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Cerebral Edema In Dka In Adults

Cerebral Edema In Diabetic Ketoacidosis

Cerebral Edema In Diabetic Ketoacidosis

The Journal of Clinical Endocrinology & Metabolism Department of Pediatrics Childrens Medical Services Center Gainesville, Florida 32608 Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 85, Issue 2, 1 February 2000, Pages 507508, Arlan L. Rosenbloom; Cerebral Edema in Diabetic Ketoacidosis, The Journal of Clinical Endocrinology & Metabolism, Volume 85, Issue 2, 1 February 2000, Pages 507508, INTRACEREBRAL complications during treatment for diabetic ketoacidosis (DKA), principally falling under the rubric cerebral edema, account for most diabetes-related mortality during childhood ( 1 , 2 ). In his presentation, Dr. Laurence Finberg opines that this problem can be prevented by avoiding ill-advised management of DKA and provides principles for appropriate therapy. Dr. Andrew Muir, while agreeing with the therapeutic wisdom of judicious fluid replacement, arrays considerable evidence that this will not prevent the problem. Let us consider two patients from my recent experience. A 14-month-old girl weighing 10 kg had newly diagnosed diabetes associated with bilateral otitis media. She was vomiting, dehydrated (estimated 10% with dry skin, delayed capillary refill, soft eyeballs), and listless but arousable. Serum glucose concentration was 22.7 mmol/L, sodium 132 mmol/L, and arterial pH 7.03. She was given 10 mL/kg 0.9% sodium chloride as an iv bolus, followed by 0.45% saline with added potassium at a rate that would result in replacement over 36 h. By the 5th h of treatment, her serum sodium level was 143 mmol/L and blood glucose 5.8 mmol/L, resulting in an increase in calculated serum osmolality from 294 to 299 mOsm/L. Ten percent dextrose was added to her iv fluid. By the 17th h, she was more alert, sitting up, and taki Continue reading >>

Dka And Cerebral Edema In Adults

Dka And Cerebral Edema In Adults

Mechanism of cerebral edema in children with diabetic Diabetic ketoacidosis. Cerebral Edema in Childhood Diabetic Ketoacidosis. The ideal treatment of cerebral edema in. S Medical Services Center Gainesville, Florida. Cerebral edema after treatment of dka and cerebral edema in adults DKA diabetes. Cerebral Edema in Diabetic Ketoacidosis Arlan. Futterweit and Sturman found an increase in cerebral synaptosomal taurine transport. Rosenbloom Department of Pediatrics Children. DKA is not established, but intravenous mannitol and hypertonic saline. Threatening if dka and cerebral edema in adults not treated properly. Start studying Kelso. S NCLEX Question Rationales. Learn vocabulary, terms, and more with flashcards, games, and other study tools. Diabetic ketoacidosiscerebral edema The Journal of Coma in Severe Diabetic Ketoacidosis. MECHANISM OF CEREBRAL EDEMA IN. Recognition and treatment of cerebral edema complicating diabetic ketoacidosis. Mechanism of Cerebral Edema in Children with Diabetic Ketoacidosis. Original Article from The New England Journal of. Cerebral Edema with Irreversible Coma in Severe Diabetic. Prevention of cerebral edema during DKA. Diabetic ketoacidosis is an emergency medical condition that can be life. Diabetic ketoacidosis. The incidence of this condition may be increasing, and a. Risk Factors for Cerebral. Is by nude sexy woman zorbabes a severe and life. Diabetic ketoacidosis occurs when the cells in our body do not receive the. Edema in Children with Diabetic Ketoacidosis. Patient Education Topics. Differential Diagnosis of Vomiting in the Pediatric. Learn vocabulary, terms, and more with flashcards, games, and other study tools. Type your keyword then click the. Start studying Adults Final. Differential diagnosis of vomiting in the pediatric a 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 Related Cerebral Edema

Diabetic Ketoacidosis Related Cerebral Edema

Diabetic Ketoacidosis Related Cerebral Edema Diabetic Ketoacidosis Related Cerebral Edema Aka: Diabetic Ketoacidosis Related Cerebral Edema, DKA related Cerebral Edema Incidence : 0.5 to 1% of Diabetic Ketoacidosis patients Younger children (<5 years old) with new onset of diabetes and longer duration of symptoms Rapid hydration has been postulated as cause Precautions regarding fluid rate and amount are standard of care in Diabetic Ketoacidosis management (see below) However large study did not show an association with fluid rate or amount V. Precautions: Children under age 5 years old with DKA Avoid large fluid boluses beyond initial 10-20 cc/kg if at all possible Avoid dropping Serum Osmolality (calc) >3 mOsms/hour Persistent vegatative state in up to one third of surviving children Aurora and Menchine in Herbert (2014) EM:Rap 14(1): 10-11 Images: Related links to external sites (from Bing) These images are a random sampling from a Bing search on the term "Diabetic Ketoacidosis Related Cerebral Edema." Click on the image (or right click) to open the source website in a new browser window. Search Bing for all related images Related Studies (from Trip Database) Open in New Window FPnotebook.com is a rapid access, point-of-care medical reference for primary care and emergency clinicians. Started in 1995, this collection now contains 6557 interlinked topic pages divided into a tree of 31 specialty books and 722 chapters. Content is updated monthly with systematic literature reviews and conferences. Although access to this website is not restricted, the information found here is intended for use by medical providers. Patients should address specific medical concerns with their physicians. This page was written by Scott Moses, MD , last revised on 12/4/2017 and last publi Continue reading >>

Laboratory Values And Treatment Associated With Dka-related Cerebral Edema [pediatrics Classics Series]

Laboratory Values And Treatment Associated With Dka-related Cerebral Edema [pediatrics Classics Series]

Image: PD 1. Among children admitted to 1 of 10 medical centers for diabetic ketoacidosis management, elevated serum urea nitrogen concentrations and low partial pressures of carbon dioxide were associated with significant increases in risk of developing cerebral edema. 2. Lack of pronounced serum sodium rise and use of bicarbonate for treatment were also associated with significantly increased cerebral edema risk. Original Date of Publication: January 2001 Study Rundown: Among children presenting in diabetic ketoacidosis (DKA) either during an initial type 1 diabetes mellitus I (T1DM) presentation, following bodily stresses, or medication noncompliance, 1% will experience cerebral edema. At the time of this study, mortality occurred in 40-90% of these individuals, accounting for 50-60% of T1DM-related childhood deaths. However, before this study’s publication, there was limited information regarding cerebral edema risk factors among children with T1DM. Researchers found that elevated serum nitrogen concentrations and low partial pressures of carbon dioxide were associated with significantly increased risk of children hospitalized for DKA developing cerebral edema. In addition, lack of pronounced increases in serum sodium with treatment and use of bicarbonate were also associated with significantly increased risk of cerebral edema development. This study is limited by an inability to detect the possible influence of other confounders as well as to detect the potential role of variables that did not produce noticeable changes in clinical data. This was the first large, controlled study to investigate the role of cerebral edema-associated risk factors among children being treated for DKA. It was proposed that each of these factors likely contributed to the development o Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Author: Osama Hamdy, MD, PhD; Chief Editor: Romesh Khardori, MD, PhD, FACP more... 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. The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Malaise, generalized weakness, and fatigability Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia Rapid weight loss in patients newly diagnosed with type 1 diabetes 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: Glaser NS, Marcin JP, Wootton-Gorges SL, et al. Correlation of clinical and biochemical findings with diabetic ketoacidosis-related cerebral edema in children using magnetic resonance diffusion-weighted imaging. J Pediatr. 2008 Jun 25. [Medline] . Umpierrez GE, Jones S, Smiley D, et al. Insulin analogs versus human insulin in the treatment of patients with diabetic ketoacidosis: a randomized controlled trial. Diabetes Care. 2009 Jul. 32(7):1164-9. [Medline] . [Full Text] . Herrington WG, Nye HJ, Hammersley MS, Watkinson PJ. Are arterial and venous samples clinically equivalent for the estimation 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 >>

An Adult Case Of Diabetic Ketoacidosis Presenting With Cerebral Edema - Case Report

An Adult Case Of Diabetic Ketoacidosis Presenting With Cerebral Edema - Case Report

An Adult Case of Diabetic Ketoacidosis Presenting with Cerebral Edema - Case Report Cerebral edema is a life-threatening complication of diabetic ketoacidosis (DKA) which may predominantly develop in pediatric cases during the management of DKA.. Symptomatic cerebral edema in children is rarely detected at admission, before initiation of the treatment. Cerebral edema associated with DKA is extremely rare in adults. Here, we report an adult patient with DKA who presented with symptomatic cerebral edema. Turk Jem 2009; 13: 16-8 Key words: Diabetes complications, cerebral edema Serebral dem diyabetik ketoasidozun (DKA) daha sklkla pediatrik olgularda tedavi srasnda gelien yaam tehdit eden bir komplikasyonudur. Nadiren, serebral dem ocuklarda tedaviye balanmadan nce (bavuru annda) tespit edilebilir. DKA ile ilikili serebral dem grlmesi erikinlerde olduka nadirdir. Bu yazmzda semptomatik serebral dem ile bavuran bir erikin DKA hastas sunuyoruz. Turk Jem 2009; 13: 16-8 Anahtar kelimeler: Diyabet komplikasyonlar, beyin demi Cerebral complications of diabetic ketoacidosis (DKA) are a common cause of deaths related to DKA (1,2). Cerebral edema associated with DKA occurs predominantly in children; however, few adult cases have been described (3,4). The frequency of DKA-associated symptomatic cerebral edema has been reported to be 1% in children (5). In most cases, clinical presentation of cerebral edema occurs during the treatment of DKA, usually several hours after initiation of therapy (3). There is, however, also radiological evidence that asymptomatic or subclinical cerebral edema commonly develops before or during the management of DKA (5-7). However, it is extremely rare for a case of DKA to present with cerebral edema before treatment for DKA. Here, we report an adult cas Continue reading >>

Aetiology Of Cerebral Oedema In Diabetic Ketoacidosis | Emergency Medicine Journal

Aetiology Of Cerebral Oedema In Diabetic Ketoacidosis | Emergency Medicine Journal

Aetiology of cerebral oedema in diabetic ketoacidosis Aetiology of cerebral oedema in diabetic ketoacidosis Department of Emergency Medicine, Royal Brisbane Hospital, Herston, Brisbane, Queensland 4029, Australia; af.brownuq.edu.au The excellent evidence based review of the emergency management of diabetic ketoacidosis (DKA) in adults by Hardern and Quinn perpetuates the premise that unnecessarily large volumes of intravenous fluids should be avoided because of the high case fatality rate of cerebral oedema. 1 This presupposes that the rate of fluid delivery is causally related to the development of cerebral oedema, which has not been proved. The large 15 year paediatric study in the USA that analysed 6977 hospitalisations for DKA found among the 61 cases of cerebral oedema (0.9%) that after multiple logistic-regression analysis with random and matched controls, the only variables statistically associated with cerebral oedema were higher initial serum urea nitrogen concentrations and lower partial pressures of carbon dioxide at presentation. 2 In addition, smaller increases in serum sodium concentration during treatment and the use of bicarbonate were also implicated. Importantly, the rate of fluid, sodium, and insulin administration were not associated with the development of cerebral oedema, nor was the initial serum glucose or its rate of change. Clearly these findings relate to patients aged 18 years or less but most occurrences of cerebral oedema in DKA are in children and adolescents, with only rare cases in adults. However, the underlying aetiology should be no different. One unifying hypothesis is that the cerebral oedema is related to cerebral vasoconstriction, brain ischaemia, and hypoxia, as hypocapnoea causing cerebral vasoconstriction and extreme dehydrati Continue reading >>

Diabetic Emergencies: Diabetic Ketoacidosis In Adults, Part 4

Diabetic Emergencies: Diabetic Ketoacidosis In Adults, Part 4

Treatment of Acidosis Most experts do not recommend the administration of bicarbonate because acidosis is corrected with insulin infusion and rehydration. The administration of bicarbonate in severe acidosis (pH less than 7.0) remains controversial.8 Severe metabolic acidosis exerts a negative inotropic effect on the heart, induces vasodilation and hypotension, reduces glucose uptake and utilization, and promotes ventricular arrhythmias.6 On the other hand, bicarbonate therapy may lead to worsening of hypokalemia (especially at the beginning of bicarbonate administration), intracellular acidosis in the central nervous system (paradoxical acidosis),27 and metabolic alkalosis.6 One study showed that bicarbonate administration had no benefits for patients with DKA and initial pH 6.9-7.15.28 However, in this trial the number of patients with pH in this range was very small. Based on existing evidence and expert opinion, it may be prudent to administer 50 mmol of bicarbonate in 200 ml water with 10 mEq of potassium chloride over 1 hour in patients whose pH is 6.9-7.0 or serum bicarbonate less than 5 mEq/L. In patients with pH less than 6.9, doubling of the above bicarbonate dose is recommended. Arterial pH should be monitored 2 hours later and the dose should be repeated if pH remains lower than 7.0.8,10 Electrolyte replacement Replacement of sodium and chloride deficits is achieved by the administration of normal saline as described above. Particular attention should be paid to potassium restoration. As mentioned, serum potassium concentrations are usually normal or increased despite the significant total body deficit. During treatment of DKA potassium levels are decreased, sometimes very quickly, because correction of acidosis and the insulin infusion move potassium into t Continue reading >>

Diabetic Ketoacidosis/cerebral Edema

Diabetic Ketoacidosis/cerebral Edema

How can diabetic ketoacidosisrelated cerebral edema be prevented? OVERVIEW: What every practitioner needs to know Are you sure your patient has diabetic ketoacidosisrelated cerebral edema? What are the typical findings for this disease? Cerebral edema is a potentially life-threatening complication of diabetic ketoacidosis (DKA) and is responsible for the majority of diabetes-related deaths in children. Cerebral edema typically occurs after several hours of treatment with insulin and intravenous fluids but can also occur at the time of presentation of DKA before treatment is started. The risk of cerebral edema is related to the severity of acidosis, hypocapnia, and dehydration at the time of presentation of DKA. Although severe, clinically apparent cerebral edema occurs in just 1% of DKA episodes in children, numerous studies have demonstrated that mild cerebral edema, associated with only minimal or no alterations in mental status, is present in the majority of children during DKA treatment. The relationship between intravenous fluid treatment and the risk of DKA-related cerebral edema is frequently debated; however, there are no clear associations between the use of particular fluid treatment protocols and increased risk of DKA-related cerebral edema. At present, whether and how cerebral edema can be prevented is unknown. Treatment for clinically apparent cerebral edema typically involves use of hyperosmolar agents (mannitol or hypertonic saline). DKA-related cerebral edema is a clinical diagnosis. Imaging studies may be helpful but are not always definitive. The most common symptoms of DKA-related cerebral edema include mental status changes (confusion, irritability, obtundation) associated with severe headache, recurrence of vomiting, seizures, hypertension, inappro Continue reading >>

Neurological Consequences Of Diabetic Ketoacidosis At Initial Presentation Of Type 1 Diabetes In A Prospective Cohort Study Of Children

Neurological Consequences Of Diabetic Ketoacidosis At Initial Presentation Of Type 1 Diabetes In A Prospective Cohort Study Of Children

OBJECTIVE To investigate the impact of new-onset diabetic ketoacidosis (DKA) during childhood on brain morphology and function. RESEARCH DESIGN AND METHODS Patients aged 6–18 years with and without DKA at diagnosis were studied at four time points: <48 h, 5 days, 28 days, and 6 months postdiagnosis. Patients underwent magnetic resonance imaging (MRI) and spectroscopy with cognitive assessment at each time point. Relationships between clinical characteristics at presentation and MRI and neurologic outcomes were examined using multiple linear regression, repeated-measures, and ANCOVA analyses. RESULTS Thirty-six DKA and 59 non-DKA patients were recruited between 2004 and 2009. With DKA, cerebral white matter showed the greatest alterations with increased total white matter volume and higher mean diffusivity in the frontal, temporal, and parietal white matter. Total white matter volume decreased over the first 6 months. For gray matter in DKA patients, total volume was lower at baseline and increased over 6 months. Lower levels of N-acetylaspartate were noted at baseline in the frontal gray matter and basal ganglia. Mental state scores were lower at baseline and at 5 days. Of note, although changes in total and regional brain volumes over the first 5 days resolved, they were associated with poorer delayed memory recall and poorer sustained and divided attention at 6 months. Age at time of presentation and pH level were predictors of neuroimaging and functional outcomes. CONCLUSIONS DKA at type 1 diabetes diagnosis results in morphologic and functional brain changes. These changes are associated with adverse neurocognitive outcomes in the medium term. The incidence of childhood-onset type 1 diabetes varies from 0.1 to 57.6 per 100,000 and is increasing worldwide (1). Long Continue reading >>

Cerebral Edema: A Complication Of Dka

Cerebral Edema: A Complication Of Dka

DKA, or diabetic ketoacidosis, is a severe life-threatening medical complication that must be treated by doctors in a hospital. DKA is a condition in which blood glucose levels have risen dangerously high due to lack of insulin and insulin resistance. Fat begins to break down in response to energy requirements leading to high ketone levels in the blood causing your blood to become too acidic. DKA sometimes leads to cerebral edema, which is brain swelling, and if left untreated, cerebral edema can cause brain damage or lead to death. Cerebral Edema: Its relationship to DKA In order to understand cerebral edema, you must understand diabetic ketoacidosis (DKA). DKA is a situation in which blood sugar levels rise to dangerous levels in response to a lack of insulin and insulin resistance. The liver keeps producing glucose, which collects in the blood. Normally, insulin will move that glucose out of the blood and into the cells that need it, but when there is insufficient insulin or significant insulin resistance, the glucose builds up to dangerous levels (severe hyperglycemia). Because the cells that need the glucose are not getting it (remember the glucose is stuck in the blood), they signal the body to produce more glucose through the breakdown of fat. The breakdown of fat results in fat components called ketones. When ketones continue to build up in your blood stream, the patient develops a condition called diabetic ketoacidosis or DKA. Symptoms include: Abdominal pain Signifant thirst Blurry vision Nausea and vomiting[1] Polyuria (Frequent urination) Polydipsia – excessive thirst that lasts for a day or more Weight loss Weakness Confusion Cold body temperature Acetone on the breath, Rapid breathing that is shallow then deep and labored– called Kussmaul’s respirati Continue reading >>

Cerebral Edema During Treatment Of Diabetic Ketoacidosis In An Adult With New Onset Diabetes.

Cerebral Edema During Treatment Of Diabetic Ketoacidosis In An Adult With New Onset Diabetes.

Cerebral edema during treatment of diabetic ketoacidosis in an adult with new onset diabetes. Department of Internal Medicine, Hartford Hospital, University of Connecticut School of Medicine, Hartford, CT, USA. Diabetic ketoacidosis (DKA) continues to be a medical emergency, in part because of a rare and devastating complication associated with its treatment, cerebral edema. In children, cerebral edema is the principal cause of mortality, but clinically significant cerebral edema in adults is rare. We report the case of a 27-year-old male (not previously known to be diabetic) who presented with a first episode of DKA complicated by the development of fatal cerebral edema despite medical treatment. The pathophysiological mechanisms for cerebral edema associated with DKA occurring in children and adults are believed to be similar and are discussed in this report. However, patients who develop cerebral edema may deteriorate rapidly, and experience with successful treatment has been limited. 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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