Alternative Names Acidosis - metabolic Causes Metabolic acidosis develops when too much acid is produced in the body. There are several types of metabolic acidosis: Diabetic acidosis also called diabetic ketoacidosis and DKA develops when substances called ketone bodies which are acidic build up during uncontrolled diabetes.
Hyperchloremic acidosis is caused by the loss of too much sodium bicarbonate from the body, which can happen with severe diarrhea. Kidney disease uremia, distal renal tubular acidosis or proximal renal tubular acidosis.
Lactic acidosis. Poisoning by aspirin, ethylene glycol found in antifreeze , or methanol. Severe dehydration. It can be caused by: Cancer Carbon monoxide poisoning Drinking too much alcohol Exercising vigorously for a very long time Liver failure Low blood sugar hypoglycemia Medicines, such as salicylates, metformin, anti-retrovirals MELAS a very rare genetic mitochondrial disorder that affects energy production Prolonged lack of oxygen from shock, heart failure, or severe anemia Seizures Symptoms Most symptoms are caused by the underlying disease or condition that is causing the metabolic acidosis.
Exams and Tests These tests can help diagnose acidosis. Tests may include: Arterial 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 Other tests may be needed to determine the cause of the acidosis.
Treatment Treatment is aimed at the health problem causing the acidosis. Outlook Prognosis The outlook will depend on the underlying disease causing the condition. Possible Complications Very severe metabolic acidosis can lead to shock or death.
When to Contact a Medical Professional Seek medical help if you have symptoms of any disease that can cause metabolic acidosis. Prevention Diabetic ketoacidosis can be prevented by keeping type 1 diabetes under control.
These results suggest the frequent coexistence of acidosis-induced hypochloremic alkalosis with DKA, and also the important roles of ketoacids in its pathogenesis.
The association of hypochloremia in AG acidosis has been reported in both nephrectomized uremic rats and heminephrectomized rats with H 2 SO 4 or D,L-lactate infusion This has also been reported in critically ill neonates and infants 21 , 22 , as well as DKA in adults The mechanism of acidosis-induced hypochloremic alkalosis remains unclear.
Based on the occurrence of acidosis-induced hypochloremia in nephrectomized and volume-controlled uremic rats, Madias et al 20 concluded that there was no reduction in Cl stores. Instead, they suggested the possibility that an internal ion shift occurred, either of chloride of the extracellular space or of sodium and water into the extracellular fluid. In the present study, the positive BE Cl might have occurred because of a chloride shift from plasma to erythrocytes or interstitial fluids, despite low bicarbonate state, and the negative BE FW might have followed an internal shift of free water 24 , Thus, our results support the argument proposed by Madias et al 20 , and it is likely that these responses might be secondary to ketoacidosis, rather than being compensatory or adaptive An inverse relationship has been noted between the concentrations of plasma bicarbonate and plasma chloride in many clinical situations 20 , 26 , Based on this, the chloride ion has been treated as a passive participant that simply replaces the lost negative charge of the outward-moving bicarbonate.
However, this relationship has not been proven in the context of increased unmeasured anions. In the present study, serum chloride was positively correlated with plasma bicarbonate, which is consistent with the negative correlation between BE Cl and plasma bicarbonate. This may suggest an important role of the ingoing chloride ion in the acid-base balance of the blood 24 , 27 , Therefore, we quantitatively proved the coexistence of hypochloremic alkalosis in DKA, and that serum ketones contributed directly to its pathogenesis.
Therefore, each parameter by the modified BE method can be simply calculated from the reference values for serum sodium and chloride, and comparable with those of other institutions. These represent a practical tool for analyzing acid-base and electrolyte disorders.
Therefore, these could be used as a surrogate of circulating ketoacids. In clinical practice, the BE XA could substitute for the other parameters.
In contrast, several factors including prior hypercapnea, volume contraction, potassium deficiency, chloruretic diuretics, persistent mineralocorticoid excess, etc. In the present study, only two patients with pneumonia showed pCO 2 greater than 44 mm Hg And significant effects of diuretics or ARB were not observed. However, volume contraction with decreased renal function due to dehydration was present on admission, as suggested by the increased mean values of BUN and Hb and decreased eGFR Table 1.
It was consistent with the previous study that the initial renal function seemed to be responsible for the retention of plasma ketones 1. And thus, it seems possible that decreased eGFR might affect on acid-base disorders secondarily through hyperketonemia.
Such dehydration must undoubtedly induce renin-angiotensin-aldosterone system activation, and it may participate in the higher admission systolic BP compared with those after treatment. Although these results did not suggest the direct participation of these factors in the generation and maintenance of acidosis-induced hypochloremic alkalosis, further basic and clinical studies including balance study should be needed for the elucidation of mechanism of acidosis-induced hypochloremic alkalosis.
Finally, the modified BE method could provide useful information for fluid therapy in DKA, when large volumes of saline are generally needed. Although repletion of sodium and chloride is reasonable, there is the possibility that hyperchloremic acidosis can occur 31 , That is, negative BE Cl suggests chloride excess, and thus, it would be the sign for alteration of replacement fluid from normal saline to balance crystalloid solution.
However, we could not clarify the alterations of these parameters during treatment as the present study had the limitation that this was a retrospective study. Further prospective studies are needed to assess the application of the modified BE method. Moreover, the modified BE method was able to detect the independent effects of serum sodium and chloride on acid-base disturbances.
Therefore, subject to prospective study, we recommend this simple and useful tool for acid-base analysis in clinical practice.
Plasma acid-base pattern in diabetic ketoacidosis. N Engl J Med. Google Scholar. Acid-base and electrolyte disturbances in patients with diabetic ketoacidosis. Diabetes Res Clin Pract. Hyperglycemic crisis in adult patients with diabetes. Diabetes Care. Mixed acid-base abnormalities in diabetes. Electrolyte and acid-base disturbances in patients with diabetes mellitus. Wyckoff J , Abrahamson MJ.
Diabetic ketoacidosis and hyperosmolar hyperglycemic state. Joslin's Diabetes Mellitus. Google Preview. Anion gap and hypoalbuminemia. Crit Care Med. Physiological approach to assessment of acid-base disturbance.
Delays in correction of hyponatremia and the use of bicarbonate during DKA treatment are additional risk factors. In patients suspected of having diabetic ketoacidosis, serum electrolytes, blood urea nitrogen BUN and creatinine, glucose, ketones, and osmolarity should be measured.
Urine should be tested for ketones. Patients who appear significantly ill and those with positive ketones should have arterial blood gas measurement.
DKA is diagnosed by an arterial pH 7. Acidemia is serum pH A presumptive diagnosis can be made when urine glucose and ketones are strongly positive. Urine test strips and some assays for serum ketones may underestimate the degree of ketosis because they detect acetoacetic acid and not beta-hydroxybutyric acid, which is usually the predominant ketoacid.
Symptoms and signs of a triggering illness should be pursued with appropriate studies eg, cultures, imaging studies. Adults should have an ECG to screen for acute myocardial infarction and to help determine the significance of abnormalities in serum potassium. Other laboratory abnormalities include hyponatremia, elevated serum creatinine, and elevated plasma osmolality. Hyperglycemia may cause dilutional hyponatremia, so measured serum sodium is corrected by adding 1.
As acidosis is corrected, serum potassium drops. An initial potassium level 4. Rarely IV sodium bicarbonate if pH 7 after 1 hour of treatment. The most urgent goals for treating diabetic ketoacidosis are rapid intravascular volume repletion, correction of hyperglycemia and acidosis, and prevention of hypokalemia 1 Treatment reference Diabetic ketoacidosis DKA is an acute metabolic complication of diabetes characterized by hyperglycemia, hyperketonemia, and metabolic acidosis. Hyperglycemia causes an osmotic diuresis with Identification of precipitating factors is also important.
Treatment should occur in intensive care settings because clinical and laboratory assessments are initially needed every hour or every other hour with appropriate adjustments in treatment. Intravascular volume should be restored rapidly to raise blood pressure and ensure glomerular perfusion; once intravascular volume is restored, remaining total body water deficits are corrected more slowly, typically over about 24 hours.
Initial volume repletion in adults is typically achieved with rapid IV infusion of 1 to 3 L of 0. Adults with diabetic ketoacidosis typically need a minimum of 3 L of saline over the first 5 hours. When blood pressure is stable and urine flow adequate, normal saline is replaced by 0. Pediatric maintenance fluids Maintenance requirements Dehydration is significant depletion of body water and, to varying degrees, electrolytes.
Symptoms and signs include thirst, lethargy, dry mucosa, decreased urine output, and, as the degree Initial fluid therapy should be 0. Hyperglycemia is corrected by giving regular insulin 0. Insulin adsorption onto IV tubing can lead to inconsistent effects, which can be minimized by preflushing the IV tubing with insulin solution. Children should be given a continuous IV insulin infusion of 0. In periods of fasting or starvation when blood glucose is low and insulin production is consequently switched off, fat is metabolized as an alternative energy source.
There are several hormones, the so-called counterregulatory hormones, which oppose the action of insulin; the most important of these is glucagon also produced within the pancreas but, by contrast to insulin, in response to a falling blood glucose.
Glucagon increases blood glucose by promoting the liver production of glucose from non-carbohydrate sources and stored glycogen. Other hormones which oppose the action of insulin include the stress hormones produced by the adrenal glands cortisol and catecholamines growth hormone and estrogen. By integration of the combined action of insulin and the counterregulatory hormones, blood glucose is maintained within narrow limits and cells continue to be supplied with a sufficient source of potential energy to function normally.
In the absence of insulin, glucose in blood cannot enter tissue cells where it is needed to provide energy, and the liver inappropriately continues to release glucose produced from non-carbohydrate sources and breakdown of glycogen to the blood. The inevitable consequence is a rising blood glucose concentration. Most of the clinical signs and symptoms which characterize DKA can be attributed to either raised blood glucose hyperglycemia or lack of glucose within cells.
The abnormalities in results of blood gas analysis stem mainly from lack of glucose within cells but first, for completeness, the consequences of hyperglycemia will be addressed.
Since glucose is an osmotically active substance, this loss of glucose in urine is associated with an osmotic diuresis and resulting dehydration, as an increasing volume of water is lost from the body in urine. Rising plasma osmolarity due to dehydration invokes the thirst response to correct the water deficit. The water deficit reduces blood volume, thereby decreasing blood pressure, so that hypotension is a presenting feature of DKA.
Osmotic diuresis is associated with large losses of electrolytes in urine, so that patients with DKA typically have a whole-body sodium and potassium deficit of mmol and mmol, respectively.
If the fluid losses remain uncorrected, reduced renal blood flow consequent on reduced blood volume threatens renal function. This in turn reduces renal excretion of glucose, thereby exacerbating hyperglycemia and all its deleterious consequences. In extreme cases, patients may present in acute renal failure. In summary, hyperglycemia in DKA causes an osmotic diuresis, which results in severe fluid and electrolyte deficit.
FIG 2. Osmotic diuresis in DKA causes polyuria, glycosuria and electrolyte depletion. These metabolic changes are an extension of the normal physiological response to starvation, when glucose is also in short supply, in this case not because of insulin deficiency, but because dietary carbohydrate, from which glucose is derived, is restricted. When glucose is in short supply, an alternative energy source is provided for in stored fat, and it is this switch to fat metabolism which lies at the root of the disturbance of acid-base balance in patients with DKA.
Fat is stored as triglycerides in adipocytes, the specialized cells of which adipose fat tissue is composed. The mobilization of fat as an alternative energy source begins with the breakdown lipolysis of triglycerides to its constituent free fatty acids and glycerol by the hormone-sensitive enzyme, lipase. Insulin inhibits lipolysis, whilst the counterregulatory hormones promote lipolysis.
In patients with DKA, therefore, lipolysis and the resulting production of free fatty acids proceed relatively unhindered. Free fatty acids are transported, bound to albumin, from adipocytes to tissues around the body where they are oxidized in cell mitochondria to acetyl CoA, providing much needed energy in the form of adenosine triphosphate ATP in the process.
Acetyl CoA is further metabolized to carbon dioxide and water in the citric acid cycle, yielding more energy-rich ATP. The liver provides an alternative fate for acetyl CoA if, as is the case in severe insulin deficiency, its production exceeds the metabolic capacity of the citric acid cycle. In this case, the liver converts some of the acetyl CoA derived from oxidation of fatty acids to the ketoacid, acetoacetic acid.
Collectively, the two ketoacids and acetone are known as ketone bodies or simply ketones. They are released from the liver to blood and delivered to peripheral tissues where the two ketoacids are utilized as energy substrates.
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