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Paradoxical Hyperkalemia In Dka

Management Of Adult Diabetic Ketoacidosis

Management Of Adult Diabetic Ketoacidosis

Go to: Abstract Diabetic ketoacidosis (DKA) is a rare yet potentially fatal hyperglycemic crisis that can occur in patients with both type 1 and 2 diabetes mellitus. Due to its increasing incidence and economic impact related to the treatment and associated morbidity, effective management and prevention is key. Elements of management include making the appropriate diagnosis using current laboratory tools and clinical criteria and coordinating fluid resuscitation, insulin therapy, and electrolyte replacement through feedback obtained from timely patient monitoring and knowledge of resolution criteria. In addition, awareness of special populations such as patients with renal disease presenting with DKA is important. During the DKA therapy, complications may arise and appropriate strategies to prevent these complications are required. DKA prevention strategies including patient and provider education are important. This review aims to provide a brief overview of DKA from its pathophysiology to clinical presentation with in depth focus on up-to-date therapeutic management. Keywords: DKA treatment, insulin, prevention, ESKD Go to: Introduction In 2009, there were 140,000 hospitalizations for diabetic ketoacidosis (DKA) with an average length of stay of 3.4 days.1 The direct and indirect annual cost of DKA hospitalizations is 2.4 billion US dollars. Omission of insulin is the most common precipitant of DKA.2,3 Infections, acute medical illnesses involving the cardiovascular system (myocardial infarction, stroke) and gastrointestinal tract (bleeding, pancreatitis), diseases of the endocrine axis (acromegaly, Cushing’s syndrome), and stress of recent surgical procedures can contribute to the development of DKA by causing dehydration, increase in insulin counter-regulatory hor Continue reading >>

Canine Diabetic Ketoacidosis - Acvim 2008 - Vin

Canine Diabetic Ketoacidosis - Acvim 2008 - Vin

Diabetic ketoacidosis (DKA) is a severe form of complicated diabetes mellitus (DM) which requires emergency care. Ketones are synthesized from fatty acids as a substitute form of energy, because glucose is not effectively entered into the cells. Excess keto-acids results in acidosis and severe electrolyte abnormalities, which can be life threatening. Ketone bodies are synthesized as an alternative source of energy, when intracellular glucose concentration can not meet metabolic demands. Ketone bodies are synthesized from acetyl-CoA which is a product of mitochondrial -oxidation of fatty acids. Synthesis of acetyl-CoA is facilitated by decreased insulin concentration and increased glucagon concentration. In non-diabetics acetyl-CoA and pyruvate enter the citric acid cycle to form ATP. However, in diabetics, production of pyruvate by glycolysis is decreased. The activity of the citric acid cycle is therefore diminished resulting in decreased utilization of Acetyl-CoA. The net effect of increased production and decreased utilization of acetyl-CoA is an increase in the concentration of acetyl-CoA which is the precursor for ketone body synthesis.1 The three ketone bodies synthesized from acetyl-CoA include beta hydroxybutyrate, acetoacetate, and acetone. Acetoacetate and beta-hydroxybutyrate are anions of moderately strong acids. Therefore, accumulation of these ketone bodies results in ketotic acidosis. Metabolic acidosis and the electrolyte abnormalities which ensue are important determinants in the outcome of patients with DKA.2 One of the beliefs regarding the pathophysiology of DKA had been that individuals that develop DKA have zero or undetectable endogenous insulin concentration. However, in a study that included 7 dogs with DKA it was shown that 5 of 7 dogs with DK Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Figure 3. Timeline in DKA management. GCS:Glascow Coma Scale, CBC:Complete Blood Counting, ECG:Electrocardiogram, HR:Heart Rate, BP:Blood Pressure, BUN:Blood Urea Nitrogen, Cr: Creatinine, WBC:White Blood Cell, CRP:C-reactive protein, CE:Cerebral edema (adapted from reference 165) Figure 4. A 15 years old male patient firstly diagnosed T1DM with DKA infected by rhino-orbita-cerebral mucormycozis (Picture from the reference [218]) 1. Introduction A chronic autoimmune destruction of the pancreatic beta cells results in decreasing endogenous insulin secretion and the clinical manifestation of type 1 diabetes mellitus (T1DM). The clinical onset of the disease is often acute in children and adolescents and diabetic ketoacidosis (DKA) is present in 20-74% of the patients [1-7]. DKA is a serious condition that requiring immediate intervention. Even with appropriate intervention, DKA is associated with significant morbidity and possible mortality in diabetic patients in the pediatric age group [8]. Young age and female sex have been associated with an increased frequency of DKA [3,9]. The triad of uncontrolled hyperglycemia, metabolic acidosis and increased total body ketone concentration characterizes DKA [10]. In addition to possible acute complications, it may also influence the later outcome of diabetes [11]. 2. Epidemiology Worldwide, an estimated 65 000 children under 15 years old develop T1DM each year, and the global incidence in children continues to increase at a rate of 3% a year [12,13]. The current incidence in the UK is around 26/100 000 per year [14]. Patterson et al. were aimed to establish 15-year incidence trends for childhood T1DM in European centres with EURODIAB study. 29 311 new cases of T1DM were diagnosed in children before their 15th birthday during a 1 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 >>

Treatment And Prevention Of Hyperkalemia In Adults

Treatment And Prevention Of Hyperkalemia In Adults

INTRODUCTION Hyperkalemia is a common clinical problem that is most often a result of impaired urinary potassium excretion due to acute or chronic kidney disease (CKD) and/or disorders or drugs that inhibit the renin-angiotensin-aldosterone system (RAAS). Therapy for hyperkalemia due to potassium retention is ultimately aimed at inducing potassium loss [1,2]. In some cases, the primary problem is movement of potassium out of the cells, even though the total body potassium may be reduced. Redistributive hyperkalemia most commonly occurs in uncontrolled hyperglycemia (eg, diabetic ketoacidosis or hyperosmolar hyperglycemic state). In these disorders, hyperosmolality and insulin deficiency are primarily responsible for the transcellular shift of potassium from the cells into the extracellular fluid, which can be reversed by the administration of fluids and insulin. Many of these patients have a significant deficit in whole body potassium and must be monitored carefully for the development of hypokalemia during therapy. (See "Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment", section on 'Potassium replacement'.) The treatment and prevention of hyperkalemia will be reviewed here. The causes, diagnosis, and clinical manifestations of hyperkalemia are discussed separately. (See "Causes and evaluation of hyperkalemia in adults" and "Clinical manifestations of hyperkalemia in adults".) DETERMINING THE URGENCY OF THERAPY The urgency of treatment of hyperkalemia varies with the presence or absence of the symptoms and signs associated with hyperkalemia, the severity of the potassium elevation, and the cause of hyperkalemia. Our approach to therapeutic urgency is as follows (algorithm 1): Continue reading >>

Diabetic Emergencies: Diabetic Ketoacidosis In Childhood And Adolescence, Part 3 Of 3

Diabetic Emergencies: Diabetic Ketoacidosis In Childhood And Adolescence, Part 3 Of 3

Severe acidosis is reversible by fluid and insulin replacement. Insulin stops lipolysis and further ketone production and allows ketoacids to be metabolized, generating bicarbonate.4 Moreover, treatment of hypovolemia improves tissue perfusion and renal function, thereby increasing the excretion of organic acids. Controlled trials have shown no clinical benefit from bicarbonate administration 3,4 and there are well-recognized serious adverse effects, including paradoxical CNS acidosis 28,29 and hypokalemia from rapid acidosis correction. 30,31 Nevertheless, there may be selected patients who may profit from cautious alkali administration, such as patients with severe acidemia (arterial pH < 6.9) in whom decreased cardiac contractility and peripheral vasodilatation can further impair tissue perfusion, and patients with life-threatening hyperkalemia. 4,32…. If bicarbonate is considered necessary, cautiously give 1-2 mmol/kg over 60 minutes. 3,4 Follow-up management — transition to per os fluid intake and SC insulin injections Oral fluids should be introduced only when substantial clinical improvement has occurred and when oral fluids are well tolerated; IV fluid administration should then be reduced. The most convenient time to change to SC insulin is just before a mealtime, provided that ketoacidosis has resolved (venous pH > 7.3 and serum bicarbonate > 18 mmol/L), plasma glucose is < 200 mg/dl (11.1 mmol/L), and oral fluid intake is well tolerated. To prevent rebound hyperglycemia, the first SC insulin injection should be given 15-30 minutes (with rapid-acting insulin analog) or 1-2 hours (with regular insulin) before stopping the insulin infusion to allow sufficient time for the insulin to be absorbed. With intermediate or long-acting insulin the overlap should be Continue reading >>

Topics By Science.gov

Topics By Science.gov

Bellazzini, Marc A; Meyer, Tom Hyperkalemia-induced electrocardiogram changes such as dysrhythmias and altered T wave morphology are well described in the medical literature. Pseudo-infarction hyperkalemia-induced changes are less well known, but present a unique danger for the clinician treating these critically ill patients. This article describes a case of pseudo anteroseptal myocardial infarction in a type 1 diabetic with hyperkalemia. The most common patterns of pseudo-infarct and their associated potassium concentrations are then summarized from a literature review of 24 cases. ... urine test is positive, contact your child's diabetes health care team. Tests done by a lab or hospital can confirm whether a child has diabetic ketoacidosis , if necessary. Some ... blood for ketones. Ask the diabetes health care team if such a meter is a good ... Katz, J. R.; Edwards, R.; Khan, M.; Conway, G. S. 1996-01-01 Diabetes in acromegaly is usually non-insulin dependent and is secondary to insulin resistance caused by growth hormone excess. Diabetic ketoacidosis is a result of relative insulin deficiency and is a rare feature of acromegaly. We describe a case of acromegaly presenting with diabetic ketoacidosis. We demonstrate that growth hormone excess can cause diabetic ketoacidosis in the presence of relative, but not absolute insulin deficiency. PMID:8944212 Gupta, Arvin; Rohrscheib, Mark; Tzamaloukas, Antonios H 2008-10-01 A patient on hemodialysis for end-stage renal disease secondary to diabetic nephropathy was admitted in a coma with Kussmaul breathing and hypertension (232/124 mmHg). She had extreme hyperglycemia (1884 mg/dL), acidosis (total CO(2) 4 mmol/L), hyperkalemia (7.2 mmol/L) with electrocardiographic abnormalities, and hypertonicity (330.7 mOsm/kg). Initial t Continue reading >>

Diabetic Ketoacidosis | Tintinallis Emergency Medicine: A Comprehensive Study Guide, 8e | Accessmedicine | Mcgraw-hill Medical

Diabetic Ketoacidosis | Tintinallis Emergency Medicine: A Comprehensive Study Guide, 8e | Accessmedicine | Mcgraw-hill Medical

Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus. DKA occurs predominantly in patients with type 1 (insulin-dependent) diabetes mellitus, but 10% to 30% of cases occur in newly diagnosed type 2 (noninsulin-dependent) diabetes mellitus, especially in African Americans and Hispanics. 1 , 2 Between 1993 and 2003, the yearly rate of U.S. ED visits for DKA was 64 per 10,000 with a trend toward an increased rate of visits among the African American population compared with the Caucasian population. 3 Europe has a comparable incidence. A better understanding of the pathophysiology of DKA and an aggressive, uniform approach to its diagnosis and management have reduced mortality to <5% of reported episodes in experienced centers. 4 However, mortality is higher in the elderly due to underlying renal disease or coexisting infection and in the presence of coma or hypotension. Figure 225-1 illustrates the complex relationships between insulin and counterregulatory hormones. DKA is a response to cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess ( Figure 225-1 ). Insulin is the only anabolic hormone produced by the endocrine pancreas and is responsible for the metabolism and storage of carbohydrates, fat, and protein. Counterregulatory hormones include glucagon, catecholamines, cortisol, and growth hormone. Complete or relative absence of insulin and the excess counterregulatory hormones result in hyperglycemia (due to excess production and underutilization of glucose), osmotic diuresis, prerenal azotemia, worsening hyperglycemia, ketone formation, and a wide-anion-gap metabolic acidosis. 4 Insulin deficiency. Pathogenesis of diabetic ketoacidosis secondary to relative insulin def Continue reading >>

Usmle Endocrine I

Usmle Endocrine I

Home > Preview Clinical Features: coarse facial features, arthralgias, uncontrolled hypertension, enlargement of the digits·, carpal tunnel syndrome. This condition is caused by excessive secretion of growth hormone (GH), usually due to a pituitary somatotroph adenoma. Other common features include malocclusion of the jaw, hyperhidrosis, heart failure, macroglossia, and local mass-effect symptoms (eg, headache, visual field defects). GH stimulates hepatic insulin-like growth factor 1 (IGF-1) secretion, which is responsible for most of the clinical manifestations of acromegaly. IGF-1 levels in acromegaly are consistently elevated throughout the day. In contrast, GH levels can fluctuate widely and cannot be used alone to diagnose acromegaly. As a result, IGF-1 is the preferred initial test. Patients with elevated IGF-1 should undergo confirmatory testing with an oral glucose suppression test Once acromegaly is confirmed with a glucose suppression test, patients should have an MRI of the brain to identify a pituitary mass. Acromegaly causes concentric myocardial hypertrophy leading to diastolic dysfunction, along with left ventricular dilation and global hypokinesis. This cardiomyopathy is worsened by concurrent hypertension, obstructive sleep apnea , and valvular heart disease, which are common in acromegaly. Complications include heart failure (eg, dyspnea, crackles at bases) and arrhythmias. Cardiovascular disease is the leading cause of death in patients with acromegaly, but normalization of growth hormone levels following successful treatment markedly reduces cardiovascular mortality. a congenital cardiomyopathy that should be distinguished from myocardial hypertrophy due to other cardiovascular diseases (eg, hypertensive, valvular, ischemic) - is characterized by as Continue reading >>

Hyperkalemia (high Blood Potassium)

Hyperkalemia (high Blood Potassium)

How does hyperkalemia affect the body? Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart. It is also important for normal transmission of electrical signals throughout the nervous system within the body. Normal blood levels of potassium are critical for maintaining normal heart electrical rhythm. Both low blood potassium levels (hypokalemia) and high blood potassium levels (hyperkalemia) can lead to abnormal heart rhythms. The most important clinical effect of hyperkalemia is related to electrical rhythm of the heart. While mild hyperkalemia probably has a limited effect on the heart, moderate hyperkalemia can produce EKG changes (EKG is a reading of theelectrical activity of the heart muscles), and severe hyperkalemia can cause suppression of electrical activity of the heart and can cause the heart to stop beating. Another important effect of hyperkalemia is interference with functioning of the skeletal muscles. Hyperkalemic periodic paralysis is a rare inherited disorder in which patients can develop sudden onset of hyperkalemia which in turn causes muscle paralysis. The reason for the muscle paralysis is not clearly understood, but it is probably due to hyperkalemia suppressing the electrical activity of the muscle. Common electrolytes that are measured by doctors with blood testing include sodium, potassium, chloride, and bicarbonate. The functions and normal range values for these electrolytes are described below. Hypokalemia, or decreased potassium, can arise due to kidney diseases; excessive losses due to heavy sweating Continue reading >>

Chapter 225: Diabetic Ketoacidosis

Chapter 225: Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus. DKA occurs predominantly in patients with type 1 (insulin-dependent) diabetes mellitus, but 10% to 30% of cases occur in newly diagnosed type 2 (non–insulin-dependent) diabetes mellitus, especially in African Americans and Hispanics.1,2 Between 1993 and 2003, the yearly rate of U.S. ED visits for DKA was 64 per 10,000 with a trend toward an increased rate of visits among the African American population compared with the Caucasian population.3 Europe has a comparable incidence. A better understanding of the pathophysiology of DKA and an aggressive, uniform approach to its diagnosis and management have reduced mortality to <5% of reported episodes in experienced centers.4 However, mortality is higher in the elderly due to underlying renal disease or coexisting infection and in the presence of coma or hypotension. Figure 225-1 illustrates the complex relationships between insulin and counterregulatory hormones. DKA is a response to cellular starvation brought on by relative insulin deficiency and counterregulatory or catabolic hormone excess (Figure 225-1). Insulin is the only anabolic hormone produced by the endocrine pancreas and is responsible for the metabolism and storage of carbohydrates, fat, and protein. Counterregulatory hormones include glucagon, catecholamines, cortisol, and growth hormone. Complete or relative absence of insulin and the excess counterregulatory hormones result in hyperglycemia (due to excess production and underutilization of glucose), osmotic diuresis, prerenal azotemia, worsening hyperglycemia, ketone formation, and a wide-anion-gap metabolic acidosis.4 Insulin deficiency. Pathogenesis of diabetic ketoacidosis secondary to relative insulin deficienc Continue reading >>

Hypokalemia

Hypokalemia

Hypokalemia, also spelled hypokalaemia, is a low 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 below 3.5 mmol/L defined as hypokalemia.[1][2] Mildly low levels do not typically cause symptoms.[3] Symptoms may include feeling tired, leg cramps, weakness, and constipation.[1] It increases the risk of an abnormal heart rhythm, which are often too slow, and can cause cardiac arrest.[1][3] Causes of hypokalemia include diarrhea, medications like furosemide and steroids, dialysis, diabetes insipidus, hyperaldosteronism, hypomagnesemia, and not enough intake in the diet.[1] It is classified as severe when levels are less than 2.5 mmol/L.[1] Low levels can also be detected on an electrocardiogram (ECG).[1] Hyperkalemia refers to a high level of potassium in the blood serum.[1] The speed at which potassium should be replaced depends on whether or not there are symptoms or ECG changes.[1] Mildly low levels can be managed with changes in the diet.[3] Potassium supplements can be either taken by mouth or intravenously.[3] If given by intravenous, generally less than 20 mmol are given over an hour.[1] High concentration solutions (>40 mmol/L) should be given in a central line if possible.[3] Magnesium replacement may also be required.[1] Hypokalemia is one of the most common water–electrolyte imbalances.[4] It affects about 20% of people admitted to hospital.[4] The word "hypokalemia" is from hypo- means "under"; kalium meaning potassium, and -emia means "condition of the blood".[5] Play media Video explanation Signs and symptoms[edit] Mild hypokalemia is often without symptoms, although it may cause elevation of blood pressure,[6] and can provoke the development of an abnormal heart rhythm. Se 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 >>

Paradoxical Glucose-induced Hyperkalemia. Combined Aldosterone-insulin Deficiency.

Paradoxical Glucose-induced Hyperkalemia. Combined Aldosterone-insulin Deficiency.

Paradoxical glucose-induced hyperkalemia. Combined aldosterone-insulin deficiency. Goldfarb S , Strunk B , Singer I , Goldberg M . Severe hyperkalemia associated with spontaneous hyperglycemia as well as with the intravenous infusions of glucose occurred in an insulin-requiring diabetic patient in the absence of potassium administration, the use of diuretics which inhibit urinary potassium excretion or acidemia. Metabolic balance studies revealed, in addition to diabets, the presence of isolated aldosterone deficiency of the hyporeninemic type. Intravenous glucose infusions (0.5 g/kg body weight) produced significant hyperkalemia but desoxycortisone acetate (DOCA) therapy (10 mg/day) prevented the glucose-induced hyperkalemia. In this patient, the serum potassium concentration increases after the intravenous infusions of glucose because there is insufficient aldosterone and insulin to reverse the transfer of potassium to the extracellular fluid which normally occurs after hypertonic infusions of glucose. Although DOCA replacement modifies the distribution of potassium in the extracellular fluid and blunts the hyperkalemic effect of intravenous infusions of glucose, a rise in the insulin level is required for the usual hypokalemic response to intravenously administered glucose. These studies illustrate the risk of raising blood glucose levels in patients with combined aldosterone and insulin deficiency and the tendency towards hyperkalemia in diabetic patients under certain clinical conditions. Continue reading >>

Diabetic Ketoacidosis Dka

Diabetic Ketoacidosis Dka

Facts: Complication seen in patients with DM I Hyperglycemia-induced crisis Lack of available glucose, leads to breaking down of FAs Production of ketone bodies History / PE: H/O recent URI Mild leukocytosis Kussmaul respirations (rapid, deep breathing) Polyuria Dehydration Fruity, acetone breath odor Decreased level of consciousness Diffuse abdominal pain Diagnosis: Hyperglycemia (glucose > 250 mg/dL) Metabolic acidosis (pH<7.3 or bicarbonate < 15-20mmol/L) Plasma ketones Paradoxical hyperkalemia (extracellular K+ shift) Treatment: Normal (0.9%) saline (restore intravascular volume) Regular insulin (correct hyperglycemia) Potassium (correct electrolytes) Treat precipitating factors (eg. antibiotics ) Bicarbonate (if pH < 7.0) ***Best indicator of metabolic recovery is arterial ph or anion gap Associated With: Continue reading >>

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