodes of DKA.2,3 The mortality appears to be greatest among patients at first presentation,1,3,4 if there has been a long history of symptoms prior to admission,3 and during the first 24 hours of treatment.4 In a recently published retrospective multicentre analysis of children with DKA, low pco2 levels and high serum sodium concentration at presentation were identified as particular risk factors for the development of cerebral oedema, together with bicarbonate therapy.5 However, in the accompanying editorial, Dunger and Edge point out that this may simply be revealing an association between severe DKA and dehydration and the risk of cerebral oedema.6 The pathogenesis of cerebral oedema remains poorly understood but there may be many contributing factors.7 The aim of management of DKA is to restore metabolic homoeostasis while minimising the risks of complications including hypoglycaemia, hypokalaemia, cardiac failure, and in children the development of cerebral oedema. How best to achieve this remains contentious, with particular controversy centred on optimal fluid management. The most appropriate volume, type, and rate of fluid to be given have all been the subject of debate. A survey in 1994 of UK paediatricians found a threefold variation in the amount of fluid recommended within the first 12 hours.8 Since then national guidelines have been developed by the B Continue reading >>
Cerebral Edema In Diabetic Ketoacidosis: A Look Beyond Rehydration
The Journal of Clinical Endocrinology & Metabolism Cerebral Edema in Diabetic Ketoacidosis: A Look Beyond Rehydration Department of Pediatrics University of Florida Gainesville, Florida 32610 Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 85, Issue 2, 1 February 2000, Pages 509513, Andrew Muir; Cerebral Edema in Diabetic Ketoacidosis: A Look Beyond Rehydration, The Journal of Clinical Endocrinology & Metabolism, Volume 85, Issue 2, 1 February 2000, Pages 509513, INJUDICIOUS fluid resuscitation is frequently suggested as the cause of the cerebral edema that is the most common cause of mortality among pediatric patients with diabetic ketoacidosis (DKA) ( 1 ). The evidence, however, supports the hypothesis that neurological demise in DKA is a multifactorial process that cannot be reliably prevented by cautious rehydration protocols. Mortality and severe morbidity can, however, be reduced when healthcare providers watch vigilantly for and respond rapidly to the sentinel neurological signs and symptoms that precede, often by hours, the dramatic collapse that is typically described in these patients. Children being treated for DKA develop clinically important neurological compromise about 0.21.0% of the time ( 2 ). Subclinical neurological pathology, causing raised intracranial pressure, likely precedes the initiation of therapy in almost all cases of DKA ( 3 5 ). Intracranial hypertension has been considered to be aggravated by therapy of the DKA ( 4 , 6 , 7 ), but in keeping with the physicians perplexity about the problem, even this widely held tenet has recently been challenged ( 8 ). The pathogenic mechanism for this terrifying complication remains unknown. Hypothetical causes of cerebral edema in children with DKA m Continue reading >>
