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How Does Ketoacidosis Cause Hyperkalemia

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 >>

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 >>

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 >>

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 >>

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

Professor of Pediatric Endocrinology University of Khartoum, Sudan Introduction DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. Epidemiology DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa. DKA at the time of first diagnosis of diabetes mellitus is reported in only 2-3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries . Consequences The latter observation is annoying because it implies the following: The late diagnosis of type 1 diabetes in many developing countries particularly in Africa. The late presentation of DKA, which is associated with risk of morbidity & mortality Death of young children with DKA undiagnosed or wrongly diagnosed as malaria or meningitis. Pathophysiology Secondary to insulin deficiency, and the action of counter-regulatory hormones, blood glucose increases leading to hyperglycemia and glucosuria. Glucosuria causes an osmotic diuresis, leading to water & Na loss. In the absence of insulin activity the body fails to utilize glucose as fuel and uses fats instead. This leads to ketosis. Pathophysiology/2 The excess of ketone bodies will cause metabolic acidosis, the later is also aggravated by Lactic acidosis caused by dehydration & poor tissue perfusion. Vomiting due to an ileus, plus increased insensible water losses due to tachypnea will worsen the state of dehydr 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 >>

Hypokalemia And Hyperkalemia

Hypokalemia And Hyperkalemia

Sort Adrenal causes of hyperkalemia? Adrenal gland is important in secreting hormones such as cortisol and aldosterone. Aldosterone causes the kidneys to retain sodium and fluid while excreting potassium in the urine. Therefore diseases of the adrenal gland, such as Addison's disease, that lead to decreased aldosterone secretion can decrease kidney excretion of potassium, resulting in body retention of potassium, and hence hyperkalemia. How trauma leads to hyperkalemia Another cause of hyperkalemia is tissue destruction, dying cells release potassium into the blood circulation. Examples of tissue destruction causing hyperkalemia include: trauma, burns, surgery, hemolysis (disintegration of red blood cells), massive lysis of tumor cells, and rhabdomyolysis (a condition involving destruction of muscle cells that is sometimes associated with muscle injury, alcoholism, or drug abuse). What is role of potassium binders (Sodium polystyrene suffocate: SPS) SPS exchanges sodium for potassium and binds it in the gut, primarily in the large intestine, decreasing the total body potassium level by approximately 0.5-1 mEq/L. Multiple doses are usually necessary. Onset of action ranges from 2 to 24 hours after oral administration and is even longer after rectal administration. The duration of action is 4-6 hours. Do not use SPS as a first-line therapy for severe life-threatening hyperkalemia; use it in the second stage of therapy. Continue reading >>

Pseudoinfarction Pattern In A Patient With Hyperkalemia, Diabetic Ketoacidosis And Normal Coronary Vessels: A Case Report

Pseudoinfarction Pattern In A Patient With Hyperkalemia, Diabetic Ketoacidosis And Normal Coronary Vessels: A Case Report

Abstract A rare electrocardiographic finding of hyperkalemia is ST segment elevation or the so called 'pseudoinfarction' pattern. It has been suggested that hyperkalemia causes the 'pseudoinfarction' pattern not only through its direct myocardial effects, but also through other mechanisms, such as anoxia, acidosis, and coronary artery spasm. A 33-year-old Caucasian woman with insulin-treated diabetes presented with continuous epigastric pain of four hours duration. Her coronary heart disease risk factors apart from diabetes included hypercholesterolemia and smoking. Her initial electrocardiogram revealed ST segment elevation in the anteroseptal leads consistent with anterior myocardial infarction. Blood tests revealed hyperglycemia, hyperkalemia, metabolic acidosis and urine ketones, while a bed-side cardiac echocardiogram showed no segmental wall motion abnormality. We provisionally diagnosed diabetic ketoacidosis that was possibly precipitated by acute myocardial infarction, as there were findings in favor of (epigastric pain, electrocardiogram pattern, presence of 3 coronary heart disease risk factors) and against (young age, normal echocardiogram) the diagnosis of acute myocardial infarction. We performed cardiac angiography in order to exclude an anterior acute myocardial infarction, which could lead to myocardial damage and possible severe complications should there be a delay in treatment. Angiography revealed normal coronary arteries. During the procedure, ST segment elevation in the anteroseptal leads was still present in our patient's electrocardiogram results. ST segment elevation is a rare manifestation of hyperkalemia. In our patient, coronary spasm did not contribute to such an electrocardiography finding. Introduction It has been reported that hyperkalemi 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 >>

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 >>

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 >>

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Diabetic ketoacidosis is a complicated condition which can be caused if you are unable to effectively treat and manage your diabetes. In this condition, ketones are accumulated in the blood which can adversely affect your health. It can be a fatal condition and may cause a lot of complications. One such complication in diabetic ketoacidosis is the onset of hyperkalemia or the high levels of potassium in the blood. In this article, we shall try to understand as to why hyperkalemia is caused in diabetic ketoacidosis? So, read on “Why is There Hyperkalemia in Diabetic Ketoacidosis?” What is Diabetic Ketoacidosis and Hyperkalemia? Diabetic ketoacidosis is a serious complication that is faced by many patients suffering from diabetes. In this condition, excess blood acids called ketones are produced by the body. The above condition should not be taken lightly and should be immediately treated as the same can cause diabetic coma, and eventually the death of the patient. Hyperkalemia refers to abnormally high levels of potassium in the blood of an individual. For a healthy individual, the level of potassium is around 3.5 to 5 milliequivalents per liter. If you have potassium levels higher than that, that is somewhere in between 5.1 to 6 milliequivalents per liter, then you have a mild level of hyperkalemia. Similarly, if the level of potassium in your blood is somewhere between 6.1 to 7 milliequivalents per liter, you have moderate hyperkalemia. Anything above that, you may be suffering from what is known as severe hyperkalemia. Relation Between Diabetic Ketoacidosis and Hyperkalemia There appears to be a strong relationship between hyperkalemia and diabetic ketoacidosis. In the paragraph that follows, we shall try to analyze and understand the same: If you have diabetes an 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 >>

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 >>

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