The following signs and symptoms are commonly seen in patients having lactic acidosis:

• Nausea
• Weakness
• Tachypnea
• Hypotension
• Confusion
• Oliguria
• Kussmaul’s breathing
• Lethargy

The following diagnostic modalities and tests are implored in patients suspected of having lactic acidosis:

• Arterial blood gases (ABG): This test allows for the determination of blood pH and anion gap.
• Lactate assays: This kind of test determines the exact concentration of lactate in the blood and serum.
• Serum lactate levels: Venous or arterial serum samples are used to determine the levels of lactate in the blood. Lactate levels beyond 4-5 mmol/L is indicative for lactic acidosis. A 10% lactate clearance within 2 hours from the start of resuscitation is associated with a good prognosis [9].

Patients diagnosed with lactic acidosis may benefit from the intravenous administration of sodium bicarbonate. This therapeutic intervention is proven to decrease the carbon dioxide concentration in the pulmonary artery and increase the pH of the serum. Some patients may be given dichloroacetate to stimulate the production of lactate dehydrogenase to eliminate the accumulation of lactate and pyruvate.

Carbicarb has used as a potent buffering agent for the treatment of acidemic events in the body. In the face of a worsening lactic acidosis with impending renal failure or cardiovascular failure, hemodialysis seem to be the only option to prevent fluid overload and the needless accumulation of carbon dioxide in the serum [10]. Patients may be given thiamine (vitamin B1) supplements to help oxidize serum acids.

Patients presenting with serum levels of lactate above 2.5 mmol/L are associated with an increased risk for morbidity and mortality [7]. Hyperlactatemia associated with anti-retroviral therapy hardly causes any mortality. However, critically ill patients with pH below 7.35 and serum level of lactate beyond 5 mmol/L have a very poor prognosis. Patients having hyperlactatemia with concurrent metabolic acidosis have more than double the risk of dying than those without indications for metabolic acidosis [8].

The following medical conditions can result in the accumulation of lactate in the serum:

• Intense exercise [1]
• Malignancies
• Acquired immune deficiency syndrome (AIDS)
• Renal failure
• Respiratory failure
• Sepsis
• Drugs and toxins
• Cardiac failure
• Anemia
• Carbon monoxide poisoning
• Diabetes mellitus
• Malaria
• Alcohol
• In born errors of metabolism [2]
• Hyperlactemia [3]
• Oral hypoglycemic agents [4]

The exact prevalence and incidence rate of lactic acidosis is hard to document for they usually occur in the critically ill patients who are sensitively unavailable for research interviews and examinations. Prevalence of lactic acidosis abounds in the high dependency areas of the hospitals [5]. There is an increasing trend in symptomatic lactic acidemia among patients under anti-retroviral therapy for AIDS [6]. Patient incidence rating reaches up to 35 cases per 1000 population under anti-retroviral regimens.

In general lactic acidosis appear in conjunction with several disease conditions that afflict mankind. The state of hyperlactatemia has been associated with the progression and deterioration of the underlying primary disease. In some medical condition like cardiopulmonary failure, lactic acidosis worsens as an effect of drugs and toxins used to allay the primary disease conditions. With severe and vigorous exercise, lactate accumulation is an imperative byproduct of the anaerobic respiration of the muscle cells. The body’s inability to keep up in naturally eliminating the lactic acid in the tissue causes the adverse symptoms of lactic acidosis. The progressive failure of the body’s acid buffering system to counteract the lactate accumulation has been elucidated as the primary culprit in lactic acidosis observed in intense exercise and intake of certain drugs.

The occurrence of lactic acidosis is easily preventable when there is a prompt diagnosis and therapeutic intervention done on the primary underlying illness. Athletes should do pre-activity stretching to avoid muscular injuries that might aggravate the accumulation of lactate in the muscles. A post-activity sports massage on the affected extremities will assist the rapid disposal of the lactic acid accumulation.

Alcohol use should be taken in moderation to avoid lactate accumulation in the serum. Diabetics and patients with impending cardiovascular disorders must submit to frequent physician’s follow-up and comply regularly with maintenance medications to avoid complications like lactic acidosis and metabolic acidosis. Patients with impending infection should be treated adequately with the appropriate antibiotic therapy to avoid the occurrence of septicemia. An annual tumor body scan to promptly diagnose ongoing and occult malignancies.

Lactic acidosis is a type of metabolic acidosis due to the inadequate disposal of lactic acid by the body leading to its accumulation in the serum. Lactate is a common byproduct of anaerobic respiration which is essentially cleared in the liver, kidneys, and the muscles. Lactic acidosis occurs when the natural buffering system of the body fails and serum pH falls below 7.25. Accumulation of lactate in the serum is also eminent at >2 mmol/L technically referred to as hyperlactataemia.

• Definition: Lactic acidosis is a type of metabolic acidosis brought about by the inadequate elimination of lactic acid by the body causing a decreased blood pH.
• Cause: Lactic acidosis can be brought about by factors like intense exercise and intake of certain kinds of drugs. Factors like kidney, respiratory, and heart failure can also lead to lactic acidosis. Uncontrolled sepsis with can lead to both lactic acidosis and metabolic acidosis. Malignancies can lead to the accumulation of acidic ions in the serum. 
• Symptoms: Patients with diagnosed lactic acidosis presents with nausea, tachypnea, hypotension, lethargy, oliguria, weakness, and confusion.
• Diagnosis: Lactic acidemic states are investigated upon using ABG, lactate assays, and serum lactate level determination.
• Treatment and follow-up: Patients suffering from lactic acidosis will benefit directly from the administration of sodium bicarbonate, dichloroacetate, and carbicarbs. Patients with kidney and heart failure can be alleviated with hemodialysis. Thiamine supplementation may be used as an oxidizing agent to treat the acidemic state. 

1. Vary TC, Drnevich D, Jurasinski C, Brennan WA Jr. Mechanisms regulating skeletal muscle glucose metabolism in sepsis. Shock. Jun 1995; 3(6):403-10.
2. Inborn Errors of Metabolism; Intensive Care Nursery House Staff Manual, UCSF Children's Hospital
3. Siegel JH, Cerra FB, Coleman B, et al. Physiological and metabolic correlations in human sepsis. Invited commentary. Surgery. Aug 1979; 86(2):163-93.
4. Salpeter SR, Greyber E, Pasternak GA, Salpeter Posthumous EE. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. Jan 20 2010; CD002967.
5. Suistomaa M, Ruokonen E, Kari A, et al; Time-pattern of lactate and lactate to pyruvate ratio in the first 24 hours of intensive care emergency admissions. Shock. 2000 Jul; 14(1):8-12.
6. Hernandez Perez E, Dawood H; Stavudine-induced hyperlactatemia/lactic acidosis at a tertiary communicable diseases clinic in South Africa. J Int Assoc Physicians AIDS Care (Chic). 2010 Mar-Apr; 9(2):109-12. 
7. Gunnerson KJ, Saul M, He S, Kellum JA. Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients. Crit Care. Feb 10 2006; 10(1):R22.
8. Fall PJ, Szerlip HM. Lactic acidosis: from sour milk to septic shock. J Intensive Care Med. Sep-Oct 2005; 20(5):255-71.
9. Jones AE. Lactate clearance for assessing response to resuscitation in severe sepsis. Acad Emerg Med. Aug 2013; 20(8):844-7.
10. Finkle SN. Should dialysis be offered in all cases of metformin-associated lactic acidosis? Crit Care. 2009; 13(1):110.