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Why Do You Get Hyperkalemia In Dka?

How Iv Insulin Can Kill Your Patient

How Iv Insulin Can Kill Your Patient

You have a patient that comes up to your unit with a blood sugar of 952. The labs are sent off and the patient is found to be in severe diabetic ketoacidosis (DKA). The doctor puts in the orders for serial lab work, fluid boluses, electrolyte replacements, and an insulin drip. As a newer nurse, you are familiar with labs, boluses, your replacement protocols, but have never administered insulin through an IV. What nursing interventions do you need to perform to safely care for this patient? How Does Insulin Work? Insulin is a hormone created by the pancreas. It allows your body to use glucose to provide the body's cells with the necessary energy they need. Insulin production from the pancreas is based off of your blood sugar levels. If you are getting hyperglycemic, the pancreas is signaled and insulin is released into the bloodstream. Insulin then signals different cells to absorb the glucose and use it as energy or store it for later use. When insulin facilitates glucose being pulled into a cell, a potassium cation is also pulled from extracellular fluid (meaning the bloodstream) into the intracellular fluid. How does this affect our patients? Initially, patients in DKA have an increased extracellular potassium level due to the hyperglycemia and acidosis they are experiencing. This potassium level is quickly decreased as blood glucose is pulled into the cells. Administration As with all critical care medications, be sure to check your hospital's policy for administration. I have seen two main situations in which IV insulin (meaning regular insulin, not Lantus, Aspart, etc.) is given. Treatment of DKA: It seems like each hospital has a different protocol they use to manage DKA patients with. Commonly patients are treated with a bolus of regular insulin IV and then place 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 >>

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 >>

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Diabetic Ketoacidosis Producing Extreme Hyperkalemia In A Patient With Type 1 Diabetes On Hemodialysis

Hodaka Yamada1, Shunsuke Funazaki1, Masafumi Kakei1, Kazuo Hara1 and San-e Ishikawa2[1] Division of Endocrinology and Metabolism, Jichi Medical University Saitama Medical Center, Saitama, Japan [2] Division of Endocrinology and Metabolism, International University of Health and Welfare Hospital, Nasushiobara, Japan Summary Diabetic ketoacidosis (DKA) is a critical complication of type 1 diabetes associated with water and electrolyte disorders. Here, we report a case of DKA with extreme hyperkalemia (9.0 mEq/L) in a patient with type 1 diabetes on hemodialysis. He had a left frontal cerebral infarction resulting in inability to manage his continuous subcutaneous insulin infusion pump. Electrocardiography showed typical changes of hyperkalemia, including absent P waves, prolonged QRS interval and tented T waves. There was no evidence of total body water deficit. After starting insulin and rapid hemodialysis, the serum potassium level was normalized. Although DKA may present with hypokalemia, rapid hemodialysis may be necessary to resolve severe hyperkalemia in a patient with renal failure. Patients with type 1 diabetes on hemodialysis may develop ketoacidosis because of discontinuation of insulin treatment. Patients on hemodialysis who develop ketoacidosis may have hyperkalemia because of anuria. Absolute insulin deficit alters potassium distribution between the intracellular and extracellular space, and anuria abolishes urinary excretion of potassium. Rapid hemodialysis along with intensive insulin therapy can improve hyperkalemia, while fluid infusions may worsen heart failure in patients with ketoacidosis who routinely require hemodialysis. Background Diabetic ketoacidosis (DKA) is a very common endocrinology emergency. It is usually associated with severe circulatory 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 >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Definition: A hyperglycemic, acidotic state caused by insulin deficiency. The disease state consists of 3 parameters: Hyperglycemia (glucose > 250 mg/dl) Acidosis Ketosis Epidemiology Incidence of ~ 10,000 cases/year in US Mortality rate: 2-5% (prior to insulin was 100%) (Lebovitz 1995) Pathophysiology Insulin deficiency leads to serum glucose rise Increased glucose load in kidney leads to increased glucose in urine and osmotic diuresis Osmotic diuresis is accompanied by loss of electrolytes including sodium, magnesium, calcium and potassium Volume depletion leads to impaired glomerular filtration rate (GFR) Inability to properly metabolize glucose results in fatty acid breakdown with resultant ketone bodies (acetoacetate + beta-hydroxybutyrate) Causes: An acute insult leads to decompensation of a chronic disease. Can also be first manifestation of new onset diabetes (particularly in children). Below are common triggers Infection (particularly sepsis) Myocardial ischemia or infarction Medication non-compliance Clinical Presentation History Polydipsia, polyuria, polyphagia Weakness Weight loss Nausea/Vomiting Abdominal Pain Physical Examination Acetone odor on breath (“fruity” smell) Kussmaul’s respirations – deep fast breathing (tachypnea and hyperpnea) Tachycardia Hypotension Altered mental status Abdominal tenderness Diagnostic Testing Definitive diagnosis is established by laboratory criteria as detailed above (hyperglycemia, ketosis and acidosis) Essential Diagnostic Tests Serum glucose Typically > 350 mg/dL Euglycemic DKA (< 300 mg/dL) reported in up to 18% of patients Blood gas Patients will exhibit an anion gap metabolic Electrolytes: hypo/hyper/normokalemia, hyponatremia Arterial or venous blood gas can be used (Savage 2011) Urinalysis Glucosuria Ketonur 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 >>

Em Basic- Hyperkalemia

Em Basic- Hyperkalemia

(This document doesn’t reflect the views or opinions of the Department of Defense, the US Army, or the Fort Hood Post command © 2012 EM Basic, Steve Carroll DO. May freely distribute with proper attribution) Hyperkalemia- high serum potassium - #1 cause = pseudohyperkalemia -Due to hemolysis of blood sample -RBCs hit wall of blood tube and lyse -This falsely elevates potassium level PEARL- ALWAYS check hemolysis level before acting on a potassium level. BUT take it in clinical context- a potassium of 5.2 (upper limit of normal 5) with 2+ hemolysis not worrisome, potassium of 8 with 1+ hemolysis is very worrisome First step- Check the patient to ensure stability (ABCs, neuro status) Next step- get a STAT EKG -Look for EKG changes -First sign- peaked T waves -Progression to widened QRS -Highest potassium level- sine wave PEARL- Only 20-30% of patients with serious hyperkalemia will have EKG changes. Although the graphic says it- can’t accurately predict potassium level based solely on the EKG Symptoms of Hyperkalemia -Can be non-specific -Nausea, vomiting, weakness, fatigue, altered mental status Causes of Hyperkalemia -Most of the time- renal failure -Medications- spironolactone, beta blockers, cyclosporine, insulin deficiency (mostly in DKA), crush injuries (rhabdo) Treatment of hyperkalemia Mnemonic- C BIG K DIE Mechanism Calcium Stabilizes cardiac membrane β-agonists/Bicarb Pushes K into the cell Insulin SAME Glucose SAME Kayexalate (polystyrene sulfonate) Eliminates from the body (causes diarrhea) DIE- Dialysis Eliminates from the body Calcium -Calcium gluconate- start with 3 amps IV -Calcium chloride- 3 times more calcium, should be given through central line or good peripheral (18 gague AC, NOT a small hand vein) -Mechanism- stabilizes the cardi Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Sort What are the two main reasons you must treat a DKA patient with adequate fluids? replenish volume so that the kidneys can keep working and so that insulin can reach its target tissues to finally stop hormone sensitive lipase from initiating lipolysis Also need to keep in mind that in their DKA they are in a state of volume depletion because of the glycosuria. this means the capillaries in the peripheral tissues vasoconstrict in order to maintain blood (and glucose) flow to the brain. if you don't achieve volume expansion at a safe rate, and you keep giving the patient increasing doses of insulin, all of the sudden when their capillaries become reperfused they get massive amounts of insulin, which causes the potassium channel to swing open with potassium influx, leading to hypokalemia, which can be deadly. This is why it's so important to address volume expansion first and foremost, more than tweaking glucose and potassium levels on your own. What are some conditions that place a patient at risk for hypoglycemic episodes while being treated in the hospital? sudden NPO status without adjustment of insulin accordingly unexpected transport after rapid-acting insulin is given enteral feeding, TPN or intravenous dextrose discontinued premeal rapid insulin given without actually having the meal reduction of corticosteroid use (steroids increase your sugars because they cause insulin resistance) 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 >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

I. Review of normal lipid metabolism Triglycerides in adipose ==lipolysis==> Long-chain FAs Long-chain FAs==hepatic beta-oxidation==>Acetyl CoA Acetyl CoA==hepatic ketogenesis==>ketone bodies Ketone bodies are Beta-hydroxybutyrate and Acetoacetate Beta-OHB is oxidized to AcAc-; their relative concentrations depend on redox state of cell; Beta-OHB predominates in situation favoring reductive metabolism (e.g. decreased tissue perfusion, met. acidosis, catabolic states--like DKA!) Typical ratio Beta-OHB:AcAc- is 3:1; us. increases in DKA II. Hormonal influences on glucose and lipid metabolism Insulin In liver, increases glu uptake from portal blood; stimulates glycogenesis, inhibits glycogenolysis and gluconeogenesis In skeletal muscle, increases glu uptake from blood, stimulates protein synth, inhibits proteolysis In adipose tissue, required for glu and lipoprotein uptake from blood; stimulates lipogenesis, inhibits lipolysis Tissues which don't require insulin to transport glucose into cells: brain, renal medulla, formed blood elements Counterregulatory hormones: glucagon (major player in DKA), epi/norepi, cortisol, growth hormone (no acute effects, only over days-weeks) Glucagon: increases hepatic beta-oxidation, ketogenesis, gluconeogenesis and glycogenolysis; decreases hepatic FA synth. Epi/Norepi: increase hepatic gluconeogenesis & glycogenolysis; increases adipose lipolysis; decreases peripheral glu utilization Cortisol: major effect is decreased peripheral glu utiliz; little effect on production Growth hormone: increases hepatic gluconeogenesis and glycogenolysis; increases adipose lipolysis In high counterreg. hormone states (see above), require high levels of insulin to avoid progressive hyperglycemia and ketoacidosis--glucagon levels in DKA are 5-6 x nl* III. Pa Continue reading >>

Pulmcrit- Dominating The Acidosis In Dka

Pulmcrit- Dominating The Acidosis In Dka

Management of acidosis in DKA is an ongoing source of confusion. There isn’t much high-quality evidence, nor will there ever be (1). However, a clear understanding of the physiology of DKA may help us treat this rationally and effectively. Physiology of ketoacidosis in DKA Ketoacidosis occurs due to an imbalance between insulin dose and insulin requirement: Many factors affect the insulin requirement: Individuals differ in their baseline insulin resistance and insulin requirements. Physiologic stress (e.g. hypovolemia, inflammation) increases the level of catecholamines and cortisol, which increases insulin resistance. Hyperglycemia and metabolic acidosis themselves increase insulin resistance (Souto 2011, Gosmanov 2014). DKA treatment generally consists of two phases: first, we must manage the ketoacidosis. Later, we must prepare the patient to transition back to their home insulin regimen. During both phases, success depends on balancing insulin dose and insulin requirement. Phase I (Take-off): Initial management of the DKA patient with worrisome acidosis Let’s start by considering a patient who presents in severe DKA with worrisome acidosis. This is uncommon. Features that might provoke worry include the following: bicarbonate < 7 mEq/L pH < 7 (if measured; there is generally little benefit from measuring pH) clinically ill-appearing (e.g., dyspnea, marked Kussmaul respirations) These patients generally have severe metabolic acidosis with respiratory compensation. This creates two concerns: If the metabolic acidosis worsens, they may decompensate. The patient is depending on respiratory compensation to maintain their pH. If they should fatigue and lose the ability to hyperventilate, their pH would drop. It is important to reverse the acidosis before the patient m 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 >>

Diagnosis And Treatment Of Diabetic Ketoacidosis (dka) In Dogs And Cats

Diagnosis And Treatment Of Diabetic Ketoacidosis (dka) In Dogs And Cats

What is DKA in Dogs and Cats? Diabetic Ketoacidosis (DKA) is a serious and life-threatening complication of diabetes mellitus that can occur in dogs and cats. DKA is characterized by hyperglycemia, ketonemia, +/- ketonuria, and metabolic acidosis. Ketone bodies are formed by lipolysis (breakdown) of fat and beta-oxidation when the metabolic demands of the cells are not met by the limited intracellular glucose concentrations. This provides alternative energy sources for cells, which are most important for the brain. The three ketones that are formed include beta-hydroxybutyrate, acetoacetate and acetone. Beta-hydroxybutyrate (BHB) and acetoacetate are anions of moderately strong acids contributing most to the academia (low blood pH). Acetone is the ketone body that can be detected on breath. In a normal animal, glucose enters the cell (with help of insulin) – undergoes glycolysis to pyruvate within cytosol – pyruvate moves into mitochondria (energy generating organelle in the cell) to enter the TCA cycle and ATP is formed. ATP is the main energy source of the body. When glucose cannot enter the cell, free fatty acids are broken down (lipolysis) and move into the cell to undergo beta-oxidation (creation of pyruvate). The pyruvate then moves into the mitochondria to enter the TCA cycle (by conversion to Acetyl-CoA first). However, when the TCA cycle is overwhelmed, the Acetyl-CoA is used in ketogenesis to form ketone bodies. Summary Diabetic Ketoacidosis (DKA) in Dogs and Cats When there is no insulin the body cannot utilize glucose and there is no intracellular glucose. The body then uses ketone bodes as an alternate source. When there is decreased insulin and increased counterregulatory hormones fatty acids are converted to AcCoA and then ketones. In the non-diabetic 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 >>

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