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Does Ketoacidosis Cause Hyperkalemia

Lactic Acidosis In A Patient With Type 2 Diabetes Mellitus

Lactic Acidosis In A Patient With Type 2 Diabetes Mellitus

Introduction A 49-year-old man presented to the emergency department complaining of dyspnea for 2 days. He had a history of hypertension, type 2 diabetes mellitus, atrial fibrillation, and a severe dilated cardiomyopathy. He had been hospitalized several times in the previous year for decompensated congestive heart failure (most recently, 1 month earlier). The plasma creatinine concentration was 1.13 mg/dl on discharge. Outpatient medications included insulin, digoxin, warfarin, spironolactone, metoprolol succinate, furosemide (80 mg two times per day; increased from 40 mg daily 1 month earlier), metolazone (2.5 mg daily; added 1 month earlier), and metformin (2500 mg in three divided doses; increased from 1000 mg 1 month earlier). Physical examination revealed an obese man in moderate respiratory distress. The temperature was 36.8°C, BP was 119/83 mmHg, and heart rate was 96 per minute. Peripheral hemoglobin oxygen saturation was 97% on room air, with a respiratory rate of 26 per minute. The heart rhythm was irregularly irregular; there was no S3 or murmur. Jugular venous pressure was about 8 cm. There was 1+ edema at the ankles. A chest radiograph showed cardiomegaly and central venous prominence. The N-terminal pro-B-type natriuretic peptide level was 5137 pg/ml (reference range = 1–138 pg/ml). The peripheral hemoglobin concentration was 12.5 g/dl, the white blood cell count was 12,500/µl (76% granulocytes), and the platelet count was 332,000/µL. Initial plasma chemistries are shown in Table 1. The impression was decompensated congestive heart failure. After administration of furosemide (160 mg intravenously), the urine output increased to 320 ml over the next 1 hour. There was no improvement in the dyspnea. Within 2 hours, the patient’s BP fell to 100/64 mmHg 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 >>

) And Reflects A Severe Shift From Glycolysis To Lipolysis For Energy Needs.

) And Reflects A Severe Shift From Glycolysis To Lipolysis For Energy Needs.

Acidosis Hyperkalemia Ketosis Lead Beta Blocker s Prostaglandin Inhibitor Methyldopa Carbonic anhydrase inhibitor Acetazolamide Mefenamic acid Post-hypocapnia Excessive Normal Saline infused (liters) Hyperkalemia[fpnotebook.com] It is due to the accumulation of ketoacids (via excessive ketosis) and reflects a severe shift from glycolysis to lipolysis for energy needs.[en.wikipedia.org] Causes: Metabolic Acidosis and Elevated Anion Gap (Mnemonic: "MUD PILERS") Methanol , Metformin Uremia Diabetic Ketoacidosis (DKA), Alcohol ic ketoacidosis or starvation ketosis[fpnotebook.com] Metabolic Acidosis Hyperkalemia Correction of hyperkalemia leads to correction of metabolic acidosis in many patients, pointing to the central role of hyperkalemia in the pathogenesis of this acidosis.[emedicine.medscape.com] 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[merckmanuals.com] The acidosis and hyperkalemia, however, are out of proportion to the degree of renal failure.[emedicine.medscape.com] List represents a sample of symptoms, diseases, and other queries. Updated weekly. Hungry Bones Syndrome Altitude Sickness Cavernous Sinus Thrombosis Posterior Subcapsular Cataract Cellulitis Splenic Infarction Megaloblastic Anemia Islet Cell Tumor Chronic Phase of Chronic Myeloid Leukemia Penile Fracture Tuberous Sclerosis Primary Sclerosing Cholangitis Odynophagia, unilateral throat pain Costovertebral Angle Tenderness Dyspepsia Tenesmus Oliguria Scrotal Ulcer Choledochal Cyst Anal Fistula Essential Hypertension Enthesitis-Related Arthritis Glioblastoma Multiforme Leiomyosarcoma Brain Neoplasm Hyperventilation Wolff-Parkinson-White Syndrome Ethmoid Sinusitis Dementia with 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 >>

Management Of Diabetic Ketoacidosis

Management Of Diabetic Ketoacidosis

Diabetic ketoacidosis is an emergency medical condition that can be life-threatening if not treated properly. The incidence of this condition may be increasing, and a 1 to 2 percent mortality rate has stubbornly persisted since the 1970s. Diabetic ketoacidosis occurs most often in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus); however, its occurrence in patients with type 2 diabetes (formerly called non–insulin-dependent diabetes mellitus), particularly obese black patients, is not as rare as was once thought. The management of patients with diabetic ketoacidosis includes obtaining a thorough but rapid history and performing a physical examination in an attempt to identify possible precipitating factors. The major treatment of this condition is initial rehydration (using isotonic saline) with subsequent potassium replacement and low-dose insulin therapy. The use of bicarbonate is not recommended in most patients. Cerebral edema, one of the most dire complications of diabetic ketoacidosis, occurs more commonly in children and adolescents than in adults. Continuous follow-up of patients using treatment algorithms and flow sheets can help to minimize adverse outcomes. Preventive measures include patient education and instructions for the patient to contact the physician early during an illness. Diabetic ketoacidosis is a triad of hyperglycemia, ketonemia and acidemia, each of which may be caused by other conditions (Figure 1).1 Although diabetic ketoacidosis most often occurs in patients with type 1 diabetes (formerly called insulin-dependent diabetes mellitus), more recent studies suggest that it can sometimes be the presenting condition in obese black patients with newly diagnosed type 2 diabetes (formerly called non–insulin-depe Continue reading >>

Hyperglycemic Crisis: Regaining Control

Hyperglycemic Crisis: Regaining Control

CE credit is no longer available for this article. Expired July 2005 Originally posted April 2004 VERONICA CRUMP, RN, BSN VERONICA CRUMP is a nurse on the surgical unit of Morristown Memorial Hospital in Morristown, N.J. She's also a subacute care nurse in the hospital's rehabilitation division. KEY WORDS: hyperosmolar hyperglycemic syndrome (HHS), diabetic ketoacidosis (DKA), hepatic glucose production, proteolysis, hepatic gluconeogenesis, ketone bodies, metabolic acidosis, hyperkalemia, hypokalemia When a patient presents with markedly high blood glucose levels, the consequences can be fatal. Here's how to get your patient through the crisis. Edith Schafer, age 71, has just been admitted to your ICU with pneumonia, which she developed at home. She has a history of Type 2 diabetes. In addition to a temperature of 102° F (38.9° C), she has rapid, shallow breathing and dry, flushed skin. Her blood pressure is 96/70 mm Hg, and she's so lethargic that she's unable to keep her eyes open. Her lab results show a serum glucose level of 900 mg/dL. In addition to the pneumonia, Mrs. Schafer is suffering from hyperosmolar hyperglycemic syndrome (HHS). Severe hyperglycemia is a complication of both Type 1 and Type 2 diabetes. It can indicate HHS or diabetic ketoacidosis (DKA), another life-threatening condition. HHS tends to occur in patients with Type 2 diabetes, like Mrs. Schafer, while Type 1 diabetics are more likely to develop DKA. However, DKA can occur in Type 2 diabetes as well.1 HHS and DKA can be set off by infection, stress, missed medication, and other causes. In Mrs. Schafer's case, the trigger was pneumonia, a common cause of hyperglycemia in patients with diabetes. No matter what the cause, though, a case of HHS or DKA can turn deadly if not caught in time. The m Continue reading >>

Serum Potassium In Lactic Acidosis And Ketoacidosis

Serum Potassium In Lactic Acidosis And Ketoacidosis

Abstract METABOLIC acidosis has been thought to elevate serum potassium concentration.1 , 2 However, hyperkalemia was not found in recent studies in patients with postictal lactic acidosis3 or in dogs infused with lactic acid4 , 5 or 3-hydroxybutyric acid5 — observations that raise questions about the association between metabolic acidosis and hyperkalemia: Does metabolic acidosis cause hyperkalemia or is the latter an epiphenomenon? Does metabolic acidosis (or acidemia) cause hyperkalemia only when acidosis is due to excess "mineral acids," and not to excess organic acids? With the hope of providing some clarification of these questions, I have reviewed initial laboratory data and clinical findings in . . . Continue reading >>

The Emedicinehealth Doctors Ask About Hyperkalemia (high Blood Potassium):

The Emedicinehealth Doctors Ask About Hyperkalemia (high Blood Potassium):

What Causes Hyperkalemia? Excess potassium in the bloodstream can result from diseases of the kidneys or adrenal glands as well as from certain medications. Hyperkalemia can also be the result of potassium moving out of its usual location within cells into the bloodstream. The majority of potassium within the body is located within cells, with only a small amount located in the bloodstream. A number of conditions can cause potassium to move out of the cells into the blood circulation, thereby increasing the measured level of potassium in the blood, even though the total amount of potassium in the body has not changed. Diabetic ketoacidosis, an emergency that can develop in people with type I diabetes, is an example of a condition in which potassium is drawn out of cells and into the bloodstream. Similarly, any condition in which there is massive tissue destruction can result in elevated levels of blood potassium as the damaged cells release their potassium. Examples of tissue destruction include: Moreover, difficulty in drawing blood from veins for testing can traumatize red blood cells, releasing potassium into the serum of the blood sample to cause a falsely elevated reading of hyperkalemia on the blood test. Any condition that decreases kidney function can result in hyperkalemia, since the kidneys rid the body of excess potassium by excreting it in the urine. Examples of conditions that decrease kidney function are glomerulonephritis, acute or chronic renal failure, transplant rejection, and obstructions within the urinary tract (such as the presence of stones). The adrenal glands secrete many hormones important for proper body function. Among these is aldosterone, which regulates the retention of sodium and fluid in the kidneys along with the excretion of potassium Continue reading >>

Hyperkalemia

Hyperkalemia

Hyperkalemia, also spelled hyperkalaemia, is an elevated level of potassium (K+) in the blood serum.[1] Normal potassium levels are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels above 5.5 mmol/L defined as hyperkalemia.[3][4] Typically this results in no symptoms.[1] Occasionally when severe it results in palpitations, muscle pain, muscle weakness, or numbness.[1][2] An abnormal heart rate can occur which can result in cardiac arrest and death.[1][3] Common causes include kidney failure, hypoaldosteronism, and rhabdomyolysis.[1] A number of medications can also cause high blood potassium including spironolactone, NSAIDs, and angiotensin converting enzyme inhibitors.[1] The severity is divided into mild (5.5-5.9 mmol/L), moderate (6.0-6.4 mmol/L), and severe (>6.5 mmol/L).[3] High levels can also be detected on an electrocardiogram (ECG).[3] Pseudohyperkalemia, due to breakdown of cells during or after taking the blood sample, should be ruled out.[1][2] Initial treatment in those with ECG changes is calcium gluconate.[1][3] Medications that might worsen the condition should be stopped and a low potassium diet should be recommended.[1] Other medications used include dextrose with insulin, salbutamol, and sodium bicarbonate.[1][5] Measures to remove potassium from the body include furosemide, polystyrene sulfonate, and hemodialysis.[1] Hemodialysis is the most effective method.[3] The use of polystyrene sulfonate, while common, is poorly supported by evidence.[6] Hyperkalemia is rare among those who are otherwise healthy.[7] Among those who are in hospital, rates are between 1% and 2.5%.[2] It increases the overall risk of death by at least ten times.[2][7] The word "hyperkalemia" is from hyper- meaning high; kalium meaning potassium; and -emia, meaning "in th Continue reading >>

What Are The Causes Of High Potassium In Dogs?

What Are The Causes Of High Potassium In Dogs?

Potassium is an electrolyte that is found in the cells and in the blood of your dog's body. An ideal potassium level is essential for controlling your dog's nerve impulses, brain function and muscle activity. It also plays a vital role in regulating your dog's heart function. The normal reference range for a dog's blood potassium level falls between 3.6 and 5.5 mEq/L. When your dog's potassium level dips too low, the condition is referred to as hypokalemia. Conversely, if his potassium level climbs too high, your dog is suffering from hyperkalemia. Your dog's potassium level is determined by performing a blood chemistry profile. Your dog's kidneys are responsible for filtering wastes from your dog's blood so that they may be expelled from your dog's body when he urinates. Optimal kidney function is vital to maintaining healthy levels of enzymes, minerals and other important substances, including potassium. Your veterinarian will perform an electrocardiogram on your dog to assess his heart rate and rhythm. He or she will review your dog's medical history and ask questions regarding your dog's recent activities, including drinking and urinating frequencies. Diagnostic tests will include a complete blood count, a blood chemistry profile and a urinalysis. Additional blood tests and radiographs may be ordered to determine the underlying cause of hyperkalemia. When your dog's kidneys no longer function optimally, potassium and other wastes build up in your dog's system. Acute anuric, meaning insufficient urine production, and acute oliguric, meaning complete shut down of kidney function, kidney failures are the most frequent causes of hyperkalemia in dogs. Some common causes of acute kidney failure include antifreeze ingestion and leptospirosis infection. Chronic renal failur Continue reading >>

Causes And Evaluation Of Hyperkalemia In Adults

Causes And Evaluation Of Hyperkalemia In Adults

INTRODUCTION Hyperkalemia is a common clinical problem. Potassium enters the body via oral intake or intravenous infusion, is largely stored in the cells, and is then excreted in the urine. The major causes of hyperkalemia are increased potassium release from the cells and, most often, reduced urinary potassium excretion (table 1). This topic will review the causes and evaluation of hyperkalemia. The clinical manifestations, treatment, and prevention of hyperkalemia, as well as a detailed discussion of hypoaldosteronism (an important cause of hyperkalemia), are presented elsewhere. (See "Clinical manifestations of hyperkalemia in adults" and "Treatment and prevention of hyperkalemia in adults" and "Etiology, diagnosis, and treatment of hypoaldosteronism (type 4 RTA)".) BRIEF REVIEW OF POTASSIUM PHYSIOLOGY An understanding of potassium physiology is helpful when approaching patients with hyperkalemia. Total body potassium stores are approximately 3000 meq or more (50 to 75 meq/kg body weight) [1]. In contrast to sodium, which is the major cation in the extracellular fluid and has a much lower concentration in the cells, potassium is primarily an intracellular cation, with the cells containing approximately 98 percent of body potassium. The intracellular potassium concentration is approximately 140 meq/L compared with 4 to 5 meq/L in the extracellular fluid. The difference in distribution of the two cations is maintained by the Na-K-ATPase pump in the cell membrane, which pumps sodium out of and potassium into the cell in a 3:2 ratio. The ratio of the potassium concentrations in the cells and the extracellular fluid is the major determinant of the resting membrane potential across the cell membrane, which sets the stage for the generation of the action potential that is e Continue reading >>

Serum Potassium In Lactic Acidosis And Ketoacidosis

Serum Potassium In Lactic Acidosis And Ketoacidosis

This article has no abstract; the first 100 words appear below. METABOLIC acidosis has been thought to elevate serum potassium concentration.1 , 2 However, hyperkalemia was not found in recent studies in patients with postictal lactic acidosis3 or in dogs infused with lactic acid4 , 5 or 3-hydroxybutyric acid5 — observations that raise questions about the association between metabolic acidosis and hyperkalemia: Does metabolic acidosis cause hyperkalemia or is the latter an epiphenomenon? Does metabolic acidosis (or acidemia) cause hyperkalemia only when acidosis is due to excess "mineral acids," and not to excess organic acids? With the hope of providing some clarification of these questions, I have reviewed initial laboratory data and clinical findings in . . . We are indebted to Dr. Henry Hoberman, of the Department of Biochemistry, Albert Einstein College of Medicine, for the lactate and 3-hydroxybutyrate analyses. From the Department of Medicine, Albert Einstein College of Medicine, and the Bronx Municipal Hospital Center (address reprint requests to Dr. Fulop at the Department of Medicine, Bronx Municipal Hospital Center, Pelham Parkway South and Eastchester Road, Bronx, NY 10461). Continue reading >>

Merck And The Merck Manuals

Merck And The Merck Manuals

Hyperkalemia is a serum potassium concentration > 5.5 mEq/L, usually resulting from decreased renal potassium excretion or abnormal movement of potassium out of cells. There are usually several simultaneous contributing factors, including increased potassium intake, drugs that impair renal potassium excretion, and acute kidney injury or chronic kidney disease. Hyperkalemia can also occur in metabolic acidosis as in diabetic ketoacidosis. Clinical manifestations are generally neuromuscular, resulting in muscle weakness and cardiac toxicity that, when severe, can degenerate to ventricular fibrillation or asystole. Diagnosis is by measuring serum potassium. Treatment may involve decreasing potassium intake, adjusting drugs, giving a cation exchange resin and, in emergencies, calcium gluconate, insulin, and dialysis. A common cause of increased serum potassium concentration is probably pseudohyperkalemia, which is most often caused by hemolysis of RBCs in the blood sample. This can also occur from prolonged application of a tourniquet or excessive fist clenching when drawing venous blood. Thrombocytosis can cause pseudohyperkalemia in serum (platelet potassium is released during clotting), as can extreme leukocytosis. Normal kidneys eventually excrete potassium loads, so sustained, nonartifactual hyperkalemia usually implies diminished renal potassium excretion. However, other factors usually contribute. They can include increased potassium intake, increased potassium release from cells, or both (see Table: Factors Contributing to Hyperkalemia). When sufficient potassium chloride is rapidly ingested or given parenterally, severe hyperkalemia may result even when renal function is normal, but this is usually temporary. Hyperkalemia due to total body potassium excess is parti Continue reading >>

St-segment Elevation Resulting From Hyperkalemia

St-segment Elevation Resulting From Hyperkalemia

A 20-year-old man with a history of type 1 diabetes mellitus presented to the emergency department with nausea, vomiting, and abdominal pain of 8 hours’ duration. Diabetic ketoacidosis was diagnosed based on a glucose of 68.8 mmol/L (1240 mg/dL), bicarbonate of 5 mmol/L, pH of 6.92, and a positive urine dipstick for ketones. Serum potassium measured 9.4 mmol/L. An ECG (Figure 1) revealed ST-segment elevation (asterisks); a wide QRS complex tachycardia; absent P waves; and tall, peaked, and tented T waves (arrows). One hour after the patient received intravenous fluid, calcium gluconate, bicarbonate, and insulin, the electrocardiographic abnormalities had resolved (Figure 2), leaving only sinus tachycardia secondary to volume depletion and minimal peaking of the T waves (arrows). Serum potassium now measured 5.7 mmol/L. Creatine kinase, creatine kinase-MB, and troponin I values were normal. At the time of discharge, the patient was in good condition, with a normal ECG. Figure 1. ECG obtained on presentation to the emergency department demonstrating a wide complex tachycardia, absent P waves, peaked T waves (arrows), and ST-segment elevation (asterisks) in leads V1, V2, and aVR. Serum potassium measured 9.4 mmol/L. Hyperkalemia can cause several characteristic ECG abnormalities that are often progressive. Initially, the T wave becomes tall, symmetrically peaked, and tented. Widening of the QRS complex with an intraventricular conduction delay then occurs. Additional elevation of serum potassium leads to a decrease in the amplitude of the P wave and its eventual disappearance from the ECG. Rarely, ST-segment elevation mimicking myocardial infarction, described as a “pseudoinfarction” pattern, is present. Further progression of hyperkalemia leads to a sine wave appear Continue reading >>

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 >>

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