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Metabolic Acidosis Abdominal Pain Mechanism

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 >>

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 >>

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 And Hyperglycemic Hyperosmolar Syndrome

Diabetic Ketoacidosis And Hyperglycemic Hyperosmolar Syndrome

In Brief Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic syndrome (HHS) are two acute complications of diabetes that can result in increased morbidity and mortality if not efficiently and effectively treated. Mortality rates are 2–5% for DKA and 15% for HHS, and mortality is usually a consequence of the underlying precipitating cause(s) rather than a result of the metabolic changes of hyperglycemia. Effective standardized treatment protocols, as well as prompt identification and treatment of the precipitating cause, are important factors affecting outcome. The two most common life-threatening complications of diabetes mellitus include diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar syndrome (HHS). Although there are important differences in their pathogenesis, the basic underlying mechanism for both disorders is a reduction in the net effective concentration of circulating insulin coupled with a concomitant elevation of counterregulatory hormones (glucagon, catecholamines, cortisol, and growth hormone). These hyperglycemic emergencies continue to be important causes of morbidity and mortality among patients with diabetes. DKA is reported to be responsible for more than 100,000 hospital admissions per year in the United States1 and accounts for 4–9% of all hospital discharge summaries among patients with diabetes.1 The incidence of HHS is lower than DKA and accounts for <1% of all primary diabetic admissions.1 Most patients with DKA have type 1 diabetes; however, patients with type 2 diabetes are also at risk during the catabolic stress of acute illness.2 Contrary to popular belief, DKA is more common in adults than in children.1 In community-based studies, more than 40% of African-American patients with DKA were >40 years of age and more than 2 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 >>

<< Guidelines For The Ed Management Of Pediatric Diabetic Ketoacidosis (dka)

<< Guidelines For The Ed Management Of Pediatric Diabetic Ketoacidosis (dka)

Epidemiology, Etiology, And Pathophysiology Epidemiology and Etiology "Type 1" and "Type 2" Diabetes in Children Type 1 diabetes is the most common type of diabetes seen in children today. The primary metabolic derangement in type 1 diabetes is an absolute insulin deficiency. These patients will have a life-long dependence on insulin injections. The overall incidence of insulin-dependent diabetes is about 15 cases per 100,000 people per year (about 50,000 are diagnosed with type 1 diabetes each year). An estimated 3 children of every 1000 will develop insulin-dependent diabetes by the age of 20. Type 1 diabetes is primarily a disease of Caucasians. The worldwide incidence is highest in Finland and Sardinia and lowest in the Asian and black populations. Type 1 diabetes is more frequently diagnosed in the winter months (the reason for this is not known.) Interestingly, twins affected by type 1 diabetes are often discordant in the development of the disease.13 About 95% of cases of type 1 diabetes are the result of a genetic defect of the immune system, exacerbated by environmental factors.13 The autoimmune destruction of the beta cells of the pancreas results in the inability to produce insulin. Inheritance of type 1 diabetes is carried in genes of the major histocompatibility complex, the human leukocyte antigen (HLA) system. Eventually, this research may lead to a vaccine using the insulin B chain 8-24 peptides to actually prevent type 1 diabetes.13 It is currently thought that islet cells damaged by a virus produce a membrane antigen that may stimulate a response by T killer cells of the immune system in the genetically susceptible patient. The T killer cells misidentify the beta cell as foreign and destroy it. As the beta cells in the pancreas are destroyed, the remai Continue reading >>

Systemic Causes Of Abdominal Pain

Systemic Causes Of Abdominal Pain

Emergency registrar Mechanisms of abdominal symptoms : Thyrotoxicosis abdominal complaints are fairly common in thyrotoxicosis. include nausea, vomiting, loose frequent stools, and weight loss. Perhaps they are overlooked because of the protean and more lifethreatening derangements of this disease. In 1 retrospective series, GI symptoms occurred in 36% of cases. Although most patients with abdominal pain and thyrotoxicosis have no demonstrable intra-abdominal pathologic condition, in 1 case series, 16% had an intra-abdominal cause requiring surgery, serving as a reminder that the search for serious medical conditions that have precipitated thyroid storm should not be overlooked. 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 >>

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 >>

Understanding The Presentation Of Diabetic Ketoacidosis

Understanding The Presentation Of Diabetic Ketoacidosis

Hypoglycemia, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar nonketotic syndrome (HHNS) must be considered while forming a differential diagnosis when assessing and managing a patient with an altered mental status. This is especially true if the patient has a history of diabetes mellitus (DM). However, be aware that the onset of DKA or HHNS may be the first sign of DM in a patient with no known history. Thus, it is imperative to obtain a blood glucose reading on any patient with an altered mental status, especially if the patient appears to be dehydrated, regardless of a positive or negative history of DM. In addition to the blood glucose reading, the history — particularly onset — and physical assessment findings will contribute to the formulation of a differential diagnosis and the appropriate emergency management of the patient. Pathophysiology of DKA The patient experiencing DKA presents significantly different from one who is hypoglycemic. This is due to the variation in the pathology of the condition. Like hypoglycemia, by understanding the basic pathophysiology of DKA, there is no need to memorize signs and symptoms in order to recognize and differentiate between hypoglycemia and DKA. Unlike hypoglycemia, where the insulin level is in excess and the blood glucose level is extremely low, DKA is associated with a relative or absolute insulin deficiency and a severely elevated blood glucose level, typically greater than 300 mg/dL. Due to the lack of insulin, tissue such as muscle, fat and the liver are unable to take up glucose. Even though the blood has an extremely elevated amount of circulating glucose, the cells are basically starving. Because the blood brain barrier does not require insulin for glucose to diffuse across, the brain cells are rece Continue reading >>

Metabolic Acidosis

Metabolic 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. See also separate Lactic Acidosis and Arterial Blood Gases - Indications and Interpretations articles. Description Metabolic acidosis is defined as an arterial blood pH <7.35 with plasma bicarbonate <22 mmol/L. Respiratory compensation occurs normally immediately, unless there is respiratory pathology. Pure metabolic acidosis is a term used to describe when there is not another primary acid-base derangement - ie there is not a mixed acid-base disorder. Compensation may be partial (very early in time course, limited by other acid-base derangements, or the acidosis exceeds the maximum compensation possible) or full. The Winter formula can be helpful here - the formula allows calculation of the expected compensating pCO2: If the measured pCO2 is >expected pCO2 then additional respiratory acidosis may also be present. It is important to remember that metabolic acidosis is not a diagnosis; rather, it is a metabolic derangement that indicates underlying disease(s) as a cause. Determination of the underlying cause is the key to correcting the acidosis and administering appropriate therapy[1]. Epidemiology It is relatively common, particularly among acutely unwell/critical care patients. There are no reliable figures for its overall incidence or prevalence in the population at large. Causes of metabolic acidosis There are many causes. They can be classified according to their pathophysiological origin, as below. The table is not exhaustive but lists those that are most common or clinically important to detect. Increased acid Continue reading >>

Metabolic Acidosis: Causes, Symptoms, And Treatment

Metabolic Acidosis: Causes, Symptoms, And Treatment

The Terrible Effects of Acid Acid corrosion is a well-known fact. Acid rain can peel the paint off of a car. Acidifying ocean water bleaches and destroys coral reefs. Acid can burn a giant hole through metal. It can also burn holes, called cavities, into your teeth. I think I've made my point. Acid, regardless of where it's at, is going to hurt. And when your body is full of acid, then it's going to destroy your fragile, soft, internal organs even more quickly than it can destroy your bony teeth and chunks of thick metal. What Is Metabolic Acidosis? The condition that fills your body with proportionately too much acid is known as metabolic acidosis. Metabolic acidosis refers to a physiological state characterized by an increase in the amount of acid produced or ingested by the body, the decreased renal excretion of acid, or bicarbonate loss from the body. Metabolism is a word that refers to a set of biochemical processes within your body that produce energy and sustain life. If these processes go haywire, due to disease, then they can cause an excess production of hydrogen (H+) ions. These ions are acidic, and therefore the level of acidity in your body increases, leading to acidemia, an abnormally low pH of the blood, <7.35. The pH of the blood mimics the overall physiological state in the body. In short, a metabolic process is like a power plant producing energy. If a nuclear power plant goes haywire for any reason, then we know what the consequences will be: uncontrolled and excessive nuclear energetic reactions leading to the leakage of large amounts of radioactive material out into the environment. In our body, this radioactive material is acid (or hydrogen ions). Acidemia can also occur if the kidneys are sick and they do not excrete enough hydrogen ions out of th 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 >>

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 >>

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 >>

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