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Abdominal Pain In Metabolic Acidosis

Question 2 Of 11

Question 2 Of 11

A 65-year-old man with past medical history of schizophrenia complains of vomiting for the past 24 hours. He reports feeling very hot for several days, but denies other symptoms including abdominal pain, chest pain, and shortness of breath. You are unable to obtain further details as he is having trouble hearing the questions. Vital signs: temperature 101°F, heart rate 130/min, respiratory rate 35/min, blood pressure 120/80 mm Hg, pulse oximetry 100% on room air. You would also expect this patient to have: A respiratory alkalosis with a metabolic acidosis. A respiratory acidosis with metabolic alkalosis. A 40-degree right axis deviation manifested by a terminal r wave in AVR on ECG. An intracranial hemorrhage on CT scan of the brain. An elevated lithium level. Answer Explanation : Aspirin intoxication caused a mixed acid base disturbance. Stimulation of the central respiratory center in the medulla leads to a respiratory alkalosis. Metabolic acidosis can be severe and is caused via several mechanisms. Uncoupling of oxidative phosphorylation leads to an increase in oxygen use and CO2 production. Pyruvate and lactate are by-products of anaerobic respiration. Increased CO2 increases the respiratory rate further. It also causes the kidneys to increase excretion of bicarbonate causing a metabolic acidosis. Additionally the Krebs cycle is disrupted leading to increased lipolysis and gluconeogenesis. The by-product of these pathways is increased ketone production, which contributes to the acidosis. Of note, children typically do not develop respiratory alkalosis with salicylate intoxication: they usually present with only a metabolic acidosis. Treatment should be aggressive. Charcoal is indicated in a patient with an adequate mental status. Avoid intubation if possible, as de Continue reading >>

Quiz Page June 2011

Quiz Page June 2011

Jump to Section A 62-year-old white man presented to the emergency department with profound abdominal pain. He had end-stage renal disease (ESRD) secondary to diabetic nephropathy and had been started on maintenance hemodialysis therapy 5 months earlier. The patient noted the onset of intermittent abdominal pain 3 days before admission, associated with nausea and diarrhea, but he denied vomiting or alleviating or worsening factors. He refused to go to dialysis therapy the day before admission because of abdominal pain, which progressively worsened. On examination, blood pressure was 239/97 mm Hg, heart rate was 126 beats/min, respiratory rate was 26 breaths/min, temperature was 35.2°C, and oxygen saturation was 96% on room air. He was in moderate distress and had a diffusely tender abdomen focused in the epigastric area, but no peritoneal signs. The rest of the examination findings were unremarkable. Initial laboratory results (Table 1) showed profound metabolic acidosis with the following values: arterial pH, 6.74; bicarbonate, 2.3 mEq/L (2.3 mmol/L); anion gap, 44 mEq/L (44 mmol/L); osmolar gap, 20 mOsm/kg; and lactate, 189.2 mg/dL (21 mmol/L). Chest radiograph and computed tomography of the abdomen and pelvis with intravenous contrast were normal. After receiving morphine intravenously, blood pressure decreased to 162/84 mm Hg. Table 1Laboratory Studies Parameter Value Reference Range Sodium (mEq/L) 145 135-145 Potassium (mEq/L) 5.2 3.6-5.2 Chloride (mEq/L) 99 101-111 Bicarbonate (mEq/L) <5 22-29 Anion gap (mEq/L) 44a 10-15 SUN (mg/dL) 75 9-21 Creatinine (mg/dL) 10.4 0.6-1.3 eGFR (mL/min/1.73 m2) 5.4b >60 Glucose (mg/dL) 44 70-110 Calcium (mg/dL) 10.3 8.4-10.2 Phosphorus (mg/dL) 2.4 2.5-4.5 Albumin (g/dL) 4.7 3.4-4.8 Lactate (mg/dL) 189.2 4.5-19.8 Serum osmolality ( Continue reading >>

Acidosis: The Kiss Of Death!

Acidosis: The Kiss Of Death!

WHAT CAUSES A CONDITION CALLED "ACIDOSIS"? WHAT IS ACIDOSIS? Acidosis Definition: Acidosis is an increased acidity in the blood and other body tissue. Acidosis is said to occur when arterial pH falls below 7.35. The pH level of our blood affects every cell in our body. Chronic acidosis corrodes body tissue, and if left unchecked, will interrupt all cellular activities and functions. WHAT CAUSES ACIDOSIS? HIGH ACID-FORMING FOODS and DIETS all lead to ACIDOSIS. Living a fast-paced daily lifestyle, such as eating on the run and excessive over stimulation, will lead people to face a constant symptoms of indigestion and growing endangerment of over-acidification (Acidosis) of the body cells, which will interrupt cellular activities and functions. It is a major root of sickness and disease. Having our cells constantly exposed to an acidic environment leads to acidosis and then chronic acidosis and finally various forms of disease such as cancer and many more! Studies have shown that an acidic, anaerobic (which is also the lack of oxygen) body environment encourages the breeding of fungus, mold, bacteria, and viruses. As a result, our inner biological terrain shifts from a healthy oxygenated, alkaline environment to an unhealthy acidic one (acidic pH scale). This forces the body to constantly deplete its cellular energy to neutralize and detoxify these acids before they can act as poisons in and around the cells, ultimately changing the environment of each cell and finally compromising its immune system leaving it vulnerable to the ravages of disease to take a foothold in the body. When our body pH becomes overly acidic, it starts to set up defense mechanisms to keep the damaging acids from entering the vital organs. Modern Day Athletes and Acid-Forming Foods Unfortunately, Mo Continue reading >>

Systemic Causes Of Abdominal Pain

Systemic Causes Of Abdominal Pain

a Department of Emergency Medicine, Thomas Jefferson University Hospital, 1020 Sansom Street, Thompson Building 239, Philadelphia, PA 19107, USA b Division of Emergency Ultrasonography, Department of Emergency Medicine, University of Pennsylvania Medical Center, 3400 Spruce Street, Philadelphia, PA 19104, USA Abstract A variety of systemic and extra-abdominal diseases can cause symptoms within the abdominal cavity. Systemic and extra-abdominal diseases may include abdominal symptoms caused by several mechanisms. This article discusses the most important and common of these causes, namely the metabolic/endocrine causes, hematologic causes, inflammatory causes, infectious causes, functional causes, and the neurogenic causes. Keywords A variety of systemic and extra-abdominal diseases can cause symptoms within the abdominal cavity (Box 1). This article discusses the most important and common of these diseases. Systemic and extra-abdominal diseases may include abdominal symptoms caused by several mechanisms listed in Table 1. Mechanisms include direct pathologic effects on intra-abdominal organs (eg, gallstone formation in sickle cell disease); conversely, systemic illnesses (eg, congestive heart failure, diabetic ketoacidosis [DKA], or addisonian crisis) may themselves be precipitated by diseases in the abdomen. Some systemic illnesses have a direct (eg, constipation in hypercalcemia) or indirect (eg, nausea and vomiting in diabetic or alcoholic ketoacidosis [AKA]) effect on the functioning of the gastrointestinal (GI) tract. Abdominal symptoms may be caused by disease in contiguous organs outside the abdomen (eg, diaphragmatic irritation from disease of adjacent structures in the lung and mediastinum).1–4 Finally, symptoms may be referred to the abdomen from extra-abdom Continue reading >>

Blood Gases And Acute Pancreatitis

Blood Gases And Acute Pancreatitis

Summarized from Sharma V, Devi T, Sharma R et al. Arterial pH, bicarbonate levels and base deficit at presentation as markers of predicting mortality in acute pancreatitis: a single-centre prospective study. Gastroenterol Rep (Oxf) 2014; 2(3): 226-31 Acute pancreatitis, i.e. acute inflammation of the pancreas, causes sudden onset of severe upper abdominal pain often radiating to the back. Other symptoms include vomiting, constipation and pyrexia. Two main causes - alcohol abuse and gall stone disease – account for the majority (~80 %) of cases. The condition has a variable course. In many cases inflammation resolves with little or no intervention over a period of a few days to a week, with no long-term consequences, but in others the condition can be severe, progressing rapidly to systemic inflammation, sepsis and multiple organ failure. Severe acute pancreatitis is thus a potentially fatal condition that warrants immediate admission to intensive care. A major problem for initial emergency room management of patients presenting with acute pancreatitis is to distinguish those whose course is likely to be benign from those who are likely to suffer severe disease and therefore require admission to intensive care. There is currently no single reliable prognostic test and clinicians must depend on rather cumbersome clinical scoring systems to predict outcome. The authors of a recently published study sought to examine the value of admission acid-base parameters (pH, bicarbonate and base excess) in predicting outcome among patients with acute pancreatitis. The notion that these might be useful prognostic markers is based partially on the observation that metabolic acidosis (characterized by reduced pH, bicarbonate and base excess) is a frequent complication of severe acute Continue reading >>

7,929 Possible Causes For Acidosis + Abdominal Pain + Bronchial Spasm In Usa

7,929 Possible Causes For Acidosis + Abdominal Pain + Bronchial Spasm In Usa

Anaphylaxis Acidosis Abdominal Pain pain a weak and rapid pulse runny nose and sneezing swollen tongue or lips wheezing or difficulty breathing a sense that something is wrong with your body tingling hands,[healthline.com] pain.[medical-dictionary.thefreedictionary.com] […] reactions such as hives, flushed skin, or pale skin suddenly feeling too warm feeling like you have a lump in your throat or difficulty swallowing nausea, vomiting, or diarrhea abdominal[healthline.com] Acute Intermittent Porphyria Acute Respiratory Failure Arm Pain Arsenic Poisoning Arterial Blood pH Decreased Aspiration Pneumonia Asthenia Autonomic Neuropathy Back Pain Bilateral Diaphragmatic Elevation Blepharoptosis Brucellosis Bulbar Poliomyelitis Cardiac Arrhythmia Cerebrospinal Fluid Abnormality Cerebrospinal Fluid Protein Increased Chronic Inflammatory Demyelinating Polyneuropathy Cranial Nerve Involvement Decreased Vital Capacity Diminished Respiratory Excursion Diplopia Dysarthria Dysesthesia Encephalocele Facial Nerve Disorder Fahr's Syndrome Fecal Incontinence Fish Poisoning Flaccid Paralysis Flaccid Paralysis of the Lower Extremity Guillain-Barré Syndrome Hypercapnia Hypertension Hyporeflexia Hypotension Influenza Japanese Encephalitis Limb Pain Low Back Pain Low Back Pain Radiating to the Posterior Leg Meningeal Tuberculosis Muscular Atrophy Myasthenia Gravis Neonatal Hypotonia Nerve Conduction Study showing Demyelination Pattern Neurologic Manifestation PO2 Decreased Paresthesia Paresthesia of Lower Extremity Paroxysmal Hypertension Patient Appears Acutely Ill Peripheral Motor Neuropathy Poikilothermia Poliomyelitis Priapism Raynaud's Disease Recent Viral Illness Reduced Abdominal Reflex Respiratory Muscle Paralysis Sensation Disorder Sensory Deficit of the Lower Extremity Shy Drager Continue reading >>

Lactic Acidosis

Lactic Acidosis

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. Description Lactic acidosis is a form of metabolic acidosis due to the inadequate clearance of lactic acid from the blood. Lactate is a byproduct of anaerobic respiration and is normally cleared from the blood by the liver, kidney and skeletal muscle. Lactic acidosis occurs when the body's buffering systems are overloaded and tends to cause a pH of ≤7.25 with plasma lactate ≥5 mmol/L. It is usually caused by a state of tissue hypoperfusion and/or hypoxia. This causes pyruvic acid to be preferentially converted to lactate during anaerobic respiration. Hyperlactataemia is defined as plasma lactate >2 mmol/L. Classification Cohen and Woods devised the following system in 1976 and it is still widely used:[1] Type A: lactic acidosis occurs with clinical evidence of tissue hypoperfusion or hypoxia. Type B: lactic acidosis occurs without clinical evidence of tissue hypoperfusion or hypoxia. It is further subdivided into: Type B1: due to underlying disease. Type B2: due to effects of drugs or toxins. Type B3: due to inborn or acquired errors of metabolism. Epidemiology The prevalence is very difficult to estimate, as it occurs in critically ill patients, who are not often suitable subjects for research. It is certainly a common occurrence in patients in high-dependency areas of hospitals.[2] The incidence of symptomatic hyperlactataemia appears to be rising as a consequence of the use of antiretroviral therapy to treat HIV infection. It appears to increase in those taking stavudine (d4T) regimens.[3] Causes of lactic acid Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is primary reduction in bicarbonate (HCO3−), typically with compensatory reduction in carbon dioxide partial pressure (Pco2); pH may be markedly low or slightly subnormal. Metabolic acidoses are categorized as high or normal anion gap based on the presence or absence of unmeasured anions in serum. Causes include accumulation of ketones and lactic acid, renal failure, and drug or toxin ingestion (high anion gap) and GI or renal HCO3− loss (normal anion gap). Symptoms and signs in severe cases include nausea and vomiting, lethargy, and hyperpnea. Diagnosis is clinical and with ABG and serum electrolyte measurement. The cause is treated; IV sodium bicarbonate may be indicated when pH is very low. Acidemia (arterial pH < 7.35) results when acid load overwhelms respiratory compensation. Causes are classified by their effect on the anion gap (see The Anion Gap and see Table: Causes of Metabolic Acidosis). High anion gap acidosis Ketoacidosis is a common complication of type 1 diabetes mellitus (see diabetic ketoacidosis), but it also occurs with chronic alcoholism (see alcoholic ketoacidosis), undernutrition, and, to a lesser degree, fasting. In these conditions, the body converts from glucose to free fatty acid (FFA) metabolism; FFAs are converted by the liver into ketoacids, acetoacetic acid, and beta-hydroxybutyrate (all unmeasured anions). Ketoacidosis is also a rare manifestation of congenital isovaleric and methylmalonic acidemia. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Lactate accumulation results from a combination of excess formation and decreased utilization of lactate. Excess lactate production occurs during states of anaerobic metabolism. The most serious form occurs during the various types o Continue reading >>

Abdominal Pain, Vomiting, And Confusion

Abdominal Pain, Vomiting, And Confusion

In the latest Case Record of the Massachusetts General Hospital, a 54-year-old woman with type 2 diabetes mellitus was admitted to the hospital because of abdominal pain, vomiting, and confusion. Initial laboratory evaluation revealed a serum lactate level of 20.3 mmol per liter and a venous blood pH of 6.62. A diagnosis was made. Metformin is excreted unmetabolized in the urine. Therefore, impaired kidney function may result in the accumulation of metformin in the plasma, causing lactic acidosis. In patients who have toxic effects of metformin, the mechanism of lactic acidosis is multifactorial, including enhanced conversion of glucose to lactate in the small intestine and inhibition of gluconeogenesis by lactate, pyruvate, and alanine. Clinical Pearls Conditions that may cause a very large anion gap acidosis include lactic acidosis, aspirin overdose, methanol or ethylene glycol toxicity, diabetic ketoacidosis, and uremia. Altered mental status, including lethargy, stupor, and even coma, can be a direct consequence of acidosis. Acidemia may lead to increased vasodilatation and warm skin, and may also be associated with a paradoxical hypothermia, which is a known complication of profound acidosis. Cardiovascular consequences of acidosis include cardiac failure and catecholamine release, which may lead to arrhythmia and some degree of respiratory compromise. Acidemia can also cause gastric atony, nausea, vomiting, and abdominal pain. Morning Report Questions Q: What is a nonhypoxic (type B) lactic acidosis? A: Type B lactic acidosis refers to the impaired lactate metabolism that can occur in association with the administration of certain medications (e.g., metformin, salicylate, isoniazid, and zidovudine) or in association with certain cancers (e.g., lymphoma and leukemi Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Practice Essentials Metabolic acidosis is a clinical disturbance characterized by an increase in plasma acidity. Metabolic acidosis should be considered a sign of an underlying disease process. Identification of this underlying condition is essential to initiate appropriate therapy. (See Etiology, DDx, Workup, and Treatment.) Understanding the regulation of acid-base balance requires appreciation of the fundamental definitions and principles underlying this complex physiologic process. Go to Pediatric Metabolic Acidosis and Emergent Management of Metabolic Acidosis for complete information on those topics. Continue reading >>

Acid-base Physiology

Acid-base Physiology

Case 15 : An old man with abdominal pain and shock Clinical Details An 85 year old man was admitted with severe abdominal pain and shock. The abdominal pain had started about 1500hrs and quickly became quite severe. There was no radiation to the back. The patient was known to have an abdominal aortic aneurysm (AAA). On arrival at hospital, the patient was shocked with peripheral circulatory failure and hypotension (BP 70-80 systolic). His abdomen was guarded and quite tender. He was distressed but able to talk and could understand instructions. Past history was of hypertension (on metoprolol and prazosin) and angina (on Isordil). Prior to this event, the patient was mobile and independent. A ruptured AAA was diagnosed clinically and he was transferred to theatre for emergency laparotomy. On arrival in theatre, BP was 120 systolic. The patient was talking but distressed by pain with rapid respirations at a rate of 30/min. It was noted that neck veins were very distended. An external jugular triple lumen central line and a brachial arterial line were placed before the surgical team had arrived in theatre. CVP was +40 mmHg. The blood gases were collected from an arterial line during preoxygenation with 100% oxygen at 1738 hrs (i.e. about 4.5 hours after onset of symptoms). Investigations: Biochemistry at 1520hrs was Na+ 138, K+ 4.9, Cl- 107, Bicarbonate 20, Glucose 11.2, Urea 12.8, creatinine 0.188, lactate 8.3 (all results in mmol/l). Haemoglobin 133 G/l. pH 7.35 pCO2 24 mmHg pO2 182 mmHg HCO3 13.8 mmol/l Assessment Initial clinical assessment The clinical expectation was an acute metabolic acidosis (lactic acidosis) due to peripheral circulatory failure, and respiratory alkalosis due to pain-induced hyperventilation. Respiratory compensation for the metabolic acidosis wo Continue reading >>

Abdominal Pain In Patients With Hyperglycemic Crises.

Abdominal Pain In Patients With Hyperglycemic Crises.

Abstract BACKGROUND: The aim of the study was to evaluate the incidence and prognosis of abdominal pain in patients with diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic state (HHS). Abdominal pain, sometimes mimicking an acute abdomen, is a frequent manifestation in patients with DKA. The prevalence and clinical significance of gastrointestinal symptoms including abdominal pain in HHS have not been prospectively evaluated. MATERIALS AND METHODS: This is a prospectively collected evaluation of 200 consecutive patients with hyperglycemic crises admitted to a large inner-city teaching hospital in Atlanta, GA.We analyzed the admission clinical characteristics, laboratory studies, and hospital course of 189 consecutive episodes of DKA and 11 cases of HHS during a 13-month period starting in October 1995. RESULTS: Abdominal pain occurred in 86 of 189 patients with DKA (46%). In 30 patients, the cause of abdominal pain was considered to be secondary to the precipitating cause of metabolic decompensation. Five of them required surgical intervention including 1 patient with Fournier's necrotizing fasciitis, 1 with cholecystitis, 1 with acute appendicitis, and 2 patients with perineal abscess. The presence of abdominal pain was not related to the severity of hyperglycemia or dehydration; however, a strong association was observed between abdominal pain and metabolic acidosis. In DKA patients with abdominal pain, the mean serum bicarbonate (9 +/- 1 mmol/L) and blood pH (7.12 +/- 0.02) were lower than in patients without pain (15 +/- 1 mmol/L and 7.24 +/- 0.09, respectively, both P <.001). Abdominal pain was present in 86% of patients with serum bicarbonate less than 5 mmol/L, in 66% of patients with levels of 5 to less than 10 mmol/L, in 36% of patients with Continue reading >>

Metabolic Acidosis: Causes, Symptoms, Diagnosis, Treatment, Prognosis, Prevention

Metabolic Acidosis: Causes, Symptoms, Diagnosis, Treatment, Prognosis, Prevention

Acidosis- A medical condition in which the fluids present in the body start to develop increased amount of acidic content making the body fluids acidic. There are two types of Acidosis- Respiratory Acidosis and Metabolic Acidosis. Respiratory Acidosis occurs as a result of malfunction of lungs. Metabolic Acidosis occurs as a result of malfunction of the kidneys. In this article, we will look into about Metabolic Acidosis. We will look into the causes, diagnosis, and treatment of Metabolic Acidosis. As stated, Metabolic Acidosis is a medical disorder in which the body starts producing excessive amounts of acid and/or the kidneys are not able to remove enough acidic content from the body. If not corrected at the appropriate time, Metabolic Acidosis can lead to a medical condition called acidemia in which pH scale in the blood gets low as a result of the kidneys being unable to form bicarbonates in the body. Causes Of Metabolic Acidosis The amount of acid in the blood can is determined by measuring the pH. A lower value of the pH means that the blood is acidic and a higher value of pH means that rhe blood is basic. Ideal pH value in the blood should be around 7.5. There are many processes in an individual's body which produces acid. Usually, the lungs and the kidneys take care of the excess production of acid; however, if there is a malfunction of these organs it results in Acidosis. As stated, Metabolic Acidosis begins in the kidneys. It develops when the kidneys are not able to discard excessive acid or in cases when they discard too much basic content from the body. Metabolic Acidosis is of three types: Diabetic Acidosis: This occurs in poorly controlled diabetes patients. In this form, there is formation of excess ketones making the blood acidic. Hyperchloremic Acidosi Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>

Hyperglycaemic Crises And Lactic Acidosis In Diabetes Mellitus

Hyperglycaemic Crises And Lactic Acidosis In Diabetes Mellitus

Hyperglycaemic crises are discussed together followed by a separate section on lactic acidosis. DIABETIC KETOACIDOSIS (DKA) AND HYPERGLYCAEMIC HYPEROSMOLAR STATE (HHS) Definitions DKA has no universally agreed definition. Alberti proposed the working definition of “severe uncontrolled diabetes requiring emergency treatment with insulin and intravenous fluids and with a blood ketone body concentration of >5 mmol/l”.1 Given the limited availability of blood ketone body assays, a more pragmatic definition comprising a metabolic acidosis (pH <7.3), plasma bicarbonate <15 mmol/l, plasma glucose >13.9 mmol/l, and urine ketostix reaction ++ or plasma ketostix ⩾ + may be more workable in clinical practice.2 Classifying the severity of diabetic ketoacidosis is desirable, since it may assist in determining the management and monitoring of the patient. Such a classification is based on the severity of acidosis (table 1). A caveat to this approach is that the presence of an intercurrent illness, that may not necessarily affect the level of acidosis, may markedly affect outcome: a recent study showed that the two most important factors predicting mortality in DKA were severe intercurrent illness and pH <7.0.3 HHS replaces the older terms, “hyperglycaemic hyperosmolar non-ketotic coma” and “hyperglycaemic hyperosmolar non-ketotic state”, because alterations of sensoria may be present without coma, and mild to moderate ketosis is commonly present in this state.4,5 Definitions vary according to the degree of hyperglycaemia and elevation of osmolality required. Table 1 summarises the definition of Kitabchi et al.5 Epidemiology The annual incidence of DKA among subjects with type 1 diabetes is between 1% and 5% in European and American series6–10 and this incidence appear Continue reading >>

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