what is normal anion gap metabolic acidosis

What are the reasons for high anion gap?

This is referred to as a high anion gap. Acidosis with a large anion gap is usually caused by an excess of organic acids or a proportionate reduction in anion excretion. Lactic acidosis, ketoacidosis, toluene intoxication, metabolic alkalosis, respiratory alkalosis, and severe hyperphosphatemia cause a spike in the anion gap.

What is the normal urine anion gap?

What is the normal range for anion gap? Normal results are 3 to 10 mEq/L, although the normal level may vary from lab to lab. If your results are higher, it may mean that you have metabolic acidosis. Hypoalbuminemia means you have less albumin protein than normal. If you have this condition, your expected normal result must be lower.

What are the symptoms of high anion gap?

• nausea.
• vomiting.
• malaise.
• hyperpnea (long, deep breaths at a normal rate)
• fatigue.
• cardiac dysfunction with hypotension, shock, ventricular arrhythmias.

What does an abnormal "anion gap" indicate?

A high anion gap value means that your blood is more acidic than normal. It may indicate that you have acidosis. Conditions that can cause acidosis (and therefore a high anion gap value) include: diabetic ketoacidosis, a condition requiring immediate medical attention. overdose of salicylates, such as aspirin.

What is high anion gap metabolic acidosis?

High anion gap metabolic acidosis is a form of metabolic acidosis characterized by a high anion gap (a medical value based on the concentrations of ions in a patient's serum). Metabolic acidosis occurs when the body produces too much acid, or when the kidneys are not removing enough acid from the body.

Is anion gap high or low in metabolic acidosis?

Several types of medical conditions can cause abnormal anion gap test results. Your provider will use the results of the anion gap test, your medical history, and other tests to make a diagnosis. A high anion gap test result may mean that you may have acidosis (blood that is more acidic than normal).

What is a normal anion gap?

Normal results are 3 to 10 mEq/L, although the normal level may vary from lab to lab. If your results are higher, it may mean that you have metabolic acidosis.

What anion gap is considered high?

Although there are differences between laboratories and assays, the normal anion gap has traditionally been set between 8 mEq/L to 12 mEq/L. If the anion gap is greater than 12, this suggests an increased presence of unmeasured anions.

What are the lab values for metabolic acidosis?

In metabolic acidosis, the distinguishing lab value is a decreased bicarbonate (normal range 21 to 28 mEq/L). The normal anion gap is 12. Therefore, values greater than 12 define an anion gap metabolic acidosis.

What labs show metabolic acidosis?

Tests may include:Arterial or venous blood gas.Basic metabolic panel, (a group of blood tests that measure your sodium and potassium levels, kidney function, and other chemicals and functions)Blood ketones.Lactic acid test.Urine ketones.Urine pH.

What is severe metabolic acidosis?

What is metabolic acidosis? The buildup of acid in the body due to kidney disease or kidney failure is called metabolic acidosis. When your body fluids contain too much acid, it means that your body is either not getting rid of enough acid, is making too much acid, or cannot balance the acid in your body.

What is considered too low for anion gap?

Results: Based on current clinical data, an anion gap value of < 3 mEq/L should be considered low. A low anion gap is a useful diagnostic tool, but its clinical significance is often unrecognized.

How do you interpret anion gap?

The anion gap is the difference between the number of cations versus anions. An anion gap can be high, normal, or low (rare). A high anion gap indicates the presence of more anions than cations, or acidosis....High anion gap acidosis may be caused by:ketoacidosis.lactic acidosis.renal failure.toxic ingestions.

Should I worry about a high anion gap?

A high anion gap value means that your blood is more acidic than normal. It may indicate that you have acidosis. Conditions that can cause acidosis (and therefore a high anion gap value) include: diabetic ketoacidosis, a condition requiring immediate medical attention.

What medications cause high anion gap?

The most common drugs and chemicals that induce the anion gap type of acidosis are biguanides, alcohols, polyhydric sugars, salicylates, cyanide and carbon monoxide.

How is anion gap metabolic acidosis treated?

Treatment / Management Primary treatment of high anion gap metabolic acidosis requires correction of the underlying cause. In mild to moderate acidosis, treatment could be limited to supportive measures including intravenous fluids and respiratory support.

Why does anion gap increase in acidosis?

An increased or normal anion gap metabolic acidosis is typically due to excess acid and/or decreased base. A reduction in the anion gap is most commonly due to decreased albumin concentration as albumin is the primary unmeasured anion.

What does a low anion gap indicate?

If your blood results reveal a low anion gap, it may mean you have a lower-than-normal level of albumin (hypoalbuminemia). Albumin is an essential protein in your blood. Low albumin may indicate the following conditions: Kidney issues. Heart disease.

What does an anion gap of 6 mean?

The anion gap tells you if your electrolytes are unbalanced, which can cause changes in the acid levels in the blood. An anion gap result can be low, normal, or high. A low anion gap (less than 6 mEq/L) may indicate: Low levels of albumin in the blood (hypoalbuminemia)

Is 17 a high anion gap?

and a normal anion gap is approximately 10—16 mEq/L. An anion gap of 17 or higher represents an increased anion gap, and an anion gap of 9 or lower represents a decreased anion gap. Acid-base disturbances that are characterized by an increased, normal, or decreased anion gap have little mechanistically in common.

What is normal anion gap acidosis?

Normal anion gap acidosis is an acidosis that is not accompanied by an abnormally increased anion gap .

What is the differential diagnosis of anion gap acidosis?

The differential diagnosis of normal anion gap acidosis is relatively short (when compared to the differential diagnosis of acidosis ): Diarrhea: due to a loss of bicarbonate. This is compensated by an increase in chloride concentration, thus leading to a normal anion gap, or hyperchloremic, metabolic acidosis.

What is renal tubular acidosis?

Renal tubular acidosis. Diarrhea: due to a loss of bicarbonate. This is compensated by an increase in chloride concentration, thus leading to a normal anion gap, or hyperchloremic, metabolic acidosis.

Can lactated ringer's solution be used instead of normal saline?

This scenario can be avoided if formulations such as lactated Ringer’s solution are used instead of normal saline to replace GI losses. Hyperparathyroidism – can cause hyperchloremia and increase renal bicarbonate loss, which may result in a normal anion gap metabolic acidosis.

What causes anion gap acidosis in neonates?

The most frequent causes of increased anion-gap metabolic acidosis in the neonate are as follows: hypoxemia or ischemia secondary to perinatal asphyxia; severe lung disease; volume depletion; vasoregulatory disturbances; and myocardial dysfunction caused by immaturity, sepsis, or asphyxia. Severe metabolic acidosis caused by a neonatal metabolic disorder is rare but should always be considered. As discussed earlier, preterm neonates frequently present with a mild to moderate normal anion-gap acidosis, which is almost always the consequence of the low renal bicarbonate threshold of the premature kidney.20,25,26 However, the use of carbonic anhydrase inhibitors and parenteral alimentation, as well as the maturation-related decreased sensitivity to aldosterone, may also contribute to the development of normal anion-gap acidosis in the neonate.2,26,33

How to diagnose metabolic acidosis?

The key to the differential diagnosis of metabolic acidosis is calculating the serum anion gap (Na + − [Cl − + HCO 3−]). This calculation, normally 10 to 15 mmol/L, represents the unmeasured negative ions, predominantly albumin, in blood. Normal anion gap acidosis (low serum HCO3 but normal anion gap) is caused by excess bicarbonate loss from either the gut (diarrhea) or kidney (renal tubular acidosis). An elevated or so-called positive anion gap suggests the presence of another unmeasured anion. Incidentally, a low serum anion gap may be seen in extreme hypoalbuminemia, as occurs in nephrotic syndrome (see Chapters 68 and 71Chapter 68Chapter 71 ).

How does pH restore normal?

Restoration of pH toward normal initially occurs through elimination of the volatile element of the carbonic acid–bicarbonate system via the lungs. This process may be severely compromised in the sick preterm and term neonate with parenchymal lung disease.

Why is the urinary anion gap negative?

Thus, with metabolic acidosis, the urinary anion gap should be negative because of the presence of high levels of ammonium, an unmeasured cation.

What happens to glucose in the absence of oxygen?

In the absence of oxygen, incomplete oxidation of glucose occurs, resulting in the production of lactate and hydrogen ions, which is known as lactic acidosis. 7 (The incomplete oxidation of fatty acids results in the production of ketoacids .) Lactate production is a normal process that occurs in many tissues in the body, such as red blood cells, skin, brain, and muscle. In the liver, this lactate is metabolized to carbon dioxide and water or is used to produce glucose. Both processes consume hydrogen ions, and both generate bicarbonate (see Eq. 31-3 ). Thus, the lactate anion can be considered a precursor of bicarbonate. Lactate is normally present in low levels (<2 mmol/l) in plasma.

Why is urine pH above 6.0?

Urine pH can be misleading and in chronic diarrhea may be above 6.0 because of substantial increases in renal ammonia metabolism that result in increased urine pH from the buffering ability of the ammonia. Although the clinical history should distinguish between these two possibilities, in a patient with surreptitious laxative abuse, this may not be helpful because diarrhea may not be reported. Colonoscopy may be required to demonstrate characteristic findings of laxative abuse (such as melanosis coli), if this diagnosis is being considered.

What is the normal range of anions?

The normal range is 10 to 14 mmol/l. Sometimes potassium is included in the calculation, in which case the normal range is 14 to 18 mmol/l. Most unmeasured anions arise from negative charges carried on plasma proteins, particularly albumin. Thus, a low plasma concentration of albumin reduces the anion gap. For every 10 g/l decrease in plasma albumin concentration, the anion gap is reduced by 4 mmol/l.

How many patients have low anion gap?

In a study of over 67,000 calculations of the anion gap, the prevalence of a low anion gap value was found in only 304 (0.8%) out of the 39,360 patients whose electrolyte blood levels were studied, and only 19 of them had a repeatedly low anion gap [ 37 ].

What is the anion gap?

The anion gap is a value that represents the difference between positively charged ions (cations) and negatively charged ions (anions) in the blood. The anion gap cannot be directly measured, instead, it is calculated from the results of an electrolyte panel, another type of blood test. The anion gap is calculated using the concentrations ...

What is the term for the concentration of cations and anions in the blood?

Although the term anion gap usually refers to the concentrations of cations and anions in the blood, it can also refer to their concentrations in the urine, which is also clinically useful [ 3 ].

What is the purpose of anion gap?

The anion gap is primarily used to determine the cause of metabolic acidosis, a condition where the body is producing too much acid or not enough acid is being removed from the body.

What should the total positive charge from cations equal?

In the body, the total positive charge from cations should equal the total negative charge from anions in the blood to maintain overall neutrality.

How to treat metabolic acidosis?

Some possible treatments for metabolic acidosis include detoxification if caused by drugs or toxins and insulin if the condition is caused by diabetes [ 9 ].

What is the condition where the body produces too much lactic acid?

Lactic acidosis – a condition where the body produces too much lactic acid [ 9, 10, 11] Diabetic ketoacidosis – a serious, life-threatening complication of diabetes resulting from excess production of ketones, which are byproducts of fat breakdown used as an alternative energy source [ 12, 13]

How to calculate anion gap?

Starting with a basic metabolic panel (BMP) or serum electrolyte panel, the anion gap (AG) should be calculated by subtracting the major anions (chloride & bicarbonate) from the major cation (sodium). Some sources argue for the use of potassium, but it has traditionally been omitted.  Consider integrating it in patients with grossly abnormal potassium values. The single largest source of unmeasured anions in the healthy population is albumin, which is why evaluation of, and correction for, hypo/hyperalbuminemia will improve the accuracy of the high anion gap Metabolic Acidosis evaluation. The correction factor of +2.5 mEq per 1 g/dL of albumin below the baseline of four is standard. Therefore, failure to correct for a low albumin would falsely depress the AG, potentially masking the presence of high anion gap Metabolic Acidosis.

What is high anion gap?

High anion gap metabolic acidosis is one of the most common metabolic derangements seen in critical care patients. Exact numbers are not readily available.

What is the best treatment for high anion gap?

In mild to moderate acidosis, treatment could be limited to supportive measures including intravenous fluids and respiratory support. Alkalization therapy should be reserved for those individuals with severe acidosis (pH less than 7.1). In the case of diabetic ketoacidosis (DKA), this value is even lower (pH less than 6.9). The most common alkalizing agent is sodium bicarbonate, but sodium and potassium citrate are alternative options. In the event of severe, recalcitrant acidosis, it may be appropriate to treat empirically with alcohol dehydrogenase inhibitors (fomepizole or ethanol) and prepare the patient for emergent hemodialysis. Fomepizole prevents the conversion of alcohols into toxic metabolites through competitive inhibition of alcohol dehydrogenase. Ethanol is not preferred, but it has a similar mechanism of action because alcohol dehydrogenase has a greater affinity for ethanol than for methanol or ethylene glycol.  Importantly, fomepizole has the greatest impact on outcomes when given within six hours of presentation; however, given it is frequently in short supply and prohibitively expensive, universal treatment of all high anion gap metabolic acidosis with fomepizole is not advised.

What is the toxic metabolite of acetaminophen?

Oxoproline (pyr oglutamic acid, the toxic metabolite of excessive acetaminophen or paracetamol)

What is the treatment for DKA?

Treatment of the underlying disorder may require glucose and insulin in the case of DKA, antibiotics and goal-directed fluid administration in the case of sepsis or administration of specific antitoxins (e.g., fomepizole or n-acetylcysteine) in the case of toxic ingestions.

Does microscopy show anion gap?

Microscopy has limited value in the evaluation of high anion gap metabolic acidosis.  One exception is the ingestion of ethylene glycol. Given that the breakdown products of ethylene glycol include oxalate, sufficient doses can produce calcium oxalate monophosphate crystal that deposits into tissues (e.g., kidneys, brain) and precipitates in the urine.  Calcium oxalate monophosphate can be seen on urine microscopy and are shaped like dumbbells, spindles, ovals or picket fences. These are differentiated from calcium oxalate diphosphate crystals, which are octahedral and traditionally described as "envelope shaped."

Is metformin a cause of lactic acidosis?

In fact, a Cochrane review found substantial evidence that metformin was not a cause of lactic acidosis. The same could not be said of the older biguanide, phenformin, which does increase the incidence of lactic acidosis by approximately tenfold.

What is normal anion gap acidosis?

In renal physiology , normal anion gap acidosis, and less precisely non-anion gap acidosis, is an acidosis that is not accompanied by an abnormally increased anion gap . The most common cause of normal anion gap acidosis is diarrhea with a renal tubular acidosis being a distant second. The differential diagnosis of normal anion gap acidosis is relatively short (when compared to the differential diagnosis of acidosis): Diarrhea : due to a loss of bicarbonate. This is compensated by an increase in chloride concentration, thus leading to a normal anion gap, or hyperchloremic, metabolic acidosis. The pathophysiology of increased chloride concentration is the following: fluid secreted into the gut lumen contains higher amounts of Na+ than Cl; large losses of these fluids, particularly if volume is replaced with fluids containing equal amounts of Na+ and Cl, results in a decrease in the plasma Na+ concentration relative to the Clconcentration. This scenario can be avoided if formulations such as lactated Ringers solution are used instead of normal saline to replace GI losses. [2] Continue reading >>

What is non-gapped metabolic acidosis?

Non-gap metabolic acidosis, or hyperchloremic metabolic acidosis, are a group of disorders characterized by a low bicarbonate, hyperchloremia and a normal anion gap (10 -12). A non-gapped metabolic acidosis fall into three categories: 1) loss of base (bicarbonate) from the gastrointestinal (GI) tract or 2) loss of base (bicarbonate) from the kidneys, 3) intravenous administration of sodium chloride solution. Bicarbonate can be lost from the GI tract (diarrhea) or from the kidneys (renal tubular acidosis) or displaced by chloride. A. What is the differential diagnosis for this problem? Proximal renal tubular acidosis: (low K+) Distal renal tubular acidosis: (low or high K+) Prostaglandin Inhibitors, (aspirin, nonsteroidal anti-inflammatory drugs, cyclooxygenase 2 inhibitors) Adrenal insufficiency (primary or secondary) (high K+) Pseudoaldosteronism, type 2 (Gordon's syndrome) B. Describe a diagnostic approach/method to the patient with this problem. Metabolic acidosis can be divided into two groups based on anion gap. If an anion gap is elevated (usually greater than 12), see gapped metabolic acidosis. Diagnosis of the cause of non-gapped metabolic acidosis is usually clinically evident - as it can be attributed to diarrhea, intravenous saline or by default, renal tubular acidosis. Occasionally, it may not be clear whether loss of base occurs due to the kidney or bowel. In such a case, one should calculate the urinary anion gap. The urinary anion gap (UAG) = sodium (Na+)+K+- chloride (Cl-). Caution if ketonuria or drug anions are in the urine as it would invalidate the calculation. As an aid, UAG is neGUTive when associated with bowel causes. Non-gapped metabolic acidosis can further be divided into two categories: 1. Historical information important in the diagnosis of Continue reading >>

What is the cause of acute non anion gap acidosis?

Acute non-anion gap metabolic acidosis, also termed hyperchloremic acidosis, is frequently detected in seriously ill patients. The most common mechanisms leading to this acid–base disorder include loss of large quantities of base secondary to diarrhea and administration of large quantities of chloride-containing solutions in the treatment of hypovolemia and various shock states. The resultant acidic milieu can cause cellular dysfunction and contribute to poor clinical outcomes. The associated change in the chloride concentration in the distal tubule lumen might also play a role in reducing the glomerular filtration rate. Administration of base is often recommended for the treatment of acute non-anion gap acidosis. Importantly, the blood pH and/or serum bicarbonate concentration to guide the initiation of treatment has not been established for this type of metabolic acidosis; and most clinicians use guidelines derived from studies of high anion gap metabolic acidosis. Therapeutic complications resulting from base administration such as volume overload, exacerbation of hypertension and reduction in ionized calcium are likely to be as common as with high anion gap metabolic acidosis. On the other hand, exacerbation of intracellular acidosis due to the excessive generation of carbon dioxide might be less frequent than in high anion gap metabolic acidosis because of better tissue perfusion and the ability to eliminate carbon dioxide. Further basic and clinical research is needed to facilitate development of evidence-based guidelines for therapy of this important and increasingly common acid–base disorder. Introduction Acute metabolic acidosis (defined temporally as lasting minutes to a few days) has traditionally been divided into two major categories based on the level Continue reading >>

What causes a decrease in pH?

Decrease in pH due to decrease in serum HCO3- Related to either loss of HCO3- or gain of H+ caused by: -Exogenous acid=e.g. ethylene glycol overdose -Kidneys=e.g. proximal renal tubular acidosis (Type 2 RTA) 3. Inability to excrete normal daily acid production by kidneys-e.g. advanced kidney disease, distal renal tubular acidosis (Type 1 RTA) Laboratory Findings in Metabolic Acidosis Decreased pCO2 (to compensate for low HCO3-) Clinically divide metabolic acidoses based on whether patient has elevated anion gap or normal anion gap Anion Gap=difference between measured cations and anions What are the common circulating cations and anions? Cations: Sodium, Potassium, Calcium, Magnesium, Proteins Anions: Chloride, Bicarbonate, Sulfates, Phosphates, Albumin, Other proteins Not practical to measure all of these, so the ones easiest to measure/in greatest abundance are measured=Sodium, Chloride, and Bicarbonate Normal Anion Gap Metabolic Acidosis (Hypercholermic metabolic acidosis) Normal anion gap metabolic acidosis characterized by decrease in bicarbonate and increase in chloride =HCl+NaHCO3-> NaCl +H2CO3-> CO2+ H2O+ NaCl H+ +Cl- +HCO3- -> Cl- + H2CO3-> H2O+CO2 +Cl- Net result=loss of bicarbonate and gain of chloride HCO3- replaced by measured anion (Cl-), so sum of Cl- + HCO3- remains unchanged=no change in anion gap What are the main causes of normal anion gap metabolic acidosis? Decreased ability to excrete H+ by kidney What are metabolic consequences of diarrhea or renal HCO3- wasting? 2. In response to volume loss and to maintain electroneutrality the kidney will hold on to Cl- 3. Sum result is loss of HCO3- and gain of Cl- What are metabolic consequences of the kidneys inability to excrete adequate H+? 2. Is buffered by HCO3- (H+ +HCO3- ->H2CO3-> H2O+CO2) Occurs when Continue reading >>

What is the pathophysiology of metabolic acidosis?

Practice Essentials This article covers the pathophysiology and causes of hyperchloremic metabolic acidoses, in particular the renal tubular acidoses (RTAs). [1, 2] It also addresses approaches to the diagnosis and management of these disorders. A low plasma bicarbonate (HCO3-) concentration represents, by definition, metabolic acidosis, which may be primary or secondary to a respiratory alkalosis. Loss of bicarbonate stores through diarrhea or renal tubular wasting leads to a metabolic acidosis state characterized by increased plasma chloride concentration and decreased plasma bicarbonate concentration. Primary metabolic acidoses that occur as a result of a marked increase in endogenous acid production (eg, lactic or keto acids) or progressive accumulation of endogenous acids when excretion is impaired by renal insufficiency are characterized by decreased plasma bicarbonate concentration and increased anion gap without hyperchloremia. The initial differentiation of metabolic acidosis should involve a determination of the anion gap (AG). This is usually defined as AG = (Na+) - [ (HCO3- + Cl-)], in which Na+ is plasma sodium concentration, HCO3- is bicarbonate concentration, and Cl- is chloride concentration; all concentrations in this formula are in mmol/L (mM or mEq/L) (see also the Anion Gap calculator). The AG value represents the difference between unmeasured cations and anions, ie, the presence of anions in the plasma that are not routinely measured. An increased AG is associated with renal failure, ketoacidosis, lactic acidosis, and ingestion of certain toxins. It can usually be easily identified by evaluating routine plasma chemistry results and from the clinical picture. A normal AG acidosis is characterized by a lowered bicarbonate concentration, which is counte Continue reading >>

What is the mnemonic for non-anion gap?

Mnemonic for NON-Anion Gap Metabolic Acidosis As I've mentioned previously on this blog, the "MUDPALES" mnemonic for anion gap metabolic acidosis is one of the most successful medical mnemonic's of all time. A less successful (and admittedly less useful) mnemonic exists for non-anion gap metabolic acidoses (NAGMA), which I learned as a resident. It's "HARDUP", which stands for the following: H = hyperalimentation (e.g., starting TPN). R = renal tubular acidosis (Type I = distal; Type II = proximal; Type IV = hyporeninemic hypoaldosteronism. U = uretosigmoid fistula (because the colon will waste bicarbonate). P = pancreatic fistula (because of alkali loss--the pancreas secretes a bicarbonate-rich fluid). Practically speaking however, the two main causes you really have to remember for NAGMA are DIARRHEA or RENAL TUBULAR ACIDOSIS, which 90% of the time you can distinguish between based on the history alone. Another way to think about the differential diagnosis of NAGMA is to ask whether or not there is GI LOSS or RENAL LOSS of bicarbonate. If the history does not provide an obvious explanation, one can distinguish between GI versus renal bicarbonate losses by determining the urine anion gap (urine AG = urine Na + urine K - urine Cl), where a positive value indicates renal bicarbonate loss whereas a largely negative value indicates extra-renal bicarbonate loss. Continue reading >>

What is acid base disorder?

Content currently under development Acid-base disorders are a group of conditions characterized by changes in the concentration of hydrogen ions (H+) or bicarbonate (HCO3-), which lead to changes in the arterial blood pH. These conditions can be categorized as acidoses or alkaloses and have a respiratory or metabolic origin, depending on the cause of the imbalance. Diagnosis is made by arterial blood gas (ABG) interpretation. In the setting of metabolic acidosis, calculation of the anion gap is an important resource to narrow down the possible causes and reach a precise diagnosis. Treatment is based on identifying the underlying cause. Continue reading >>

Why is anion gap metabolic acidosis important?

Anion gap metabolic acidosis is frequently due to anaerobic metabolism and lactic acid accumulation. While lactate is part of many mnemonics for metabolic acidosis, it is important to distinguish it is not a separate etiology, but rather a consequence of a condition.

What causes non-gap metabolic acidosis?

Non-gap metabolic acidosis is primarily due to the loss of bicarbonate, and the main causes of this condition are diarrhea and renal tubular acidosis. Additional and rarer etiologies include Addison’s disease, ureterosigmoid or pancreatic fistulas, acetazolamide use, and hyperalimentation through TPN initiation.  GI and renal losses of bicarbonate can be distinguished via urine anion gap analysis:

What is the pH of acidosis?

Determining the type of metabolic acidosis can help clinicians narrow down the cause of the disturbance. Acidemia refers to a pH less than the normal range of 7.35 to 7.45. In addition, metabolic acidosis requires a bicarbonate value less than 24 mEq/L. Further classification of metabolic acidosis is based on the presence or absence of an anion gap, or concentration of unmeasured serum anions. Plasma neutrality dictates that anions must balance cations to maintain a neutral charge. Therefore, sodium (Na), the primary plasma cation, is balanced by the sum of the anions bicarbonate and chloride in addition to the unmeasured anions, which represent the anion gap. Unmeasured anions include lactate and acetoacetate, and these are often some of the main contributors to metabolic acidosis. [7][8][9]

What is metabolic acidosis?

Metabolic acidosis is characterized by an increase in the hydrogen ion concentration in the systemic circulation that results in an abnormally low serum bicarbonate level. Metabolic acidosis signifies an underlying disorder that needs to be corrected to minimize morbidity and mortality.

What is the term for the total acid-base status of the serum pH?

The term acidemia is used to define the total acid-base status of the serum pH. For example, a patient can have multiple acidoses contributing to a net acidemia. Its origin classifies acidosis as either a respiratory acidosis which involves changes in carbon dioxide, or metabolic acidosis which is influenced by bicarbonate (HCO3).[1][2][3] ...

What are the mechanisms of metabolic acidosis?

The many etiologies of metabolic acidosis are classified into 4 main mechanisms: increased production of acid, decreased excretion of acid, acid ingestion, and renal or gastrointestinal (GI) bicarbonate losses. [4][5][6]

Why is acid-base interpretation important?

Acid-base interpretation is crucial to identify and correct disturbances in acid-base equilibrium that have profound consequences on patient health. The following steps use lab values and equations to determine if a patient has metabolic acidosis and any additional acid-base disturbances.

How to correct metabolic acidosis in infants?

Infants will try to correct metabolic acidosis by a reflex respiratory alkalosis using hyperventilation and Kussmaul respirations. More severe uncompensated acidosis can decrease peripheral vascular resistance and cardiac ventricular function, leading to hypotension, pulmonary edema, and tissue hypoxia, which will further complicate the picture by increasing lactate production because of hypoxia ...

Why does acidosis occur in neonates?

Metabolic acidosis in the neonate can be caused by several reasons, including increased acid intake from exogenous sources; increased endogenous production of an acid, such as seen in an inborn error of metabolism (IEM); inadequate excretion of acid by the kidneys; or excessive loss of bicarbonate in urine or stool.

What is the difference between anions and cations?

Anions are molecules that contain a negative charge. Cations are molecules that contain a positive charge. Generally, the total amount of anions and cations in plasma, serum, or urine are equivalent. The anion gap (AG) is the difference between the measured anions and cations and can be calculated by subtracting the concentrations ...

What is the average pH of neonates?

Neonates have an average arterial pH of 7.37 (range of 7.35–7.45). The average bicarbonate level in a neonate is 20 mEq/L. A diagnosis of metabolic acidosis can be made when the pH is less than 7.35 and a base deficit greater than 5 exists. 1. + +.

What is a normal AG?

A normal AG is typically less than 12 mEq/L. 1 If the AG is elevated (ie, > 15 mEq/L), then there are anions that have not been accounted for, and an investigation must be performed to search for the culprit.

How to calculate AG?

The AG equation can be written as AG = ( [Na + ]) − ( [Cl −] + [HCO 3− ]). A normal AG is typically less than 12 mEq/L. 1 If the AG is elevated (ie, > 15 mEq/L), then there are anions that have not been accounted for, and an investigation must be performed to search for the culprit. Common anions that result in an elevated AG include lactate and the ketone bodies β-hydroxybutyrate and acetoacetate. Neonates with intoxication IEMs usually have elevated AGs from accumulation of the toxic organic acid, such as isovaleric acid in isovaleric acidemia (IVA), in addition to lactate and ketone bodies secondary to clinical decompensation.