-
Critical Care Clinics Apr 2002Metabolic acidosis is a common occurrence in critically ill patients. Understanding the pathological mechanisms underlying the generation of protons will enable the... (Review)
Review
Metabolic acidosis is a common occurrence in critically ill patients. Understanding the pathological mechanisms underlying the generation of protons will enable the clinician to quickly recognize these disorders and establish an acceptable treatment strategy. This article presents a logical approach to metabolic acidosis.
Topics: Acid-Base Imbalance; Acidosis; Acidosis, Lactic; Chlorides; Diabetic Ketoacidosis; Ethanol; Humans; Intensive Care Units; Poisoning; Renal Insufficiency
PubMed: 12053835
DOI: 10.1016/s0749-0704(01)00012-4 -
Drug Safety May 2010Metabolic acidosis may occasionally develop in the course of treatment with drugs used in everyday clinical practice, as well as with the exposure to certain chemicals.... (Review)
Review
Metabolic acidosis may occasionally develop in the course of treatment with drugs used in everyday clinical practice, as well as with the exposure to certain chemicals. Drug-induced metabolic acidosis, although usually mild, may well be life-threatening, as in cases of lactic acidosis complicating antiretroviral therapy or treatment with biguanides. Therefore, a detailed medical history, with special attention to the recent use of culprit medications, is essential in patients with acid-base derangements. Effective clinical management can be handled through awareness of the adverse effect of certain pharmaceutical compounds on the acid-base status. In this review, we evaluate relevant literature with regard to metabolic acidosis associated with specific drug treatment, and discuss the clinical setting and underlying pathophysiological mechanisms. These mechanisms involve renal inability to excrete the dietary H+ load (including types I and IV renal tubular acidoses), metabolic acidosis owing to increased H+ load (including lactic acidosis, ketoacidosis, ingestion of various substances, administration of hyperalimentation solutions and massive rhabdomyolysis) and metabolic acidosis due to HCO3- loss (including gastrointestinal loss and type II renal tubular acidosis). Determinations of arterial blood gases, the serum anion gap and, in some circumstances, the serum osmolar gap are helpful in delineating the pathogenesis of the acid-base disorder. In all cases of drug-related metabolic acidosis, discontinuation of the culprit medications and avoidance of readministration is advised.
Topics: Acid-Base Equilibrium; Acidosis; Acidosis, Lactic; Acidosis, Renal Tubular; Bicarbonates; Diabetic Ketoacidosis; Humans
PubMed: 20397738
DOI: 10.2165/11533790-000000000-00000 -
Anaesthesia Apr 2008The correct identification of the cause, and ideally the individual acid, responsible for metabolic acidosis in the critically ill ensures rational management. In Part 2... (Review)
Review
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.
Topics: Acid-Base Equilibrium; Acidosis; Acidosis, Lactic; Acidosis, Renal Tubular; Critical Illness; Humans; Prognosis
PubMed: 18336491
DOI: 10.1111/j.1365-2044.2007.05371.x -
Anaesthesia Mar 2008Metabolic acidaemia (pH < 7.35 not primarily related to hypoventilation) is common amongst the critically ill and it is essential that clinicians caring for such... (Review)
Review
Metabolic acidaemia (pH < 7.35 not primarily related to hypoventilation) is common amongst the critically ill and it is essential that clinicians caring for such patients have an understanding of the common causes. The exclusive elimination routes of volatile (carbon dioxide), organic (lactic and ketone) and inorganic (phosphate and sulphate) acids mean compensation for a defect in any one is limited and requires separate provision during critical illness. We discuss the models available to diagnose metabolic acidosis including CO2/HCO3(-) and physical chemistry-derived (Stewart or Fencl-Stewart) approaches, but we propose that the base excess and anion gap, corrected for hypoalbuminaemia and iatrogenic hyperchloraemia, remain most appropriate for clinical usage. Finally we provide some tips for interpreting respiratory responses to metabolic acidosis and how to reach a working diagnosis, the consequences of which are considered in Part 2 of this review.
Topics: Acid-Base Equilibrium; Acidosis; Chemical Phenomena; Chemistry, Physical; Critical Illness; Humans; Hydrogen-Ion Concentration
PubMed: 18289237
DOI: 10.1111/j.1365-2044.2007.05370.x -
American Journal of Kidney Diseases :... Nov 2021
Topics: Acidosis; Humans; Hyponatremia; Melanoma
PubMed: 34688455
DOI: 10.1053/j.ajkd.2021.05.025 -
Nephrology, Dialysis, Transplantation :... May 2023Guidelines recommend treatment of metabolic acidosis (MA) in patients with chronic kidney disease (CKD), but the diagnosis and treatment rates in real-world settings are...
BACKGROUND
Guidelines recommend treatment of metabolic acidosis (MA) in patients with chronic kidney disease (CKD), but the diagnosis and treatment rates in real-world settings are unknown. We investigated the frequency of MA treatment and diagnosis in patients with CKD.
METHODS
In this retrospective cohort study, we examined administrative health data from two US databases [Optum's de-identified Integrated Claims + Clinical Electronic Health Record Database (US EMR cohort; 1 January 2007 to 30 June 2019) and Symphony Health Solutions IDV® (US claims cohort; 1 May 2016 to 30 April 2019)] and population-level databases from Manitoba, Canada (1 April 2006 to 31 March 2018). Patients who met laboratory criteria indicative of CKD and chronic MA were included: two consecutive estimated glomerular filtration results <60 mL/min/1.73 m2 and two serum bicarbonate results 12 to <22 mEq/L over 28-365 days. Outcomes included treatment of MA (defined as a prescription for oral sodium bicarbonate) and a diagnosis of MA (defined using administrative records). Outcomes were assessed over a 3-year period (1 year pre-index, 2 years post-index).
RESULTS
A total of 96 184 patients were included: US EMR, 6179; Manitoba, 3223; US Claims, 86 782. Sodium bicarbonate treatment was prescribed for 17.6%, 8.7% and 15.3% of patients, and a diagnosis was found for 44.7%, 20.9% and 20.9% of patients, for the US EMR, Manitoba and US Claims cohorts, respectively.
CONCLUSIONS
This analysis of 96 184 patients with laboratory-confirmed MA from three independent cohorts of patients with CKD and MA highlights an important diagnosis and treatment gap for this disease-modifying complication.
Topics: Humans; Sodium Bicarbonate; Retrospective Studies; Acidosis; Renal Insufficiency, Chronic; Bicarbonates
PubMed: 36323446
DOI: 10.1093/ndt/gfac299 -
Mineral and Electrolyte Metabolism 1998Metabolic acidosis increases protein degradation resulting in muscle wasting and a negative nitrogen balance. The branched-chain amino acids serve as useful markers of... (Review)
Review
Metabolic acidosis increases protein degradation resulting in muscle wasting and a negative nitrogen balance. The branched-chain amino acids serve as useful markers of these changes and their catabolism is increased in acidosis, particularly for the spontaneous acidosis associated with renal failure. As a result, the neutral nitrogen balance is compromised and malnutrition results. Glucocorticoids mediate these changes through the recently discovered ATP-dependent ubiquitin-proteasome pathway. Therapy necessitates correction of the underlying acidosis either through adjustment of the alkalinity of the dialysate for the patient on dialysis or through dietary protein restriction and sodium bicarbonate supplements for the predialysis patient.
Topics: Acidosis; Amino Acids, Branched-Chain; Dietary Proteins; Humans; Kidney Failure, Chronic; Muscle Proteins; Proteins; Sodium Bicarbonate; Ubiquitins
PubMed: 9397412
DOI: 10.1159/000057345 -
The Veterinary Clinics of North... Mar 2017High anion gap (AG) metabolic acidoses can be identified by a decrease in pH, decrease in HCO or base excess, and an increased AG. The AG represents the difference... (Review)
Review
High anion gap (AG) metabolic acidoses can be identified by a decrease in pH, decrease in HCO or base excess, and an increased AG. The AG represents the difference between unmeasured cations and unmeasured anions; it increases secondary to the accumulation of anions other than bicarbonate and chloride. The most common causes of high AG acidosis are renal failure, diabetic ketoacidosis, and lactic acidosis. Severe increases in concentration of phosphorus can cause hyperphosphatemic acidosis.
Topics: Acid-Base Equilibrium; Acidosis; Acidosis, Lactic; Algorithms; Animals; Diabetic Ketoacidosis
PubMed: 28017408
DOI: 10.1016/j.cvsm.2016.11.002 -
Kidney International. Supplement Jul 2005In patients with chronic kidney disease, metabolic acidosis can occur as a result of insufficient ammoniagenesis within the damaged kidney. This, in turn, can bring... (Review)
Review
In patients with chronic kidney disease, metabolic acidosis can occur as a result of insufficient ammoniagenesis within the damaged kidney. This, in turn, can bring about a variety of sequella that have their basis in hormonal and cellular abnormalities that effect stunted growth, loss of muscle and bone mass, and negative nitrogen balance. Cellular mechanisms accounting for these findings are reviewed. In bone, metabolic acidosis causes direct dissolution of bone; ostoeclastic activity is increased while osteoblastic activity is suppressed. In muscle, branched-chain amino acid oxidation is increased and the ubiquitin-proteasome pathway is activated: muscle wasting results. Even a modest degree of metabolic acidosis can be harmful and can initiate a series of maladaptive responses that are not easily reversed, although there is evidence that alkali therapy can be beneficial in reversing these responses.
Topics: Acidosis; Chronic Disease; Humans; Kidney Diseases
PubMed: 15954945
DOI: 10.1111/j.1523-1755.2005.00450.x -
Nefrologia : Publicacion Oficial de La... 2012In the chronic kidney disease population metabolic acidosis is prevalent presenting already in the early stages of renal dysfunction. The pathogenesis associates the... (Review)
Review
In the chronic kidney disease population metabolic acidosis is prevalent presenting already in the early stages of renal dysfunction. The pathogenesis associates the lack of bicarbonate production with the accumulation of organic/inorganic acids and the development of tubulointerstitial damage through ammonium retention and complement deposition. The empiric use of oral sodium bicarbonate represents an interesting therapeutic option that has been documented in a few clinical trials in human subjects. The availability of oral sodium, in its diverse forms, represents an inexpensive and simple way of treating an entity that could hasten the progression of kidney disease, as well as protein catabolism, bone disease and mortality.
Topics: Acidosis; Animals; Disease Progression; Humans; Incidence; Renal Insufficiency, Chronic
PubMed: 23169354
DOI: 10.3265/Nefrologia.pre2012.Jul.11515