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Dka Hypernatremia

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 >>

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 >>

Diabetic Ketoacidosis And Cerebral Edema

Diabetic Ketoacidosis And Cerebral Edema

Elliot J. Krane, M.D. Departments of Pediatrics and Anesthesiology Stanford University Medical Center Introduction In 1922 Banting and Best introduced insulin into clinical practice. A decade later the first reported case of cerebral edema complicating diabetic ketoacidosis (DKA) was reported by Dillon, Riggs and Dyer writing in the pathology literature. While the syndrome of cerebral edema complicating DKA was either not seen, ignored, or was unrecognized by the medical community until 3 decades later when the complication was again reported by Young and Bradley at the Joslin Clinic, there has since been a flurry of case reports in the 1960's and 1970's and basic and clinical research from the 1970's to the 1990's leading to our present day acceptance of this as a known complication of DKA, or of the management of DKA. In fact, we now recognize that the cerebral complications of DKA (including much less frequent cerebral arterial infarctions, venous sinus thrombosis, and central nervous system infections) are the most common cause of diabetic-related death of young diabetic patients (1), accounting for 31% of deaths associated with DKA and 20% of all diabetic deaths, having surpassed aspiration, electrolyte imbalance, myocardial infarction, etc. Furthermore, diabetes mellitus remains an important cause of hospitalization of young children. The prevalence rate of diabetes continues to grow in all Western developed nations, nearly doubling every decade, resulting in 22,000 hospital admissions in children under 15 years of age for diabetes in the United States in 1994, the majority of which were due to ketoacidosis. With approximately 4 hospital admissions of children for DKA per 100,000 population per year (2), every PICU located in a major metropolitan center will conti Continue reading >>

Diabetic Ketoacidosis

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 And Hyperosmolar Hyperglycemia — A Brief Review

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemia — A Brief Review

Diabetic Ketoacidosis and Hyperosmolar Hyperglycemia — A Brief Review SPECIAL FEATURE By Richard J. Wall, MD, MPH, Pulmonary Critical Care & Sleep Disorders Medicine, Southlake Clinic, Valley Medical Center, Renton, WA. Dr. Wall reports no financial relationships relevant to this field of study. Financial Disclosure: Critical Care Alert's editor, David J. Pierson, MD, nurse planner Leslie A. Hoffman, PhD, RN, peer reviewer William Thompson, MD, executive editor Leslie Coplin, and managing editor Neill Kimball report no financial relationships relevant to this field of study. INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two of the most common and serious acute complications of diabetes mellitus. DKA is responsible for more than 500,000 hospital days annually in the United States, at an estimated annual cost of $2.4 billion. Both conditions are part of the spectrum of uncontrolled hyperglycemia, and there is sometimes overlap between them. This article will discuss and compare the two conditions, with a focus on key clinical features, diagnosis, and treatment. DIAGNOSTIC FEATURES In DKA, there is an accumulation of ketoacids along with a high anion gap metabolic acidosis (see Table below).1 The acidosis usually evolves quickly over a 24-hour period. The pH is often < 7.20 and initial bicarbonate levels are often < 20 mEq/L. DKA patients (especially children) often present with nausea, vomiting, hyperventilation, and abdominal pain. Blood sugar levels in DKA tend to be 300-800 mg/dL, but they are sometimes much higher when patients present in a comatose state. In HHS, there is no (or little) ketonemia but the plasma osmolality may reach 380 mOsm/kg, and as a result, patients often have neurologic complications such as coma. Bica Continue reading >>

Management Of The Complicated Diabetic

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 >>

Severe Hypercalcemia In Diabetic Ketoacidosis: A Case Report

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 >>

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 >>

Management Of Diabetic Ketoacidosis In The Picu

Management Of Diabetic Ketoacidosis In The Picu

DKA - A common PICU diagnosis Incidence 4.6 – 8 per 1000 person years among people with diabetes Pediatric mortality rate is 1-2% DKA causes profound dehydration Hyperglycemia leads to osmotic diuresis Often 10-15% down from baseline weight Profound urinary free water and electrolyte loss Free water follows glucose into urine Electrolytes follow free water into urine Electrolyte abnormalities Pseudo-hyponatremia with hyperglycemia Sodium should rise with correction of glucose Profound total-body K+ depletion Urinary loss, decreased intake, emesis Initial K+ may be high due to acidosis, low insulin Aggressive K+ replacement necessary to prevent arrhythmias Phosphate, magnesium, calcium require replacement Initial DKA management - ED Resuscitation aimed at shock reversal Begin with 10-20 mL/kg NS bolus, may repeat if signs of shock persist Bolus fluids only necessary if signs of shock present Avoid overly-aggressive fluid resuscitation Concern for inciting cerebral edema, though no clear data Initial DKA management - ED NEVER give bicarbonate Increases risk of cerebral edema Begin insulin infusion at 0.1 units/kg/hr Should be initiated prior to leaving ED SQ or bolus insulin not indicated Pre-PICU arrival Order several bags of dextrose-containing and non-dextrose-containing IVF pre-PICU arrival Often takes pharmacy 1 hour to custom-make IVF No dextrose-containing fluids stocked in PICU Fluid Management - PICU 3 components to replacement fluids Deficit (often 10-15% total body water deficit) Ongoing losses (polyuria, emesis) Maintenance Possible to calculate the above, or give: 1.5X maintenance if moderately dehydrated 2X maintenance if severely dehydrated Isotonic fluid with potassium NS + 20 mEq/L KCl + 20 mEq/L KPhos Start with 40 mEq/L of potassium if K+ < 5 K+ Continue reading >>

Diabetic Ketoacidosis In Children And Adolescents: An Update And Revised Treatment Protocol

Diabetic Ketoacidosis In Children And Adolescents: An Update And Revised Treatment Protocol

Standardized pediatric-specific treatment is required to ensure safe correction of metabolic derangements associated with DKA. ABSTRACT: British Columbia has an estimated 150 to 200 new cases of type 1 diabetes in children annually. In these cases, 10% to 20% of patients will present in diabetic ketoacidosis (DKA). DKA is associated with significant fluid and biochemical derangements, necessitating a thoughtful, structured approach to its management. Recent gains have been made in knowledge about the pathophysiology and medical care of DKA and its most significant complication, cerebral edema. In response, BC Children’s Hospital has devised an updated medical protocol for managing DKA in infants, children, and adolescents that conforms to new international consensus guidelines. The protocol assists the medical practitioner in calculating fluid and electrolyte replacement needs for individual patients and outlines a plan for initial assessment and ongoing monitoring. Accompanying resources have also been developed to aid nursing, laboratory, and pharmacy colleagues to ensure that all children presenting with DKA in this province are managed following scientifically established guidelines. Canada has one of the highest rates of type 1 diabetes (T1D) in the world. The estimated incidence of T1D in Canadian children aged 0 to 14 years is 21.7 per 100000 per year.[1] Using 2008 census data,[2] prevalence in this age group in British Columbia is estimated to be about 1029 established cases of T1D or about 150 new cases per year. Much publicity has been given to the rising incidence of type 2 diabetes (T2D) in youth and young adults in North America, a phenomenon that we are also observing in our province, but the fact that there has also been a 2% to 3% annual increase in t Continue reading >>

I’ll See Your Ketoacidosis And Raise You A Renal Failure

I’ll See Your Ketoacidosis And Raise You A Renal Failure

A while back I posted on a paper that appeared in The Lancet about an obese woman who came to the emergency room with gastroenteritis and was misdiagnosed as being in diabetic ketoacidosis (a life-threatening disorder). She was misdiagnosed because the pinheads covering the ER couldn’t get past the fact that she had been on a low-carb diet. At the time I posted on this travesty I noted that this Lancet paper would from here on out be waved in the face of anyone who was following or advocated a low-carb diet as proof that such a diet is dangerous and can cause diabetic ketoacidosis (DKA). Well, now we’ve got an answer. Next time someone tells you that it has been proven that low-carb diets are dangerous and can cause ketoacidosis, you can resort to poker terminology and reply that you’ll see their ketoacidosis and raise them a renal failure. A few days ago I got wind of a paper published a few years ago that can be used as a counterpoint to the above mentioned idiotic paper in The Lancet that has given low-carbers such a bad time. This paper, published in the journal Renal Failure in 1998, is, like the other paper, a case report. The short version is as follows: An obese young man arrived comatose in the emergency room. In an effort to lose weight he had been consuming a high-carbohydrate canned beverage as his sole source of nutrition for the two weeks prior. His blood sugar–at about 20 times normal–was extremely elevated and led to a diagnosis of diabetic ketoacidosis. The physicians on staff treated the patient appropriately, and he, over the next 20 hours or so, regained consciousness as his blood sugar levels and other lab parameters began to normalize. During a lab analysis 22 hours after admission the doctors found the patient to be breaking down and rel Continue reading >>

Cerebral Edema In Diabetic Ketoacidosis: A Look Beyond Rehydration

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 >>

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 >>

Does Fluid Choice Make Any Difference In Dka?

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

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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