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Why Is Bicarb Low In Dka

Pulmcrit – Four Dka Pearls

Pulmcrit – Four Dka Pearls

Introduction I have a confession to make: I love treating DKA. It’s satisfying to take a patient from severe acidosis, electrolytic disarray, and hypovolemia to normal physiology during an ICU shift. Although it's usually straightforward, there are some pitfalls and a few tricks that may help your patients improve faster.0 Pearl #1: Avoid normal saline A common phenomenon observed when starting a DKA resuscitation with normal saline (NS) is worseningof the patient’s acidosis with decreasing bicarbonate levels (example below). This occurs despite an improvement in the anion gap, and is explained by a hyperchloremic metabolic acidosis caused by bolusing with NS. This could be a real problem for a patient whose initial bicarbonate level is extremely low.1 A while ago I made the switch from NS to lactated ringers (LR) for resuscitation of DKA patients, and have not observed this phenomenon when using LR. Example of the effect of normal saline resuscitation during the initial phase of DKA resuscitation. This patient received approximately 3 liters normal saline between admission labs and the next set of labs as well as an insulin infusion, all textbook management per American Diabetes Association guidelines. The anion gap decreased from 33 mEq/L to 30 mEq/L, indicating improvement of ketoacidosis. However, the bicarbonate decreased from 8 mEq/L to 5 mEq/L due to a hyperchloremic metabolic acidosis caused by the normal saline. Note the increase in chloride over four hours. Failure of the potassium to decrease significantly despite insulin infusion may reflect potassium shifting out of the cells in response to the hyperchloremic metabolic acidosis. There is only one randomized controlled trial comparing NS to LR for resuscitation in DKA (Zyl et al, 2011). These authors fou Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

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

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

Diabetic Ketoacidosis

Initial Evaluation Initial evaluation of patients with DKA includes diagnosis and treatment of precipitating factors (Table 14–18). The most common precipitating factor is infection, followed by noncompliance with insulin therapy.3 While insulin pump therapy has been implicated as a risk factor for DKA in the past, most recent studies show that with proper education and practice using the pump, the frequency of DKA is the same for patients on pump and injection therapy.19 Common causes by frequency Other causes Selected drugs that may contribute to diabetic ketoacidosis Infection, particularly pneumonia, urinary tract infection, and sepsis4 Inadequate insulin treatment or noncompliance4 New-onset diabetes4 Cardiovascular disease, particularly myocardial infarction5 Acanthosis nigricans6 Acromegaly7 Arterial thrombosis, including mesenteric and iliac5 Cerebrovascular accident5 Hemochromatosis8 Hyperthyroidism9 Pancreatitis10 Pregnancy11 Atypical antipsychotic agents12 Corticosteroids13 FK50614 Glucagon15 Interferon16 Sympathomimetic agents including albuterol (Ventolin), dopamine (Intropin), dobutamine (Dobutrex), terbutaline (Bricanyl),17 and ritodrine (Yutopar)18 DIFFERENTIAL DIAGNOSIS Three key features of diabetic acidosis are hyperglycemia, ketosis, and acidosis. The conditions that cause these metabolic abnormalities overlap. The primary differential diagnosis for hyperglycemia is hyperosmolar hyperglycemic state (Table 23,20), which is discussed in the Stoner article21 on page 1723 of this issue. Common problems that produce ketosis include alcoholism and starvation. Metabolic states in which acidosis is predominant include lactic acidosis and ingestion of drugs such as salicylates and methanol. Abdominal pain may be a symptom of ketoacidosis or part of the inci Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic Ketoacidosis Definition Diabetic ketoacidosis is a dangerous complication of diabetes mellitus in which the chemical balance of the body becomes far too acidic. Description Diabetic ketoacidosis (DKA) always results from a severe insulin deficiency. Insulin is the hormone secreted by the body to lower the blood sugar levels when they become too high. Diabetes mellitus is the disease resulting from the inability of the body to produce or respond properly to insulin, required by the body to convert glucose to energy. In childhood diabetes, DKA complications represent the leading cause of death, mostly due to the accumulation of abnormally large amounts of fluid in the brain (cerebral edema). DKA combines three major features: hyperglycemia, meaning excessively high blood sugar kevels; hyperketonemia, meaning an overproduction of ketones by the body; and acidosis, meaning that the blood has become too acidic. Insulin deficiency is responsible for all three conditions: the body glucose goes largely unused since most cells are unable to transport glucose into the cell without the presence of insulin; this condition makes the body use stored fat as an alternative source instead of the unavailable glucose for energy, a process that produces acidic ketones, which build up because they require insulin to be broken down. The presence of excess ketones in the bloodstream in turn causes the blood to become more acidic than the body tissues, which creates a toxic condition. Causes and symptoms DKA is most commonly seen in individuals with type I diabetes, under 19 years of age and is usually caused by the interruption of their insulin treatment or by acute infection or trauma. A small number of people with type II diabetes also experience ketoacidosis, but this is rare give 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 >>

Bicarbonate In Diabetic Ketoacidosis - A Systematic Review

Bicarbonate In Diabetic Ketoacidosis - A Systematic Review

Abstract This study was designed to examine the efficacy and risk of bicarbonate administration in the emergent treatment of severe acidemia in diabetic ketoacidosis (DKA). PUBMED database was used to identify potentially relevant articles in the pediatric and adult DKA populations. DKA intervention studies on bicarbonate administration versus no bicarbonate in the emergent therapy, acid-base studies, studies on risk association with cerebral edema, and related case reports, were selected for review. Two reviewers independently conducted data extraction and assessed the citation relevance for inclusion. From 508 potentially relevant articles, 44 were included in the systematic review, including three adult randomized controlled trials (RCT) on bicarbonate administration versus no bicarbonate in DKA. We observed a marked heterogeneity in pH threshold, concentration, amount, and timing for bicarbonate administration in various studies. Two RCTs demonstrated transient improvement in metabolic acidosis with bicarbonate treatment within the initial 2 hours. There was no evidence of improved glycemic control or clinical efficacy. There was retrospective evidence of increased risk for cerebral edema and prolonged hospitalization in children who received bicarbonate, and weak evidence of transient paradoxical worsening of ketosis, and increased need for potassium supplementation. No studies involved patients with an initial pH < 6.85. The evidence to date does not justify the administration of bicarbonate for the emergent treatment of DKA, especially in the pediatric population, in view of possible clinical harm and lack of sustained benefits. Introduction Diabetic ketoacidosis (DKA) is a serious medical emergency resulting from relative or absolute insulin deficiency and the u Continue reading >>

* Diabetic Ketoacidosis

* Diabetic Ketoacidosis

* Diabetic Ketoacidosis #155767 malak - 01/24/07 22:35 Diabetic Ketoacidosis In children under 10 years of age, diabetic ketoacidosis causes 70% of diabetes-related deaths. Diabetic ketoacidosis is defined by the triad of hyperglycemia, acidosis, and ketosis. Clinical Presentation Diabetes is newly diagnosed in 20% of cases of diabetic ketoacidosis. The remainder of cases occur in known diabetics in whom ketosis develops because of a precipitating factor, such as infection or noncompliance with insulin. Symptoms of DKA include polyuria, polydipsia, fatigue, nausea, and vomiting, developing over 1 to 2 days. Abdominal pain is prominent in 25%. Physical Exam Patients are typically flushed, tachycardic, and tachypneic. Kussmaul's respiration, with deep breathing and air hunger, occurs when the serum pH is between 7.0 and 7.24. A fruity odor on the breath indicates the presence of acetone, a by-product of diabetic ketoacidosis. Fever is seldom present even though infection is common. Hypothermia and hypotension may also occur. Eighty percent of patients with diabetic ketoacidosis have altered mental status. Most are awake but confused; 10% are comatose. Laboratory Findings Serum glucose level >250 mg/dL pH <7.35 Bicarbonate level below normal with an elevated anion gap Presence of ketones in the serum Indications for Hospital Admission of Patients with Diabetic Ketoacidosis Hyperglycemia (glucose >250 mg/dL) Arterial pH <7.35, or venous pH <7.30, or serum bicarbonate <15 mEq/L Ketonuria, ketonemia, or both Differential Diagnosis Differential Diagnosis of Ketosis-Causing Conditions Alcoholic ketoacidosis does not cause an elevated serum glucose. Alcoholic ketoacidosis occurs with heavy drinking and vomiting. Starvation ketosis occurs after 24 hours without food and is not us Continue reading >>

Hyperglycemic Crises In Diabetes

Hyperglycemic Crises In Diabetes

Ketoacidosis and hyperosmolar hyperglycemia are the two most serious acute metabolic complications of diabetes, even if managed properly. These disorders can occur in both type 1 and type 2 diabetes. The mortality rate in patients with diabetic ketoacidosis (DKA) is <5% in experienced centers, whereas the mortality rate of patients with hyperosmolar hyperglycemic state (HHS) still remains high at ∼15%. The prognosis of both conditions is substantially worsened at the extremes of age and in the presence of coma and hypotension (1–10). This position statement will outline precipitating factors and recommendations for the diagnosis, treatment, and prevention of DKA and HHS. It is based on a previous technical review (11), which should be consulted for further information. PATHOGENESIS Although the pathogenesis of DKA is better understood than that of HHS, the basic underlying mechanism for both disorders is a reduction in the net effective action of circulating insulin coupled with a concomitant elevation of counterregulatory hormones, such as glucagon, catecholamines, cortisol, and growth hormone. These hormonal alterations in DKA and HHS lead to increased hepatic and renal glucose production and impaired glucose utilization in peripheral tissues, which result in hyperglycemia and parallel changes in osmolality of the extracellular space (12,13). The combination of insulin deficiency and increased counterregulatory hormones in DKA also leads to the release of free fatty acids into the circulation from adipose tissue (lipolysis) and to unrestrained hepatic fatty acid oxidation to ketone bodies (β-hydroxybutyrate [β-OHB] and acetoacetate), with resulting ketonemia and metabolic acidosis. On the other hand, HHS may be caused by plasma insulin concentrations that are in Continue reading >>

Electrolyte Imbalance In Diabetic Ketoacidosis

Electrolyte Imbalance In Diabetic Ketoacidosis

If you have diabetes, it's important to be familiar with diabetic ketoacidosis (DKA). DKA is a serious complication of diabetes that occurs when lack of insulin and high blood sugar lead to potentially life-threatening chemical imbalances. The good news is DKA is largely preventable. Although DKA is more common with type 1 diabetes, it can also occur with type 2 diabetes. High blood sugar causes excessive urination and spillage of sugar into the urine. This leads to loss of body water and dehydration as well as loss of important electrolytes, including sodium and potassium. The level of another electrolyte, bicarbonate, also falls as the body tries to compensate for excessively acidic blood. Video of the Day Insulin helps blood sugar move into cells, where it is used for energy production. When insulin is lacking, cells must harness alternative energy by breaking down fat. Byproducts of this alternative process are called ketones. High concentrations of ketones acidify the blood, hence the term "ketoacidosis." Acidosis causes unpleasant symptoms like nausea, vomiting and rapid breathing. Bicarbonate is an electrolyte that normally counteracts blood acidity. In DKA, the bicarbonate level falls as ketone production increases and acidosis progresses. Treatment of DKA includes prompt insulin supplementation to lower blood sugar, which leads to gradual restoration of the bicarbonate level. Potassium may be low in DKA because this electrolyte is lost due to excessive urination or vomiting. When insulin is used to treat DKA, it can further lower the blood potassium by pushing it into cells. Symptoms associated with low potassium include fatigue, muscle weakness, muscle cramps and an irregular heart rhythm. Severely low potassium can lead to life-threatening heart rhythm abnorm Continue reading >>

Emergency Management Of Diabetic Ketoacidosis In Adults

Emergency Management Of Diabetic Ketoacidosis In Adults

Diabetic ketoacidosis (DKA) is a potentially fatal metabolic disorder presenting most weeks in most accident and emergency (A&E) departments.1 The disorder can have significant mortality if misdiagnosed or mistreated. Numerous management strategies have been described. Our aim is to describe a regimen that is based, as far as possible, on available evidence but also on our experience in managing patients with DKA in the A&E department and on inpatient wards. A literature search was carried out on Medline and the Cochrane Databases using “diabetic ketoacidosis” as a MeSH heading and as textword. High yield journals were hand searched. Papers identified were appraised in the ways described in the Users’ guide series published in JAMA. We will not be discussing the derangements in intermediary metabolism involved, nor would we suggest extrapolating the proposed regimen to children. Although some of the issues discussed may be considered by some to be outwith the remit of A&E medicine it would seem prudent to ensure that A&E staff were aware of the probable management of such patients in the hours after they leave the A&E department. AETIOLOGY AND DEFINITION DKA may be the first presentation of diabetes. Insulin error (with or without intercurrent illness) is the most common precipitating factor, accounting for nearly two thirds of cases (excluding those where DKA was the first presentation of diabetes mellitus).2 The main features of DKA are hyperglycaemia, metabolic acidosis with a high anion gap and heavy ketonuria (box 1). This contrasts with the other hyperglycaemic diabetic emergency of hyperosmolar non-ketotic hyperglycaemia where there is no acidosis, absent or minimal ketonuria but often very high glucose levels (>33 mM) and very high serum sodium levels (>15 Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

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 Pre-diabetes (Impaired Glucose Tolerance) article more useful, or one of our other health articles. See also the separate Childhood Ketoacidosis article. Diabetic ketoacidosis (DKA) is a medical emergency with a significant morbidity and mortality. It should be diagnosed promptly and managed intensively. DKA is characterised by hyperglycaemia, acidosis and ketonaemia:[1] Ketonaemia (3 mmol/L and over), or significant ketonuria (more than 2+ on standard urine sticks). Blood glucose over 11 mmol/L or known diabetes mellitus (the degree of hyperglycaemia is not a reliable indicator of DKA and the blood glucose may rarely be normal or only slightly elevated in DKA). Bicarbonate below 15 mmol/L and/or venous pH less than 7.3. However, hyperglycaemia may not always be present and low blood ketone levels (<3 mmol/L) do not always exclude DKA.[2] Epidemiology DKA is normally seen in people with type 1 diabetes. Data from the UK National Diabetes Audit show a crude one-year incidence of 3.6% among people with type 1 diabetes. In the UK nearly 4% of people with type 1 diabetes experience DKA each year. About 6% of cases of DKA occur in adults newly presenting with type 1 diabetes. About 8% of episodes occur in hospital patients who did not primarily present with DKA.[2] However, DKA may also occur in people with type 2 diabetes, although people with type 2 diabetes are much more likely to have a hyperosmolar hyperglycaemic state. Ketosis-prone type 2 diabetes tends to be more common in older, overweight, non-white people with type 2 diabetes, and DKA may be their Continue reading >>

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Diagnosis And Treatment Of Diabetic Ketoacidosis And The Hyperglycemic Hyperosmolar State

Go to: Pathogenesis In both DKA and HHS, the underlying metabolic abnormality results from the combination of absolute or relative insulin deficiency and increased amounts of counterregulatory hormones. Glucose and lipid metabolism When insulin is deficient, the elevated levels of glucagon, catecholamines and cortisol will stimulate hepatic glucose production through increased glycogenolysis and enhanced gluconeogenesis4 (Fig. 1). Hypercortisolemia will result in increased proteolysis, thus providing amino acid precursors for gluconeogenesis. Low insulin and high catecholamine concentrations will reduce glucose uptake by peripheral tissues. The combination of elevated hepatic glucose production and decreased peripheral glucose use is the main pathogenic disturbance responsible for hyperglycemia in DKA and HHS. The hyperglycemia will lead to glycosuria, osmotic diuresis and dehydration. This will be associated with decreased kidney perfusion, particularly in HHS, that will result in decreased glucose clearance by the kidney and thus further exacerbation of the hyperglycemia. In DKA, the low insulin levels combined with increased levels of catecholamines, cortisol and growth hormone will activate hormone-sensitive lipase, which will cause the breakdown of triglycerides and release of free fatty acids. The free fatty acids are taken up by the liver and converted to ketone bodies that are released into the circulation. The process of ketogenesis is stimulated by the increase in glucagon levels.5 This hormone will activate carnitine palmitoyltransferase I, an enzyme that allows free fatty acids in the form of coenzyme A to cross mitochondrial membranes after their esterification into carnitine. On the other side, esterification is reversed by carnitine palmitoyltransferase I Continue reading >>

Acid–base Problems In Diabetic Ketoacidosis

Acid–base Problems In Diabetic Ketoacidosis

Disclosure forms provided by the authors are available with the full text of this article at NEJM.org. Dr. Halperin reports holding a patent on the use of sodium-linked glucose transporter 2 inhibitors to increase the excretion of water in patients with hyponatremia (US 8,518,895,B2) and a pending patent application on the use of sodium-linked glucose transporter 2 inhibitors to increase urine volume and lower solute concentration in the urine (08578 11286 PSP). No other potential conflict of interest relevant to this article was reported. We thank Drs. Arlan Rosenbloom, Brian Robinson, and Robert Jungas for their critique and helpful suggestions in the preparation of an earlier version of the manuscript, and S.Y. Lee for secretarial assistance. From the Renal Division, St. Michael’s Hospital and University of Toronto, and Keenan Research Center, Li Ka Shing Knowledge Institute of St. Michael’s Hospital, University of Toronto, Toronto. Address reprint requests to Dr. Halperin at the Department of Medicine, University of Toronto Keenan Research Center, Li Ka Shing Knowledge Institute of St. Michael’s Hospital, 30 Bond St., Rm. 408, Toronto, ON M5B 1W8, Canada, or at [email protected] Continue reading >>

Diabetic Emergencies-diagnosis And Clinical Management: Diabetic Ketoacidosis In Adults, Part 2

Diabetic Emergencies-diagnosis And Clinical Management: Diabetic Ketoacidosis In Adults, Part 2

Hyperglycemia Hyperglycemia in DKA is the result of reduced glucose uptake and utilization from the liver, muscle, and fat tissue and increased gluconeogenesis as well as glycogenolysis. The lack of insulin results in an increase in gluconeogenesis, primarily in the liver but also in the kidney, and increased glycogenolysis in liver and muscle.8,9 In addition, the inhibitory effect of insulin on glucagon secretion is abolished and plasma glucagon levels increase. The increase of glucagon aggravates hyperglycemia by enhancing gluconeogenesis and glycogenolysis. In parallel, the increased concentrations of the other counter-regulatory hormones enhance further gluconeogenesis. In addition to increased gluconeogenesis, in DKA there is excess production of substances which are used as a substrate for endogenous glucose production. Thus, the amino acids glutamine and alanine increase because of enhanced proteolysis and reduced protein synthesis.8,9 Hyperglycemia-induced osmotic diuresis leads to dehydration, hyperosmolality, electrolyte loss (Na+, K +, Mg 2 +, PO 4 3+, Cl−, and Ca+), and eventually decline in glomerular filtration rate. With decline in renal function, glucosuria diminishes and hyperglycemia worsens. Dehydration results in augmentation of plasma osmolality, which results in water movement out of the cells to the extracellular space. Osmotic diuresis caused by hyperglycemia results in loss of sodium in urine; in addition, the excess of glucagon aggravates hyponatremia because it inhibits reabsorption of sodium in the kidneys. With impaired insulin action and hyperosmolality, utilization of potassium by skeletal muscles is markedly decreased leading to intracellular potassium deficiency. Potassium is also lost due to osmotic diuresis. In addition, metabolic ac Continue reading >>

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