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Abdominal Pain In Metabolic Acidosis

Lactic Acidosis And Pancreatitis

Lactic Acidosis And Pancreatitis

All nukes (d4T, ddI, abacavir, tenofovir, FTC, 3TC, AZT), hydroxyurea and ribavirin, have been linked to reports of lactic acidosis and/or pancreatitis. PIs and efavirenz have also been associated with pancreatitis. Lactic acidosis Lactic acidosis is a very serious side effect but it is no longer reported in countries that no longer use d4T, ddI and AZT. Although other nukes are linked to lactic acidosis one or more of these nukes are linked to most cases. Lactic acid is a by-product formed when the body breaks down starches and sugars. Levels of lactic acid are normally carefully regulated by the liver. Small increases in lactic acid (called hyperlactataemia) are relatively frequent, and are temporary, especially after exercise. If they reach a higher level, there is a risk of lactic acidosis. This is a potentially fatal side effect related to nucleoside/tide analogues. It is now rarely reported. Not only are nukes included in nearly all HIV combinations, but the symptoms of lactic acidosis are common side effects or symptoms. Symptoms Symptoms include: Unexplained tiredness, often severe Sickness (vomiting) and nausea Pain in the stomach, abdomen and/or liver Unexplained weight loss Difficulty breathing Poor blood circulation – cold hands or feet or bluish skin colour Sudden peripheral neuropathy Before combination therapy was available, this was only very rarely seen in HIV, and might well have been under diagnosed. Drug packaging now includes a clearer warning about this risk. Pregnancy might be an additional risk factor for lactic acidosis when using nukes. For this reason d4T or ddI are not recommended during pregnancy when alternative drugs are available. Lactic acidosis is diagnosed through examination, lab tests and an abdominal CT scan or liver biopsy. Altho Continue reading >>

Nonanion Gap Metabolic Acidosis In A Patient With A Pancreaticopleural Fistula | The Journal Of The American Osteopathic Association

Nonanion Gap Metabolic Acidosis In A Patient With A Pancreaticopleural Fistula | The Journal Of The American Osteopathic Association

NonAnion Gap Metabolic Acidosis in a Patient With a Pancreaticopleural Fistula Benjamin Eovaldi, OMS IV ; Claude Zanetti, MD From the Department of Medicine at Midwestern University/Chicago College of Osteopathic Medicine in Downers Grove, Illinois, and the Department of Pulmonary Medicine at Swedish Covenant Hospital in Chicago, Illinois. Address correspondence to Benjamin Eovaldi, OMS IV, 555 31st Street, Downers Grove, IL 60615-1235.E-mail: [email protected] . NonAnion Gap Metabolic Acidosis in a Patient With a Pancreaticopleural Fistula The Journal of the American Osteopathic Association, May 2011, Vol. 111, 344-345. doi:10.7556/jaoa.2011.111.5.344 The Journal of the American Osteopathic Association, May 2011, Vol. 111, 344-345. doi:10.7556/jaoa.2011.111.5.344 Eovaldi B, Zanetti C. NonAnion Gap Metabolic Acidosis in a Patient With a Pancreaticopleural Fistula. J Am Osteopath Assoc 2011;111(5):344345. doi: 10.7556/jaoa.2011.111.5.344. NonAnion Gap Metabolic Acidosis in a Patient With a Pancreaticopleural Fistula You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account While acid-base disturbances are known to occur with chronic pancreatitis, few cases have been reported in which nonanion gap metabolic acidosis is caused by pancreaticopleural fistula, a known complication of chronic pancreatitis. The current report describes the case of a 49-year-old African American woman who presented with severe pleuritic chest pain and dyspnea at rest. The patient had a history of alcohol-induced chronic pancreatitis. Her chest radiograph was positive for a large left-sided pleural effusion. Magnetic resonance cholangiopancreatography revealed a small connection between the pancreas a 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 >>

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 >>

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 >>

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

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 >>

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 >>

5,194 Possible Causes For Acidosis + High Pitched Bowel Sounds + Severe Abdominal Pain In Usa

5,194 Possible Causes For Acidosis + High Pitched Bowel Sounds + Severe Abdominal Pain In Usa

Small Bowel Obstruction Severe Abdominal Pain Acidosis High Pitched Bowel Sounds The classic physical examination findings of abdominal distension, tympany to percussion, and high-pitched bowel sounds suggest the diagnosis.[medbullets.com] Positive findings on examination were limited to a softly distended non-tender abdomen and loud high-pitched bowel sounds.[saudijgastro.com] Symptoms include Severe abdominal pain or cramping Vomiting Bloating Loud bowel sounds Swelling of the abdomen Inability to pass gas Constipation A complete intestinal obstruction[medlineplus.gov] Intestinal Obstruction Severe Abdominal Pain High Pitched Bowel Sounds Clinical signs include abdominal distention, tympany due to an air-filled stomach and high-pitched bowel sounds. [ 9 ] History There is considerable overlap with the presentation[patient.info] Decreased pH and C02 content (metabolic acidosis ) reflect lactic acidosis occurring with bowel infarction Increased pH and C02 content (metabolic alkalosis) secondary to[diagnose-me.com] Because of the serious complications that can develop from small bowel obstruction, seek immediate medical care if you have severe abdominal pain or the other symptoms listed[virginiamason.org] Abdominal Distension Abdominal Fullness Abdominal Pain Abdominal Pain Worsens after Meals Acute Abdomen Acute Pancreatitis Acute Peritonitis Amylase Increased Arterial Blood pH Decreased Aspiration Pneumonia Bezoar Bilious Vomiting Blind Loop Syndrome Bowel Distention Colic Colonic Diverticulosis Complete Blood Count Abnormal Constipation Crohn's Disease Dehydration Dyspepsia Flatulence, Bloating and Distension Hernia Hyperactive Bowel Sounds Hypokalemia Hyponatremia Hypovolemic Shock Ileus Increased Abdominal Girth Inguinal Hernia Intestinal Adhesions Intestinal Diseas 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 >>

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 >>

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 >>

Diagnosis Of Acute Abdominal Pain In Older Patients

Diagnosis Of Acute Abdominal Pain In Older Patients

COREY LYON, LCDR, MC, USN, U.S. Naval Hospital Sigonella, Sigonella, Italy DWAYNE C. CLARK, M.D., Fond du Lac Regional Clinic, Fond du Lac, Wisconsin Acute abdominal pain is a common presenting complaint in older patients. Presentation may differ from that of the younger patient and is often complicated by coexistent disease, delays in presentation, and physical and social barriers. The physical examination can be misleadingly benign, even with catastrophic conditions such as abdominal aortic aneurysm rupture and mesenteric ischemia. Changes that occur in the biliary system because of aging make older patients vulnerable to acute cholecystitis, the most common indication for surgery in this population. In older patients with appendicitis, the initial diagnosis is correct only one half of the time, and there are increased rates of perforation and mortality when compared with younger patients. Medication use, gallstones, and alcohol use increase the risk of pancreatitis, and advanced age is an indicator of poor prognosis for this disease. Diverticulitis is a common cause of abdominal pain in the older patient; in appropriately selected patients, it may be treated on an outpatient basis with oral antibiotics. Small and large bowel obstructions, usually caused by adhesive disease or malignancy, are more common in the aged and often require surgery. Morbidity and mortality among older patients presenting with acute abdominal pain are high, and these patients often require hospitalization with prompt surgical consultation. Acute abdominal pain (generally defined as pain of less than one week’s duration) is a common presenting complaint among older patients. Approximately one fourth of patients who present to the emergency department are older than 50 years.1 The presentatio Continue reading >>

Lactic Acidosis

Lactic Acidosis

Type B Lactic acidosis type B is associated with certain diseases (e.g., diabetes mellitus), some drugs—notably biguanides, certain toxins, and some inborn errors of metabolism (Table I). Tissue hypoxia and hypotension are not obvious features of type B lactic acidosis but may supervene as a consequence of the acidemia. The incidence of lactic acidosis among patients with diabetes has declined since the biguanide phenformin (phenylethybiguanide) was withdrawn in many countries during the 1970s. Lactic acidosis occurred approximately 10–15 times more frequently during phenformin therapy than with metformin. An inherited inability to hydroxylate phenformin may explain the higher risk of lactic acidosis than with metformin. Lactic acidosis complicating metformin (dimethylbiguanide) occurs much less commonly, with most cases being reported among patients in whom biguanide therapy is contraindicated (e.g., renal impairment or hypoxic states). LACTIC ACIDOSIS Lactic acidosis occurs whenever lactate production exceeds its utilization. This can occur with tissue hypoxia or in nonhypoxemic conditions when cellular metabolism is impaired. Type A lactic acidosis is the hypoxic form. It can occur with true hypoxemia, severe anemia, reduced oxygen delivery from poor perfusion, or from dramatically increased tissue demand from exercise, convulsions, or heat stroke.1,3,4,7 Type B lactic acidosis is the nonhypoxic form. It occurs in the face of adequate oxygen delivery when mitochondrial oxidative function is abnormal. This can occur with drugs or toxins, hypoglycemia, diabetes mellitus, liver failure, renal failure, lymphosarcoma, sepsis, and inborn errors of metabolism (Box 60-1).1,2,4 PROGNOSIS AND FUTURE PERSPECTIVES Primary lactic acidosis of the neonate usually ends in death Continue reading >>

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