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How Does Ketoacidosis Cause Hyperkalemia

What Are The Causes Of High Potassium In Dogs?

What Are The Causes Of High Potassium In Dogs?

Potassium is an electrolyte that is found in the cells and in the blood of your dog's body. An ideal potassium level is essential for controlling your dog's nerve impulses, brain function and muscle activity. It also plays a vital role in regulating your dog's heart function. The normal reference range for a dog's blood potassium level falls between 3.6 and 5.5 mEq/L. When your dog's potassium level dips too low, the condition is referred to as hypokalemia. Conversely, if his potassium level climbs too high, your dog is suffering from hyperkalemia. Your dog's potassium level is determined by performing a blood chemistry profile. Your dog's kidneys are responsible for filtering wastes from your dog's blood so that they may be expelled from your dog's body when he urinates. Optimal kidney function is vital to maintaining healthy levels of enzymes, minerals and other important substances, including potassium. Your veterinarian will perform an electrocardiogram on your dog to assess his heart rate and rhythm. He or she will review your dog's medical history and ask questions regarding your dog's recent activities, including drinking and urinating frequencies. Diagnostic tests will include a complete blood count, a blood chemistry profile and a urinalysis. Additional blood tests and radiographs may be ordered to determine the underlying cause of hyperkalemia. When your dog's kidneys no longer function optimally, potassium and other wastes build up in your dog's system. Acute anuric, meaning insufficient urine production, and acute oliguric, meaning complete shut down of kidney function, kidney failures are the most frequent causes of hyperkalemia in dogs. Some common causes of acute kidney failure include antifreeze ingestion and leptospirosis infection. Chronic renal failur Continue reading >>

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

Why Is There Hyperkalemia In Diabetic Ketoacidosis?

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

What 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 >>

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 >>

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 >>

Causes And Evaluation Of Hyperkalemia In Adults

Causes And Evaluation Of Hyperkalemia In Adults

INTRODUCTION Hyperkalemia is a common clinical problem. Potassium enters the body via oral intake or intravenous infusion, is largely stored in the cells, and is then excreted in the urine. The major causes of hyperkalemia are increased potassium release from the cells and, most often, reduced urinary potassium excretion (table 1). This topic will review the causes and evaluation of hyperkalemia. The clinical manifestations, treatment, and prevention of hyperkalemia, as well as a detailed discussion of hypoaldosteronism (an important cause of hyperkalemia), are presented elsewhere. (See "Clinical manifestations of hyperkalemia in adults" and "Treatment and prevention of hyperkalemia in adults" and "Etiology, diagnosis, and treatment of hypoaldosteronism (type 4 RTA)".) BRIEF REVIEW OF POTASSIUM PHYSIOLOGY An understanding of potassium physiology is helpful when approaching patients with hyperkalemia. Total body potassium stores are approximately 3000 meq or more (50 to 75 meq/kg body weight) [1]. In contrast to sodium, which is the major cation in the extracellular fluid and has a much lower concentration in the cells, potassium is primarily an intracellular cation, with the cells containing approximately 98 percent of body potassium. The intracellular potassium concentration is approximately 140 meq/L compared with 4 to 5 meq/L in the extracellular fluid. The difference in distribution of the two cations is maintained by the Na-K-ATPase pump in the cell membrane, which pumps sodium out of and potassium into the cell in a 3:2 ratio. The ratio of the potassium concentrations in the cells and the extracellular fluid is the major determinant of the resting membrane potential across the cell membrane, which sets the stage for the generation of the action potential that is e Continue reading >>

How Does Diabetes Cause Hyperkalemia?

How Does Diabetes Cause Hyperkalemia?

Potassium and Hyperkalemia Potassium is a mineral in your body cells that performs several important body functions. Hyperkalemia is the condition when your blood has too much potassium in it. Adrenal glands are tiny structures that sit on the top parts of your kidneys. They secrete (hide and release) a chemical called “aldosterone”. Aldosterone signals the kidneys to release potassium along with urine. By doing so, the body is able to keep up a constant level of potassium in the blood. However, if your adrenals are not working properly, the levels of aldosterone start to fall and your kidneys are no longer able to release the potassium in your urine. When aldosterone starts to fall and the kidneys are no longer able to release potassium in the urine, the potassium starts to accumulate in the blood causing hyperkalemia- high blood potassium. Why Diabetes Causes Hyperkalemia? If you have diabetes, your body is unable to produce insulin- the chemical that regulates sugar levels in your blood. This triggers the fat cells to break down and release ketones. Ketones are chemicals that increase the acidity of your blood. High blood acidity, combined with high blood sugar, acts to force the potassium in your body cells to move out into your blood. Therefore, the potassium content of your blood increases. Further, high blood glucose in diabetes is capable of destroying the blood vessels in the kidneys and the adrenal glands. This reduces their capacity to release potassium with urine and eventually you develop hyperkalemia. This is how your diabetes may lead to hyperkalemia. Symptoms of hyperkalemia are: Muscle Fatigue Weakness Paralysis Heart beating in an irregular way Nausea If you have any of these symptoms, talk to your doctor. Your doctor may order blood tests to diagn Continue reading >>

Chapter 4. Disorders Of Potassium Balance: Hypokalemia & Hyperkalemia

Chapter 4. Disorders Of Potassium Balance: Hypokalemia & Hyperkalemia

Potassium is the principal cation of the intracellular fluid (ICF) where its concentration is between 120 and 150 mEq/L. The extracellular fluid (ECF) and plasma potassium concentration [K] is much lower—in the 3.5–5.0 mEq/L range. The very large transcellular gradient is maintained by active K transport via the Na-K-ATPase pumps present in all cell membranes and the ionic permeability characteristics of these membranes. The resulting greater than 40-fold transmembrane [K] gradient is the principal determinant of the transcellular resting potential gradient, about −90 mV with the cell interior negative (Figure 4–1). Normal cell function requires maintenance of the ECF [K] within a relatively narrow range. This is particularly important for excitable cells such as myocytes and neurons. The pathophysiologic effects of dyskalemia on these cells result in most of the clinical manifestations. Transcellular ion movement. Most cells contain these pumps, antiporters, and channels. The effects of insulin, catecholamines, and thyroid hormones on K transport are shown. Individual potassium intakes vary widely—a typical Western diet provides between 50 and 100 mEq K per day. Under steady-state conditions, an equal amount is excreted, mainly in urine (about 90%), and to a lesser extent in stool (5–10%) and sweat (1–10%). Normally, homeostatic mechanisms maintain plasma [K] precisely between 3.5 and 5.0 mEq/L. Rapid regulation of potassium concentration is needed to prevent potentially fatal hyperkalemia after every meal and is largely due to transcellular K shifts. The normal postprandial rise in insulin concentration moves both K and glucose into the intracellular compartment, where 98% of total body K (˜3000 mEq) is located. Postprandial insulin release is primarily Continue reading >>

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 >>

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 >>

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 >>

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 >>

Hypokalemia And Hyperkalemia

Hypokalemia And Hyperkalemia

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

Hyperkalemia And Hypokalemia

Hyperkalemia And Hypokalemia

Hyperkalemia is defined as a serum potassium concentration (serum [K+]) greater than 5.0 mEq/L. In critically ill patients, hyperkalemia is less frequent than hypokalemia but more likely to cause serious complications. Severe hyperkalemia requires rapid correction to prevent serious cardiovascular complications. The measured value for serum [K+] can be elevated as a result of in vitro phenomena, usually the release of K+ from cells during the clotting process. Pseudohyperkalemia should be recognized and considered in patients with marked elevations of white blood cell or platelet count.3 Simultaneous measurements of plasma (unclotted) and serum (clotted) [K+] should identify this problem. A serum [K+] that is 0.2 to 0.3 mEq/L greater than plasma [K+] is indicative of pseudohyperkalemia. Pseudohyperkalemia also may result from hemolysis of a blood specimen after collection; this event is usually identified in the laboratory and reported. True hyperkalemia occurs by two mechanisms: (1) impaired K+ excretion and (2) shifts in intracellular and extracellular K+ (Box 14-1). Renal insufficiency is the most common cause of altered K+ excretion. With acute oliguric renal failure, elevated potassium level, if not treated, is life threatening. In most patients with nonoliguric chronic renal failure, mild hyperkalemia is evident.4 With some causes of chronic renal failure, such as diabetes mellitus and tubulointerstitial diseases, hyperkalemia is more pronounced and is probably related to low circulating renin and aldosterone levels.5 Decreased aldosterone production promotes the development of hyperkalemia. Patients with acquired adrenal insufficiency develop hyperkalemia despite normal renal function. Various drugs used in the intensive care unit (ICU) can produce hyperkalemia b Continue reading >>

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 >>

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