Most cases of metabolic acidosis present with non-specific signs and symptoms. These symptomatology and signs are most commonly seen among patients with established metabolic acidosis:

• Hyperventilation: The respiratory centers are stimulated to cause hyperventilation to help eliminate carbon dioxide from the blood during acidotic states. 
• Dyspnea: Breathing will be too fast and shallow impairing adequate oxygen exchange in the lungs.
• Chest pain: The acidic plasma triggers the release of some cytokines that may cause angina and temporary coronary vasospasm.
• Palpitation: The compensatory tachycardia will be felt as palpitation.
• Neurologic signs: Headache and confusion are common findings when the cerebrospinal fluid becomes acidic.
• Fatigue and weakness: Sodium channels are impaired during metabolic acidosis causing an essential hyponatremia in the extracellular space lowering the action potential in muscles.
• Nausea and vomiting: The toxic state of metabolic acidosis is exemplified as nausea and vomiting among children.
• Bone pains: The acidotic state causes vasospasm of the smaller arterioles that supply the bones presenting as sharp bone pains. Chronic calcium depletion with the acidemic state can also cause untimely osteoporosis among patients. 

The following laboratory examinations and tests are utilized for the work up of patients with metabolic acidosis:

• Serum electrolytes: The bicarbonate (HCO3) ion is usually inadequate during metabolic acidosis. 
• Arterial blood gases (ABG): Blood gases analysis will reveal a pH level less than 7.4 during acidotic states. Concentration of HCO3 can also be determined in the ABG [4].
• Urinalysis: Urine pH may be determined from the urinalysis. Electrolytes such as sodium, chloride, and potassium can also be measured in the urine [5]. The determination of ketones in the urine is associated with diabetic, starvation, and alcoholic ketoacidosis.
• Anion gap: An increasing anion gap (AG) is indicative of an acidemic state where there is an increased number of undetected ions in the serum [6]. 
• Complete blood count: An elevated white blood cell (WBC) count may connote septicemia which could cause lactic acidosis.
• Blood urea nitrogen (BUN): This renal function test is sensitive in assessing the degree of metabolic acidosis during renal failure [7].
• Serum lactate level: An elevation of up to 3 times the normal serum lactate level is indicative of lactic ketoacidosis. 
• Salicylate level in serum: An elevated serum level of salicylate from oral medications can induce metabolic acidosis.
• Iron serum level: Iron levels exceeding 300 mg/dl is already considered toxic and could consequently lead to metabolic acidosis. 
• Electrocardiography (ECG): This test will detect rhythm abnormalities in the heart during eg. hyperkalemia.

The goal in the treatment of metabolic acidosis is to raise the serum pH to more than 7.2 to prevent life-threatening complications like cardiac arrhythmia. The most common drug used to balance metabolic acidosis is sodium bicarbonate [8]. Bicarbonate deficit is generally computed as desired HCO3 is equal to HCO3 deficit per Liter multiplied by 0.5 times body weight.

This computation will give a crude estimate of the HCO3 deficit in serum where sodium bicarbonate is administered intravenously to correct the imbalance. In the same way potassium citrate can also be given to correct metabolic acidosis with hypokalemia. Oral sodium bicarbonate is indicated for metabolic acidosis states that requires exogenous bases or alkalis to correct [9]. Researches have determined that potassium citrate may be superior to sodium bicarbonate because it requires lesser volume and does propagate the unnecessary excretion of calcium ion in the urine [10].

In general, the prognosis of metabolic acidosis is related to the underlying condition that gave rise to it. Cohort studies have shown that mortality with metabolic acidosis is usually caused by unabated acidotic states from hyperchloremia [3]. Significant morbidity is also observable among patients with uncorrected and late correction of acid-base imbalances from the time of admission. Severe uncorrected metabolic acidosis can lead to shock or death.

Medical conditions that lead to the buildup of acid in the body can potentially cause metabolic acidosis. These medical conditions include:

• Diabetic ketoacidosis
• Hyperchloremic acidosis
• Alcoholism
• Malignancy
• Liver failure
• Intense exercise
• Sepsis
• Heart failure
• Acidic medications
• Renal tubular acidosis
• Renal failure [1]
• Poisoning
• Severe dehydration

There are no exact epidemiologic data that give the incidence and prevalence of metabolic acidosis. The relative prevalence of this metabolic state is reflected in each primary disease etiology that result in this acidemic state. Moreover, metabolic acidosis is oftentimes underdiagnosed and underdocumented because metabolic acidosis is just a mere sign of a primary disease process.

In general, the basic pathophysiology of metabolic acidosis is two folds. There could be an increased acid production within any organ system or there is an inadequate production of bicarbonates from the buffering systems of the body [2]. The body regulates plasma acidity by means of these buffering systems: the bicarbonate buffering system, renal compensatory system, respiratory compensatory system, and the intracellular absorption of hydrogen atoms. The bicarbonate system receives the hydrogen from the acidic compounds and neutralizes them into carbon dioxide and water. Any imbalance in the buffering system moves the pH lower than 7.4 making the serum acidic.

Prevention of metabolic acidosis is grossly dependent on the primary prevention of its underlying causes. Diabetic control is essential to prevent diabetic ketoacidosis from ensuing. Alcohol should be taken in moderation to avoid alcoholic ketoacidosis from taking place. Athletic sports and exercises should be done in moderation to prevent lactic acidosis from developing. The injudicious use of salicylate-base pain relievers and iron supplements must be checked to prevent it’s toxicity that may lead to metabolic acidosis.

Metabolic acidosis is defined as a medical condition where there is an imbalance of the acid-base ions causing plasma acidity. The metabolic acidosis state is usually a sign of underlying disease process. Correction of the primary cause of the metabolic imbalance will normalize or reverse the metabolic state. An indepth understanding of the nature of the acid-base regulation mechanism is required to understand the complex processes that give rise to metabolic acidosis.

• Definition: Metabolic acidosis is defines as a clinical condition where there is an imbalance of the acid-base ions causing too much acid in plasma.
• Cause: Ketoacidosis is the leading cause of metabolic acidosis which could be brought about by diabetes, alcoholism, starvation, and cancer. Hyperchloremic states with diarrhea and vomiting may also induce acidemic states in the serum.
• Symptoms: Acidotic patients will present with varying degrees of dyspnea, hyperventilation, chest pains, palpitation, and bone pain. 
• Diagnosis: The ideal workup for metabolic acidosis include ABG, CBC, serum lactate levels, and ECG readings. 
• Treatment and follow-up: The prompt correction of the acidemic state is imperative to prevent life-threatening arrhythmia. Patients may be given sodium bicarbonate intravenously, oral sodium bicarbonate, and potassium citrate to correct the metabolic acidosis.

1. Morimatsu H, Toda Y, Egi M, 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.
2. Mitch WE. Metabolic and clinical consequences of metabolic acidosis. J Nephrol. 2006; 19 Suppl 9:S70-5 (ISSN: 1121-8428)
3. 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.
4. Schauer KL, Freund DM, Prenni JE, Curthoys NP. Proteomic profiling and pathway analysis of the response of rat renal proximal convoluted tubules to metabolic acidosis. Am J Physiol Renal Physiol. 2013; 305(5):F628-40 
5. Pereira PC, Miranda DM, Oliveira EA, Silva AC. Molecular pathophysiology of renal tubular acidosis. Curr Genomics. Mar 2009; 10(1):51-9.
6. Reddy P, Mooradian AD. Clinical utility of anion gap in deciphering acid-base disorders. Int J Clin Pract. Oct 2009; 63(10):1516-25.
7. Mathur RP, Dash SC, Gupta N, Prakash S. Effects of correction of metabolic acidosis on blood urea and bone metabolism in patients with mild to moderate chronic kidney disease: a prospective randomized single blind controlled trial. Ren Fail. 2006; 28(1):1-5.
8. Goraya N, Simoni J, Jo CH, Wesson DE. A comparison of treating metabolic acidosis in CKD stage 4 hypertensive kidney disease with fruits and vegetables or sodium bicarbonate. Clin J Am Soc Nephrol. Mar 2013; 8(3):371-81.
9. Abramowitz MK, Melamed ML, Bauer C, Raff AC, Hostetter TH. Effects of oral sodium bicarbonate in patients with CKD. Clin J Am Soc Nephrol. May 2013; 8(5):714-20.
10. Starke A, Corsenca A, Kohler T, Knubben J, Kraenzlin M, Uebelhart D, et al. Correction of metabolic acidosis with potassium citrate in renal transplant patients and its effect on bone quality. Clin J Am Soc Nephrol. Sep 2012; 7(9):1461-72.