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Hypokalemia Dka

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with significant fluid and electrolyte loss. DKA occurs mostly in type 1 diabetes mellitus (DM). It causes nausea, vomiting, and abdominal pain and can progress to cerebral edema, coma, and death. DKA is diagnosed by detection of hyperketonemia and anion gap metabolic acidosis in the presence of hyperglycemia. Treatment involves volume expansion, insulin replacement, and prevention of hypokalemia. Diabetic ketoacidosis (DKA) is most common among patients with type 1 diabetes mellitus and develops when insulin levels are insufficient to meet the body’s basic metabolic requirements. DKA is the first manifestation of type 1 DM in a minority of patients. Insulin deficiency can be absolute (eg, during lapses in the administration of exogenous insulin) or relative (eg, when usual insulin doses do not meet metabolic needs during physiologic stress). Common physiologic stresses that can trigger DKA include Some drugs implicated in causing DKA include DKA is less common in type 2 diabetes mellitus, but it may occur in situations of unusual physiologic stress. Ketosis-prone type 2 diabetes is a variant of type 2 diabetes, which is sometimes seen in obese individuals, often of African (including African-American or Afro-Caribbean) origin. People with ketosis-prone diabetes (also referred to as Flatbush diabetes) can have significant impairment of beta cell function with hyperglycemia, and are therefore more likely to develop DKA in the setting of significant hyperglycemia. SGLT-2 inhibitors have been implicated in causing DKA in both type 1 and type 2 DM. 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 >>

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Lack of insulin, thus no proper metabolism of glucose, ketones form, pH goes down, H+ concentration rises, our body tries to compensate by exchanging K+ from inside the cells for H+ outside the cells, hoping to lower H+ concentration, but at the same time elevating serum potassium. Most people are seriously dehydrated, so are in acute kidney failure, thus the kidneys aren’t able to excrete the excess of potassium from the blood, compounding the problem. On the other hand, many in reality are severely potassium depleted, so once lots of fluid so rehydration and a little insulin is administered serum potassium will plummet, so needs to be monitored 2 hourly - along with glucose, sodium and kidney function - to prevent severe hypokalemia causing fatal arrhythmias, like we experienced decades ago when this wasn’t so well understood yet. In practice, once the patient started peeing again, we started adding potassium chloride to our infusion fluids, the surplus potassium would be peed out by our kidneys so no risk for hyperkalemia. Continue reading >>

Hypokalemic Respiratory Arrest In Diabetic Ketoacidosis

Hypokalemic Respiratory Arrest In Diabetic Ketoacidosis

THE OCCURRENCE of life-threatening hypokalemic hypoventilatory respiratory failure requiring intubation and respiratory support in diabetic ketoacidosis (DKA) is exceedingly rare. In none of the reported cases have serum phosphate levels been assessed within 12 hours of respiratory failure and in only one case have serial arterial blood gas measurements been performed to document hypoventilation.1 The recent documentation of severe hypophosphatemia as a cause of hypoventilation and the fact that decrements in serum phosphate and serum potassium levels frequently parallel one another in DKA call into question the importance of hypokalemia to the respiratory response in DKA. We report a case of DKA in a young, otherwise healthy man whose treatment was complicated by severe hypokalemia and a hypoventilatory respiratory arrest without severe hypophosphatemia. We further discuss issues relating to the assessment and treatment of the hypokalemic patient with DKA at risk for ventilatory failure. Report of a Case Continue reading >>

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Hodaka Yamada1, Shunsuke Funazaki1, Masafumi Kakei1, Kazuo Hara1 and San-e Ishikawa2[1] Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan [2] Division of Endocrinology and Metabolism, International University of Health and Welfare Hospital, Nasushiobara, Japan Summary Diabetic ketoacidosis (DKA) is a critical complication of type 1 diabetes associated with water and electrolyte disorders. Here, we report a case of DKA with extreme hyperkalemia (9.0 mEq/L) in a patient with type 1 diabetes on hemodialysis. He had a left frontal cerebral infarction resulting in inability to manage his continuous subcutaneous insulin infusion pump. Electrocardiography showed typical changes of hyperkalemia, including absent P waves, prolonged QRS interval and tented T waves. There was no evidence of total body water deficit. After starting insulin and rapid hemodialysis, the serum potassium level was normalized. Although DKA may present with hypokalemia, rapid hemodialysis may be necessary to resolve severe hyperkalemia in a patient with renal failure. Patients with type 1 diabetes on hemodialysis may develop ketoacidosis because of discontinuation of insulin treatment. Patients on hemodialysis who develop ketoacidosis may have hyperkalemia because of anuria. Absolute insulin deficit alters potassium distribution between the intracellular and extracellular space, and anuria abolishes urinary excretion of potassium. Rapid hemodialysis along with intensive insulin therapy can improve hyperkalemia, while fluid infusions may worsen heart failure in patients with ketoacidosis who routinely require hemodialysis. Background Diabetic ketoacidosis (DKA) is a very common endocrinology emergency. It is usually associated with severe circulatory Continue reading >>

Profound Hypokalemia Associated With Severe Diabetic Ketoacidosis

Profound Hypokalemia Associated With Severe Diabetic Ketoacidosis

Go to: Abstract Hypokalemia is common during the treatment of diabetic ketoacidosis (DKA); however, severe hypokalemia at presentation prior to insulin treatment is exceedingly uncommon. A previously healthy 8-yr-old female presented with new onset type 1 diabetes mellitus, severe DKA (pH = 6.98), and profound hypokalemia (serum K = 1.3 mmol/L) accompanied by cardiac dysrhythmia. Insulin therapy was delayed for 9 h to allow replenishment of potassium to safe serum levels. Meticulous intensive care management resulted in complete recovery. This case highlights the importance of measuring serum potassium levels prior to initiating insulin therapy in DKA, judicious fluid and electrolyte management, as well as delaying and/or reducing insulin infusion rates in the setting of severe hypokalemia. Keywords: diabetic ketoacidosis, hypokalemia, insulin, low-dose insulin drip, pediatric Nearly one third of children with newly diagnosed type 1 diabetes present in diabetic ketoacidosis (DKA). Higher proportions of young children and those from disadvantaged socioeconomic groups present with DKA (1). DKA is the leading cause of mortality among children with diabetes, and electrolyte abnormalities are a recognized complication of DKA contributing to morbidity and mortality (2, 3). Total body potassium deficiency of 3-6 mEq/kg is expected at presentation of DKA due to osmotic diuresis, emesis, and secondary hyperaldosteronism; however, pretreatment serum potassium levels are usually not low due to the extracellular shift of potassium that occurs with acidosis and insulin deficiency (3, 4). After insulin treatment is initiated, potassium shifts intracellularly and serum levels decline. Replacement of potassium in intravenous fluids is the standard of care in treatment of DKA to prevent Continue reading >>

Prevalence And Potential Risk Factors Of Hypokalemia In Pediatric Patients With Diabetic Ketoacidosis

Prevalence And Potential Risk Factors Of Hypokalemia In Pediatric Patients With Diabetic Ketoacidosis

Aims To examine the local prevalence of hypokalemia in patients with diabetic ketoacidosis (DKA), both at presentation and during treatment, and to investigate the potential risk factors leading to significant hypokalemia during treatment of DKA. Methods Retrospective review of 114 consecutive patient-episodes. Univariate analyses were performed to study any difference in mean between the group with nadir of potassium (Kn) >= 3.0mmol/L from group with Kn < 3.0mmol/L for predictors concerning patients’ demographics, the baseline characteristics, the therapies for DKA (including average insulin infusion rate before Kn), and the pace of recovery from DKA. Predictors deemed statistical significant in univariate analyses were subjected to multivariate analysis. Results The period prevalence of hypokalemia at presentation and during treatment of DKA were 13.8% and 92.5% respectively. Univariate analysis showed patients who were younger, with lower mean body weight, lower mean plasma bicarbonate at presentation, lower mean serum potassium level at presentation, higher urine output per unit body weight (in the first 24 hours of admission), higher amount of potassium supplement given before Kn, shorter time lag of starting potassium supplements (as reference to time of start of insulin) and longer duration of metabolic acidosis were independently associated with risk of developing Kn < 3.0mmol/L. Multivariate analysis showed that duration of metabolic acidosis was the sole risk factor for having Kn < 3.0mmol/L. Conclusions In our cohort, the longer duration of metabolic acidosis predicts significant hypokalemia during DKA treatment, which could have represented a persistent accumulation of free fatty acid and an on-going stimulus for aldosterone secretion, hence kaliuresis-rel Continue reading >>

Diabetic Ketoacidosis (dka) Myths

Diabetic Ketoacidosis (dka) Myths

Recently, I was asked to give a lecture to both my residents and nurses at the University of Texas Health Science Center at San Antonio (UTHSCSA) on some common DKA myths. Now this topic was originally covered by my good friend Anand Swaminathan on multiple platforms and I did ask his permission to create this blogpost with the idea of improving patient care and wanted to express full disclosure of that fact. I specifically covered four common myths that I still see people doing in regards to DKA management: We should get ABGs instead of VBGs After Intravenous Fluids (IVF), Insulin is the Next Step Once pH <7.1, Patients Need Bicarbonate Therapy We Should Bolus Insulin before starting the infusion DKA Myths Case: 25 y/o female with PMH of Type I DM who presents via EMS with AMS. Per EMS report, the patient ran out of her insulin 3 days ago….. Vital Signs: BP 86/52 HR 136 RR 30 O2Sat 97% on room air Temp 99.1 Accucheck: CRITICAL HIGH EMS was not able to establish IV access, so decided to just bring her to the ED due to how sick she looks. Your nurses are on point today and get you two large bore 18G IVs and start to draw blood work to send to the lab. You state I need a blood gas, and the nurse turns to you and asks do you need an ABG or VBG? Myth #1: We should get ABGs instead of VBGs in DKA So you do a literature review and come across two studies that specifically look at ABG vs VBG in an ED population: Study #1: Kelly AM et al. Review Article – Can Venous Blood Gas Analysis Replace Arterial in Emergency Medical Care. Emery Med Australas 2010; 22: 493 – 498. PMID: 21143397 For pH, 3 studies of patients with DKA (265 patients) were reviewed showing a weighted mean difference of 0.02 pH units. Only one study, which was the largest study (200 patients) reported 95% Continue reading >>

Diabetic Ketoacidosis Treatment & Management

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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Print Overview Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) — a major source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. If you have diabetes or you're at risk of diabetes, learn the warning signs of diabetic ketoacidosis — and know when to seek emergency care. Symptoms Diabetic ketoacidosis signs and symptoms often develop quickly, sometimes within 24 hours. For some, these signs and symptoms may be the first indication of having diabetes. You may notice: Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Weakness or fatigue Shortness of breath Fruity-scented breath Confusion More-specific signs of diabetic ketoacidosis — which can be detected through home blood and urine testing kits — include: High blood sugar level (hyperglycemia) High ketone levels in your urine When to see a doctor If you feel ill or stressed or you've had a recent illness or injury, check your blood sugar level often. You might also try an over-the-counter urine ketones testing kit. Contact your doctor immediately if: You're vomiting and unable to tolerate food or liquid Your blood sugar level is higher than your target range and doesn't respond to home treatment Your urine ketone level is moderate or high Seek emergency care if: Your blood sugar level is consistently higher than 300 milligrams per deciliter (mg/dL), or 16.7 mill Continue reading >>

Episode 60.0 – Aggressive Resuscitation Of Diabetic Ketoacidosis

Episode 60.0 – Aggressive Resuscitation Of Diabetic Ketoacidosis

Show Notes Take Home Points DKA should be suspected in any patient with altered mental status and hyperglycemia. Get a VBG (ABG not necessary) to confirm the diagnosis. Hypokalemia kills in DKA. Aggresively replete potassium and consider holding insulin, which drops serum potassium, until K is greater than 3.5 The insulin bolus isn’t necessary and appears to cause more episodes of hypokalemia. Just start insulin as an infusion at 0.14 units/kg Be vigilant about cerebral edema. Any change or deterioration in mental status should prompt treatment and evaluation. Mannitol in the euvolemic, normotensive patient and 3% hypertonic saline in the hypotensive/hypovolemic patient Finally, don’t forge to always hunt down the underlying cause of the DKA. Infection and non-compliance is the most common so liberally administer broad spectrum antibiotics if you’ve got even a hint of infection brewing Additional Reading References Aurora S et al. Prevalence of hypokalemia in ED patients with diabetic ketoacidosis. Am J Emerg Med 2012; 30: 481-4. PMID: 21316179 Boyd JC et al. Relationship of potassium and magnesium concentrations in serum to cardiac arrhythmias. Clin Chem 1984; 30(5): 754-7. PMID: 6713638 Duhon B et al. Intravenous sodium bicarbonate therapy in severely acidotic diabetic ketoacidosis. Ann Pharmacother 2013; 47: 970-5. PMID: 23737516 Fagan MJ et al. Initial fluid resuscitation for patients with diabetic ketoacidosis: how dry arethey? Clin Ped 2008; 47(9): 851-6. PMID: Goyal N et al. Utility of Initial Bolus insulin in the treatment of diabetic ketoacidosis. J Emerg Med 2010; 38(4): 422-7. PMID: 18514472 Green SM et al. Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis. Ann Emergency Medicine 1998; 31: 41-48. PMID: 943734 Continue reading >>

Myths In Dka Management

Myths In Dka Management

Anand Swaminathan, MD, MPH (@EMSwami) is an assistant professor and assistant program director at the NYU/Bellevue Department of Emergency Medicine in New York City. Review questions are available at the end of this post. Background Each year, roughly 10,000 patients present to the Emergency Department in diabetic ketoacidosis (DKA). Prior to the advent of insulin, the mortality rate of DKA was 100% although in recent years, that rate has dropped to approximately 2-5%.1 Despite clinical advances, the mortality rate has remained constant over the last 10 years. With aggressive resuscitative measures and appropriate continued management this trend may change. DKA is defined as: Hyperglycemia (glucose > 250 mg/dl) Acidosis (pH < 7.3) Ketosis In the absence of insulin, serum glucose rises leading to osmotic diuresis. This diuresis leads to loss of electrolytes including sodium, magnesium, calcium and phosphorous. The resultant volume depletion leads to impaired glomerular filtration rate (GFR) and acute renal failure. In patients with DKA, fatty acid breakdown produces 2 different ketone bodies, first acetoacetate, which then further converts to beta-hydroxybutyrate, the latter being the ketone body largely produced in DKA patients. With this background in mind, let’s take a look at four urban legends in the management of DKA and the evidence that dispels these legends. Here’s our case: Although this presentation likely represents DKA, a blood gas is typically obtained to confirm the diagnosis. Often, the question arises as to whether an arterial or venous blood gas is adequate. Urban Legend #1 – An ABG is necessary for the diagnosis and treatment of DKA ABG gets you pH, PaO2, PaCO2, HCO3, Lactate, electrolytes and O2Sat VBG gets all this except for PaO2 (but we have Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Abbas E. Kitabchi, PhD., MD., FACP, FACE Professor of Medicine & Molecular Sciences and Maston K. Callison Professor in the Division of Endocrinology, Diabetes & Metabolism UT Health Science Center, 920 Madison Ave., 300A, Memphis, TN 38163 Aidar R. Gosmanov, M.D., Ph.D., D.M.Sc. Assistant Professor of Medicine, Division of Endocrinology, Diabetes & Metabolism, The University of Tennessee Health Science Center, 920 Madison Avenue, Suite 300A, Memphis, TN 38163 Clinical Recognition Omission of insulin and infection are the two most common precipitants of DKA. Non-compliance may account for up to 44% of DKA presentations; while infection is less frequently observed in DKA patients. Acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke, acute thrombosis) and gastrointestinal tract (bleeding, pancreatitis), diseases of endocrine axis (acromegaly, Cushing`s syndrome, hyperthyroidism) and impaired thermo-regulation or recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hormones, and worsening of peripheral insulin resistance. Medications such as diuretics, beta-blockers, corticosteroids, second-generation anti-psychotics, and/or anti-convulsants may affect carbohydrate metabolism and volume status and, therefore, could precipitateDKA. Other factors: psychological problems, eating disorders, insulin pump malfunction, and drug abuse. It is now recognized that new onset T2DM can manifest with DKA. These patients are obese, mostly African Americans or Hispanics and have undiagnosed hyperglycemia, impaired insulin secretion, and insulin action. A recent report suggests that cocaine abuse is an independent risk factor associated with DKA recurrence. Pathophysiology In 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 >>

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 >>

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