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Does Ketoacidosis Cause Hypokalemia

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

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 >>

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 (dka)

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 >>

Starvation Ketoacidosis: A Cause Of Severe Anion Gap Metabolic Acidosis In Pregnancy

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 >>

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 >>

Episode 60.0 – Aggressive Resuscitation Of Diabetic Ketoacidosis

Episode 60.0 – Aggressive Resuscitation Of Diabetic Ketoacidosis

Show Notes Take Home Points DKA should be suspected in any patient with altered mental status and hyperglycemia. Get a VBG (ABG not necessary) to confirm the diagnosis. Hypokalemia kills in DKA. Aggresively replete potassium and consider holding insulin, which drops serum potassium, until K is greater than 3.5 The insulin bolus isn’t necessary and appears to cause more episodes of hypokalemia. Just start insulin as an infusion at 0.14 units/kg Be vigilant about cerebral edema. Any change or deterioration in mental status should prompt treatment and evaluation. Mannitol in the euvolemic, normotensive patient and 3% hypertonic saline in the hypotensive/hypovolemic patient Finally, don’t forge to always hunt down the underlying cause of the DKA. Infection and non-compliance is the most common so liberally administer broad spectrum antibiotics if you’ve got even a hint of infection brewing Additional Reading References Aurora S et al. Prevalence of hypokalemia in ED patients with diabetic ketoacidosis. Am J Emerg Med 2012; 30: 481-4. PMID: 21316179 Boyd JC et al. Relationship of potassium and magnesium concentrations in serum to cardiac arrhythmias. Clin Chem 1984; 30(5): 754-7. PMID: 6713638 Duhon B et al. Intravenous sodium bicarbonate therapy in severely acidotic diabetic ketoacidosis. Ann Pharmacother 2013; 47: 970-5. PMID: 23737516 Fagan MJ et al. Initial fluid resuscitation for patients with diabetic ketoacidosis: how dry arethey? Clin Ped 2008; 47(9): 851-6. PMID: Goyal N et al. Utility of Initial Bolus insulin in the treatment of diabetic ketoacidosis. J Emerg Med 2010; 38(4): 422-7. PMID: 18514472 Green SM et al. Failure of adjunctive bicarbonate to improve outcome in severe pediatric diabetic ketoacidosis. Ann Emergency Medicine 1998; 31: 41-48. PMID: 943734 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

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 >>

Cardiovascular Complications Of Ketoacidosis

Cardiovascular Complications Of Ketoacidosis

US Pharm. 2016;41(2):39-42. ABSTRACT: Ketoacidosis is a serious medical emergency requiring hospitalization. It is most commonly associated with diabetes and alcoholism, but each type is treated differently. Some treatments for ketoacidosis, such as insulin and potassium, are considered high-alert medications, and others could result in electrolyte imbalances. Several cardiovascular complications are associated with ketoacidosis as a result of electrolyte imbalances, including arrhythmias, ECG changes, ventricular tachycardia, and cardiac arrest, which can be prevented with appropriate initial treatment. Acute myocardial infarction can predispose patients with diabetes to ketoacidosis and worsen their cardiovascular outcomes. Cardiopulmonary complications such as pulmonary edema and respiratory failure have also been seen with ketoacidosis. Overall, the mortality rate of ketoacidosis is low with proper and urgent medical treatment. Hospital pharmacists can help ensure standardization and improve the safety of pharmacotherapy for ketoacidosis. In the outpatient setting, pharmacists can educate patients on prevention of ketoacidosis and when to seek medical attention. Metabolic acidosis occurs as a result of increased endogenous acid production, a decrease in bicarbonate, or a buildup of endogenous acids.1 Ketoacidosis is a metabolic disorder in which regulation of ketones is disrupted, leading to excess secretion, accumulation, and ultimately a decrease in the blood pH.2 Acidosis is defined by a serum pH <7.35, while a pH <6.8 is considered incompatible with life.1,3 Ketone formation occurs by breakdown of fatty acids. Insulin inhibits beta-oxidation of fatty acids; thus, low levels of insulin accelerate ketone formation, which can be seen in patients with diabetes. Extr 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 >>

Dka/hhns

Dka/hhns

Sort Metabolic acidosis HCO3 <22 pH <7.35 paCO2 normal (uncompensated) paCO2 <35 (partially compensated) pH 7.35-7.39 (acidic normal) & paCO2 <35 (fully compensated) "If ill, take your insulin and drink clear liquids with carbohydrate." The client must be familiar with "sick day" management. He should take his insulin, check his blood glucose every 1 to 4 hr, and if unable to eat solid food, take in small frequent amounts of fluids and glucose-containing beverages. Which of the following is an appropriate client instruction regarding DKA prevention? Abdominal pain The client with HHNS would not have abdominal pain, a symptom of acidosis. Confusion from dehydration would be present, as would thirst and frequent urination. Which of the following signs and symptoms is least likely in HHNS? Metabolic acidosis secondary to breakdown of fats for energy manifested by ketosis is most likely. Rapid, deep respirations (Kussmaul's respirations) will show compensation for the acidosis as the body "blows off" carbon dioxide, a respiratory acid. What type of acid-base imbalance is likely in a client with DKA? How would the nurse recognize compensation for this acid-base disorder? Physical and/or psychological stress stimulates the sympathetic nervous system's fight or flight response. This results in an increased production of catecholamines (epinephrine and norepinephrine), which stimulate the release of cortisol. This results in glycolysis, the breakdown of glycogen into glucose. What is the relationship between stress and blood glucose levels in a client with diabetes? The nurse's first action should be to assess whether the client is adherent to the currently prescribed diet and medications. The client's current diet and medication use have not been successful in keeping glucose Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious complication of diabetes mellitus and should be regarded as a medical emergency. DKA is defined as a severe metabolic acidosis of blood (pH <7.35) which occurs secondary to sustained fatty acid (ketones) release from fat stores in response to energy demands experienced by feline diabetic patients. Classically, DKA is characterised by metabolic acidosis, ketosis and ketonuria. It can sometimes be confused with feline hyperosmolar hyperglycaemic state. The two main ketones are acetoacetate and β-hydroxybutyrate, which are produced by the liver and serve as an energy source for tissue in times of low insulin levels. (prolonged fasting, starvation, diabetes mellitus) or insulin resistance[1]. Clinical signs Clinical signs include sudden collapse, dehydration, weakness, depression, vomiting, and an increased respiratory rate. DKA can occur at any age and there is no breed or gender predisposition with this disease. It appears commonly in obese cats or cats with a history of sudden weight gain. Concurrent disease predispose cats, especially diabetic ones to developing DKA. Concurrent illnesses include chronic renal disease, hepatic lipidosis, acute pancreatitis, bacterial or viral infections and neoplasia[2]. Hyperglycaemia and hypoinsulinaemia contribute significantly to a shift of potassium to the extracellular fluid. However, with rehydration, potassium ions are lost from the extracellular fluid and hypokalemia develops rapidly. Insulin therapy may worsen hypokalemia because insulin shifts potassium into cells. The most important clinical significance of hypokalemia in DKA is profound muscle weakness, which may result in ventroflexion of the neck and, in extreme cases, respiratory paralysis. In one study of cats with DKA, most cats Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

4 Evaluation 5 Management Defining features include hyperglycemia (glucose > 250mg/dl), acidosis (pH < 7.3), and ketonemia/ketonuria Leads to osmotic diuresis and depletion of electrolytes including sodium, magnesium, calcium and phosphorous. Further dehydration impairs glomerular filtration rate (GFR) and contributes to acute renal failure Due to lipolysis / accumulation of of ketoacids (represented by increased anion gap) Compensatory respiratory alkalosis (i.e. tachypnea and hyperpnea - Kussmaul breathing) Breakdown of adipose creates first acetoacetate leading to conversion to beta-hydroxybutyrate Causes activation of RAAS in addition to the osmotic diuresis Cation loss (in exchange for chloride) worsens metabolic acidosis May be the initial presenting of an unrecognized T1DM patient Presenting signs/symptoms include altered mental status, tachypnea, abdominal pain, hypotension, decreased urine output. Perform a thorough neurologic exam (cerebral edema increases mortality significantly, especially in children) Assess for possible inciting cause (especially for ongoing infection; see Differential Diagnosis section) Ill appearance. Acetone breath. Drowsiness with decreased reflexes Tachypnea (Kussmaul's breathing) Signs of dehydration with dry mouth and dry mucosa. Perform a thorough neurologic exam as cerebral edema increases mortality significantly, especially in children There may be signs from underlying cause (eg pneumonia) Differential Diagnosis Insulin or oral hypoglycemic medication non-compliance Infection Intra-abdominal infections Steroid use Drug abuse Pregnancy Diabetic ketoacidosis (DKA) Diagnosis is made based on the presence of acidosis and ketonemia in the setting of diabetes. Bicarb may be normal due to compensatory and contraction alcoholosis so the 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 >>

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