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How Does Ketoacidosis Cause Hypokalemia

Hypokalemia And The Heart

Hypokalemia And The Heart

An article from the E-Journal of the ESC Council for Cardiology Practice Practicing cardiologists must keep potassium levels within normal limits in all their cardiac patients. Unrecognised hypokalemia is a leading cause of iatrogenic mortality among cardiac patients who have an inherent risk for arrhythmias and who frequently use medications that increase the risks of hypokalemia and/or arrhythmia. Symptomatic or severe hypokalemia should be corrected with a solution of intravenous potassium: 10-40 mEq infused over 2-3 h (infusion rate should not to exceed 40 mEq/h). In less urgent situations, oral supplementation is preferred and safer: 50-100 mEq/d divided two-four times per day. Long-term treatment should be based on the recognition of the hypokalemia cause. Hypokalemia and the heart Potassium is the most abundant intracellular cation and is necessary for maintaining a normal charge difference between intracellular and extracellular space. Potassium homeostasis is important for normal cellular function and is regulated by ion-exchange pumps (primarily cellular, membrane-bound, sodium-potassium ATPase pumps). Derangements of potassium regulation often lead to neuromuscular, gastrointestinal and cardiac rhythm abnormalities. The normal level of plasma potassium is 3,8 – 5,1 mmol/l. The deviations to both extremes (hypo- and hyperkalemia) are related to the risk of cardiac arrhythmias. Potassium levels below 3,0 mmol/l cause significant Q-T interval prolongation with subsequent risk of torsade des pointes, ventricular fibrillation and sudden cardiac death. Potassium levels above 6,0 mmol/l cause peaked T waves, wider QRS komplexes and may result in bradycardia, asystole and sudden death. Hyperkalemia is most frequently caused by renal failure (frequently a trigger is 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 >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Snap Shot A 12 year old boy, previously healthy, is admitted to the hospital after 2 days of polyuria, polyphagia, nausea, vomiting and abdominal pain. Vital signs are: Temp 37C, BP 103/63 mmHg, HR 112, RR 30. Physical exam shows a lethargic boy. Labs are notable for WBC 16,000, Glucose 534, K 5.9, pH 7.13, PCO2 is 20 mmHg, PO2 is 90 mmHg. Introduction Complication of type I diabetes result of ↓ insulin, ↑ glucagon, growth hormone, catecholamine Precipitated by infections drugs (steroids, thiazide diuretics) noncompliance pancreatitis undiagnosed DM Presentation Symptoms abdominal pain vomiting Physical exam Kussmaul respiration increased tidal volume and rate as a result of metabolic acidosis fruity, acetone odor severe hypovolemia coma Evaluation Serology blood glucose levels > 250 mg/dL due to ↑ gluconeogenesis and glycogenolysis arterial pH < 7.3 ↑ anion gap due to ketoacidosis, lactic acidosis ↓ HCO3- consumed in an attempt to buffer the increased acid hyponatremia dilutional hyponatremia glucose acts as an osmotic agent and draws water from ICF to ECF hyperkalemia acidosis results in ICF/ECF exchange of H+ for K+ moderate ketonuria and ketonemia due to ↑ lipolysis β-hydroxybutyrate > acetoacetate β-hydroxybutyrate not detected with normal ketone body tests hypertriglyceridemia due to ↓ in capillary lipoprotein lipase activity activated by insulin leukocytosis due to stress-induced cortisol release H2PO4- is increased in urine, as it is titratable acid used to buffer the excess H+ that is being excreted Treatment Fluids Insulin with glucose must prevent resultant hypokalemia and hypophosphatemia labs may show pseudo-hyperkalemia prior to administartion of fluid and insulin due to transcellular shift of potassium out of the cells to balance the H+ be 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 >>

Understanding And Treating Diabetic Ketoacidosis

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 >>

Hyperglycemia & Low Potassium

Hyperglycemia & Low Potassium

Hyperglycemia, or high blood sugar, is a potentially serious health condition affecting individuals with diabetes. Hyperglycemia can trigger a severe depletion of potassium, a mineral that serves many critical functions in the human body. Carefully follow medical advice for diabetes management including dietary restrictions and medication to minimize the impact of hyperglycemia and the potential for total body potassium depletion. Video of the Day Potassium is a necessary dietary mineral which must be consumed daily, as it is easily soluble and flushes out in the urine, according to Dr. Elson M. Haas of Periodic Paralysis International. Potassium is the primary mineral found inside of human body cells, while sodium is the primary mineral found outside the body cells. Potassium and sodium must be maintained in careful balance. Potassium is plentiful in fresh fruits, vegetables and whole grains, but is easily lost in the cooking process. Consuming an excess of sodium in relation to potassium can lead to high blood pressure and other negative health consequences. Hyperglycemia, or high serum glucose levels, happens occasionally in nearly all diabetics but must be carefully monitored and corrected as it may lead to serious complications like diabetic ketoacidosis and diabetic coma, according to the MayoClinic.com. In addition to high blood glucose levels, symptoms of hyperglycemia include frequent urination and increased thirst. Hyperglycemia results from too little insulin or inefficient insulin use and may also occur due to stress or illness, according to the American Diabetes Association. Low Potassium Effects Potassium deficiency can be caused by dietary insufficiency, chronic illness, heavy sweating, or the prolonged use of diuretics or laxatives, according to Dr. Elso Continue reading >>

Diabetic Ketoacidosis

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 >>

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 >>

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

Diabetic Ketoacidosis And Hyperglycaemic Hyperosmolar State

The hallmark of diabetes is a raised plasma glucose resulting from an absolute or relative lack of insulin action. Untreated, this can lead to two distinct yet overlapping life-threatening emergencies. Near-complete lack of insulin will result in diabetic ketoacidosis, which is therefore more characteristic of type 1 diabetes, whereas partial insulin deficiency will suppress hepatic ketogenesis but not hepatic glucose output, resulting in hyperglycaemia and dehydration, and culminating in the hyperglycaemic hyperosmolar state. Hyperglycaemia is characteristic of diabetic ketoacidosis, particularly in the previously undiagnosed, but it is the acidosis and the associated electrolyte disorders that make this a life-threatening condition. Hyperglycaemia is the dominant feature of the hyperglycaemic hyperosmolar state, causing severe polyuria and fluid loss and leading to cellular dehydration. Progression from uncontrolled diabetes to a metabolic emergency may result from unrecognised diabetes, sometimes aggravated by glucose containing drinks, or metabolic stress due to infection or intercurrent illness and associated with increased levels of counter-regulatory hormones. Since diabetic ketoacidosis and the hyperglycaemic hyperosmolar state have a similar underlying pathophysiology the principles of treatment are similar (but not identical), and the conditions may be considered two extremes of a spectrum of disease, with individual patients often showing aspects of both. Pathogenesis of DKA and HHS Insulin is a powerful anabolic hormone which helps nutrients to enter the cells, where these nutrients can be used either as fuel or as building blocks for cell growth and expansion. The complementary action of insulin is to antagonise the breakdown of fuel stores. Thus, the relea Continue reading >>

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 >>

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 >>

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 >>

Diabetic Ketoacidosis (dka) Myths

Diabetic Ketoacidosis (dka) Myths

Recently, I was asked to give a lecture to both my residents and nurses at the University of Texas Health Science Center at San Antonio (UTHSCSA) on some common DKA myths. Now this topic was originally covered by my good friend Anand Swaminathan on multiple platforms and I did ask his permission to create this blogpost with the idea of improving patient care and wanted to express full disclosure of that fact. I specifically covered four common myths that I still see people doing in regards to DKA management: We should get ABGs instead of VBGs After Intravenous Fluids (IVF), Insulin is the Next Step Once pH <7.1, Patients Need Bicarbonate Therapy We Should Bolus Insulin before starting the infusion DKA Myths Case: 25 y/o female with PMH of Type I DM who presents via EMS with AMS. Per EMS report, the patient ran out of her insulin 3 days ago….. Vital Signs: BP 86/52 HR 136 RR 30 O2Sat 97% on room air Temp 99.1 Accucheck: CRITICAL HIGH EMS was not able to establish IV access, so decided to just bring her to the ED due to how sick she looks. Your nurses are on point today and get you two large bore 18G IVs and start to draw blood work to send to the lab. You state I need a blood gas, and the nurse turns to you and asks do you need an ABG or VBG? Myth #1: We should get ABGs instead of VBGs in DKA So you do a literature review and come across two studies that specifically look at ABG vs VBG in an ED population: Study #1: Kelly AM et al. Review Article – Can Venous Blood Gas Analysis Replace Arterial in Emergency Medical Care. Emery Med Australas 2010; 22: 493 – 498. PMID: 21143397 For pH, 3 studies of patients with DKA (265 patients) were reviewed showing a weighted mean difference of 0.02 pH units. Only one study, which was the largest study (200 patients) reported 95% Continue reading >>

Myths In Dka Management

Myths In Dka Management

Anand Swaminathan, MD, MPH (@EMSwami) is an assistant professor and assistant program director at the NYU/Bellevue Department of Emergency Medicine in New York City. Review questions are available at the end of this post. Background Each year, roughly 10,000 patients present to the Emergency Department in diabetic ketoacidosis (DKA). Prior to the advent of insulin, the mortality rate of DKA was 100% although in recent years, that rate has dropped to approximately 2-5%.1 Despite clinical advances, the mortality rate has remained constant over the last 10 years. With aggressive resuscitative measures and appropriate continued management this trend may change. DKA is defined as: Hyperglycemia (glucose > 250 mg/dl) Acidosis (pH < 7.3) Ketosis In the absence of insulin, serum glucose rises leading to osmotic diuresis. This diuresis leads to loss of electrolytes including sodium, magnesium, calcium and phosphorous. The resultant volume depletion leads to impaired glomerular filtration rate (GFR) and acute renal failure. In patients with DKA, fatty acid breakdown produces 2 different ketone bodies, first acetoacetate, which then further converts to beta-hydroxybutyrate, the latter being the ketone body largely produced in DKA patients. With this background in mind, let’s take a look at four urban legends in the management of DKA and the evidence that dispels these legends. Here’s our case: Although this presentation likely represents DKA, a blood gas is typically obtained to confirm the diagnosis. Often, the question arises as to whether an arterial or venous blood gas is adequate. Urban Legend #1 – An ABG is necessary for the diagnosis and treatment of DKA ABG gets you pH, PaO2, PaCO2, HCO3, Lactate, electrolytes and O2Sat VBG gets all this except for PaO2 (but we have Continue reading >>

Diabetic Ketoacidosis

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 >>

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