Type B lactic acidosis: a rare oncological emergency.

Type B lactic acidosis is a rare metabolic complication of malignancy, more commonly in haematological malignancies. Due to the lack of formal prospective trials, treatment of lactic acidosis associated with malignancy is based on case reports. Given the poor prognosis, early recognition of type B lactic acidosis and prompt treatment are crucial. We report the first case of type B lactic acidosis in metastatic melanoma, followed by a brief literature review on the proposed pathophysiology and treatment.

A Case of Renal Involvement in B Lymphoblastic Lymphoma Leukemia.

BACKGROUND: Renal involvement is rare in B lymphoblastic lymphoma (B-LBL). The authors describe a rare case of renal involvement in a 21-year-old male patient with B lymphoblastic lymphoma leukemia, presenting with severe lactic acidosis. METHODS: Hematologic investigation, bone marrow aspirate and biopsy, cytogenetic analysis and renal biopsy were performed. RESULTS: The patient achieved complete hematological remission (CHR) after induction therapy with the regimen of VDCP and received consolidation chemotherapy regularly. He remained CHR until now. CONCLUSIONS: Renal biopsy, bone marrow aspirate, and biopsy are important to confirm a correct diagnosis. Renal involvement in B-LBL as a prognostic factor needs further studies.

Type B lactic acidosis secondary to thiamine deficiency in a child with malignancy.

Type B lactic acidosis is an underrecognized clinical entity that must be distinguished from type A (hypoxic) lactic acidosis. We present the case of a 4-year-old boy with medulloblastoma who presented with lactic acidosis in the setting of septic shock. His hyperlactatemia persisted to high levels even after his hemodynamic status improved. After administration of intravenous thiamine, his lactate level rapidly normalized and remained stable. It was determined that his total parenteral nutrition was deficient in vitamins due to a national shortage. Because thiamine is an important cofactor for pyruvate dehydrogenase, he was unable to use glucose through aerobic metabolism pathways. We briefly review type A versus type B lactic acidosis in this case report.

Type B lactic acidosis associated with multiple myeloma.

We present a 58-year-old man with recurrent multiple myeloma treated with 2 autologous stem cell transplantations. He was admitted for dyspnea and found to have severe type B lactic acidosis with serum lactate level of 193.6 mg/dL. This case reviews malignancy-associated type B lactic acidosis and discusses its etiology, pathogenesis, and management.

The role of serum lactate in the acute care setting.

Acute care services are increasingly faced with the double burden of high patient acuity and limited resources. Early identification of patients who are sick or who have the potential to deteriorate rapidly is crucial so that these resources may be allocated to those in greatest need. Traditional measures of illness and end points of resuscitation, such as vital signs, often fail to identify occult hypoperfusion with certain disease processes associated with high morbidity and mortality. Thus, biochemical markers that may predict illness earlier are becoming more relevant. We present a review of the evidence behind use of the serum lactate level in this setting.

Type B lactic acidosis and insulin-resistant hyperglycemia in an adolescent following cardiac surgery.

OBJECTIVE: To report the presence of type B lactic acidosis and insulin-resistant hyperglycemia following cardiopulmonary bypass in a pediatric patient. DESIGN: Case report. SETTING: Tertiary referral children's hospital pediatric intensive care unit. PATIENT: Fourteen-year-old child with hyperlactatemia and hyperglycemia following cardiac surgery. INTERVENTIONS AND RESULTS: We report a patient who following cardiopulmonary bypass for repair of his congenital heart disease developed type B lactic acidosis and hyperglycemia resistant to insulin therapy. Resolution of his hyperlactatemia and hyperglycemia occurred approximately 24 hrs postoperatively without apparent ill effect. CONCLUSIONS: Type B lactic acidosis is a phenomenon that may occur in the pediatric population in conjunction with insulin-resistant hyperglycemia. We observed that its resolution corresponded to improvement in the patient's hyperglycemia.

Type B lactic acidosis following cardiopulmonary bypass.

OBJECTIVE: To describe, characterize, and identify the associations of postcardiac surgical lactic acidosis occurring in the absence of clinical evidence of tissue hypoperfusion. DESIGN: The preliminary study is a report of a series of observations in 12 patients. The prospective study is also observational, involving the structured collection of hemodynamic and metabolic variables in a prescribed series of patients. SETTING: Cardiac surgical intensive care unit of a university teaching hospital. PATIENTS: Twelve patients who developed an unexplained lactic acidosis after cardiac surgery are reported in the preliminary study. The prospective study involved observations in 112 consecutive patients undergoing cardiopulmonary bypass for cardiac surgery. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Preliminary study: Cardiac index was increased before, during and after recovery from lactic acidosis. Recovery from lactic acidosis was associated with a decrease in oxygen transport index and significant increases in oxygen consumption index and oxygen extraction ratio. PROSPECTIVE STUDY: Hemodynamic, oxygen transport, and oxygen consumption variables, together with arterial blood gas and lactate concentrations, were assessed every 6 hrs for 24 hrs after surgery. Sixteen patients developed lactic acidosis (peak lactate concentration > 5.0 mmol/L). Compared with the remainder of the patients, this subgroup had longer duration of cardiopulmonary bypass (116 +/- 31 vs. 76 +/- 31 mins, p < .01), greater intraoperative hypothermia (24.9 +/- 2.0 degrees vs. 26.6 +/- 2.3 degrees C, p < .01), more frequent requirement for vasopressor agents (14/16 vs. 35/96, p < .05) and a higher frequency of hyperglycemia (15/16 vs. 28/96, p < .01). Hemodynamic variables, including cardiac index, were remarkably similar in the acidotic and nonacidotic groups. All of the acidotic patients, in both parts of this study, recovered from their acidosis. Eleven of the patients in the preliminary study and all of the 16 acidotic patients in the prospective study were ultimately discharged from the hospital. CONCLUSIONS: This report documents the occurrence of lactic acidosis in a subgroup of patients undergoing cardiopulmonary bypass. The pathogenesis of this disorder is uncertain, but it appears to not relate to inadequate oxygen delivery. Systemic vasodilation and reduced oxygen extraction appear to be features of this disorder, which has an excellent prognosis.

Type B lactic acidosis in an AIDS patient treated with zidovudine.

Human immunodeficiency virus type 1 (HIV 1) infection has been shown to cause myopathy. Zidovudine, a nucleoside analogue, has also been shown to cause myopathy in HIV-infected patients. Dalakas et al., were unable to distinguish the myopathy associated with HIV infection from the toxic mitochondrial myopathy caused by zidovudine. In a recent report, Chattha et al., described seven patients with Acquired Immunodeficiency Syndrome (AIDS) who developed type B lactic acidosis. Four of these patients were treated with zidovudine. A 100% mortality over a period of 15 months was observed. Zidovudine disrupts the mitochondrial deoxyribonucleic acid (DNA) that encodes for the respiratory chains, inhibiting the transport of lactate into the mitochondria. This may cause the accumulation of lactate in the cytoplasm, producing a severe metabolic acidosis. We present an AIDS patient with servere type B lactic acidosis which could have been associated with, or precipitated by, zidovudine.

[Lactic acidosis and hyperlactatemia]. / Acidose lactique et hyperlactatémie.

Lactic acidosis is a relatively frequent acid-base disorder in a hospital setting. It is defined by the association of an arterial pH inferior to 7.35 and an arterial lactate level superior to 5 mmol/l. Classically, 2 types of acidosis are distinguished on the basis of their mechanisms of onset: the type A, with evident clinical signs of tissue hypoperfusion and the type B, more are, without apparent hypoxia. This last category is observed in various circumstances such as diabetes, acute liver failure, poisoning and, more rarely, inborn errors of carbohydrate metabolism. Treatment aims primarily at the correction of the cause. The efficacy of sodium bicarbonate is presently debated, considering the risk to worsen hyperlactatemia and to induce hyperosmolarity or rebound alkalosis. The administration of dichloroacetate, an activator of pyruvate dehydrogenase, permits to correct partially the lactic acidosis but is not harmless especially in case of prolonged administration. Other therapeutic modalities are evoked. Arterial lactate level is a reliable prognostic index of shock, because blood values do not depend only of the oxygen debt but also of the efficacy of hepatic and renal lactate uptake. Sequential measurements are recommended.

Lactate metabolism.

Lactate is the end product of the anaerobic metabolism of glucose, and its accumulation in the blood signals an increase in production or a decrease in utilization, or both. The most common etiology of lactic acidosis is hypoperfusion, which represents an imbalance between systemic oxygen demand and oxygen availability with resultant tissue hypoxia. A wide variety of other etiologies of hyperlactatemia have been identified or implicated. However, most of these are uncommon causes, and many actually represent an associated perfusion failure. Clinical recognition of hyperlactatemia is facilitated by an awareness of the clinical settings in which it is likely to occur. Serum electrolyte and arterial blood gas studies are helpful to recognize lactic acidosis, but direct assay of blood lactate is necessary to identify milder degrees of lactate elevation, to confirm and quantitate the severity of more severe degrees, and to monitor the progress of therapy. Therapy should be directed toward measures to ensure adequate systemic oxygen delivery and specific treatment of the underlying causes.