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Why Does Metabolic Acidosis Cause Abdominal Pain

Jaime Moo-young, Md

Jaime Moo-young, Md

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

Chapter 16: Acid-base Imbalances

Chapter 16: Acid-base Imbalances

Sort What is the function of a buffer? a) To excrete weak acids b) To secrete hydrogen ions c) To convert strong acids to weak acids d) To convert ammonia to ammonium ions c) To convert strong acids to weak acids -Buffers convert strong acids to weak acids. Excretion of weak acids, secretion of hydrogen ions into the renal tubule, and conversion of ammonia to ammonium ions takes place in the kidneys. A nurse is caring for a patient three days after abdominal surgery who continues to have poorly controlled abdominal pain with green bilious nasogastric output. The patient's respiratory rate is 32 and heart rate is 128. Which acid-base imbalance does the nurse suspect is occurring? a) Mixed acidosis b) Mixed alkalosis c) Metabolic alkalosis d) Respiratory acidosis b) Mixed alkalosis -Mixed alkalosis can occur in a patient who is losing CO2 via hyperventilation (possibly related to pain) while also losing acid by another method, such as prolonged suctioning with a nasogastric tube. Respiratory acidosis occurs when the primary loss of acid is via a respiratory "blow off" of CO2. Metabolic alkalosis occurs with a systemic loss of acid via a metabolic process such as vomiting or suctioning with a nasogastric tube. Mixed acidosis occurs when acid is retained by both respiratory and metabolic systems, such as in a critically ill patient in shock with hypoperfusion and hypoventilation, and will often cause a more profoundly acidotic pH than either condition could independently create. The nurse is caring for a patient that is in respiratory acidosis. What cardiovascular condition should the nurse closely monitor the patient for? a) Diarrhea b) Confusion c) Abdominal pain d) Ventricular fibrillation d) Ventricular fibrillation -Respiratory acidosis causes compensatory hyperkalemia Continue reading >>

Alcoholic Ketoacidosis

Alcoholic Ketoacidosis

Alcoholic ketoacidosis is a metabolic complication of alcohol use and starvation characterized by hyperketonemia and anion gap metabolic acidosis without significant hyperglycemia. Alcoholic ketoacidosis causes nausea, vomiting, and abdominal pain. Diagnosis is by history and findings of ketoacidosis without hyperglycemia. Treatment is IV saline solution and dextrose infusion. Alcoholic ketoacidosis is attributed to the combined effects of alcohol and starvation on glucose metabolism. Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis. Counter-regulatory hormones are increased and may further inhibit insulin secretion. Plasma glucose levels are usually low or normal, but mild hyperglycemia sometimes occurs. Diagnosis requires a high index of suspicion; similar symptoms in an alcoholic patient may result from acute pancreatitis, methanol or ethylene glycol poisoning, or diabetic ketoacidosis (DKA). In patients suspected of having alcoholic ketoacidosis, serum electrolytes (including magnesium), BUN and creatinine, glucose, ketones, amylase, lipase, and plasma osmolality should be measured. Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas and serum lactate measurement. The absence of hyperglycemia makes DKA improbable. Those with mild hyperglycemia may have underlying diabetes mellitus, which may be recognized by elevated levels of glycosylated Hb (HbA1c). Typical laboratory findings include a high anion gap metabolic acidosis, ketonemia, and low levels of potassium, magnesium, and phosphorus. Detection of acidosis may be com 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 >>

Anion Gap (elevated) Differential Diagnosis

Anion Gap (elevated) Differential Diagnosis

Acetaminophen Alcoholic Ketoacidosis Diabetic Ketoacidosis Ethylene Glycol Iron Isoniazid Lactic Acidosis Metformin Methanol Paraldehyde Salicylates Related Content Editors & Reviewers Normal Anion Gap: 8 - 12 +/- 2 Associations: Glucose levels > 250 mg/dL +/- abdominal pain +/- nausea & vomiting + ketones in the urine + serum bicarbonate < 18 Pathophysiology: Insufficient presence of insulin that results in the abnormal breakdown of fatty acids that generate ketoacids. Associations: History of tuberculosis (latent or active) Pathophysiology: Due to functional deficiencies in pyridoxine (vitamin B6) that can serve as a co-factor in metabolic reactions. This leads to a metabolic acidosis. Associations: Numerous medical conditions or drugs containing propylene glycol (lorazepam; phenytoin) Pathophysiology: Lactic acid formation is a byproduct of another underlying problem that prevents its metabolism or prevent pyruvate from entering the Krebs cycle. Associations: Reports of ingestion/Suicide Attempt (or) elderly patient on chronic aspirin +/- mixed acid/base disorder Pathophysiology: Initially stimulates the medullary center in the brain and causes increased respirations leading to respiratory alkalosis. Then shifts to a metabolic acidosis and uncoupling of cellular respiration. 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 >>

Index Of Suspicioncase 1: Acute, Intermittent, And Colicky Abdominal Pain In A 12-year-old Boycase 2: Emesis Since Birth In A 2½-month-old Infantcase 3: Worsening Cough Since Birth In A 16-month-old Toddler

Index Of Suspicioncase 1: Acute, Intermittent, And Colicky Abdominal Pain In A 12-year-old Boycase 2: Emesis Since Birth In A 2½-month-old Infantcase 3: Worsening Cough Since Birth In A 16-month-old Toddler

Case 1 Presentation A 12-year-old boy presents to the emergency department with acute-onset, intermittent, colicky right lower quadrant abdominal pain for 3 to 4 hours. The pain is associated with nausea and one episode of nonbilious, nonbloody vomiting. He has not had diarrhea, constipation, fever, urinary symptoms, trauma, or past similar episodes. On examination, the boy’s temperature is 38.8°C, his heart rate is 146 beats per minute, his respiratory rate is 26 breaths per minute, and his blood pressure is 110/65 mm Hg. He looks tired. His weight is 38.8 kg (35th percentile). Abdominal examination reveals a soft and nondistended abdomen, but he is tender in the left and right lower quadrants. He has no rebound tenderness, guarding, palpable masses, or organomegaly. The findings on the rest of the physical examination are unremarkable. Initial laboratory evaluations show hemoglobin of 13.6 g/dL, a white blood cell count of 18 × 103/μL (82% neutrophils, 12% lymphocytes, 6% monocytes, and 1% eosinophils), and a platelet count of 277 × 103/μL. His blood levels are as follows: total serum bilirubin, 0.6 mg/dL; direct bilirubin, <0.1 mg/dL; alanine aminotransferase, 18 IU/L; aspartate aminotransferase, 28 IU/L; alkaline phosphatase, 175 IU/L; amylase, 34 IU/L; and lipase, 42 IU/L. Serum electrolyte levels are normal. The only abnormality on urinalysis is 1+ blood. Abdominal radiographs show a nonspecific bowel gas pattern. Ultrasonography of the abdomen reveals elongated tubular structures with hypoechoic centers in the small intestine, which suggest a diagnosis (Fig 1). An additional study confirms the diagnosis. Download figure Open in new tab Download powerpoint Case 2 Presentation A 2-month-old boy is referred to our hospitalist service from an outside hospital. Continue reading >>

Non-surgical Causes Of Acute Abdominal Pain

Non-surgical Causes Of Acute Abdominal Pain

Non-Surgical Causes of Acute Abdominal Pain Abdominal pain constitutes 5% of the causes of emergency admissions and is an important part in the practice of emergency services in all centers. Patients may suffer from acute surgical abdomen, acute abdomen with nonsurgical diseases or acute problems of chronic diseases. Abdominal pain is sometimes associated with acute trauma. Clinical assessment is a process where diagnosis and treatment must be done quickly and must be well managed. We have tried here to discuss the non-surgical causes of abdominal pain. 1. Introduction Acute abdomen describes the sudden and severe starting of abdominal pain with unexplained etiology [1]. Case management should be done fairly quickly. Nonsurgical diseases as well as surgical pathologies could be the cause of acute abdomen. Medical history and physical examination findings are very important for assessment. Abdominal pain is the most important sign of acute abdomen but might not be observed in each cases [2]. Especially the elderly and children should be considered for acute abdomen. Abdominal pain is usually a feature, but a pain-free acute abdomen can occur, particularly in older people, in children, in the immunocompromised, and in the women during their last trimester of pregnancy. Acute abdominal complaints are common [3]. The differential diagnosis of acute abdomen should be done as soon as possible with the medical history, physical examination, laboratory and radiological findings; and the diagnosis should be accelerated for patient management [4]. 2. Pathophysiology 2.1. Visceral pain Visceral pain is a kind of a pain resulting from abdominal, pelvic and thoracic organs whose mechanism is not clearly understood and thus, very difficult to identify [5]. Visceral pain is a common, Continue reading >>

Mksap Quiz: Abdominal Pain In A Type 1 Diabetic

Mksap Quiz: Abdominal Pain In A Type 1 Diabetic

A 40-year-old woman is evaluated in the emergency department at 1 a.m. for a 7-hour history of gradually worsening generalized abdominal pain, hyperventilation, and lethargy. Her husband reports difficulty awakening her on several occasions since onset of symptoms, both during the evening and at night. The patient has a 3-day history of nausea and anorexia. She has a 22-year history of type 1 diabetes mellitus treated with insulin. Because she has been unable to eat or drink for the past 3 days, she has reduced her dosage of basal insulin by half and taken no premeal rapid-acting insulin during this period. Her only other medical problem is hypertriglyceridemia. Medications before coming to the emergency department were insulin glargine, prandial insulin glulisine, gemfibrozil, niacin, and daily fish oil. Physical examination shows a lethargic but arousable woman. Temperature is 96.8 °C (36.0 °F), blood pressure is 105/70 mm Hg, pulse rate is 118/min, and respiration rate is 28/min; BMI is 36. Deep sighing respirations are noted, but the chest is clear to auscultation. She has a sweet smell on her breath. Abdominal examination reveals generalized abdominal tenderness with guarding but no rebound tenderness. Bowel sounds are heard in all four quadrants. Laboratory studies show hemoglobin 14.7 g/dL (147 g/L), leukocyte count 23,000/µL (23 × 109/L) with 90% polymorphonuclear leukocytes, sodium 149 mEq/L (149 mmol/L), potassium 5.1 mEq/L (5.1 mmol/L), chloride 92 mEq/L (92 mmol/L), bicarbonate 4 mEq/L (4 mmol/L), fasting glucose 615 mg/dL (34.1 mmol/L), amylase 1168 units/L. Urinalysis shows 4+ glucose, 4+ ketones, no bacteria or leukocytes. A chest radiograph is normal. Besides administering intravenous fluids and insulin, which of the following is the most appropriate Continue reading >>

7,954 Possible Causes For Acidosis + Hyperpnea + Abdominal Pain + Kussmaul Respiration In Usa

7,954 Possible Causes For Acidosis + Hyperpnea + Abdominal Pain + Kussmaul Respiration In Usa

Methanol Poisoning Kussmaul Respiration Acidosis Hyperpnea Abdominal Pain Metabolic Acidosis Symptoms may include a decreased level of consciousness, poor coordination, vomiting, abdominal pain, and a specific smell on the breath.[en.wikipedia.org] After a latency period of 6 to 30 hours, the effects of the toxic metabolites of methanol can cause vomiting, vertigo, abdominal pain, diarrhoea, dyspnoea, acidosis (Kussmaul's[inchem.org] Other symptoms such as hyperpnea, and later, Kussmaul breathing, are indicative of acidosis (see page 10 for a differential diagnosis of acidosis).[nap.edu] Abdominal Cramps Abnormal Renal Function Acid-Base Imbalance Acute Respiratory Failure Agitated Delirium Agitation Anion Gap Increased Arterial Blood pH Decreased Asthenia Bilateral Visual Field Contraction Blurred Vision Brain Edema Central Scotoma Cerebral Edema Chorea Coma Confusion Cortical Blindness Diplopia Dizziness Epigastric Pain Erosive Gastritis Fatigue Frontal Headache Fundoscopy Abnormal Gastric Lavage Giddiness and Lightheadedness Grand Mal Epilepsy Headache Hyperpigmented Optic Disc Hyperventilation Hypocapnia Jaundice Leg Cramp Lethargy Loss of Vision Macula Edema Manic Behavior Muscle Cramp Muscle Weakness Nausea Optic Neuritis Patient Appears Acutely Ill Pediatric Disorder Photophobia Pupillary Abnormality Raw Throat Respiratory Failure Secondary Optic Atrophy Secondary Parkinsonism Seizure Stupor Suicidal Depression Suicidal Ideation Suicide Attempt Tachypnea Toxic Amblyopia Toxic Effect of Methyl Alcohol Toxic Hepatitis Toxic Nephropathy Toxic Retinopathy Transient Blindness Vertigo Visual Acuity Decreased Vomiting Abdominal Pain Caused by Alcohol Abdominal Pain Radiating to the Back Abdominal Pain Radiating to the Inguinal Region Abdominal Pain Relieved by Antacids Continue reading >>

The Evaluation Of Acute Abdominal Pain In The Elderly Patient

The Evaluation Of Acute Abdominal Pain In The Elderly Patient

Abstract Obstetrician/Gynecologists frequently encounter older patients complaining of acute abdominal pain. Because of physiologic changes, medication use, and preexisting conditions, the elderly patient often does not manifest overt signs of disease. Also, while appendicitis is the most common cause of abdominal pain in the general population, biliary disease, small bowel obstruction and perforated viscus constitute the leading etiologies in the geriatric population. The older patient's physical findings often do not correlate with the severity of disease; however, mental status changes, hypothermia, bandemia, and metabolic acidosis are helpful indicators of significant derangement. Emergent abdominal pain, defined as hemodynamic instability such as that caused by massive hemorrhage, requires immediate surgery. Otherwise, the most effective work-up includes a detailed history and physical examination, and selective screening laboratory tests. When the diagnosis is still unclear, repeat physical examination, in-patient observation, and consultation should be considered. The decision of whether to perform diagnostic laparoscopy or laparotomy should be individualized after assessing the patient's entire clinical presentation and progress. Acute abdominal pain in the older patient is associated with low diagnostic accuracy, but high mortality. Therefore, as a primary care physician, the obstetrician/gynecologist must be proficient in the evaluation of acute abdominal pain in the elderly patient. Continue reading >>

Acid-base Imbalances: Metabolic Acidosis And Alkalosis

Acid-base Imbalances: Metabolic Acidosis And Alkalosis

Acid-Base Imbalances: Metabolic Acidosis and Alkalosis; Respiratory Acidosis and Alkalosis The hydrogen ion concentration ([H+]) of the body, described as the pH or negative log of the [H+], is maintained in a narrow range to promote health and homeostasis. The body has many regulatory mechanisms that counteract even a slight deviation from normal pH. An acid-base imbalance can alter many physiological processes and lead to serious problems or, if left untreated, to coma and death. A pH below 7.35 is considered acidosis and above 7.45 is alkalosis. Alterations in hydrogen ion concentration can be metabolic or respiratory in origin or they may have a mixed origin. Metabolic acidosis, a pH below 7.35, results from any nonpulmonary condition that leads to an excess of acids over bases. Renal patients with chronic acidemia may show signs of skeletal problems as calcium and phosphate are released from bone to help with the buffering of acids. Children with chronic acidosis may show signs of impaired growth. Metabolic alkalosis, a pH above 7.45, results from any nonpulmonary condition that leads to an excess of bases over acids. Metabolic alkalosis results from one of two mechanisms: an excess of bases or a loss of acids. Patients with a history of congestive heart failure and hypertension who are on sodium-restricted diets and diuretics are at greatest risk for metabolic alkalosis. Metabolic alkalosis can also be caused by prolonged vomiting, hyperaldosteronism, and diuretic therapy. Respiratory acidosis is a pH imbalance that results from alveolar hypoventilation and an accumulation of carbon dioxide. It can be classified as either acute or chronic. Acute respiratory acidosis is associated with a sudden failure in ventilation. Chronic respiratory acidosis is seen in patient Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Practice Essentials Diabetic ketoacidosis (DKA) is an acute, major, life-threatening complication of diabetes that mainly occurs in patients with type 1 diabetes, but it is not uncommon in some patients with type 2 diabetes. This condition is a complex disordered metabolic state characterized by hyperglycemia, ketoacidosis, and ketonuria. Signs and symptoms The most common early symptoms of DKA are the insidious increase in polydipsia and polyuria. The following are other signs and symptoms of DKA: Nausea and vomiting; may be associated with diffuse abdominal pain, decreased appetite, and anorexia History of failure to comply with insulin therapy or missed insulin injections due to vomiting or psychological reasons or history of mechanical failure of insulin infusion pump Altered consciousness (eg, mild disorientation, confusion); frank coma is uncommon but may occur when the condition is neglected or with severe dehydration/acidosis Signs and symptoms of DKA associated with possible intercurrent infection are as follows: See Clinical Presentation for more detail. Diagnosis On examination, general findings of DKA may include the following: Characteristic acetone (ketotic) breath odor In addition, evaluate patients for signs of possible intercurrent illnesses such as MI, UTI, pneumonia, and perinephric abscess. Search for signs of infection is mandatory in all cases. Testing Initial and repeat laboratory studies for patients with DKA include the following: Serum electrolyte levels (eg, potassium, sodium, chloride, magnesium, calcium, phosphorus) Note that high serum glucose levels may lead to dilutional hyponatremia; high triglyceride levels may lead to factitious low glucose levels; and high levels of ketone bodies may lead to factitious elevation of creatinine levels. Continue reading >>

Hyperphosphatemia, A Cause Of High Anion Gap Metabolic Acidosis: Report Of A Case And Review Of The Literature

Hyperphosphatemia, A Cause Of High Anion Gap Metabolic Acidosis: Report Of A Case And Review Of The Literature

(Department of Nephrology, Jerry L Pettis VA Medical Center, Loma Linda, USA) BACKGROUND: Hyperphosphatemia is a common problem in patients with kidney failure. It is usually mild and rarely severe enough to cause metabolic acidosis on its own. Besides kidney failure, use of phosphate containing enemas, rhabdomyolysis, and tumor lysis syndrome are common causes of severe hyperphosphatemia. CASE REPORT: A 74-year-old man with a history of diabetes mellitus type II, arterial hypertension, and end stage renal disease, who was on hemodialysis and who had undergone hemicolectomy for ischemic bowel disease, and had not eaten for several days, developed severe metabolic acidosis, with an anion gap (AG) of 31 meq/L, uncorrected for serum albumin. At that time he had a high level of beta-hydroxybutyrate and severe hyperphosphatemia (16.5 mg/dL). Metabolic acidosis and hyperphosphatemia were corrected with hemodialysis, confirming the role of hyperphosphatemia in the development of high AG metabolic acidosis. CONCLUSIONS: Although our patient had many reasons to develop high AG metabolic acidosis, hyperphosphatemia played a significant role in his acidosis. Severe hyperphosphatemia is rarely mentioned as a cause of high AG acidosis. It should be added to the long list of causes of this metabolic disorder. Physiological basis of acid base changes are discussed. This paper has been published under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) allowing to download articles and share them with others as long as they credit the authors and the publisher, but without permission to change them in any way or use them commercially. 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 >>

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