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Why Is Bun Elevated In Ketoacidosis

Lab Test

Lab Test

Measurement of serum or plasma blood urea nitrogen (BUN) for the evaluation and management of volume status and renal disorders. It is performed on patients undergoing routine laboratory testing and is usually performed as part of a multiphasic automated testing process. Adults: 10-20 mg/dL (3.6-7.1 mmol/L) Elderly: may be slightly higher than adult Children: 5-18 mg/dL (1.8-6.4 mmol/L) Infant: 5-18 mg/dL Newborn: 3-12 mg/dL Cord: 21-40 mg/dL Critical Values: >100 mg/dL (indicates serious impairment of renal function) Adrenal insufficiency - moderate elevations in BUN levels are consistent with both acute and chronic adrenal insufficiency. The increased Bun is largely due to dehydration secondary to aldosterone deficiency, which leads to excretion of sodium in excess of intake and results in azotemia. Patients with secondary adrenal insufficiency are less affected because of intact aldosterone secretion. Elevation is usually reversible with restoration of normal renal hemodynamics and circulating blood volume. Community-acquired pneumonia - In one study, an elevated BUN, along with increased respiratory rate and decreased diastolic blood pressure, was predictive of mortality in patients with community-acquired pneumonia. Hemolytic uremic syndrome (HUS) - BUN level is consistently increased with the elevation usually occurring very rapidly. The combination of renal insufficiency, a catabolic state, and reabsorption of blood from the GI tract can cause BUN levels to increase as much as 50 mg/dL/day. In children with uncomplicated dehydration and diarrhea, the BUN level should fall to one half the admission level within 24 hours; if this does not occur, renal disease should be suspected. Hemorrhagic shock - Acute tubular necrosis (ATN) from prolonged hypotension results in Continue reading >>

I’ll See Your Ketoacidosis And Raise You A Renal Failure

I’ll See Your Ketoacidosis And Raise You A Renal Failure

A while back I posted on a paper that appeared in The Lancet about an obese woman who came to the emergency room with gastroenteritis and was misdiagnosed as being in diabetic ketoacidosis (a life-threatening disorder). She was misdiagnosed because the pinheads covering the ER couldn’t get past the fact that she had been on a low-carb diet. At the time I posted on this travesty I noted that this Lancet paper would from here on out be waved in the face of anyone who was following or advocated a low-carb diet as proof that such a diet is dangerous and can cause diabetic ketoacidosis (DKA). Well, now we’ve got an answer. Next time someone tells you that it has been proven that low-carb diets are dangerous and can cause ketoacidosis, you can resort to poker terminology and reply that you’ll see their ketoacidosis and raise them a renal failure. A few days ago I got wind of a paper published a few years ago that can be used as a counterpoint to the above mentioned idiotic paper in The Lancet that has given low-carbers such a bad time. This paper, published in the journal Renal Failure in 1998, is, like the other paper, a case report. The short version is as follows: An obese young man arrived comatose in the emergency room. In an effort to lose weight he had been consuming a high-carbohydrate canned beverage as his sole source of nutrition for the two weeks prior. His blood sugar–at about 20 times normal–was extremely elevated and led to a diagnosis of diabetic ketoacidosis. The physicians on staff treated the patient appropriately, and he, over the next 20 hours or so, regained consciousness as his blood sugar levels and other lab parameters began to normalize. During a lab analysis 22 hours after admission the doctors found the patient to be breaking down and rel Continue reading >>

Understanding And Treating Diabetic Ketoacidosis

Understanding And Treating Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious metabolic disorder that can occur in animals with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient's response to therapy, technicians should understand how this disorder occurs. DM is caused by a relative or absolute lack of insulin production by the pancreatic b-cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either insulin-dependent (the body is unable to produce sufficient insulin) or non-insulin-dependent (the body produces insulin, but the tissues in the body are resistant to the insulin).4 Most dogs and cats that develop DKA have an insulin deficiency. Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, the cells cannot access glucose, thereby causing them to undergo starvation.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, b-hydroxybutyric acid) can be used as energy by the tissues when there is a lack of glucose or nutritional intake.1,2 The breakdown of fat, combined with the body's inability to use glucose, causes many pets with diabetes to present with weight loss, despite having a ravenous appetite. If diabetes is undiagnosed or uncontrolled, a series of metab Continue reading >>

Diabetic Ketoacidosis Workup

Diabetic Ketoacidosis Workup

Approach Considerations Diabetic ketoacidosis is typically characterized by hyperglycemia over 250 mg/dL, a bicarbonate level less than 18 mEq/L, and a pH less than 7.30, with ketonemia and ketonuria. While definitions vary, mild DKA can be categorized by a pH level of 7.25-7.3 and a serum bicarbonate level between 15-18 mEq/L; moderate DKA can be categorized by a pH between 7.0-7.24 and a serum bicarbonate level of 10 to less than 15 mEq/L; and severe DKA has a pH less than 7.0 and bicarbonate less than 10 mEq/L. [17] In mild DKA, anion gap is greater than 10 and in moderate or severe DKA the anion gap is greater than 12. These figures differentiate DKA from HHS where blood glucose is greater than 600 mg/dL but pH is greater than 7.3 and serum bicarbonate greater than 15 mEq/L. Laboratory studies for diabetic ketoacidosis (DKA) should be scheduled as follows: Repeat laboratory tests are critical, including potassium, glucose, electrolytes, and, if necessary, phosphorus. Initial workup should include aggressive volume, glucose, and electrolyte management. It is important to be aware that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>

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 (dka)

Diabetic Ketoacidosis (dka)

Department of Obstetrics and Gynaecology Diabetic ketoacidosis is an acute metabolic and obstetric emergency that can jeopardize both mother and fetus. Normally treated in ICU. Fetal mortality as high as 50%. The clinical features of DKA are due to: Marked dehydration Acidosis Electrolyte disturbance Presenting signs and symptoms of DKA: Vomiting Polydipsia Polyuria Weakness Abdominal pain Weight loss Hyperventilation Dry mucus membranes Tachycardia Hypotension Disorientation Coma Underlying infection Laboratory Findings: Pregnant patient can develop DKA with glucose level less than 20 mg/dl. Diabetic Plasma glucose >16 mmol/l Keto Serum Acetone 1,2 or more Acidosis Arterial pH S-HCO3 Anion Gap less than 7,4 <15,1 [Na+ - (Cl- +HCO-3)] > 12 Diagnostic criteria for diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) DKA DKA DKA HHS Mild Moderate Servere . Plasma glucose (mg/dL) >250 >250 >250 >600 Arterial pH 7.25-7.30 7.00-7.24 <7,00 >7,30 Serum bicarbonate (mEq/L) 15-18 10-15 <10 >15 Urine ketones* Positive Positive Positive Small Serum ketones* Positive Positive Positive Small Effective serum osmolality (mOsm/kg) Variable Variable Variable >320 Anion gap >10 >12 >12 <12 Alteration in sensoria or mental obtundation Alert Variable/drowsy Stupor/coma Stupor/coma * Nitroprusside reaction method. Calculation: 2[measured Na (mEq/L)] + glucose (mg/dL)/18. Calculation: (Na+) - (Cl- + HCO3-) (mEq/L). See text for details. Copyright © 2006 American Diabetes Association From Diabetes Care Vol 29, Issue 12, 2006. Reprinted with permission from the American Diabetes Association. Additional Laboratory Findings Glucosuria Leukocytosis Ketonuria Elevated CPK Metabolic acidosis Elevated amylase Hyperosmolarity Elevated transaminase Hypokalemia Elevated BUN Hypomagne Continue reading >>

Hyperglycemic Emergencies

Hyperglycemic Emergencies

Lana Kravarusic Doctor of Pharmacy Candidate, University of Florida Introduction Diabetes mellitus, if uncontrolled, may lead to serious hyperglycemic emergencies. The two most serious hyperglycemic emergencies are diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). (Hyperglycemic hyperosmolar state is synonymous with hyperosmolar syndrome and hyperglycemic hyperosmolar nonketotic state which are both older names.) DKA most commonly occurs in patients with Type 1 diabetes mellitus or pancreatic disease, while HHS occurs more frequently with Type 2 diabetes. The presentation of the two syndromes can be distinguished by several factors. Both DKA and HHS patients present with hyperglycemia, but DKA is characterized by ketonemia, ketonuria, and metabolic acidosis while HHS involves dehydration without significant ketoacidosis. It is also possible that a patient presents with a mixture of DKA and HHS.1 The incidence of DKA is estimated to be 4-8 per 1000 diabetic patients, but is likely an underestimation. Up to 25% of cases in the United States are discovered at diagnosis, especially in younger children. The current mortality rate is 2-5% with treatment, and is usually a result of the underlying associated illnesses rather than DKA itself.2 For example elderly patients (>65 years) may have a mortality rate as high as 20% due to comorbid conditions. In some rare cases, however, mortality is a result of a DKA complication such as cerebral edema which is estimated to occur in 0.7-1% of DKA cases in young adults and children. Therefore, children less than 5 years of age and elderly over the age of 65 are considered high-risk DKA patients.1 Currently, the incidence of HHS in the United States is thought to be less than 1 per 1000-person years, making HHS much Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is the most common acid–base disorder and can be life threatening. It results from excessive cellular acid production, reduced acid secretion, or loss of body alkali. The body has two buffering mechanisms to counteract an increase in acid. The initial response is to increase carbon dioxide excretion by increasing ventilation. The second response is increased renal excretion of acids and renal regeneration of bicarbonate. The adequacy of compensation can be assessed by the quick check method or the Winter formula (Table 2). Metabolic acidosis can be classified into two categories using the anion gap. Each category has a distinct differential diagnosis. Anion gap = [Sodium] – ([Chloride] + [Bicarbonate]) Normally, the anion gap is approximately 12 ± 2 meq/L (12 ± 2 mmol/L). Most unmeasured anions consist of albumin. Therefore, the presence of either a low albumin level or an unmeasured cationic light chain, which occurs in multiple myeloma, results in a low anion gap. Increased hydrogen ion concentration or decreased bicarbonate concentration will increase the gap. When the primary disturbance is a metabolic acidosis, the anion gap helps to narrow the diagnostic possibilities to an increased anion gap acidosis or a normal anion gap acidosis. Increased Anion Gap Metabolic Acidosis Common causes include ketoacidosis (diabetes mellitus, alcohol abuse, starvation), lactic acidosis, chronic kidney disease, salicylate toxicity, and ethylene glycol and methanol poisoning. Diabetic ketoacidosis is the most common cause of an increased anion gap acidosis, but a normal anion gap acidosis may be present early in the disease course when the extracellular fluid (ECF) volume is nearly normal. Ketoacidosis also may develop in patients with a histor Continue reading >>

Incidence And Characteristics Of Acute Kidney Injury In Severe Diabetic Ketoacidosis

Incidence And Characteristics Of Acute Kidney Injury In Severe Diabetic Ketoacidosis

Abstract Acute kidney injury is a classical complication of diabetic ketoacidosis. However, to the best of our knowledge, no study has reported the incidence and characteristics of acute kidney injury since the consensus definition was issued. Retrospective study of all cases of severe diabetic ketoacidosis hospitalised consecutively in a medical surgical tertiary ICU during 10 years. Patients were dichotomised in with AKI and without AKI on admission according to the RIFLE classification. Clinical and biological parameters were compared in these populations. Risk factors of presenting AKI on admission were searched for. Results Ninety-four patients were included in the study. According to the RIFLE criteria, 47 patients (50%) presented acute kidney injury on admission; most of them were in the risk class (51%). At 12 and 24 hours, the percentage of AKI patients decreased to 26% and 27% respectively. During the first 24 hours, 3 patients needed renal replacement therapy. Acute renal failure on admission was associated with a more advanced age, SAPS 2 and more severe biological impairments. Treatments were not different between groups except for insulin infusion. Logistic regression found 3 risk factors of presenting AKI on admission: age (odds ratio 1.060 [1.020–1.100], p<0.01), blood glucose (odds ratio 1.101 [1.039–1.166], p<0.01) and serum protein (odds ratio 0.928 [0.865–0.997], p = 0.04). Acute kidney injury is frequently associated with severe diabetic ketoacidosis on admission in ICU. Most of the time, this AKI is transient and characterised by a volume-responsiveness to fluid infusion used in DKA treatment. Age, blood glucose and serum protein are associated to the occurrence of AKI on ICU admission. Figures Citation: Orban J-C, Maizière E-M, Ghaddab A, V 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 serious metabolic disorder that can occur in patients with diabetes mellitus (DM).1,2 Veterinary technicians play an integral role in managing and treating patients with this life-threatening condition. In addition to recognizing the clinical signs of this disorder and evaluating the patient’s response to therapy, technicians should understand how this disorder occurs. Technicians must also educate owners about the long-term care of diabetic pets. DM is caused by a relative or absolute lack of insulin production by the pancreatic β cells or by inactivity or loss of insulin receptors, which are usually found on membranes of skeletal muscle, fat, and liver cells.1,3 In dogs and cats, DM is classified as either type I (insulin dependent; the body is unable to produce sufficient insulin) or type II (non–insulin dependent; the body produces insulin, but the body’s tissues are resistant to insulin).4 Most dogs that develop DM have insulin deficiency, while cats that develop DM tend to have insulin resistance.5 DKA occurs when the body cannot use glucose for energy because of a lack of, or resistance to, insulin. When this happens, the body uses alternative energy sources, resulting in ketone production and subsequent acidosis.1 Insulin has many functions, including the enhancement of glucose uptake by the cells for energy.1 Without insulin, cells cannot use glucose, causing them to starve.2 The unused glucose remains in the circulation, resulting in hyperglycemia. To provide cells with an alternative energy source, the body breaks down adipocytes, releasing free fatty acids (FFAs) into the bloodstream. The liver subsequently converts FFAs to triglycerides and ketone bodies. These ketone bodies (i.e., acetone, acetoacetic acid, β-hydrox Continue reading >>

Exam Shows Diffuse Abdominal Tenderness With Guarding.

Exam Shows Diffuse Abdominal Tenderness With Guarding.

A 14 y/o female is brought to the emergency department by her mother after being found unresponsive at home. She had been ill the day before with nausea and vomiting, but was not running a fever. Her parents had kept her home from school that day. When her mother came home at lunchtime to check on her, she was very lethargic and not responding coherently. By the time she arrived at the hospital, she had to be brought in to the ED on a gurney. Initial evaluation showed O2 sat 100% on room air, pulse 126, respirations 30, BP 92/68, temperature 101.2 F. She appears pale, mucous membranes are dry and she only responds to painful stimuli. Exam shows diffuse abdominal tenderness with guarding. Differential diagnosis? What initial treatment would you suggest? What labs would you order? Any xrays or additional studies? CBC WBC 23,500 Hgb 14.2 g/dL Hct 45% Platelets 425,000 BMP Sodium 126 Potassium 5.2 Chloride 87 CO2 <5 BUN 32 Creatinine 1.5 Glucose 1,376 Arterial Blood Gases pH 7.19 Po2 100 mm Hg HCO3 7.5 mmo/L Pco2 20 mm Hg Sao2 98% (room air) Urine Specific gravity 1.015 Ketones 4+ Leukocytes few Glucose 4+ Nitrates 0 RBCs many Diabetic ketoacidosis (DKA) is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. DKA occurs mostly in type 1 diabetics. 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. Symptoms and signs of DKA Nausea & vomiting Abdominal pain--particularly in children Lethargy and somnolence Kussmaul respirations Hypotension Tachycardia Fruity breath Continue reading >>

Jaime Moo-young, Md

Jaime Moo-young, Md

Diabetic Ketoacidosis (DKA) Pathogenesis · Insufficient insulin for a given carbohydrate load decreased cellular metabolism of glucose · Increased gluconeogenesis, glycogenolysisHyperglycemia · Increased breakdown of free fatty acids as alternative energy source ketone and ketoacid accumulation · Hyperglycemiaserum hyperosmolality osmotic diuresis dehydration and electrolyte derangements (dehydration is most lethal!) · Seen almost exclusively in Type I diabetes; rarely in Type II Definition: Triad of 1. Hyperglycemia (usually between 500 – 800 mg/dL or 27.8-44.4 mmol/L) 2. Anion Gap Metabolic Acidosis (pH usually <7.30) 3. Ketonemia: -hydroxybutyrate, acetoacetate most significant ** Urine ketones do not make the diagnosis, but they can support it** Triggers (the “I’sâ€): Don’t forget to ask about these! · Insulin deficiency: insulin non-compliance, insufficient insulin dosing, new-onset Type I diabetes · Iatrognic: glucocorticoids, atypical antipsychotics, high-dose thiazide diuretics · Infection: UTI, pneumonia, TB · Inflammation: pancreatitis, cholecystitis · Ischemia/infarction: MI, stroke, gut ischemia · Intoxication: Alcohol, cocaine, other drugs Presentation · Symptoms · Polyuria, polydipsia, weight loss · Nausea, vomiting, abdominal pain · Fatigue, malaise · Associated trigger sx (fever/chills, chest pain, etc) · Signs · Volume depletion: skin turgor, dry axillae, dry mucus membranes, HR, BP · Altered mental status: stupor, coma · Kussmaul respirations: rapid, shallow breathing = hyperventilation to counteract metabolic acidosis · Fruity, acetone odor on breath Lab workup and findings · Hyperglycemia: > 250 mg/dL in serum, + glucose on urinalysis · Acidemia (pH <7. Continue reading >>

Evaluation Of Delirium

Evaluation Of Delirium

Diagnostic Tests Common Differential 1st Tests Other Tests Dementia the diagnosis of dementia is based predominantly on historical factors: diagnosis is clinical Pain diagnosis is clinical: causes of underlying pain should be sought (e.g., hip fracture) Stroke/cerebrovascular accident and transient ischemic attack neuroimaging (CT and/or MRI): ischemic CVA: hyperdense vessels at the site of blood clot in middle cerebral artery (MCA), posterior cerebral artery (PCA), or anterior cerebral artery (ACA); loss of insular stripe located between Sylvian fissure and basal ganglia is frequently associated with early MCA stroke; subtle mass effect; [78] hemorrhagic CVA: hyperdense to grey matter lesion at the site of hemorrhage; mass effect may also be evident but frequently subtle in early stroke more Findings frequently absent for transient ischemic attacks and ischemic strokes. Findings frequently absent for transient ischemic attacks and ischemic strokes. Myocardial infarction ECG: ST segment elevation or depression, or T wave changes serum troponin: elevated CXR: evidence of pulmonary congestion/ pleural effusion if secondary heart failure, may show enlarged cardiac shadow coronary angiogram: presence of thrombus with occlusion of the artery Acute systemic infection basic test panel (CBC, serum electrolytes, blood glucose, serum liver function tests, coagulation profile): elevated WBC count or leukopenia with sepsis; may be elevated urea and creatinine with sepsis; may be low platelets with sepsis; blood glucose may be elevated or, more rarely, low with sepsis; serum transaminases and serum bilirubin may be elevated with sepsis; may be prolonged or elevated INR, PT, aPTT more If shock is present, urgent simultaneous treatment required. WBC count may be normal in early stages Continue reading >>

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemia — A Brief Review

Diabetic Ketoacidosis And Hyperosmolar Hyperglycemia — A Brief Review

Diabetic Ketoacidosis and Hyperosmolar Hyperglycemia — A Brief Review SPECIAL FEATURE By Richard J. Wall, MD, MPH, Pulmonary Critical Care & Sleep Disorders Medicine, Southlake Clinic, Valley Medical Center, Renton, WA. Dr. Wall reports no financial relationships relevant to this field of study. Financial Disclosure: Critical Care Alert's editor, David J. Pierson, MD, nurse planner Leslie A. Hoffman, PhD, RN, peer reviewer William Thompson, MD, executive editor Leslie Coplin, and managing editor Neill Kimball report no financial relationships relevant to this field of study. INTRODUCTION Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are two of the most common and serious acute complications of diabetes mellitus. DKA is responsible for more than 500,000 hospital days annually in the United States, at an estimated annual cost of $2.4 billion. Both conditions are part of the spectrum of uncontrolled hyperglycemia, and there is sometimes overlap between them. This article will discuss and compare the two conditions, with a focus on key clinical features, diagnosis, and treatment. DIAGNOSTIC FEATURES In DKA, there is an accumulation of ketoacids along with a high anion gap metabolic acidosis (see Table below).1 The acidosis usually evolves quickly over a 24-hour period. The pH is often < 7.20 and initial bicarbonate levels are often < 20 mEq/L. DKA patients (especially children) often present with nausea, vomiting, hyperventilation, and abdominal pain. Blood sugar levels in DKA tend to be 300-800 mg/dL, but they are sometimes much higher when patients present in a comatose state. In HHS, there is no (or little) ketonemia but the plasma osmolality may reach 380 mOsm/kg, and as a result, patients often have neurologic complications such as coma. Bica Continue reading >>

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