Metabolic Acidosis Clinical Presentation

Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FACP, FASN more...

Updated: Aug 30, 2011

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History
Physical Examination
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History

Symptoms of metabolic acidosis are not specific. The respiratory center in the brainstem is stimulated, and hyperventilation develops in an effort to compensate for the acidosis. As a result, patients may report varying degrees of dyspnea. Patients may also report chest pain, palpitations, headache, confusion, generalized weakness, and bone pain. Patients, especially children, also may present with nausea, vomiting, and decreased appetite.

The clinical history in metabolic acidosis is helpful in establishing the etiology when symptoms relate to the underlying disorder. The age of onset and a family history of acidosis may point to inherited disorders, which usually start during childhood. Important points in the history include the following:

Diarrhea - GI losses of HCO₃^-
History of diabetes mellitus, alcoholism, or prolonged starvation - Accumulation of ketoacids
Polyuria, increased thirst, epigastric pain, vomiting -Diabetic ketoacidosis (DKA)
Nocturia, polyuria, pruritus, and anorexia - Renal failure^[4]
Ingestion of drugs or toxins - Salicylates, acetazolamide, cyclosporine, ethylene glycol, methanol
Visual symptoms, including dimming, photophobia, scotomata - Methanol ingestion
Renal stones - RTA or chronic diarrhea
Tinnitus, blurred vision, and vertigo - Salicylate overdose

Physical Examination

The best recognized sign of metabolic acidosis is Kussmaul respirations, a form of hyperventilation that serves to increase minute ventilatory volume. This is characterized by an increase in tidal volume rather than respiratory rate and is appreciated as deliberate, slow, deep breathing.

Chronic metabolic acidosis in children may be associated with stunted growth and rickets.

Coma and hypotension have been reported with acute severe metabolic acidosis.

Other physical signs of metabolic acidosis are not specific and depend on the underlying cause. Some examples include xerosis, scratch marks on the skin, pallor, drowsiness, fetor, asterixis, and pericardial rub for renal failure, as well as reduced skin turgor, dry mucous membranes, and fruity smell for DKA.

Proceed to Differential Diagnoses

Contributor Information and Disclosures

Author

Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics

Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Federation for Medical Research, American Heart Association, American Society of Nephrology, American Society of Transplantation, American Thoracic Society, International Society of Nephrology, and Royal College of Physicians

Disclosure: Genzyme Grant/research funds Other

Coauthor(s)

Khaled Hamawi, MD Medical Director, Department of Pancreatic Transplantation, Mayo clinic

Khaled Hamawi, MD is a member of the following medical societies: American Society of Nephrology and American Society of Transplantation

Disclosure: Nothing to disclose.

Specialty Editor Board

James W Lohr, MD Professor, Department of Internal Medicine, Division of Nephrology, Fellowship Program Director, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

James W Lohr, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, and Central Society for Clinical Research

Disclosure: Genzyme Honoraria Speaking and teaching

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Eleanor Lederer, MD Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Chief Editor

Vecihi Batuman, MD, FACP, FASN Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, and International Society of Nephrology

Disclosure: Nothing to disclose.

References

Noritomi DT, Soriano FG, Kellum JA, Cappi SB, Biselli PJ, Libório AB, et al. Metabolic acidosis in patients with severe sepsis and septic shock: a longitudinal quantitative study. Crit Care Med. Oct 2009;37(10):2733-9. [Medline].
Reddy P, Mooradian AD. Clinical utility of anion gap in deciphering acid-base disorders. Int J Clin Pract. Oct 2009;63(10):1516-25. [Medline].
Maciel AT, Park M. Differences in acid-base behavior between intensive care unit survivors and nonsurvivors using both a physicochemical and a standard base excess approach: a prospective, observational study. J Crit Care. Dec 2009;24(4):477-83. [Medline].
Morimatsu H, Toda Y, Egi M, Shimizu K, Matsusaki T, Suzuki S, et al. Acid-base variables in patients with acute kidney injury requiring peritoneal dialysis in the pediatric cardiac care unit. J Anesth. 2009;23(3):334-40. [Medline].
Walsh SB, Shirley DG, Wrong OM, Unwin RJ. Urinary acidification assessed by simultaneous furosemide and fludrocortisone treatment: an alternative to ammonium chloride. Kidney Int. Jun 2007;71(12):1310-6. [Medline].
Pereira PC, Miranda DM, Oliveira EA, Silva AC. Molecular pathophysiology of renal tubular acidosis. Curr Genomics. Mar 2009;10(1):51-9. [Medline]. [Full Text].

Table. Comparison of Types 1, 2, and 4 RTA

Table. Comparison of Types 1, 2, and 4 RTA

Characteristics	Proximal (Type 2)	Distal (Type 1)	Type 4
Primary defect	Proximal HCO₃ - reabsorption	Diminished distal H+ secretion	Diminished ammoniagenesis
Urine pH	< 5.5 when serum HCO₃ - is low	>5.5	< 5.5
Serum HCO₃ -	>15 mEq/L	Can be < 10 mEq/L	>15 mEq/L
Fractional excretion of HCO₃ - (FEHCO₃)	>15-20% during HCO₃ - load	< 5% (can be as high as 10% in children)	< 5%
Serum K₊	Normal or mild decrease	Mild-to-severe decrease*	High
Associated features	Fanconi syndrome	...	Diabetes mellitus, renal insufficiency
Alkali therapy	High doses	Low doses	Low doses
Complications	Osteomalacia or rickets	Nephrocalcinosis, nephrolithiasis	...
*K⁺ may be high if RTA is due to volume depletion.

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