Potassium Balance In Acid-base Disorders
INTRODUCTION There are important interactions between potassium and acid-base balance that involve both transcellular cation exchanges and alterations in renal function [1]. These changes are most pronounced with metabolic acidosis but can also occur with metabolic alkalosis and, to a lesser degree, respiratory acid-base disorders. INTERNAL POTASSIUM BALANCE Acid-base disturbances cause potassium to shift into and out of cells, a phenomenon called "internal potassium balance" [2]. An often-quoted study found that the plasma potassium concentration will rise by 0.6 mEq/L for every 0.1 unit reduction of the extracellular pH [3]. However, this estimate was based upon only five patients with a variety of disturbances, and the range was very broad (0.2 to 1.7 mEq/L). This variability in the rise or fall of the plasma potassium in response to changes in extracellular pH was confirmed in subsequent studies [2,4]. Metabolic acidosis — In metabolic acidosis, more than one-half of the excess hydrogen ions are buffered in the cells. In this setting, electroneutrality is maintained in part by the movement of intracellular potassium into the extracellular fluid (figure 1). Thus, metabolic acidosis results in a plasma potassium concentration that is elevated in relation to total body stores. The net effect in some cases is overt hyperkalemia; in other patients who are potassium depleted due to urinary or gastrointestinal losses, the plasma potassium concentration is normal or even reduced [5,6]. There is still a relative increase in the plasma potassium concentration, however, as evidenced by a further fall in the plasma potassium concentration if the acidemia is corrected. A fall in pH is much less likely to raise the plasma potassium concentration in patients with lactic acidosis Continue reading >>
Review Of Diabetic Ketoacidosis Management
Review of Diabetic Ketoacidosis Management Department of Clinical Health Professions Department of Clinical Health Professions ABSTRACT: Diabetic ketoacidosis (DKA) is a medical emergency caused by insulin deficiency. It is characterized by hyperglycemia, metabolic acidosis, and ketoacidosis. DKA arises from lack of insulin, with or without a precipitating event that leads to a cascade of pathophysiological changes. The goals of DKA treatment are to normalize volume status, hyperglycemia, electrolytes, and ketoacidosis. Pharmacists in community or ambulatory-care settings can assist in preventing DKA, while inpatient pharmacists play a role in management of DKA. Diabetic ketoacidosis (DKA) is a serious medical emergency caused by insulin deficiency that takes a significant toll on the U.S. healthcare system.1,2 There are over 500,000 hospital days per year and $2.4 billion in medical costs attributed to DKA alone. DKA has high rates of morbidity and mortality, especially in younger type 1 diabetic patients. It is the most common cause of death for those under the age of 24 years with type 1 diabetes.3 It is estimated that 27% to 37% of patients with DKA are newly diagnosed with diabetes, usually type 1.1 Trauma, infection, or surgery may increase the risk of DKA in patients with type 2 diabetes.3 Mortality with DKA is generally associated with the underlying illness or comorbidity.1,3,4 Generally, DKA may be characterized by significant hyperglycemia, metabolic acidosis, and ketoacidosis. However, DKA may present in various ways, from euglycemia to severe hyperglycemia with or without dehydration and coma.3-5 The treatment approach for each patient is highly individualized based on a patients clinical factors.5 Simply put, DKA is caused by too little insulin and a resp Continue reading >>
Initial Potassium Replacement In Diabetic Ketoacidosis: The Unnoticed Area Of Gap
Initial Potassium Replacement in Diabetic Ketoacidosis: The Unnoticed Area of Gap We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. Initial Potassium Replacement in Diabetic Ketoacidosis: The Unnoticed Area of Gap Diabetic ketoacidosis is an acute complication of diabetes mellitus (DM). It affects all the types of DM and hence is a continuous threat for all the diabetes patients ( 1 ). DKA is a well-studied disease. Among the precipitating causes, mostly reported factors are non-compliance of patients with the antidiabetic treatment, and infection; others, however, may not have any precipitating cause ( 1 , 2 ). The progress of disease is very simple; lack of insulin causes hyperglycemia and inability of glucose to enter the cell. In-turn, triglycerides are broken down to free fatty acids which are used as a source of energy ( 1 , 3 , 4 ). In due process, the end-product of this metabolic derangement, i.e., ketones, cause acidification of blood causing major disruption in homeostasis. Similar to pathophysiology, the treatment of DKA is also simple and encompasses administration of insulin to achieve euglycaemia, and administration of crystalloid or colloidal solution to attain euvolaemia and euelectrolytaemia ( 1 3 ). Nevertheless, by the time patient reports for medical attention, these simple derangements and the rectification pathway have had gone significant derailment with potassium being the most affected ion throughout the Continue reading >>
Diabetic Ketoacidosis
Print Overview Diabetic ketoacidosis is a serious complication of diabetes that occurs when your body produces high levels of blood acids called ketones. The condition develops when your body can't produce enough insulin. Insulin normally plays a key role in helping sugar (glucose) — a major source of energy for your muscles and other tissues — enter your cells. Without enough insulin, your body begins to break down fat as fuel. This process produces a buildup of acids in the bloodstream called ketones, eventually leading to diabetic ketoacidosis if untreated. If you have diabetes or you're at risk of diabetes, learn the warning signs of diabetic ketoacidosis — and know when to seek emergency care. Symptoms Diabetic ketoacidosis signs and symptoms often develop quickly, sometimes within 24 hours. For some, these signs and symptoms may be the first indication of having diabetes. You may notice: Excessive thirst Frequent urination Nausea and vomiting Abdominal pain Weakness or fatigue Shortness of breath Fruity-scented breath Confusion More-specific signs of diabetic ketoacidosis — which can be detected through home blood and urine testing kits — include: High blood sugar level (hyperglycemia) High ketone levels in your urine When to see a doctor If you feel ill or stressed or you've had a recent illness or injury, check your blood sugar level often. You might also try an over-the-counter urine ketones testing kit. Contact your doctor immediately if: You're vomiting and unable to tolerate food or liquid Your blood sugar level is higher than your target range and doesn't respond to home treatment Your urine ketone level is moderate or high Seek emergency care if: Your blood sugar level is consistently higher than 300 milligrams per deciliter (mg/dL), or 16.7 mill Continue reading >>
What Is Hypokalemia?
What is hypokalemia? Hypokalemia is the technical term for a low potassium level. Potassium, represented by K on the periodic table of elements, is one of the most important components of the blood. Mild hypokalemia is diagnosed with a serum potassium level less than 3.5 mEq/L, and severe hypokalemia is usually less than 2.5 mEq/L. This common condition has numerous causes; quite a few problematic symptoms; and standard, effective treatments. Causes of Hypokalemia The causes of hypokalemia fall into three categories: poor intake increased excretion and potassium shifts. Poor intake is rather easy to understand: the patient merely does not take in enough potassium. This may result from eating disorders, dental problems, and poverty. Failure to replace potassium can lead to symptoms ranging from mild to severe. Increased excretion of potassium is usually seen in the cases of vomiting and diarrhoea. In these conditions, the potassium is excreted far faster than the patient can replace it. Some medications, such as diuretics, can cause potassium loss. Excessive urination, such as that which occurs with diabetes, is another culprit. Perhaps more difficult to understand is the shift of fluids in the body that can cause a hypokalemic state. If a patient experiences paralysis for an extended period, potassium may leave the blood and leach into the interstitial space. High doses of insulin can also cause a potassium shift that decreases the availability of the nutrient in the blood. Finally, high doses of beta agonists commonly used in COPD are possible causes of low serum potassium. Symptoms of Hypokalemia As noted, symptoms can range from mild to severe, most falling in the mild category. In fact, many patients are hypokalemic for long periods and have few to no symptoms becau Continue reading >>
Hypothermia And Hypokalemia In A Patient With Diabetic Ketoacidosis
We present the case of a 36-year-old man with type-1 diabetes who was hospitalized with diabetic ketoacidosis (DKA). On admission, he had hypothermia, hypokalemia and combined metabolic and respiratory alkalosis, in addition to hyperglycemia. Hypothermia, hypokalemia and metabolic alkalosis, with a concurrent respiratory alkalosis, are not commonly seen in DKA. After admission, intravenous infusion of 0.45% saline was administered, which resulted in the development of pure metabolic acidosis. After starting insulin infusion, hypokalemia and hypophosphatemia became evident and finally resulted in massive rhabdomyolysis. Hyperkalemia accompanying oliguric acute kidney injury (AKI) warranted initiation of hemodialysis (HD) on Day-five. On the 45th hospital day, his urine output started to increase and a total of 22 HD sessions were required. We believe that in this case severe dehydration, hypothermia and hypokalemia might have contributed to the initial symptoms of DKA as well as the prolongation of AKI. How to cite this article: Saito O, Saito T, Sugase T, Kusano E, Nagata D. Hypothermia and hypokalemia in a patient with diabetic ketoacidosis. Saudi J Kidney Dis Transpl 2015;26:580-3 Diabetic ketoacidosis (DKA) is a combination of the biochemical triad of hyperglycemia, ketonemia and metabolic acidosis. [1] Initial hypokalemia in DKA is a rare finding, with an incidence of 4-10%. [2] Hypothermia is rarely seen in patients with DKA, and the prognosis of this association is poor, with a mortality of 60% in the Western countries. [3] Also, combined metabolic and respiratory alkalosis is rarely seen in DKA, with an incidence of 7.5%. [4] We herewith report the case of a 36-year-old man with type-1 diabetes who was admitted to the hospital with DKA in association with hypothe Continue reading >>
Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome
In Brief Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated. Mortality rates are 2–5% for DKA and 15% for HHS, and mortality is usually a consequence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment protocols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. The two most common life-threatening complications of diabetes mellitus include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). Although there are important differences in their pathogenesis, the basic underlying mechanism for both disorders is a reduction in the net effective concentration of circulating insulin coupled with a concomitant elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These hyperglycemic emergencies continue to be important causes of morbidity and mortality among patients with diabetes. DKA is reported to be responsible for more than 100,000 hospital admissions per year in the United States1 and accounts for 4–9% of all hospital discharge summaries among patients with diabetes.1 The incidence of HHS is lower than DKA and accounts for <1% of all primary diabetic admissions.1 Most patients with DKA have type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness.2 Contrary to popular belief, DKA is more common in adults than in children.1 In community-based studies, more than 40% of African-American patients with DKA were >40 years of age and more than 2 Continue reading >>
Understanding And Treating Diabetic Ketoacidosis
Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab Continue reading >>
Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy
Copyright © 2014 Nupur Sinha et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Pregnancy is a diabetogenic state characterized by relative insulin resistance, enhanced lipolysis, elevated free fatty acids and increased ketogenesis. In this setting, short period of starvation can precipitate ketoacidosis. This sequence of events is recognized as “accelerated starvation.” Metabolic acidosis during pregnancy may have adverse impact on fetal neural development including impaired intelligence and fetal demise. Short periods of starvation during pregnancy may present as severe anion gap metabolic acidosis (AGMA). We present a 41-year-old female in her 32nd week of pregnancy, admitted with severe AGMA with pH 7.16, anion gap 31, and bicarbonate of 5 mg/dL with normal lactate levels. She was intubated and accepted to medical intensive care unit. Urine and serum acetone were positive. Evaluation for all causes of AGMA was negative. The diagnosis of starvation ketoacidosis was established in absence of other causes of AGMA. Intravenous fluids, dextrose, thiamine, and folic acid were administered with resolution of acidosis, early extubation, and subsequent normal delivery of a healthy baby at full term. Rapid reversal of acidosis and favorable outcome are achieved with early administration of dextrose containing fluids. 1. Introduction A relative insulin deficient state has been well described in pregnancy. This is due to placentally derived hormones including glucagon, cortisol, and human placental lactogen which are increased in periods of stress [1]. The insulin resistance increases with gestational age Continue reading >>
Successful Use Of Renal Replacement Therapy For Refractory Hypokalemia In A Diabetic Ketoacidosis Patient
Volume 2019 |Article ID 6130694 | 3 pages | Successful Use of Renal Replacement Therapy for Refractory Hypokalemia in a Diabetic Ketoacidosis Patient 1Department of Medicine, Saint Josephs University Medical Center, 703 Main St, Paterson, NJ, USA 2New York Medical College, Valhalla, NY, USA A 39-year-old African-American female presented to the emergency department with a seven-day history of right upper quadrant abdominal pain accompanied by nausea, vomiting, and diarrhea. She was noted to be alert and following commands, but tachypneic with Kussmaul respirations; and initial laboratory testing supported a diagnosis of diabetic ketoacidosis (DKA) and hypokalemia. To avoid hypokalemia-induced arrhythmias, insulin administration was withheld until a serum potassium (K) level of 3.3 mEq/L could be achieved. Efforts to increase the patients potassium level via intravenous repletion were ineffectual; hence, an attempt was made at more aggressive potassium repletion via hemodialysis using a 4 mEq/L K dialysate bath. The patient was started on Aldactone and continuous veno-venous hemodialysis (CVVH) with ongoing low-dose insulin infusion. This regimen was continued over 24 h resulting in normalization of the patients potassium levels, resolution of acidosis, and improvement in mental status. Upon resolution of her acidemia, the patient was transitioned from insulin infusion to treatment with a subcutaneous insulin aspart and insulin detemir, and did not experience further hypokalemia. Considering our success, we propose CVVH as a tool for potassium repletion when aggressive intravenous (IV) repletion has failed. Hospitalizations for diabetic ketoacidosis (DKA) have soared in incidence over the recent years, increasing 54.9% from 19.5 to 30.2 hospitalizations per 1,000 people Continue reading >>
What Causes Potassium And Sodium Loss In Diabetic Ketoacidosis (dka)?
What causes potassium and sodium loss in diabetic ketoacidosis (DKA)? Glucosuria leads to osmotic diuresis, dehydration and hyperosmolarity. Severe dehydration, if not properly compensated, may lead to impaired renal function. Hyperglycemia, osmotic diuresis, serum hyperosmolarity, and metabolic acidosis result in severe electrolyte disturbances. The most characteristic disturbance is total body potassium loss. This loss is not mirrored in serum potassium levels, which may be low, within the reference range, or even high. Potassium loss is caused by a shift of potassium from the intracellular to the extracellular space in an exchange with hydrogen ions that accumulate extracellularly in acidosis. Much of the shifted extracellular potassium is lost in urine because of osmotic diuresis. Patients with initial hypokalemia are considered to have severe and serious total body potassium depletion. High serum osmolarity also drives water from intracellular to extracellular space, causing dilutional hyponatremia. Sodium also is lost in the urine during the osmotic diuresis. Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline] . Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 2009 Jul. 32(7):1164-9. [Medline] . [Full Text] . Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation of pH, serum bicarbonate and potassium concentration in critically ill patients?. Diabet Med. 2012 Jan. 29(1):32-5 Continue reading >>
Diabetic Ketoacidosis
Introduction Diabetic ketoacidosis (DKA) is a dangerous complication of diabetes caused by a lack of insulin in the body. Diabetic ketoacidosis occurs when the body is unable to use blood sugar (glucose) because there isn't enough insulin. Instead, it breaks down fat as an alternative source of fuel. This causes a build-up of a by-product called ketones. Most cases of diabetic ketoacidosis occur in people with type 1 diabetes, although it can also be a complication of type 2 diabetes. Symptoms of diabetic ketoacidosis include: passing large amounts of urine feeling very thirsty vomiting abdominal pain Seek immediate medical assistance if you have any of these symptoms and your blood sugar levels are high. Read more about the symptoms of diabetic ketoacidosis. Who is affected by diabetic ketoacidosis? Diabetic ketoacidosis is a relatively common complication in people with diabetes, particularly children and younger adults who have type 1 diabetes. Younger children under four years of age are thought to be most at risk. In about 1 in 4 cases, diabetic ketoacidosis develops in people who were previously unaware they had type 1 diabetes. Diabetic ketoacidosis accounts for around half of all diabetes-related hospital admissions in people with type 1 diabetes. Diabetic ketoacidosis triggers These include: infections and other illnesses not keeping up with recommended insulin injections Read more about potential causes of diabetic ketoacidosis. Diagnosing diabetic ketoacidosis This is a relatively straightforward process. Blood tests can be used to check your glucose levels and any chemical imbalances, such as low levels of potassium. Urine tests can be used to estimate the number of ketones in your body. Blood and urine tests can also be used to check for an underlying infec Continue reading >>
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 >>
Diabetic Ketoacidosis (dka)
Tweet Diabetic ketoacidosis (DKA) is a dangerous complication faced by people with diabetes which happens when the body starts running out of insulin. DKA is most commonly associated with type 1 diabetes, however, people with type 2 diabetes that produce very little of their own insulin may also be affected. Ketoacidosis is a serious short term complication which can result in coma or even death if it is not treated quickly. Read about Diabetes and Ketones What is diabetic ketoacidosis? DKA occurs when the body has insufficient insulin to allow enough glucose to enter cells, and so the body switches to burning fatty acids and producing acidic ketone bodies. A high level of ketone bodies in the blood can cause particularly severe illness. Symptoms of DKA Diabetic ketoacidosis may itself be the symptom of undiagnosed type 1 diabetes. Typical symptoms of diabetic ketoacidosis include: Vomiting Dehydration An unusual smell on the breath –sometimes compared to the smell of pear drops Deep laboured breathing (called kussmaul breathing) or hyperventilation Rapid heartbeat Confusion and disorientation Symptoms of diabetic ketoacidosis usually evolve over a 24 hour period if blood glucose levels become and remain too high (hyperglycemia). Causes and risk factors for diabetic ketoacidosis As noted above, DKA is caused by the body having too little insulin to allow cells to take in glucose for energy. This may happen for a number of reasons including: Having blood glucose levels consistently over 15 mmol/l Missing insulin injections If a fault has developed in your insulin pen or insulin pump As a result of illness or infections High or prolonged levels of stress Excessive alcohol consumption DKA may also occur prior to a diagnosis of type 1 diabetes. Ketoacidosis can occasional Continue reading >>
Alcoholic Ketoacidosis
Alcoholic Ketoacidosis Damian Baalmann, 2nd year EM resident A 45-year-old male presents to your emergency department with abdominal pain. He is conscious, lucid and as the nurses are hooking up the monitors, he explains to you that he began experiencing abdominal pain, nausea, vomiting about 2 days ago. Exam reveals a poorly groomed male with dry mucous membranes, diffusely tender abdomen with voluntary guarding. He is tachycardic, tachypneic but normotensive. A quick review of the chart reveals a prolonged history of alcohol abuse and after some questioning, the patient admits to a recent binge. Pertinent labs reveal slightly elevated anion-gap metabolic acidosis, normal glucose, ethanol level of 0, normal lipase and no ketones in the urine. What are your next steps in management? Alcoholic Ketoacidosis (AKA): What is it? Ketones are a form of energy made by the liver by free fatty acids released by adipose tissues. Normally, ketones are in small quantity (<0.1 mmol/L), but sometimes the body is forced to increase its production of these ketones. Ketones are strong acids and when they accumulate in large numbers, their presence leads to an acidosis. In alcoholics, a combination or reduced nutrient intake, hepatic oxidation of ethanol, and dehydration can lead to ketoacidosis. Alcoholics tend to rely on ethanol for their nutrient intake and when the liver metabolizes ethanol it generates NADH. This NADH further promotes ketone formation in the liver. Furthermore, ethanol promotes diuresis which leads to dehydration and subsequently impairs ketone excretion in the urine. Alcoholic Ketoacidosis: How do I recognize it? Typical history involves a chronic alcohol abuser who went on a recent binge that was terminated by severe nausea, vomiting, and abdominal pain. These folk Continue reading >>
