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How Does Ketoacidosis Cause Hyperkalemia

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 >>

Hyperkalemia

Hyperkalemia

Objectives The objectives of this module will be to: Describe the classic presentation of a patient with hyperkalemia. Name the electrocardiographic manifestations of hyperkalemia. List the principles of managing a patient with hyperkalemia. Introduction Hyperkalemia is a metabolic abnormality seen frequently in the Emergency Department. The most common condition leading to hyperkalemia is missed dialysis in a patient with end stage renal disease (ESRD), but many other conditions can predispose an individual to hyperkalemia, such as acute renal failure, extensive burns, trauma, or severe rhabdomyolysis or severe acidosis. Other conditions that can be associated with hyperkalemia are acute digoxin toxicity and adrenal insufficiency. In rare circumstances, hyperkalemia can become so significant that cardiac dysrhythmias and subsequent death can occur; therefore, rapid identification and appropriate treatment are paramount to properly treating this condition. Initial Actions and Primary Survey The primary survey should focus on assessing airway, breathing and circulation. Since many patients with severe hyperkalemia will have renal dysfunction, some may be fluid overloaded and may present with pulmonary edema and respiratory distress. Traditionally, the electrocardiogram (ECG) has been used as a surrogate marker for clinically significant hyperkalemia. Patients suspected of having hyperkalemia (chronic renal failure, severe diabetic ketoacidosis, etc.) should be placed on a cardiac monitor and a 12-lead electrocardiogram should be performed immediately. Concurrently, intravenous access should be obtained and a blood sample should be sent to the laboratory for a basic metabolic profile. Differential Diagnosis Hyperkalemia Pseudohyperkalemia Thrombocytosis Erythrocytosis Leu Continue reading >>

Chapter 4. Disorders Of Potassium Balance: Hypokalemia & Hyperkalemia

Chapter 4. Disorders Of Potassium Balance: Hypokalemia & Hyperkalemia

Potassium is the principal cation of the intracellular fluid (ICF) where its concentration is between 120 and 150 mEq/L. The extracellular fluid (ECF) and plasma potassium concentration [K] is much lower—in the 3.5–5.0 mEq/L range. The very large transcellular gradient is maintained by active K transport via the Na-K-ATPase pumps present in all cell membranes and the ionic permeability characteristics of these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the transcellular resting potential gradient, about −90 mV with the cell interior negative (Figure 4–1). Normal cell function requires maintenance of the ECF [K] within a relatively narrow range. This is particularly important for excitable cells such as myocytes and neurons. The pathophysiologic effects of dyskalemia on these cells result in most of the clinical manifestations. Transcellular ion movement. Most cells contain these pumps, antiporters, and channels. The effects of insulin, catecholamines, and thyroid hormones on K transport are shown. Individual potassium intakes vary widely—a typical Western diet provides between 50 and 100 mEq K per day. Under steady-state conditions, an equal amount is excreted, mainly in urine (about 90%), and to a lesser extent in stool (5–10%) and sweat (1–10%). Normally, homeostatic mechanisms maintain plasma [K] precisely between 3.5 and 5.0 mEq/L. Rapid regulation of potassium concentration is needed to prevent potentially fatal hyperkalemia after every meal and is largely due to transcellular K shifts. The normal postprandial rise in insulin concentration moves both K and glucose into the intracellular compartment, where 98% of total body K (˜3000 mEq) is located. Postprandial insulin release is primarily 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 >>

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 >>

How Does Diabetes Cause Hyperkalemia?

How Does Diabetes Cause Hyperkalemia?

Potassium and Hyperkalemia Potassium is a mineral in your body cells that performs several important body functions. Hyperkalemia is the condition when your blood has too much potassium in it. Adrenal glands are tiny structures that sit on the top parts of your kidneys. They secrete (hide and release) a chemical called “aldosterone”. Aldosterone signals the kidneys to release potassium along with urine. By doing so, the body is able to keep up a constant level of potassium in the blood. However, if your adrenals are not working properly, the levels of aldosterone start to fall and your kidneys are no longer able to release the potassium in your urine. When aldosterone starts to fall and the kidneys are no longer able to release potassium in the urine, the potassium starts to accumulate in the blood causing hyperkalemia- high blood potassium. Why Diabetes Causes Hyperkalemia? If you have diabetes, your body is unable to produce insulin- the chemical that regulates sugar levels in your blood. This triggers the fat cells to break down and release ketones. Ketones are chemicals that increase the acidity of your blood. High blood acidity, combined with high blood sugar, acts to force the potassium in your body cells to move out into your blood. Therefore, the potassium content of your blood increases. Further, high blood glucose in diabetes is capable of destroying the blood vessels in the kidneys and the adrenal glands. This reduces their capacity to release potassium with urine and eventually you develop hyperkalemia. This is how your diabetes may lead to hyperkalemia. Symptoms of hyperkalemia are: Muscle Fatigue Weakness Paralysis Heart beating in an irregular way Nausea If you have any of these symptoms, talk to your doctor. Your doctor may order blood tests to diagn 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 >>

Hypokalemia And Hyperkalemia

Hypokalemia And Hyperkalemia

Study Points 1 . What percent of total body potassium is in the extracellular fluid? The amount of potassium present in the average human body is approximately 50 mEq/kg. Of this, 90% is found in intracellular fluid, 8% in skin and bones, and 2% in extracellular fluid [1,2,3,4,5]. The maintenance of this relatively small amount of extracellular potassium is critical; small changes can cause serious clinical consequences. Click to Review 2 . Severe hyperkalemia is defined as a serum level of A) 2 mEq/L or greater. B) 4 mEq/L or greater. C) 6 mEq/L or greater. D) 7 mEq/L or greater. Chronic hypokalemia and hyperkalemia develop in a minimum of weeks to months, and acute hypokalemia and hyperkalemia occur over hours to days. Mild hypokalemia occurs at serum levels of less than 3.5 mEq/L, but greater than 3 mEq/L; moderate hypokalemia at 2.5 to 3 mEq/L; and levels less than 2.5 mEq/L are considered severe [7,8]. Mild-to-moderate hyperkalemia is defined as a serum level of 5.5 to 6.9 mEq/L, and severe hyperkalemia is a serum level of 7 mEq/L or greater [9]. Physician consultation is indicated for serum potassium levels less than 3 mEq/L or greater than 6 mEq/L. Click to Review 3 . The main cause of hypokalemia is A) vomiting. B) decreased intake. C) the use of potassium-sparing diuretics. D) the use of non-potassium-sparing drugs. In the vast majority of cases, hypokalemia is drug induced; approximately 20% to 50% of all patients who are treated with non-potassium-sparing diuretics develop low serum potassium levels [7]. Most cases of chronic hyperkalemia are caused by renal failure; however, the increased use of spironolactone after the publication of the Randomized Aldactone Evaluation Study has resulted in a marked increase in morbidity and mortality from hyperkalemia, wit Continue reading >>

Hyperkalaemia In Adults

Hyperkalaemia In Adults

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Dietary Potassium article more useful, or one of our other health articles. Description Hyperkalaemia is defined as plasma potassium in excess of 5.5 mmol/L[1]. The European Resuscitation Guidelines further classify hyperkalaemia as: Mild - 5.5-5.9 mmol/L. Moderate - 6.0-6.4 mmol/L. Severe - >6.5 mmol/L. Potassium is the most abundant intracellular cation - 98% of it being located intracellularly. Hyperkalaemia has four broad causes: Renal causes - eg, due to decreased excretion or drugs. Increased circulation of potassium - can be exogenous or endogenous. A shift from the intracellular to the extracellular space. Pseudohyperkalaemia. Epidemiology The time of greatest risk is at the extremes of life. Reported incidence in hospitals is 1-10%, with reduced renal function causing a five-fold increase in risk in patients on potassium-influencing drugs[2]. Men are more likely than women to develop hyperkalaemia, whilst women are more likely to experience hypokalaemia. Renal causes Acute kidney injury (AKI). Chronic kidney disease (CKD): Normally all potassium that is ingested is absorbed and excretion is 90% renal and 10% alimentary. Most excretion by the gut is via the colon and in CKD this can maintain a fairly normal blood level of potassium. It seems likely that the elevated potassium levels in CKD trigger the excretion of potassium via the colon[3]. Patients with CKD must be careful of foods rich in potassium. Hyperkalaemic renal tubular acidosis. Mineralocorticoid deficiency. Medicines that interfere with potassium excretion - eg, amiloride, spironolac 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 >>

Hyperkalemia In Diabetic Ketoacidosis.

Hyperkalemia In Diabetic Ketoacidosis.

Abstract Patients with diabetic ketoacidosis tend to have somewhat elevated serum K+ concentrations despite decreased body K+ content. The hyperkalemia was previously attributed mainly to acidemia. However, recent studies have suggested that "organic acidemias" (such as that produced by infusing beta-hydroxybutyric acid) may not cause hyperkalemia. To learn which, if any, routinely measured biochemical indices might correlate with the finding of hyperkalemia in diabetic ketoacidosis, we analyzed the initial pre-treatment values in 131 episodes in 91 patients. Serum K+ correlated independently and significantly (p less than 0.001) with blood pH (r = -0.39), serum urea N (r = 0.38) and the anion gap (r = 0.41). The mean serum K+ among the men was 5.55 mmol/l, significantly higher than among the women, 5.09 mmol/l (p less than 0.005). Twelve of the 16 patients with serum K+ greater than or equal to 6.5 mmol/l were men, as were all eight patients with serum K+ greater than or equal to 7.0 mmol/l. Those differences paralleled a significantly higher mean serum urea N concentration among the men (15.1 mmol/l) than the women (11.2 mmol/l, p less than 0.01). The greater tendency to hyperkalemia among the men in this series may have been due partly to their greater renal dysfunction during the acute illness. However, other factors that were not assessed, such as cell K+ release associated with protein catabolism, and insulin deficiency per se, may also have affected serum K+ in these patients. 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 >>

Hyperkalemia And Hypokalemia

Hyperkalemia And Hypokalemia

Hyperkalemia is defined as a serum potassium concentration (serum [K+]) greater than 5.0 mEq/L. In critically ill patients, hyperkalemia is less frequent than hypokalemia but more likely to cause serious complications. Severe hyperkalemia requires rapid correction to prevent serious cardiovascular complications. The measured value for serum [K+] can be elevated as a result of in vitro phenomena, usually the release of K+ from cells during the clotting process. Pseudohyperkalemia should be recognized and considered in patients with marked elevations of white blood cell or platelet count.3 Simultaneous measurements of plasma (unclotted) and serum (clotted) [K+] should identify this problem. A serum [K+] that is 0.2 to 0.3 mEq/L greater than plasma [K+] is indicative of pseudohyperkalemia. Pseudohyperkalemia also may result from hemolysis of a blood specimen after collection; this event is usually identified in the laboratory and reported. True hyperkalemia occurs by two mechanisms: (1) impaired K+ excretion and (2) shifts in intracellular and extracellular K+ (Box 14-1). Renal insufficiency is the most common cause of altered K+ excretion. With acute oliguric renal failure, elevated potassium level, if not treated, is life threatening. In most patients with nonoliguric chronic renal failure, mild hyperkalemia is evident.4 With some causes of chronic renal failure, such as diabetes mellitus and tubulointerstitial diseases, hyperkalemia is more pronounced and is probably related to low circulating renin and aldosterone levels.5 Decreased aldosterone production promotes the development of hyperkalemia. Patients with acquired adrenal insufficiency develop hyperkalemia despite normal renal function. Various drugs used in the intensive care unit (ICU) can produce hyperkalemia b Continue reading >>

Starvation Ketoacidosis

Starvation Ketoacidosis

Etiology xxx Physiology Accumulation of Ketones Generated by Metabolism of Free Fatty Acids Diagnosis Anion Gap: usually >20 Osmolal Gap: increased Serum Ketones: positive Serum Potassium: normal (ketoacidosis does not cause hyperkalemia) Clinical Manifestations Neurologic Manifestations xxxx Renal Manifestations Anion Gap Metabolic Acidosis (AGMA) (see Metabolic Acidosis-Elevated Anion Gap, [[Metabolic Acidosis-Elevated Anion Gap]]) Diagnosis Delta Gap/Delta Bicarbonate Ratio: usually 1.1 Ketoacidosis xxx Elevated Osmolal Gap (see Serum Osmolality, [[Serum Osmolality]]) Physiology: increased (due to presence of osmotically-active, acetone) Other Manifestations xxx xxx Treatment Nutritional Support References xxx Continue reading >>

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