Data from Luft, F. C. (2001). Lactic acidosis: Update for critical care clinicians. Journal of the American Society of Nephrology, 12(Suppl 17): S15-S19; Moyle, G. (2002). Hyperlactatemia and lactic acidosis: Should routine screening be considered? AIDS Read, 12(8):344-348; and Sharma, S. (2006). Lactic acidosis. Retrieved May 29, 2006, from www.emedicine.com/med/topic1253.htm.
Type Definition Related Conditions
Type A lactic acidosis (fast) Poor tissue perfusion or oxygenation (hypoxia)
Anaerobic muscle activity Vigorous exercise, seizures
Tissue hypoperfusion Sepsis, cardiogenic or hypovolemic shock, hypotension, myocardial infraction, acute heart failure, ischemic bowel, massive pulmonary emboli
Decreased tissue delivery or utilization Hypoxemia, carbon monoxide poisoning
Type B lactic acidosis (slow) Impaired lactate metabolism without evidence of inadequate tissue oxygenation (hypoxia)
Type B1 Related to underlying disorder Cancer (especially lymphomas, leukemia, and sarcoma), AIDS, sepsis, hepatic or renal failure, diabetes mellitus
Type B2 Associated with drugs and toxins Antiretrovirals, acetaminophen, biguanide antihyperglycemics, cyanide, beta agonists, methanol, sorbitol, cocaine, parenteral nutrition, ethanol intoxication
Type B3 Related to congenital enzymatic defects of metabolism Glucose-6-phosphatase deficiency (von Gierke’s disease), pyruvate dehydrogenase deficiency, fructose-1,6-diphosphatase deficiency
Type D lactic acidosis (rare) Bacterial overgrowth of gram-positive anaerobes Jejunoileal bypass, small bowel resection, or other forms of short bowel syndrome and malabsorption

Lactate Production

Approximately 1500 mmol of lactate are produced daily by various organs in the body. Lactate is the end product of anaerobic glycolysis. Serum lactate levels reflect the balance between production and elimination of lactate. The liver and kidneys are responsible for metabolizing and eliminating lactate (Moyle, 2002); about 70% to 90% of the body’s lactate is metabolized by the liver, and 10% to 20% is eliminated by the kidneys.

The Cori cycle is the process by which lactic acid or lactate is recycled during anaerobic metabolism. When the energy needs of the body are greater than the oxygen supply, muscle cells and red blood cells produce adenosine triphosphate (ATP) through lactic acid fermentation. During anaerobic glycolysis, pyruvic acid is converted through gluconeogenesis into lactate, which is then converted into glucose for energy (Sharma, 2006). Some lactate is metabolized into CO2 and water through the citric acid cycle and ultimately eliminated from the body. In normal circumstances, the Cori cycle allows the body to focus on the production of ATP while the liver handles lactate, thereby preventing lactic acidosis through the removal of lactate in the blood. Lactate is produced from pyruvic acid through a chemical reaction with the enzyme lactate dehydrogenase (LDH).


Type A versus Type B Lactic Acidosis

Type A lactic acidosis occurs when the production of anaerobic lactic acid results in hypoxemia, or poor tissue perfusion. This deficit in oxygenation leads to difficulty generating ATP in the absence of oxygen (Moyle, 2002). Lactic acidosis induced by hypoxia is far more common than type B lactic acidosis. Etiologies of type A lactic acidosis include hypovolemic shock, sepsis, congestive heart failure, carbon monoxide poisoning, pheochromocytoma, and catecholamines (Sharma, 2006; Pignanelli & Budzinski-Braunscheidel, 1998). These etiologies can be subdivided into three primary causes: low PO2 (pulmonary), poor delivery of oxygen (circulatory), or decreased oxygen-carrying capacity (as seen with hemoglobin disorders) (Luft, 2001).

Type B lactic acidosis occurs without hypoxia. It is considered to be the result of impaired lactate metabolism secondary to drugs, toxins, and/or disease processes. Type B lactic acidosis is characterized by a pH less than 7.35 and an arterial serum lactate level greater than 5 mEq/L (5 mmol/L in SI units) (Sharma, 2006). Arterial blood gas values in patients with type B lactic acidosis typically reflect a metabolic acidosis. The hallmark signs and symptoms of this rare oncologic emergency are changes in mental status and hyperventilation (Table 33-2).

Data from Borron, S. (2005). Lactic acidosis. Retrieved May 11, 2005, from www.emedicine.com/emerg/topic291.htm; Pignanelli, A., & Budzinski-Braunscheidel, M. (1998). Lactic acidosis—type B. In C. Chernecky & B. Berger (Eds.), Advanced and critical care oncology nursing (pp. 384-397). Philadelphia: W. B. Saunders; and Vasseur, B. G., Kawanishi, H., & Shah, N., et al. (2002). Type B lactic acidosis: A rare complication of antiretroviral therapy after cardiac surgery. Annuals of Thoracic Surgery, 74(4):1251-1252.
Early Signs and Symptoms Late Signs and Symptoms
Nausea and vomiting Shortness of breath
Abdominal pain Tachypnea
Fatigue Hyperventilation
Weight loss Liver or renal failure
Enlarged liver Clotting abnormalities


Cardiac dysrhythmias


Several theories have attempted to explain the etiology of type B lactic acidosis secondary to malignancy. Some propose that in patients with a large tumor burden, anaerobic glycolysis occurs as a result of decreased oxygenation in lactate-producing areas. Intrinsically, tumor cells have a higher rate of glycolysis than normal cells (DeKeulenaer et al., 2003). According to another theory, local tissue hypoxia and anaerobic metabolism occur as a result of microvascular aggregation of leukocytes and leukostasis, which result in the production of lactate. A third theory is that in patients with liver metastasis, lactate accumulates because the liver is unable to eliminate it. Finally, still others theorize that cancer cells themselves can produce lactate.


• Liver dysfunction:

• Alcohol intoxication

• Hepatitis (B or C virus)

• Malignancies (e.g., leukemia; lymphoma; breast, colon, and lung cancer; and multiple myeloma) and AIDS. Type B lactic acidosis can occur with any malignancy.

• Cardiac or renal insufficiency

• Drug related:

• Antiretrovirals (inhibit enzymes necessary for mitochondrial DNA synthesis) (Vasseur et al., 2002):

• Stavudine (Mokrzycki et al., 2000).

• Zidovudine

• Didanosine

• Lamivudine

• Zalcitabine

• Fialuridine

• Biguanide antihyperglycemics (known to inhibit lactate metabolism)

• Metformin (Glucophage)

• Phenformin or buformin (off the market)

• Other medications: Cyanide, beta agonists, methanol, epinephrine, salicylates, acetaminophen, cocaine, valproic acid, nitroprusside infusion, propofol, and 5-flourouracil

• Diabetic ketoacidosis

• Hyperglycemia greater than 300 mg/dL

• Intravenous radiographic contrast secondary to contrast-induced nephrotoxicity

• Pancreatitis

• Obesity

• Female gender (more often than males)

• Congenital disorders:

• Glucose-6-phosphatase deficiency (von Gierke’s disease)

• Pyruvate dehydrogenase deficiency

• Fructose-1,6-diphosphatatse deficiency

• Pediatric patients: Thiamine deficiency during TPN


The prognosis for patients with type B lactic acidosis appears to be poor; the disorder is fatal in 56% to 75% of cases (Borron, 2005; Moyle, 2002). However, the severity of the acidosis can vary, and the prognosis depends on how rapidly it is identified and treated. Hyperlactemia secondary to antiretroviral therapy rarely is fatal, and it is effectively treated by discontinuing antiretroviral therapy and administering vitamins and antioxidants (Sharma, 2006). The higher the lactate level and the more acidotic the patient, the worse the prognosis. In patients with cancer, treatment should be directed at the underlying cause, not the acidosis. Cytoreduction therapy has been shown to reduce the acidosis as the tumor mass shrinks, which improves the prognosis. However, if the tumor mass recurs, the acidosis can recur, reducing survival.


1. Vital signs:

• Temperature: Normal unless infection or sepsis is present.

• Pulse: Tachycardia.

• Respirations: Tachypnea, dyspnea; may progress to compensatory hyperventilation, Kussmaul’s breathing, and/or respiratory muscle fatigue.

• Blood pressure: Hypotension (systolic blood pressure less than 90 mm Hg).

• Pulse oximetry: May be normal.

Oct 19, 2016 | Posted by in NURSING | Comments Off on 33. LACTIC ACIDOSIS, TYPE B

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