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Why Is Sodium High In Dka?

Sodium Bicarbonate And Diabetic Ketoacidosis

Sodium Bicarbonate And Diabetic Ketoacidosis

OVERVIEW The correction of the acidaemia in DKA is achieved by correcting the underlying pathophysiology with fluid replacement and insulin The role of sodium bicarbonate (NaHCO3) as a therapy for diabetic ketoacidosis (DKA) is controversial Different sources have different values for the cut off pH which requires treatment, and other sources advise against NaHCO3 use in DKA completely — there is no consensus RATIONALE Reasons proposed for use of sodium bicarbonate in DKA: treatment of severe acidaemia, which causes catecholamine resistance and myocardial depression treatment of severe hyperkalemia replacement of bicarbonate loss from Renal or GI tract — theoretical potential for giving HCO3- with renal wasting of HCO3- or GI loss if delta ratio is <1 (as is usual for DKA) ketoacids lost in urine (hence delta ratio <1) cannot be converted into HCO3- DISADVANTAGES Side effects of sodium bicarbonate Worsening of intracellular acidaemia hypernatraemia (1mmol of Na+ for every 1mmol of HCO3-) hyperosmolality (cause arterial vasodilation and hypotension) volume overload rebound or ‘overshoot’ alkalosis hypokalaemia ionised hypocalcaemia impaired oxygen unloading due to left shift of the oxyhaemoglobin dissociation curve removal of acidotic inhibition of glycolysis by increased activity of PFK CSF acidosis hypercapnia (CO2 readily passes intracellularly and worsens intracellular acidosis) severe tissue necrosis if extravasation takes place bicarbonate increases lactate production by: — increasing the activity of the rate limiting enzyme phosphofructokinase and removal of acidotic inhibition of glycolysis — shifts Hb-O2 dissociation curve, increased oxygen affinity of haemoglobin and thereby decreases oxygen delivery to tissues EVIDENCE A 2011 systematic review by C Continue reading >>

Hyperkalemia (high Blood Potassium)

Hyperkalemia (high Blood Potassium)

How does hyperkalemia affect the body? Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart. It is also important for normal transmission of electrical signals throughout the nervous system within the body. Normal blood levels of potassium are critical for maintaining normal heart electrical rhythm. Both low blood potassium levels (hypokalemia) and high blood potassium levels (hyperkalemia) can lead to abnormal heart rhythms. The most important clinical effect of hyperkalemia is related to electrical rhythm of the heart. While mild hyperkalemia probably has a limited effect on the heart, moderate hyperkalemia can produce EKG changes (EKG is a reading of theelectrical activity of the heart muscles), and severe hyperkalemia can cause suppression of electrical activity of the heart and can cause the heart to stop beating. Another important effect of hyperkalemia is interference with functioning of the skeletal muscles. Hyperkalemic periodic paralysis is a rare inherited disorder in which patients can develop sudden onset of hyperkalemia which in turn causes muscle paralysis. The reason for the muscle paralysis is not clearly understood, but it is probably due to hyperkalemia suppressing the electrical activity of the muscle. Common electrolytes that are measured by doctors with blood testing include sodium, potassium, chloride, and bicarbonate. The functions and normal range values for these electrolytes are described below. Hypokalemia, or decreased potassium, can arise due to kidney diseases; excessive losses due to heavy sweating Continue reading >>

Electrolyte Imbalance In Diabetic Ketoacidosis

Electrolyte Imbalance In Diabetic Ketoacidosis

If you have diabetes, it's important to be familiar with diabetic ketoacidosis (DKA). DKA is a serious complication of diabetes that occurs when lack of insulin and high blood sugar lead to potentially life-threatening chemical imbalances. The good news is DKA is largely preventable. Although DKA is more common with type 1 diabetes, it can also occur with type 2 diabetes. High blood sugar causes excessive urination and spillage of sugar into the urine. This leads to loss of body water and dehydration as well as loss of important electrolytes, including sodium and potassium. The level of another electrolyte, bicarbonate, also falls as the body tries to compensate for excessively acidic blood. Video of the Day Insulin helps blood sugar move into cells, where it is used for energy production. When insulin is lacking, cells must harness alternative energy by breaking down fat. Byproducts of this alternative process are called ketones. High concentrations of ketones acidify the blood, hence the term "ketoacidosis." Acidosis causes unpleasant symptoms like nausea, vomiting and rapid breathing. Bicarbonate is an electrolyte that normally counteracts blood acidity. In DKA, the bicarbonate level falls as ketone production increases and acidosis progresses. Treatment of DKA includes prompt insulin supplementation to lower blood sugar, which leads to gradual restoration of the bicarbonate level. Potassium may be low in DKA because this electrolyte is lost due to excessive urination or vomiting. When insulin is used to treat DKA, it can further lower the blood potassium by pushing it into cells. Symptoms associated with low potassium include fatigue, muscle weakness, muscle cramps and an irregular heart rhythm. Severely low potassium can lead to life-threatening heart rhythm abnorm Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

The Facts Diabetic ketoacidosis (DKA) is a condition that may occur in people who have diabetes, most often in those who have type 1 (insulin-dependent) diabetes. It involves the buildup of toxic substances called ketones that make the blood too acidic. High ketone levels can be readily managed, but if they aren't detected and treated in time, a person can eventually slip into a fatal coma. DKA can occur in people who are newly diagnosed with type 1 diabetes and have had ketones building up in their blood prior to the start of treatment. It can also occur in people already diagnosed with type 1 diabetes that have missed an insulin dose, have an infection, or have suffered a traumatic event or injury. Although much less common, DKA can occasionally occur in people with type 2 diabetes under extreme physiologic stress. Causes With type 1 diabetes, the pancreas is unable to make the hormone insulin, which the body's cells need in order to take in glucose from the blood. In the case of type 2 diabetes, the pancreas is unable to make sufficient amounts of insulin in order to take in glucose from the blood. Glucose, a simple sugar we get from the foods we eat, is necessary for making the energy our cells need to function. People with diabetes can't get glucose into their cells, so their bodies look for alternative energy sources. Meanwhile, glucose builds up in the bloodstream, and by the time DKA occurs, blood glucose levels are often greater than 22 mmol/L (400 mg/dL) while insulin levels are very low. Since glucose isn't available for cells to use, fat from fat cells is broken down for energy instead, releasing ketones. Ketones accumulate in the blood, causing it to become more acidic. As a result, many of the enzymes that control the body's metabolic processes aren't able Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Initial Evaluation Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors (Table 14–18). The most common precipitating factor is infection, followed by noncompliance with insulin therapy.3 While insulin pump therapy has been implicated as a risk factor for DKA in the past, most recent studies show that with proper education and practice using the pump, the frequency of DKA is the same for patients on pump and injection therapy.19 Common causes by frequency Other causes Selected drugs that may contribute to diabetic ketoacidosis Infection, particularly pneumonia, urinary tract infection, and sepsis4 Inadequate insulin treatment or noncompliance4 New-onset diabetes4 Cardiovascular disease, particularly myocardial infarction5 Acanthosis nigricans6 Acromegaly7 Arterial thrombosis, including mesenteric and iliac5 Cerebrovascular accident5 Hemochromatosis8 Hyperthyroidism9 Pancreatitis10 Pregnancy11 Atypical antipsychotic agents12 Corticosteroids13 FK50614 Glucagon15 Interferon16 Sympathomimetic agents including albuterol (Ventolin), dopamine (Intropin), dobutamine (Dobutrex), terbutaline (Bricanyl),17 and ritodrine (Yutopar)18 DIFFERENTIAL DIAGNOSIS Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue. Common problems that produce ketosis include alcoholism and starvation. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol. Abdominal pain may be a symptom of ketoacidosis or part of the inci 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 >>

Hyperkalaemia In Diabetic Ketoacidosis

Hyperkalaemia In Diabetic Ketoacidosis

Dear Editor, I have a brief comment on the informative ‘Lesson of the week’ by Moulik and colleagues, describing an association between hyperkalaemia and an ECG pattern suggesting acute myocardial infarction in a patient with diabetic ketoacidosis (DKA). One of the mechanisms of hyperkalaemia in DKA stated at the beginning of the Discussion is not strictly correct. It is inorganic acids, and not organic acids (including lactic acid), that cause hyperkalaemia as a result of potassium ions leaving cells in ‘exchange’ for hydrogen ion entry (and their intracellular buffering). In DKA, the key mechanism is lack of insulin, which is probably the most important short-term regulator of plasma potassium concentration (through stimulation of the cell ‘sodium’ pump – Na,K-ATPase) and defence against acute hyperkalaemia resulting from our daily intake of potassium (~80 mmol): The extracellular pool of potassium is around 65 mmol and could almost double after a single steak meal (~50 mmol), which is too rapid a change for compensatory renal excretion. In DKA, an additional mechanism is the osmotic shrinkage of cells as a result of the high plasma glucose concentration (and plasma osmolality), which steepens the intracellular to extracellular potassium concentration gradient and thereby causes an increase in potassium ion loss from cells. Of course, these observations do not materially alter the management of DKA, but only serve to emphasise the importance of inulin administration, glucose control and re-salination over the use (though not excluding it in severe metabolic acidosis) of bicarbonate, bearing in mind that such patients have usually become potassium depleted as a consequence of earlier increased renal losses, and therefore risk developing significant hypoka Continue reading >>

Keywords Dka, Diabetic Ketoacidosis, Children, Clinical Guideline

Keywords Dka, Diabetic Ketoacidosis, Children, Clinical Guideline

Version control and change history Version Date from Date to Amendment 1.0 24/02/2012 current Original version © Department for Health and Ageing, Government of South Australia. All rights reserved. Clinical Guideline Management of Diabetic Ketoacidosis (DKA) in Children Policy developed by: SA Child Health Clinical Network Approved by SA Health Safety & Strategic Governance Committee on: 1 July 2013 Next review due: 31 May 2016 Summary The Management of Diabetic Ketoacidosis (DKA) in Children Clinical Guideline is primarily aimed at medical staff working in any of primary care, local, regional, general or tertiary hospitals, however may be utilised or guide the care provided by other clinicians such as nurses. The information is current at the time of publication and provides a minimum standard for the assessment (including investigations) and management of DKA, it does not replace or remove clinical judgement or the professional care and duty necessary for each specific case. Policy history Is this a new policy? Y Does this policy amend or update an existing policy? Y Does this policy replace an existing policy? Y If so, which policies? Management of Acute Croup in Children, WCH Guideline Applies to All Health Networks CALHN, SALHN, NALHN, CHSALHN, WCHN, SAAS Staff impact All Clinical, Medical, Nursing, Allied Health, Emergency, Dental, Mental Health, Pathology PDS reference CG092 Policy South Australian Paediatric Clinical Guidelines Diabetic ketoacidosis (DKA) in children Disclaimer The South Australian Paediatric Clinical Guidelines have been prepared to promote and facilitate standardisation and consistency of practice, using a multidisciplinary approach Information in this guideline is current at the time of publication SA Health does not accept responsibility Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

DKA is an acute complication of diabetes mellitus (usually type 1 diabetes) characterized by hyperglycemia, ketonuria, acidosis, and dehydration. Insulin deficiency prevents glucose from being used for energy, forcing the body to metabolize fat for fuel. Free fatty acids, released from the metabolism of fat, are converted to ketone bodies in the liver. Increase in the secretion of glucagon, catecholamines, growth hormone, and cortisol, in response to the hyperglycemia caused by insulin deficiency, accelerates the development of DKA. Osmotic diuresis caused by hyperglycemia creates a shift in electrolytes, with losses in potassium, sodium, phosphate, and water. Serum glucose level is usually elevated over 300 mg/dL; may be as high as 1,000 mg/dL. Serum bicarbonate and pH are decreased due to metabolic acidosis, and partial pressure of carbon dioxide is decreased as a respiratory compensation mechanism. Serum sodium and potassium levels may be low, normal, or high due to fluid shifts and dehydration, despite total body depletion. Urine glucose is present in high concentration and specific gravity is increased, reflecting osmotic diuresis and dehydration. Observe for cardiac changes reflecting dehydration, metabolic acidosis, and electrolyte imbalance- hypotension; tachycardia; weak pulse; electrocardiographic changes, including elevated P wave, flattened T wave or inverted, prolonged QT interval. Administer replacement electrolytes and insulin as ordered. Flush the entire I.V. infusion set with solution containing insulin and discard the first 50 mL because plastic bags and tubing may absorb some insulin and the initial solution may contain decreased concentration of insulin. Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a potentially life-threatening complication of diabetes mellitus.[1] Signs and symptoms may include vomiting, abdominal pain, deep gasping breathing, increased urination, weakness, confusion, and occasionally loss of consciousness.[1] A person's breath may develop a specific smell.[1] Onset of symptoms is usually rapid.[1] In some cases people may not realize they previously had diabetes.[1] DKA happens most often in those with type 1 diabetes, but can also occur in those with other types of diabetes under certain circumstances.[1] Triggers may include infection, not taking insulin correctly, stroke, and certain medications such as steroids.[1] DKA results from a shortage of insulin; in response the body switches to burning fatty acids which produces acidic ketone bodies.[3] DKA is typically diagnosed when testing finds high blood sugar, low blood pH, and ketoacids in either the blood or urine.[1] The primary treatment of DKA is with intravenous fluids and insulin.[1] Depending on the severity, insulin may be given intravenously or by injection under the skin.[3] Usually potassium is also needed to prevent the development of low blood potassium.[1] Throughout treatment blood sugar and potassium levels should be regularly checked.[1] Antibiotics may be required in those with an underlying infection.[6] In those with severely low blood pH, sodium bicarbonate may be given; however, its use is of unclear benefit and typically not recommended.[1][6] Rates of DKA vary around the world.[5] In the United Kingdom, about 4% of people with type 1 diabetes develop DKA each year, while in Malaysia the condition affects about 25% a year.[1][5] DKA was first described in 1886 and, until the introduction of insulin therapy in the 1920s, it was almost univ Continue reading >>

Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Management Of Diabetic Ketoacidosis And Other Hyperglycemic Emergencies

Understand the management of patients with diabetic ketoacidosis and other hyperglycemic emergencies. ​ The acute onset of hyperglycemia with attendant metabolic derangements is a common presentation in all forms of diabetes mellitus. The most current data from the National Diabetes Surveillance Program of the Centers for Disease Control and Prevention estimate that during 2005-2006, at least 120,000 hospital discharges for diabetic ketoacidosis (DKA) occurred in the United States,(1) with an unknown number of discharges related to hyperosmolar hyperglycemic state (HHS). The clinical presentations of DKA and HHS can overlap, but they are usually separately characterized by the presence of ketoacidosis and the degree of hyperglycemia and hyperosmolarity, though HHS will occasionally have some mild degree of ketosis. DKA is defined by a plasma glucose level >250 mg/dL, arterial pH <7.3, the presence of serum ketones, a serum bicarbonate measure <18 mEq/L, and a high anion gap metabolic acidosis. The level of normal anion gap may vary slightly by individual institutional standards. The anion gap also needs to be corrected in the presence of hypoalbuminemia, a common condition in the critically ill. Adjusted anion gap = observed anion gap + 0.25 * ([normal albumin]-[observed albumin]), where the given albumin concentrations are in g/L; if given in g/dL, the correction factor is 2.5.(3) HHS is defined by a plasma glucose level >600 mg/dL, with an effective serum osmolality >320 mOsm/kg. HHS was originally named hyperosmolar hyperglycemic nonketotic coma; however, this name was changed because relatively few patients exhibit coma-like symptoms. Effective serum osmolality = 2*([Na] + [K]) + glucose (mg/dL)/18.(2) Urea is freely diffusible across cell membranes, thus it will Continue reading >>

Serum Sodium Level Corrected For Hyperglycemia

Serum Sodium Level Corrected For Hyperglycemia

"In marked hyperglycemia, ECF osmolality rises and exceeds that of ICF, since glucose penetrates cell membranes slowly in the absence of insulin, resulting in movement of water out of cells into the ECF. Serum Na concentration falls in proportion to the dilution of the ECF, declining 1.6 mEq/ L for every 100 mg/dL (5.55 mmol/L) increment in the plasma glucose level above normal. This condition has been called translational hyponatremia because no net change in total body water (TBW) has occurred. No specific therapy is indicated, because Na concentration will return to normal once the plasma glucose concentration is lowered." Source: Equation Corrected Sodium = Measured sodium + (((Serum glucose - 100)/100) x 1.6) Alternatively (equivalent equation): = Measured sodium + 0.016 x (Serum glucose - 100) All calculations must be confirmed before use. The authors make no claims of the accuracy of the information contained herein; and these suggested doses are not a substitute for clinical judgment. Neither GlobalRPh Inc. nor any other party involved in the preparation of this program shall be liable for any special, consequential, or exemplary damages resulting in whole or part from any user's use of or reliance upon this material.PLEASE READ THE DISCLAIMER CAREFULLY BEFORE ACCESSING OR USING THIS SITE. BY ACCESSING OR USING THIS SITE, YOU AGREE TO BE BOUND BY THE TERMS AND CONDITIONS SET FORTH IN THE DISCLAIMER. Read the disclaimer Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Diabetic ketoacidosis is a condition that results from when the body is deprived of the ability to use glucose as an energy source. Usually this is due to a lack of insulin. Insulin is used to uptake glucose into the cells to be used for energy. If there is no insulin or the cells are resistant to insulin, the blood sugar levels increase to dangerous levels for the patient. It seems counter intuitive that the patient wouldn't have energy with such high levels of glucose, but this glucose is essentially unusable without insulin. Because your body needs energy to survive, it starts turning to alternative fuel sources (fat). Fat cells start breaking down and, as a result, release ketones (which are acidic) into the bloodstream. Hence the name: diabetic ketoacidosis. “High levels of ketones can poison the body. When levels get too high, you can develop DKA. DKA may happen to anyone with diabetes, though it is rare in people with type 2. Treatment for DKA usually takes place in the hospital. But you can help prevent it by learning the warning signs and checking your urine and blood regularly.” Causes The most common causes of DKA are not getting enough insulin, having a severe infection, becoming dehydrated, or a combination of these issues. It seems like it occurs mainly in patients with type one diabetes. Symptoms Some of the symptoms that people experience with DKA include the following: Excessive thirst and urination (more water is pulled into the urine as a result of high ketone loss in the urine) Lethargy Breathing very quickly (patients have a very high level of acids in their bloodstream and they try to "blow" off carbon dioxide by breathing quickly) A fruity odor on their breath (ketones have a fruity smell) Nausea and vomiting (the body tries to get rid of acid Continue reading >>

Hyperglycemic Crises In Diabetes

Hyperglycemic Crises In Diabetes

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. PATHOGENESIS 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 in Continue reading >>

Hypernatraemia And Acidosis

Hypernatraemia And Acidosis

aka Metabolic Muddle 005 A 20 year old male presents with 3 days of lethargy and generalised malaise. He is confused and looks very unwell. The following blood tests are obtained: Questions Q1. Describe the acid base disturbance. Q2. What is the likely diagnosis? Q3. Describe the electrolyte abnormalities. Q4.Should the corrected sodium be used for calculating the anion gap? Q5. It emerges that the patient has recently been diagnosis with Schizophrenia and has commenced olanzepine. What is the significance of this additional history? Q6. An amylase is measured and is found to be 3 times the upper limit of normal. What is the significance of this finding? References and Links Beck, LH. Should the actual or the corrected serum sodium be used to calculate the anion gap in diabetic ketoacidosis? CLEVELAND CLINIC JOURNAL OF MEDICINE 2001; 68 (8) 673-674. (pdf) Continue reading >>

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