diabetestalk.net

Does Ketoacidosis Cause Hyperkalemia

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 >>

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 >>

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 >>

What Is Hyperkalemia?: Signs, Symptoms, Causes And Treatment

What Is Hyperkalemia?: Signs, Symptoms, Causes And Treatment

What is Hyperkalemia? It is a medical condition where the potassium levels are abnormally high. For the muscle cells and nerve cells to function properly, your body requires the right balance of a nutrient called potassium. Normal potassium levels are between 3.5 to 5.0 mmol/L. If your blood potassium level is between 5.1 mmol/L and 6.0 mmol/L, you may have mild hyperkalemia. When your potassium level is between 6.1 mmol/L and 7.0 mmol/L, you may have moderate hyperkalemia. You are said to have severe hyperkalemia if your potassium level is above 7.0 mmol/L. High potassium levels in the bloodstream can be dangerous and lead to serious heart problems. Most patients with this condition are diagnosed with mild hyperkalemia. However, it is important you seek treatment when you are diagnosed with any form of high potassium levels to prevent the condition from progressing. Severe hyperkalemia can cause cardiac arrest or even death. Potassium is vital for the proper functioning of the heart, muscles and nerves. This nutrient is responsible for controlling the activity of the skeletal muscle, smooth muscles and heart muscle. Potassium also helps in proper transmission of electrical signals in the entire nervous system of the body. Achieving a normal potassium level helps you to maintain a normal heart electrical rhythm. Signs and Symptoms Most people with high potassium levels do not show any signs and symptoms. However, if signs and symptoms appear, they are normally mild and not specific. Usually, hyperkalemia that develops slowly with time is likely to produce less signs and symptoms compared with a sudden increase in potassium levels. Sudden hyperkalemia is a life threatening condition that requires immediate medical attention. Usually, the signs and symptoms of hyperkalemi 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 >>

On The Relationship Between Potassium And Acid-base Balance

On The Relationship Between Potassium And Acid-base Balance

The notion that acid-base and potassium homeostasis are linked is well known. Students of laboratory medicine will learn that in general acidemia (reduced blood pH) is associated with increased plasma potassium concentration (hyperkalemia), whilst alkalemia (increased blood pH) is associated with reduced plasma potassium concentration (hypokalemia). A frequently cited mechanism for these findings is that acidosis causes potassium to move from cells to extracellular fluid (plasma) in exchange for hydrogen ions, and alkalosis causes the reverse movement of potassium and hydrogen ions. As a recently published review makes clear, all the above may well be true, but it represents a gross oversimplification of the complex ways in which disorders of acid-base affect potassium metabolism and disorders of potassium affect acid-base balance. The review begins with an account of potassium homeostasis with particular detailed attention to the renal handling of potassium and regulation of potassium excretion in urine. This discussion includes detail of the many cellular mechanisms of potassium reabsorption and secretion throughout the renal tubule and collecting duct that ensure, despite significant variation in dietary intake, that plasma potassium remains within narrow, normal limits. There follows discussion of the ways in which acid-base disturbances affect these renal cellular mechanisms of potassium handling. For example, it is revealed that acidosis decreases potassium secretion in the distal renal tubule directly by effect on potassium secretory channels and indirectly by increasing ammonia production. The clinical consequences of the physiological relation between acid-base and potassium homeostasis are addressed under three headings: Hyperkalemia in Acidosis; Hypokalemia w 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 >>

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 >>

Hyperkalemia In A Young Woman With Type 1 Diabetes Mellitus

Hyperkalemia In A Young Woman With Type 1 Diabetes Mellitus

A 32-year-old woman with multiple medical problems was brought to the emergency department with lethargy and weakness. The family noted progressive confusion and fatigue over 2 days, coupled with extreme weakness. The patient and family denied all other complaints as well as any traumatic or toxicologic events. The medical history included juvenile-onset diabetes mellitus, hypertension, renal insufficiency, and diabetic retinopathy with visual impairment; the patient used insulin and lisinopril as well as several other unknown medications. On examination, she was confused and lethargic but was aroused by stimuli and spoke coherently. Vital signs were: blood pressure, 188/106 mmHg; pulse, approximately 70 beats/min; respiratory rate, 24 breaths/min; temperature, 36.1°C (97°F); and oxygen saturation, 94% on room air; the ECG monitor demonstrated the rhythm strip in Figure 1. A bedside glucose test was 256 mg/dL. The remainder of the examination was unremarkable. Results of a 12-lead ECG are seen in Figure 2. Based upon the ECG findings noted in Figures 1 and 2, which of the following best describe the patient’s risk of an adverse event and the most appropriate management: A. Low risk; atropine IV and glucagon IV B. Intermediate risk; transcutaneous pacing and IV epinephrine infusion C. High risk; synchronized electrical cardioversion with amiodarone IV D. Extremely high risk; calcium IV, sodium bicarbonate IV, and dextrose/insulin IV Correct Answer: D. Extremely high risk; calcium IV, sodium bicarbonate IV, and dextrose/insulin IV Discussion Hyperkalemia presents across a spectrum of severity, ranging from asymptomatic discovery to cardiorespiratory arrest. Of the various electrolyte disorders, it is perhaps the most serious with the potential for severe adverse outco 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 >>

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 >>

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 >>

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 >>

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 >>

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 >>

More in ketosis