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Abdominal Pain In Metabolic Acidosis

Chronic Metabolic Acidosis Destroys Pancreas

Chronic Metabolic Acidosis Destroys Pancreas

Peter Melamed and Felix Melamed Biotherapy Clinic of San Francisco, USA *Corresponding Author: Biotherapy Clinic of San Francisco 2215 Post Street, Suite 1, San Francisco, CA 94115, USA Phone 1 415 3776643 Fax 1 415 4093909 [email protected] Visit for more related articles at JOP. Journal of the Pancreas Abstract One primary reason for the current epidemic of digestive disorders might be chronic metabolic acidosis, which is extremely common in the modern population. Chronic metabolic acidosis primarily affects two alkaline digestive glands, the liver, and the pancreas, which produce alkaline bile and pancreatic juice with a large amount of bicarbonate. Even small acidic alterations in the bile and pancreatic juice pH can lead to serious biochemical/biomechanical changes. The pancreatic digestive enzymes require an alkaline milieu for proper function, and lowering the pH disables their activity. It can be the primary cause of indigestion. Acidification of the pancreatic juice decreases its antimicrobial activity, which can lead to intestinal dysbiosis. Lowering the pH of the pancreatic juice can cause premature activation of the proteases inside the pancreas with the potential development of pancreatitis.The acidification of bile causes precipitation of the bile acids, which irritate the entire biliary system and create bile stone formation. Aggressive mixture of the acidic bile and the pancreatic juice can cause erratic contractions of the duodenum’s walls and subsequent bile reflux into the stomach and the esophagus. Normal exocrine pancreatic function is the core of proper digestion. Currently, there is no effective and safe treatment for enhancing the exocrine pancreatic function. Restoring normal acid-base homeostasis can be a useful toolfor pathophysi 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 >>

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 >>

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 >>

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 >>

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 >>

Metabolic Acidosis In Emergency Medicine Clinical Presentation

Metabolic Acidosis In Emergency Medicine Clinical Presentation

History Metabolic acidosis can result in a variety of nonspecific changes in several organ systems, including, but not limited to, neurologic, cardiovascular, pulmonary, gastrointestinal, and musculoskeletal dysfunction. Symptoms are often specific to and a result of the underlying etiology of the metabolic acidosis. Head, eyes, ears, nose, throat (HEENT) findings include the following: Cardiovascular findings include the following: Neurologic findings include the following: Pulmonary findings include subjective dyspnea from the patient's observation of hyperventilation. GI findings include the following: Musculoskeletal findings include the following: 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 >>

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 >>

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 >>

Metformin-associated Lactic Acidosis

Metformin-associated Lactic Acidosis

OVERVIEW metformin use is associated with lactic acidosis, but it remians controversial as a disease entity MECHANISM the mechanism of lactic acidosis is uncertain Metabolic effects of metformin include: decreased gluconeogenesis increased peripheral glucose uptake decreased fatty acid oxidation CLINICAL FEATURES presence of risk factors abdominal pain nausea and vomiting fatigue myalgias altered mental status myocardial insufficiency multi-organ failure RISK FACTORS advanced age high dose renal failure (metformin is excreted unchanged in the urine) hypoxia active alcohol intake sepsis dehydration shock acidosis INVESTIGATIONS high anion gap metabolic acidosis (HAGMA) high lactate MANAGEMENT rule out other causes of lactic acidosis (sepsis, cardiogenic shock, hypoperfusion, ischaemic bowel) withdrawal of metformin RRT RRT remove metformin and correct acidosis best performed early due to large volume of distribution of metformin use hemodialysis use HCO3 buffer CONTROVERSY Some argue that metformin itself does not cause lactic acidosis, that it is actually due to the underlying conditions such as renal failure and diabetes mellitus. However, there are definite cases of lactic acidosis from acute metformin overdose with no other underlying risk factors. References and Links Journal articles Orban JC, Fontaine E, Ichai C. Metformin overdose: time to move on. Crit Care. 2012 Oct 25;16(5):164. [Epub ahead of print] PubMed PMID: 23110819; PubMed Central PMCID: PMC3682282. Salpeter SR, Greyber E, Pasternak GA, Salpeter EE. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. 2010 Apr 14;(4):CD002967. doi: 10.1002/14651858.CD002967.pub4. Review. PubMed PMID: 20393934. FOAM and web resources Continue reading >>

What Is The Origin/mechanism Of Abdominal Pain In Diabetic Ketoacidosis?

What Is The Origin/mechanism Of Abdominal Pain In Diabetic Ketoacidosis?

Other than all papers I could find citing the depth of the keto-acidosis (and not the height of the blood glucose levels) correlating with abdominal pain, nothing else to explain how these two are linked. Decades ago, I was taught that because of the keto-acidosis causing a shift of intracellular potassium (having been exchanged for H+ protons of which in keto-acidosis there were too many of in the extracellular fluid) to the extracellular, so also the blood compartment, resulting in hyperkalemia, paralyzing the stomach, which could become grossly dilated - that’s why we often put in a nasogastric drainage tube to prevent vomiting and aspiration - and thus cause “stomach pain”. This stomach pain in the majority of cases indeed went away after the keto-acidosis was treated and serum electrolyte levels normalized. In one patient it didn’t, she remained very, very metabolically acidotic, while blood glucose levels normalized, later we found her to have a massive and fatal intestinal infarction as the underlying reason for her keto-acidosis….. 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 >>

What Is Metabolic Acidosis?

What Is Metabolic Acidosis?

Metabolic acidosis happens when the chemical balance of acids and bases in your blood gets thrown off. Your body: Is making too much acid Isn't getting rid of enough acid Doesn't have enough base to offset a normal amount of acid When any of these happen, chemical reactions and processes in your body don't work right. Although severe episodes can be life-threatening, sometimes metabolic acidosis is a mild condition. You can treat it, but how depends on what's causing it. Causes of Metabolic Acidosis Different things can set up an acid-base imbalance in your blood. Ketoacidosis. When you have diabetes and don't get enough insulin and get dehydrated, your body burns fat instead of carbs as fuel, and that makes ketones. Lots of ketones in your blood turn it acidic. People who drink a lot of alcohol for a long time and don't eat enough also build up ketones. It can happen when you aren't eating at all, too. Lactic acidosis. The cells in your body make lactic acid when they don't have a lot of oxygen to use. This acid can build up, too. It might happen when you're exercising intensely. Big drops in blood pressure, heart failure, cardiac arrest, and an overwhelming infection can also cause it. Renal tubular acidosis. Healthy kidneys take acids out of your blood and get rid of them in your pee. Kidney diseases as well as some immune system and genetic disorders can damage kidneys so they leave too much acid in your blood. Hyperchloremic acidosis. Severe diarrhea, laxative abuse, and kidney problems can cause lower levels of bicarbonate, the base that helps neutralize acids in blood. Respiratory acidosis also results in blood that's too acidic. But it starts in a different way, when your body has too much carbon dioxide because of a problem with your lungs. Continue reading >>

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 >>

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