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What Causes The Fluid And Electrolyte Disturbances In Dka?

Diabetic Ketoacidosis

Diabetic Ketoacidosis

The Facts Diabetic ketoacidosis (DKA) is a condition that may occur in people who have diabetes, most often in those who have type 1 (insulin-dependent) diabetes. It involves the buildup of toxic substances called ketones that make the blood too acidic. High ketone levels can be readily managed, but if they aren't detected and treated in time, a person can eventually slip into a fatal coma. DKA can occur in people who are newly diagnosed with type 1 diabetes and have had ketones building up in their blood prior to the start of treatment. It can also occur in people already diagnosed with type 1 diabetes that have missed an insulin dose, have an infection, or have suffered a traumatic event or injury. Although much less common, DKA can occasionally occur in people with type 2 diabetes under extreme physiologic stress. Causes With type 1 diabetes, the pancreas is unable to make the hormone insulin, which the body's cells need in order to take in glucose from the blood. In the case of type 2 diabetes, the pancreas is unable to make sufficient amounts of insulin in order to take in glucose from the blood. Glucose, a simple sugar we get from the foods we eat, is necessary for making the energy our cells need to function. People with diabetes can't get glucose into their cells, so their bodies look for alternative energy sources. Meanwhile, glucose builds up in the bloodstream, and by the time DKA occurs, blood glucose levels are often greater than 22 mmol/L (400 mg/dL) while insulin levels are very low. Since glucose isn't available for cells to use, fat from fat cells is broken down for energy instead, releasing ketones. Ketones accumulate in the blood, causing it to become more acidic. As a result, many of the enzymes that control the body's metabolic processes aren't able Continue reading >>

The Pathophysiology Of Diabetic Ketoacidosis

The Pathophysiology Of Diabetic Ketoacidosis

People still die from diabetic ketoacidosis. Poor patient education is probably the mostimportant determinant of the incidence of the catastrophe that constitutes "DKA".In several series, only about a fifth of patients with DKA are first-time presenterswith recently acquired Type I diabetes mellitus. The remainder are recognised diabeticswho are either noncompliant with insulin therapy, or have serious underlying illess thatprecipitates DKA. Most such patients have type I ("insulin dependent", "juvenile onset") diabetes mellitus, but it has recently been increasingly recognised that patients with type II diabetes mellitusmay present with ketoacidosis, and that some such patients present with "typical hyperosmolar nonketotic coma", but on closer inspection have varying degrees of ketoacidosis. DKA is best seen as a disorder that follows on an imbalance between insulin levels andlevels of counterregulatory hormones. Put simply: "Diabetic ketoacidosis is due to a marked deficiency of insulin in the face of high levels of hormones thatoppose the effects of insulin, particularly glucagon. Even small amounts of insulin can turn off ketoacid formation". Many hormones antagonise the effects of insulin. These include: In addition, several cytokines such as IL1, IL6 and TNF alpha antagonise the effects ofinsulin. [J Biol Chem 2001 Jul 13;276(28):25889-93]It is thus not surprising that many causes of stress and/or the systemic inflammatory response syndrome,appear to precipitate DKA in patients lacking insulin. Mechanisms by which these hormones and cytokinesantagonise insulin are complex, including inhibition of insulin release (catecholamines), antagonistic metaboliceffects (decreased glycogen production, inhibition of glycolysis), and promotion of peripheral resistance tothe e Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

OVERVIEW potentially life-threatening complication of diabetes melitus resulting from the consequences of insulin deficiency Diagnostic criteria pH < 7.3 ketosis (ketonemia or ketonuria) HCO3 <15 mmol/L due to high anion gap metabolic acidosis (HAGMA) hyperglycemia (may be mild; euglycemic DKA can occur) PATHOGENESIS increased glucagon, cortisol, catcholamines, GH decreased insulin -> hyperglycaemia -> hyperosmolality + glycosuria -> electrolyte loss -> ketone production from metabolism of TG -> acidosis HISTORY dry, abdominal pain, polyuria, weight loss, coma risk factors: non-compliance, illness, newly diagnosed ROS to rule find out possible precipitant (infection, MI, pneumonia, GI illness) normal insulin regime diabetic control previous DKA’s/admissions previous ICU admissions EXAMINATION volume assessment signs of cause e.g. (infection) GCS work of breathing INVESTIGATIONS ABG electrolytes osmolality urinalysis: ketones pregnancy test standard investigations to rule out cause: FBC, ECG, CXR MANAGEMENT Goals (1) establish precipitant and treat (2) assess severity of metabolic derangement (3) cautious fluid resuscitation with replacement of body H2O (4) provision of insulin (5) replacement of electrolytes Resuscitate intubation for airway protection if required O2 as required IV access fluid boluses (20mL/kg boluses of NS/HMN) urinary catheter Acid-base and Electrolyte abnormalities will have a severe metabolic acidosis with probable incomplete respiratory compensation K+ may be normal but patient will have a whole body K+ deficiency -> needs to be replaced once < 5mmol/L -> use KH2PO4 Na+ may be deranged acidaemia rarely requires HCO3- therapy and will respond to other treatments Specific therapy start insulin infusion (avoid bolus) 0.1u/kg/hr aim to lower glucose Continue reading >>

Hyperglycemic Crises: Managing Acute Complications Of Diabetes

Hyperglycemic Crises: Managing Acute Complications Of Diabetes

Authors: Kim Cathcart, MS, RN, RRT | Cheryl Duksta, RN, ADN, M.Ed | Kate Biggs, RN, MSN Hyperglycemia occurs from time to time in all people with diabetes. However, at times, hyperglycemia can lead to acute, life-threatening complications known as Hyperglycemic Crises. This course is designed to educate healthcare professionals about the emergencies associated with hyperglycemic crises, including causes, diagnosis, treatment, and prevention of Hyperosmolar Hyperglycemic State (HHS) and Diabetic Ketoacidosis (DKA). Course objectives include: Paraphrase the pathophysiology of diabetic ketoacidosis (DKA) Interpret diagnostic findings related to DKA Relate the nurse’s role in caring for patients with diabetic complications About the Authors Kim Cathcart, MS, RN, RRT, started working in the field of inhalation therapy in 1976 and by 1979 had completed her first test to become a registered respiratory therapist. She earned a bachelor's degree in general studies and a master's degree in educational administration from the University of Dayton, and later she received her bachelor's degree in nursing from Wright State University. She has taught clinicals and labs in respiratory therapy and has served as a respiratory nurse liaison. Her nursing career includes work in skilled nursing, orthopedics, and med-surg/chemical detox. She has also worked as a diabetic resource nurse and in an infectious disease/HIV clinic. Her publishing credentials include articles on respiratory care, contributions to hospital publications, and a tribute in a nursing magazine. Cheryl Duksta, RN, ADN, M.Ed, is currently a critical care nurse in an intermediate care unit in Austin, Texas. She is an active member of the American Association of Critical-Care Nurses (AACN) Greater Austin chapter. A master' Continue reading >>

Diabetic Ketoacidosis Causes, Symptoms, Treatment, And Complications

Diabetic Ketoacidosis Causes, Symptoms, Treatment, And Complications

Diabetic ketoacidosis definition and facts Diabetic ketoacidosis is a life-threatening complication of type 1 diabetes (though rare, it can occur in people with type 2 diabetes) that occurs when the body produces high levels of ketones due to lack of insulin. Diabetic ketoacidosis occurs when the body cannot produce enough insulin. The signs and symptoms of diabetic ketoacidosis include Risk factors for diabetic ketoacidosis are type 1 diabetes, and missing insulin doses frequently, or being exposed to a stressor requiring higher insulin doses (infection, etc). Diabetic ketoacidosis is diagnosed by an elevated blood sugar (glucose) level, elevated blood ketones and acidity of the blood (acidosis). The treatment for diabetic ketoacidosis is insulin, fluids and electrolyte therapy. Diabetic ketoacidosis can be prevented by taking insulin as prescribed and monitoring glucose and ketone levels. The prognosis for a person with diabetic ketoacidosis depends on the severity of the disease and the other underlying medical conditions. What is diabetic ketoacidosis? Diabetic ketoacidosis (DKA) is a severe and life-threatening complication of diabetes. Diabetic ketoacidosis occurs when the cells in our body do not receive the sugar (glucose) they need for energy. This happens while there is plenty of glucose in the bloodstream, but not enough insulin to help convert glucose for use in the cells. The body recognizes this and starts breaking down muscle and fat for energy. This breakdown produces ketones (also called fatty acids), which cause an imbalance in our electrolyte system leading to the ketoacidosis (a metabolic acidosis). The sugar that cannot be used because of the lack of insulin stays in the bloodstream (rather than going into the cell and provide energy). The kidneys f Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Professor of Pediatric Endocrinology University of Khartoum, Sudan Introduction DKA is a serious acute complications of Diabetes Mellitus. It carries significant risk of death and/or morbidity especially with delayed treatment. The prognosis of DKA is worse in the extremes of age, with a mortality rates of 5-10%. With the new advances of therapy, DKA mortality decreases to > 2%. Before discovery and use of Insulin (1922) the mortality was 100%. Epidemiology DKA is reported in 2-5% of known type 1 diabetic patients in industrialized countries, while it occurs in 35-40% of such patients in Africa. DKA at the time of first diagnosis of diabetes mellitus is reported in only 2-3% in western Europe, but is seen in 95% of diabetic children in Sudan. Similar results were reported from other African countries . Consequences The latter observation is annoying because it implies the following: The late diagnosis of type 1 diabetes in many developing countries particularly in Africa. The late presentation of DKA, which is associated with risk of morbidity & mortality Death of young children with DKA undiagnosed or wrongly diagnosed as malaria or meningitis. Pathophysiology Secondary to insulin deficiency, and the action of counter-regulatory hormones, blood glucose increases leading to hyperglycemia and glucosuria. Glucosuria causes an osmotic diuresis, leading to water & Na loss. In the absence of insulin activity the body fails to utilize glucose as fuel and uses fats instead. This leads to ketosis. Pathophysiology/2 The excess of ketone bodies will cause metabolic acidosis, the later is also aggravated by Lactic acidosis caused by dehydration & poor tissue perfusion. Vomiting due to an ileus, plus increased insensible water losses due to tachypnea will worsen the state of dehydr Continue reading >>

Understanding The Presentation Of Diabetic Ketoacidosis

Understanding The Presentation Of Diabetic Ketoacidosis

Hypoglycemia, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS) must be considered while forming a differential diagnosis when assessing and managing a patient with an altered mental status. This is especially true if the patient has a history of diabetes mellitus (DM). However, be aware that the onset of DKA or HHNS may be the first sign of DM in a patient with no known history. Thus, it is imperative to obtain a blood glucose reading on any patient with an altered mental status, especially if the patient appears to be dehydrated, regardless of a positive or negative history of DM. In addition to the blood glucose reading, the history — particularly onset — and physical assessment findings will contribute to the formulation of a differential diagnosis and the appropriate emergency management of the patient. Pathophysiology of DKA The patient experiencing DKA presents significantly different from one who is hypoglycemic. This is due to the variation in the pathology of the condition. Like hypoglycemia, by understanding the basic pathophysiology of DKA, there is no need to memorize signs and symptoms in order to recognize and differentiate between hypoglycemia and DKA. Unlike hypoglycemia, where the insulin level is in excess and the blood glucose level is extremely low, DKA is associated with a relative or absolute insulin deficiency and a severely elevated blood glucose level, typically greater than 300 mg/dL. Due to the lack of insulin, tissue such as muscle, fat and the liver are unable to take up glucose. Even though the blood has an extremely elevated amount of circulating glucose, the cells are basically starving. Because the blood brain barrier does not require insulin for glucose to diffuse across, the brain cells are rece Continue reading >>

Diabetic Ketoacidosis And Cerebral Edema

Diabetic Ketoacidosis And Cerebral Edema

Elliot J. Krane, M.D. Departments of Pediatrics and Anesthesiology Stanford University Medical Center Introduction In 1922 Banting and Best introduced insulin into clinical practice. A decade later the first reported case of cerebral edema complicating diabetic ketoacidosis (DKA) was reported by Dillon, Riggs and Dyer writing in the pathology literature. While the syndrome of cerebral edema complicating DKA was either not seen, ignored, or was unrecognized by the medical community until 3 decades later when the complication was again reported by Young and Bradley at the Joslin Clinic, there has since been a flurry of case reports in the 1960's and 1970's and basic and clinical research from the 1970's to the 1990's leading to our present day acceptance of this as a known complication of DKA, or of the management of DKA. In fact, we now recognize that the cerebral complications of DKA (including much less frequent cerebral arterial infarctions, venous sinus thrombosis, and central nervous system infections) are the most common cause of diabetic-related death of young diabetic patients (1), accounting for 31% of deaths associated with DKA and 20% of all diabetic deaths, having surpassed aspiration, electrolyte imbalance, myocardial infarction, etc. Furthermore, diabetes mellitus remains an important cause of hospitalization of young children. The prevalence rate of diabetes continues to grow in all Western developed nations, nearly doubling every decade, resulting in 22,000 hospital admissions in children under 15 years of age for diabetes in the United States in 1994, the majority of which were due to ketoacidosis. With approximately 4 hospital admissions of children for DKA per 100,000 population per year (2), every PICU located in a major metropolitan center will conti 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 >>

Fluid And Electrolyte/acid-base Flashcards

Fluid And Electrolyte/acid-base Flashcards

1. 50 year old with pneumonia, diaphoresis and a high fever Rationale: Diaphoresis and high fever can lead to free water loss through the skin, resulting in hypernatremia. Loop diuretics are more likely to result in a hypovolemic hyponatremia. Diarrhea and vomitting cause both sodium and water losses. Clients with SIADH have hyponatremia due to increased water reabsorption in the renal tubules. A client is admitted with diabetic ketoacidosis and, with treatment, has a normal blood glucose, pH, and serum osmolality. During assessment, the client complains of weakness in the legs. Which of the following is a priority nursing intervention? 1. Request a physical therapy consult from the physician. 2. Ensure the client is safe from falls and check the most recent potassium level. 3. Allow uninterrupted rest periods throughout the day. 4. Encourage the client to increase intake of dairy products and green leafy vegetables. 2. Ensure the client is safe from falls and check the most recent potassium level. Rationale: In the treatment of diabetic ketoacidosis the blood sugar is lowered, the pH is corrected, and potassium moves back into the cells, resulting in low serum potassium. Client safety and the correction of low potassium levels are a priority. The weakness in the legs is a clinical manifestation of the hypokalemia. Dairy products and green, leafy vegetables are a source of calcium. A client with a potassium level of 5.5 mEq/L is to receive sodium polystyrene sulfonate (Kayexalate) orally. After administering the drug the priority nursing action is to monitor Normal serum potassium levels are 3.5 to 5.5 mEq/L. The nurse is caring for a bedridden client admitted with multiple myeloma and a serum calcium level of 13 mg/dL. Which of the following is the most appropriate nu Continue reading >>

Diabetic Ketoacidosis: A Serious Complication

Diabetic Ketoacidosis: A Serious Complication

A balanced body chemistry is crucial for a healthy human body. A sudden drop in pH can cause significant damage to organ systems and even death. This lesson takes a closer look at a condition in which the pH of the body is severely compromised called diabetic ketoacidosis. Definition Diabetic ketoacidosis, sometimes abbreviated as DKA, is a condition in which a high amount of acid in the body is caused by a high concentration of ketone bodies. That definition might sound complicated, but it's really not. Acidosis itself is the state of too many hydrogen ions, and therefore too much acid, in the blood. A pH in the blood leaving the heart of 7.35 or less indicates acidosis. Ketones are the biochemicals produced when fat is broken down and used for energy. While a healthy body makes a very low level of ketones and is able to use them for energy, when ketone levels become too high, they make the body's fluids very acidic. Let's talk about the three Ws of ketoacidosis: who, when, and why. Type one diabetics are the group at the greatest risk for ketoacidosis, although the condition can occur in other groups of people, such as alcoholics. Ketoacidosis usually occurs in type one diabetics either before diagnosis or when they are subjected to a metabolic stress, such as a severe infection. Although it is possible for type two diabetics to develop ketoacidosis, it doesn't happen as frequently. To understand why diabetic ketoacidosis occurs, let's quickly review what causes diabetes. Diabetics suffer from a lack of insulin, the protein hormone responsible for enabling glucose to get into cells. This inability to get glucose into cells means that the body is forced to turn elsewhere to get energy, and that source is fat. As anyone who exercises or eats a low-calorie diet knows, fa 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 >>

An Exceptional Case Of Diabetic Ketoacidosis

An Exceptional Case Of Diabetic Ketoacidosis

Copyright © 2017 Celine Van de Vyver 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. Abstract We present a case of diabetic ketoacidosis, known as one of the most serious metabolic complications of diabetes. We were confronted with rapid neurological deterioration and unseen glycaemic values, which reached almost 110 mmol/L, subsequently resulting in hyperkalaemia and life-threatening dysrhythmias. This is the first reported live case with such high values of blood glucose and a favourable outcome. 1. Introduction Diabetic ketoacidosis (DKA) is known as one of the most serious complications of diabetes, besides hyperosmolar hyperglycaemic syndrome (HHS), and it is associated with significant morbidity and mortality. The symptoms are often nonspecific and there are many diseases that mimic the presentation. The clinical course usually evolves within a short time frame (<24 h). DKA exists of a triad of uncontrolled hyperglycaemia, metabolic acidosis, and increased total body ketone concentration [1]. These three criteria are needed for diagnosis. The most common precipitating factors of DKA are infections and discontinuation of or inadequate insulin therapy. Mainstays of treatment are correction of hypovolemia and hyperglycaemia, rapid administration of insulin, and electrolyte management. Glycaemic values in DKA normally do not exceed 33 mmol/L. In contrast, blood glucose in HHS is often higher [2, 3]. We present a case of severe diabetic ketoacidosis with glycaemic values of almost 110 mmol/L, leading to neurologic sequelae and requiring more aggressive treatment. A similar case report detailing th 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 >>

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 >>

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