diabetestalk.net

What Is The Cause Of Metabolic Acidosis?

Causes And Consequences Of Fetal Acidosis

Causes And Consequences Of Fetal Acidosis

The causes and consequences ofacute (minutes or hours) andchronic (days or weeks) fetal acidosis are different In the past much attention has been paid to acute acidosis during labour, but in previously normal fetuses this israrely associated with subsequent damage In contrast, chronic acidosis, which is often not detected antenatally, is associated with a significant increase in neurodevelopmental delay The identification of small for gestational age fetuses by ultrasound scans and the use of Doppler waveforms to detect which of these have placental dysfunction mean that these fetuses can be monitored antenatally Delivery before hypoxia has produced chronic acidosis, may prevent subsequent damage and good timing of delivery remains the only management option at present. What is acidosis? Acidosis means a high hydrogen ion concentration in the tissues. Acidaemia refers to a high hydrogen ion concentration in the blood and is the most easily measured indication of tissue acidosis. The unit most commonly used is pH, which is log to base 10 of the reciprocal of the hydrogen ion concentration. Whereas blood pH can change quickly, tissue pH is more stable. The cut off taken to define acidaemia in adults is a pH of less than 7.36, but after labour and normal delivery much lower values commonly occur in the fetus (pH 7.00), often with no subsequent ill effects. Studies looking at the pH of fetuses from cord blood samples taken antenatally and at delivery have established reference ranges. Other indices sometimes used to assess acidosis are the base excess or bicarbonate. Neither of these is measured by conventional blood gas machines but is calculated from the measured pH and pCO2. The major sources of hydrogen ions in the fetus are carbonic and lactic acids from aerobic and a Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

OVERVIEW a metabolic acidosis is an abnormal primary process or condition leading to an increase in fixed acids in the blood -> resulting in a fall in arterial plasma bicarbonate CAUSES pathophysiological mechanism: (i) A gain of strong acid (ii) A loss of base the gain of strong acid may be endogenous (eg ketoacids from lipid metabolism) or exogenous (NH4Cl infusion). bicarbonate loss may occur via the bowel (diarrhoea, small bowel fistulas) or via the kidneys (carbonic anhydrase inhibitors, renal tubular acidosis). CLASSIFICATION high anion gap Lactate Toxins – methanol, metformin, phenformin, paraldehyde, propylene glycol, pyroglutamic acidosis, iron, isoniazid, ethanol, ethylene glycol, salicylates, solvents Ketones Renal Normal anion gap Chloride Acetazolamide and Addisons GI causes – diarrhoea, vomiting, fistulas (pancreatic, ureterostomies, small bowel, ileostomies) Extras – RTA MAINTENANCE the disorder is maintained as long as the primary cause persists. in many cases the acid-base disturbance tends to increase in severity while the problem causing it persists though this is not absolute. EFFECTS Respiratory Effects hyperventilation (Kussmaul respirations) – this is the compensatory response shift of oxyhaemoglobin dissociation curve (ODC) to the right – due to the acidosis occurs rapidly decreased 2,3 DPG levels in red cells (shifting the ODC back to the left) -> after 6 hours of acidosis, the red cell levels of 2,3 DPG have declined enough to shift the oxygen dissociation curve (ODC) back to normal. Cardiovascular Effects depression of myocardial contractility sympathetic overactivity resistance to the effects of catecholamines peripheral arteriolar vasodilatation venoconstriction of peripheral veins vasoconstriction of pulmonary arteries (increased Continue reading >>

Metabolic Acidosis In The Critically Ill: Part 2. Causes And Treatment

Metabolic Acidosis In The Critically Ill: Part 2. Causes And Treatment

The correct identification of the cause, and ideally the individual acid, responsible for metabolic acidosis in the critically ill ensures rational management. In Part 2 of this review, we examine the elevated (corrected) anion gap acidoses (lactic, ketones, uraemic and toxin ingestion) and contrast them with nonelevated conditions (bicarbonate wasting, renal tubular acidoses and iatrogenic hyperchloraemia) using readily available base excess and anion gap techniques. The potentially erroneous interpretation of elevated lactate signifying cell ischaemia is highlighted. We provide diagnostic and therapeutic guidance when faced with a high anion gap acidosis, for example pyroglutamate, in the common clinical scenario ‘I can’t identify the acid – but I know it's there'. The evidence that metabolic acidosis affects outcomes and thus warrants correction is considered and we provide management guidance including extracorporeal removal and fomepizole therapy. In Part 1 of this review article, we considered the classification and diagnostic approach to metabolic acidosis in the critically ill, including base excess, CO2/HCO–3, and anion gap, and proposed albumin-corrected anion gap-based techniques for bedside use in the critically ill. In Part 2 we examine the types of acidosis further, using a (modified) anion gap methodology, and emphasise points of clinical relevance and common pitfalls in practice. It is often unclear whether metabolic acidosis is a ‘primary’ abnormality, i.e. the patient is unwell because they have accumulated H+, or an epiphenomenon reflecting the effects of the underlying process, or the accumulation a toxic aprote anion species. We will consider the impact that metabolic acidosis may have on prognosis, whether its treatment can improve outc Continue reading >>

Metabolic Acidosis Nclex Review Notes

Metabolic Acidosis Nclex Review Notes

Are you studying metabolic acidosis and need to know a mnemonic on how to remember the causes? This article will give you a clever mnemonic and simplify the signs and symptoms and nursing interventions on how to remember metabolic acidosis for nursing lecture exams and NCLEX. In addition, you will learn how to differentiate metabolic acidosis from metabolic alkalosis. Don’t forget to take the metabolic acidosis and metabolic alkalosis quiz. This article will cover: Metabolic acidosis simplified Lab values expected with metabolic acidosis Causes of metabolic acidosis Signs and symptoms of metabolic acidosis Nursing interventions for metabolic acidosis Lecture on Metabolic Acidosis Metabolic Acidosis Metabolic Acidosis in Simple Terms: a metabolic problem due to the buildup of acid in the body fluids which affects the bicarbonate (HCO3 levels) either from: increased acid production (ex: DKA where ketones (acids) increase in the body which decreases bicarbonate) decreased acid excretion (ex: renal failure where there is high amount of waste left in the body which causes the acids to increase and bicarb can’t control imbalance) loss of too much bicarb (diarrhea) When this acidic phenomena is taking place in the body other systems will try to compensate to increase the bicarb back to normal. One system that tries to compensate is the respiratory system. In order to compensate, the respiratory system will cause the body to hyperventilate by increasing breathing through Kussmaul’s respirations. Kussmaul respirations are deep, rapid breathes. The body hopes this will help expel CO2 (an acid) which will “hopefully” increase the pH back to normal. Lab values expected in Metabolic Acidosis: HCO3: decreased <22 Blood pH: decreased <7.35 CO2: <35 or normal (may be normal b Continue reading >>

Drug And Chemical-induced Metabolic Acidosis.

Drug And Chemical-induced Metabolic Acidosis.

Abstract Metabolic acidosis produced by drugs and/or chemicals can be conveniently divided into those with an increase in the anion gap (anion gap = Na- (Cl + HCO3)) and those with a normal anion gap. The increase in the anion gap is due to the accumulation of unmeasured organic anions, such as lactate or acetoacetate and beta-hydroxybutyrate, as occurs in ketoacidosis and lactic acidosis, or the accumulation of toxic anions such as formate or glycolate, as occurs with the ingestion of methanol or ethylene glycol. Increased concentrations of lactic acid may also be present in the toxic forms of metabolic acidosis. The most common drugs and chemicals that induce the anion gap type of acidosis are biguanides, alcohols, polyhydric sugars, salicylates, cyanide and carbon monoxide. In normal anion gap acidosis the reduction in bicarbonate is balanced by a reciprocal increase in the chloride concentration so that the sum of the two remains unchanged. Normal anion gap acidosis is caused by carbonic anhydrase inhibitors, hydrochloride salts of amino acids, toluene, amphotericin, spironolactone and non-steroidal anti-inflammatory drugs. The mechanism by which these substances produce metabolic acidosis and the therapy are discussed. Continue reading >>

Causes Of Metabolic Acidosis

Causes Of Metabolic Acidosis

In practically every CICM exam paper, the candidates are presented with an ABG (sometimes several) which expect the diagnosis of a metabolic acidosis of some sort. It is therefore essential to develop some sort of mnemonic aid to recall the differential diagnosis of metabolic acidosis. In spite of its many obvious disadvantages, the anion gap classification of metabolic acid-base disorders is useful tool. Causes of Metabolic Acidosis High anion gap Normal anion gap MUD PILES Methanol and other toxic alcohols Uraemia Diabetic (or other) ketoacidosis Pyroglutamic acidosis Iron overdose Lactic acidosis Ethylene glycol Salicylates PANDA RUSH Pancreatic secretion loss Acetazolamide Normal saline intoxication Diarrhoea Aldosterone antagonists Renal tubular acidosis Type 1 (distal) Ureteric diversion Small bowel fistula Hyperalimentation (TPN) The MUDPILES mnemonic is showing its age. Nowhere is there space for citrate, for instance. This is a problem, as several SAQs (eg. Question 3.3 from the second paper of 2013) present the candidate with a citrate-based acidosis. The "P" in PILES used to be "Paraldehyde", but paraldehyde has fallen out of favour since the 1980s, and so "Pyroglutamic acidosis" is probably a better substitute. Iron is not a cause of a high anion gap on its own (in fact, ionised iron is cationic) but it can cause the anion gap to increase when it is removed from solution by its conversion to ferric hydroxide. Also, methanol and ethylene glycol are insufficiently distinct to merit their own individual places in the mnemonic (both are toxic alcohols). In spite of these concerns, the MUDPILES meme is still propagated throughout the medical school curricula, as the educators cynically expect their graduates to never have to seriously think about acidosis. It's s Continue reading >>

Causes Of Respiratory Acidosis, Respiratory Alkalosis, Metabolic Acidosis, & Metabolic Alkalosis And 2 Others

Causes Of Respiratory Acidosis, Respiratory Alkalosis, Metabolic Acidosis, & Metabolic Alkalosis And 2 Others

RESPIRATORY ACIDOSIS ASTHMA. ATELECTASIS. BRAIN TRAUMA. BRONCHIECTASIS. BRONCHITIS. CNS DEPRESSANTS. EMPHYSEMA. HYPOVENTILATION. PULMONARY EDEMA. PNEUMONIA. PULMONARY EMBOLI. METABOLIC ACIDOSIS DIABETES MELLITUS. DIABETIC KETOACIDOSIS. EXCESSIVE DIGESTION OF ASPIRIN. HIGH-FAT DIET. INSUFFICIENT METABOLISM OF CARBS. MALNUTRITION. RENAL INSUFFICIENCY. RENAL FAILURE. SEVERE DIARRHEA. III. What causes disturbances in pH? A. Metabolic acidosis - this is quite common in medical practice. Examples include: 1. Kidney failure 2. Ketosis = excess production of ketone bodies (examples: "ketoacidosis" in diabetes) in malnutrition, people on "ketonic diets" for weight loss) 3. Lactic acidosis (over-production of lactic acid that occurs from heart failure -> hypoxia resulting in anaerobic glucose metabolism). 4. Take note of the fact that the problem doesn't necessary begin with the kidney - but it reflects difference in bicarbonate levels caused by "metabolic" processes throughout body. 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 >>

What Is Metabolic Acidosis?

What Is Metabolic Acidosis?

What keeps your blood from becoming too acidic or basic? How does the body control this? Read this lesson to learn about what happens when this balance is overthrown and the blood becomes too acidic, in a scenario called metabolic acidosis. Your body needs to stay approximately around a given equilibrium to function normally. There is a little bit of wiggle room, but not much, and when things go awry, the body begins to suffer. Our blood is literally our life source - it carries oxygen to the body and helps remove waste materials so we can function properly. Under normal conditions, our blood pH is around 7.4, but sometimes this balance is thrown off and the blood becomes more acidic. This condition is called metabolic acidosis. In this scenario, the body is either producing too much acid, not getting rid of enough acid, or fails to make enough base to neutralize the acid. (A neutral pH value is 7.0; higher numbers are more basic or alkaline and lower numbers are more acidic.) Causes of Metabolic Acidosis Metabolic acidosis sounds like something out of a horror movie - acidic blood?! What would cause the body to do this? Well, there are a few known causes, some of which we'll discuss below. Ketoacidosis: The body creates ketones when it burns fats instead of carbohydrates for energy, and ketones make the blood acidic. When you are fasting, causing your body to switch to fats for fuel, or when you drink too much alcohol, you risk the build up of ketones in the blood. Diabetics are also at risk of this condition when the body fails to produce enough insulin. Lactic acidosis: Notice an acidosis trend here? The body's cells create lactic acid when they are deprived of oxygen. You may experience bouts of lactic acidosis during intense exercise or due to heart conditions. Ren Continue reading >>

Combined Respiratory And Metabolic Acidosis Caused By Bronchospasm In Anaphylactic Shock

Combined Respiratory And Metabolic Acidosis Caused By Bronchospasm In Anaphylactic Shock

Zieliński J. · Koziorowski A. From the Department of Internal Medicine (Prof. Dr. B. Jochweds) and Department of Pathophysiology (Dr. A. Koziorowski), Institute of Tuberculosis, Warszawa Authors’ address: Dr. Jan Zielinski and Dr. Antoni Koziorowski, Instytut Gruzlicy, Klinika Chorób Wewnetrznych, Plocka 26, Warszawa (Poland) 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 >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis, defined as a venous pH < 7.35 is relatively common in dogs. The opposite condition is metabolic alkalosis. Metabolic acidosis is characterized by a decrease in plasma bicarbonate concentration < 18 mEq/L. It occurs as a result of loss of NaHCO3-rich fluids from the intestine or kidneys, increased acid production due to metabolism or reduced excretion of acids (anions). Causes include: Peritoneal dialysis Clinical signs often relate to underlying disease but depression and compensatory tachypnea may be observed. In metabolic acidosis a predisposition of cardiac abnormalities, particularly ventricular arrhythmia and ventricular fibrillation, can be observed. Treatment usually requires addressing underlying disease conditions and aggressive intravenous fluid therapy, usually with lactated Ringer's solution[11]. Only in patients with pH < 7.2, should NaHCO3 be added to the solution. In patients with respiratory acidosis secondary to hypoventilation, NaHCO3 therapy should be avoided because it inevitably decreases respiratory drive, thereby worsening acidosis and hypoxemia[12] As well, dogs with normochloremic metabolic acidosis caused by ketoacidosis are also less likely to benefit from NaHCO3 therapy[13]. In these patients, as organic acids are metabolized they form bicarbonate anions resulting in rebound alkalosis if NaHCO3 has been administered concurrently. References Continue reading >>

Metabolic Acidosis And Hyperventilation Induced By Acetazolamide In Patients With Central Nervous System Pathology

Metabolic Acidosis And Hyperventilation Induced By Acetazolamide In Patients With Central Nervous System Pathology

ACETAZOLAMIDE, a carbonic anhydrase inhibitor, is used in patients with meningeal inflammation, mild intracranial hypertension, and basal skull fractures to decrease the formation of cerebrospinal fluid (CSF). It causes mild metabolic acidosis by inhibiting the reabsorption of bicarbonate (HCO−3) ions from renal tubules. This effect has been used successfully in the treatment of patients with chronic respiratory acidosis with superimposed metabolic alkalosis 1 and central sleep apnea syndrome. 2 Life-threatening metabolic acidosis during acetazolamide therapy has been observed only in patients with renal impairment or 3 diabetes 4 and in elderly patients. 5 Severe metabolic acidosis, associated with acetazolamide, in the absence of other predisposing factors has not been reported in patients with central nervous system disease. We report three cases of severe metabolic acidosis and hyperventilation during acetazolamide therapy in normal doses in adult patients without renal impairment. A 35-yr-old man with a head injury underwent craniotomy for evacuation of a traumatic left temporal extradural hematoma. Postoperatively, the patient underwent mechanical ventilation to maintain a partial pressure of arterial carbon dioxide (Paco2) of 30–35 mmHg. On the third postoperative day, 250 mg acetazolamide administered every 8 h through a nasogastric tube was started to treat a CSF leak from the operative wound. A T-piece trial of weaning was started on the fourth postoperative day. On the fifth postoperative day, patient respiratory rate increased to 40–44 breaths/min. Arterial blood gas analysis showed metabolic acidosis resulting in compensatory hypocapnia and a normal pH (table 1). The patient was sedated and underwent artificial ventilation for the next 6 days. Attempt 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 >>

An Under Recognised Cause Of Metabolic Acidosis

An Under Recognised Cause Of Metabolic Acidosis

The MUDPALES mnemonic for raised anion gap acidosis was drilled into me from medical school. However recently after working through each category I became stumped when nothing ticked the box to identify the cause. The lady I had been asked to see was in her 80s and had fractured her hip. On admission she had normal renal function and acid base status. Post-operatively she was started on regular analgesia including paracetamol (acetaminophen) and developed a Staphlococcus Aureus wound cellulitis treated with flucloxacillin. Over the following 2 weeks she developed a raised anion gap acidosis and positive urinary anion gap. Renal function, lactate and ketones were normal. A cause of metabolic acidosis not in MUDPILES is pyroglutamic acidosis. Pyroglutamic acid (also called 5-oxoproline) is a by-product in the gamma-glutamyl cycle. This pathway is involved in the synthesis of glutathione, and is shown above from a recent paper. Glutathione provides negative feedback on the cycle by inhibiting the enzyme gamma-glutamyl-cysteine synthase. An acquired deficiency in glutathione, as with alcohol or paracetamol, results in loss of this negative feedback and increased production of 5-oxoproline leading to a metabolic acidosis. Other drugs affect the cycle at different points including flucloxacillin which inhibits 5-oxoprolinase similarly resulting in build-up of 5-oxoproline. Urine amino acid screens show high levels of 5-oxoproline, though this test is not always available. Our patient improved with withdrawal of paracetamol and flucloxacillin and oral bicarbonate which was stopped after a week. Some cases have been treated with N-acetylcysteine to replenish glutathione levels. I think this is probably an under-recognised cause of metabolic acidosis with many of the risk factor Continue reading >>

More in ketosis