Lactic acidosis in critically ill patients.

Lactic acidosis is defined as increase in blood lactate levels in association with acidemia. It should be suspected in all patients presenting with shock & decreased mayocardial contractility. The patients with lactic acidosis have high mortality. However, the prognosis and case fatality are completely dependent on underlying disease in each patient with lactic acidosis being an independent indicator of severity of shock. All efforts should be directed towards treatment of underlying cause and concomitant correction of acidosis.

A Case of Type B Lactic Acidosis in Acute Leukemia

Type B lactic acidosis is a rare condition in patients with solid tumors or hematological malignancies. Although there have been several theories to explain its mechanism, the exact cause of lactic acidosis remains to be discovered. Lactic acidosis is usually related to increased tumor burden in patients with malignancy. We experienced a case of lactic acidosis in a 39-year-old man who visited an emergency room because of dyspnea, and the cause of lactic acidosis turned out to be recurrent acute leukemia. Chemotherapy relieved the degree of lactic acidosis initially, but as the disease progressed, lactic acidosis became aggravated. Type B lactic acidosis can be a clinical presentation of acute exacerbation of acute leukemia.

Acidosis láctica severa asociada a infusión de propofol: Caso clínico / Severe lactic acidosis caused by propofol infusion: Report of one case

Propofol infusion syndrome (PRIS) is a rare but potentially lethal complications. This disorder is triggered under unknown circumstances by a propofol infusion of more than 5 mg/kg/h for more than 48 h. PRIS is characterized by a multiorgan failure and rhabdomyolysis and is induced by a disturbance in mitochondrial long chain fatty acid oxidation. We report a 43 year-old woman who underwent brain surgery due to a vascular malformation. In the immediate postoperative period, she had an unexplained and severe lactic acidosis. During anaesthesia, she received a propofol infusion of 7 mg/kg/h that continued in the UCI at a rate of 3.5 mg/kg/h, for 8 hours more. The suspicion of PRIS motivated immediate discontinuation of propofol with rapid correction of lactic acidosis and full recovery of the patient.

Metformin induced lactic acidosis in a patients with Anorexia Nervosa: a case report and literature review

Severe lactic acidosis is a rare but life threatening complication of metformin, particularly in patients with renal failure. The mortality rate of metformin induced lactic acidosis is about 50%. Metformin is usually prescribed in type 2 diabetes and is a recognized cause of lactic acidosis in predisposed diabetic patients. We present a case of anorexia nervosa [AN] admitted with severe lactic acidosis and acute renal failure induced by six months of self medication with metformin attempting further weight reduction. The patient was volume resuscitated and started on bicarbonate infusion. She underwent immediate hemodialysis with rapid and prompt recovery. The relation between metformin induced lactic acidosis and anorexia nervosa is not known before. Reversible tubular dysfunction that may mimic Fanconi syndrome has been documented in one report. AN can be considered an additional risk factor for metformin induced lactic acidosis

Metabolic acidosis.

Acute metabolic acidosis is frequently encountered in critically ill patients. Metabolic acidosis can occur as a result of either the accumulation of endogenous acids that consumes bicarbonate (high anion gap metabolic acidosis) or loss of bicarbonate from the gastrointestinal tract or the kidney (hyperchloremic or normal anion gap metabolic acidosis). The cause of high anion gap metabolic acidosis includes lactic acidosis, ketoacidosis, renal failure and intoxication with ethylene glycol, methanol, salicylate and less commonly with pyroglutamic acid (5-oxoproline), propylene glycole or djenkol bean (gjenkolism). The most common causes of hyperchloremic metabolic acidosis are gastrointestinal bicarbonate loss, renal tubular acidosis, drugs-induced hyperkalemia, early renal failure and administration of acids. The appropriate treatment of acute metabolic acidosis, in particular organic form of acidosis such as lactic acidosis, has been very controversial. The only effective treatment for organic acidosis is cessation of acid production via improvement of tissue oxygenation. Treatment of acute organic acidosis with sodium bicarbonate failed to reduce the morbidity and mortality despite improvement in acid-base parameters. Further studies are required to determine the optimal treatment strategies for acute metabolic acidosis.

Importância clínica da dosagem de lactato e contagem de eritroblastos no sangue colhido no segmento placentário da veia umbilical para o diagnóstico de hipóxia-isquemia em prematuros / Clinical value of lactate measurement and nucleated red blood cell counts in the placental segment of the umbilical vein of premature newborns for diagnosis of hypoxia-ischemia

OBJETIVO: Determinar a validade clínica das dosagens de lactato e contagem de eritroblastos quando comparados com o excesso de bases (EB) em sangue do segmento placentário da veia umbilical de prematuros. MÉTODOS: foram colhidas amostras de 25 prematuros, após ligadura e dequitação. Os prematuros foram seguidos até a alta. Estatística incluiu regressão linear, correlação de Spearman, curvas ROC, Teste de Fisher. RESULTADOS: Lactato mostrou boa correlação com pH e EB (p < 0,0001). Níveis de lactato de 4,04 mmol/L mostraram sensibilidade de 62,5 por cento e especificidade de 91,1 por cento em discriminar pH < 7,2 e EB < -10 mmol/L. Contagens de eritroblastos mostraram boa correlação com o EB (p = 0,0095), mas sensibilidade de 37,5 por cento e especificidade 82,4 por cento em discriminar EB < 10 mmol/L. CONCLUSÕES: Lactato é um marcador válido para hipóxia fetal, em amostras do segmento placentário das veias umbilicais. Contagens de eritroblastos apresentaram baixa sensibilidade na discriminação da acidose.

OBJECTIVE: To evaluate the clinical value of lactate measurement and nucleated red blood cell (NRBC) counts when compared to base excess (BE) in the blood collected from the placental segment of the umbilical vein. METHODS: 25 umbilical cords from premature babies were sampled after placental delivery and cord clamping. Babies were followed until discharge. Statistics involved linear regression, Spearman's correlation, ROC curves, and Fisher's exact test. RESULTS: The relationship between lactate in the umbilical vein blood and pH and BE was significant (p < 0.0001). A 4.04 mmol/L lactate level showed a sensitivity of 62.5 percent and a specificity of 94.1 percent in detecting pH <7.2 and BE < -10 mmol/L. NRBC counts were related to BE (p = 0.0095), but with a sensitivity of 37.5 percent and specificity of 82.4 percent in detecting BE < -10 mmol/L. CONCLUSIONS: Lactate is a valuable marker of fetal hypoxia when sampled from placental segment veins. NRBC counts demonstrated low sensitivity for the detection of acidosis.

Acidosis láctica secundaria a terapia antirretroviral en pacientes con VIH/sida / Secundary lactic acidosis to antirretroviral therapy in patients with HIV/AIDS

La acidosis láctica es una complicación infrecuente de la terapia antirretrovial para VIH. Su aparición se ha relacionado con la administración de análogos nucleósidos de la transcriptasa inversa, en especial estavudina y didanosina. Se presentan los 2 casos que se manejaron en el año 2005 en el Servicio de Medicina del Hospital México. En ambos el desenlace fue fatal, aún cuando se utilizaron todas las medidas terapéuticas recomendadas. Descriptores: Acidosis láctica, antiretroviral, lactato, L-carnitina.

Metabolic emergencies in diabetes.

Hypoglycaemia is the commonest metabolic abnormality faced by diabetic patients on hypoglycaemic therapy including insulin. Diabetic keto-acidosis (DKA) requires prompt diagnosis and all patients arriving emergency with dehydration, shock, coma, severe respiratory difficulty and evidence of any major illness should be tested for capillary blood glucose (CBG) and urinary ketones urgently not to miss DKA. Hyperosmolar non-ketotic state complicates elderly type 2 diabetes with intercurrent infections (respiratory tract infection is commonest) characterised by severe dehydration, severe hyperglycaemia and absence of acidosis and vomiting. Lactic acidosis is extremely rare; may be compounded with comorbidities like tissue hypoxia, septic shock, heart failure--metformin usage inadvertently may precipitate the condition.

Lactato sérico como marcador prognóstico em criancas gravemente doentes / Blood lactate concentration as prognostic marker in critically ill children

OBJETIVO: Verificar a utilidade do lactato como marcador de hipoperfusão tecidual e como índice prognóstico em criancas criticamente doentes. MÉTODOS: Estudo prospectivo, longitudinal, tipo observacional de 75 pacientes admitidos na UTI pediátrica do Hospital de Clínicas (UFPR) entre novembro de 1998 e maio de 1999. De acordo com o nível de lactato na admissão, os pacientes foram divididos em grupo A (lactato > 18 mg/dl) e grupo B (lactato < 18 mg/dl). Com relacão à evolucão, em sobrevivente e óbito. No grupo A, a avaliacão clínica e a coleta de amostras de sangue arterial foram realizadas na admissão, 6, 12, 24, 48 horas e, posteriormente, a cada 24 horas. No grupo B, foram realizadas nos mesmos horários e interrompidas com 48 horas após admissão. RESULTADOS: No grupo A, foram incluídos 50 pacientes, e no Grupo B, 25. O grupo A apresentou maior freqüência de sinais clínicos de hipoperfusão (24/50). Houve diferenca estatisticamente significativa da média de lactato na admissão entre os pacientes que foram a óbito nas primeiras 24 horas de internacão (95 mg/dl) quando comparados àqueles que evoluíram a óbito após 24 horas de admissão (28 mg/dl). O nível de lactato na avaliacão de 24 horas de UTI foi o que apresentou melhor sensibilidade (55,6 por cento) e especificidade (97,2 por cento) como parâmetro preditor de óbito. CONCLUSÕES: A maioria dos pacientes com lactato > 18 mg/dl evidenciou sinais clínicos de hipoperfusão na admissão. A normalizacão ou diminuicão dos níveis de lactato a partir de 24 horas de internacão esteve significativamente relacionada com a maior probabilidade de sobrevida.

Blood lactate determined by a portable device in critically ill patients.

Patients with tissue perfusion deficit usually have lactic acidosis or hyperlactacidemia and blood lactate level has been used to diagnose this condition and to monitor the disease progression. We conducted a study to examine the diagnostic accuracy of capillary and arterial lactate (C LAC and strip A LAC) obtained by using a portable lactate analyzer (Accusport) compared with the standard method (A LAC) in this condition. Forty eight patients were included in the study. Strong correlation between C LAC and A LAC as well as strip A LAC and A LAC were demonstrated (r = 0.89 and 0.98 respectively, p <0.05). When determining agreement between C LAC and strip A LAC with the standard method, all but 2 of C LAC - A LAC differences and 2 of strip A LAC - A LAC differences were within the agreement limits (mean +/- 2SD). We conclude that capillary and arterial lactate determined by the tested device, when used and interpreted cautiously, can substitute arterial lactate in the diagnosis of hyperlactacidemia and monitoring the effectiveness of therapy.

Acidosis láctica fatal en paciente con síndrome de inmunodeficiencia adquirido y tratamiento antiretroviral de alto grado de actividad: comunicación de un caso / Fatal lactic acidosis in a patient with acquired immunodeficiency syndrome treated with highly active antiretroviral therapy: case report

Type B lactic acidosis occurs without any evidence of cellular hypoxia and is associated with the use of drugs or toxins. We report a 36 years old woman with acquired immunodeficiency syndrome that was admitted to the hospital with a severe lactic acidosis. She had been treated with didanosine, stavudine and efavirenz for four months prior to admission. Despite the use of high bicarbonate doses and vasoactive drugs, the patient had a catastrophic evolution and died in shock and multiple organ failure, 68 hours after admission

Acidosis láctica: algunas consideraciones / Some reflections on lactic acidosis

La hiperlactacidemia significa clínicamente problemas para los pacientes. La acidosis láctica es un trastorno ácido-básico consecutivo a la acumulación del ácido láctico, el cual se comporta en el nivel celular, como la contrapartida reducida del ácido pirúvico. Este último, resulta de la degradación de la glucosa en el citosol, proceso que se realiza de manera anaoeróbica y que puede culminar en CO2 H2O si sigue la vía del ácido cítrico de Krebs. El diagnóstico de esta entidad se confirma al medir la concentración sanguínea del lactato, aunque existen diversas características clínicas y de laboratorio que dan indicios de la existencia de este trastorno. Las causas de acidosis láctica se dividen en las producidas por hipoxia hística (tipo A) y las no producidas por este trastorno (tipo B); dentro de estas últimas se sitúan las debidas a alteraciones sistémicas, al uso de fármacos o toxinas y a las que acompañan a errores innatos del metabolismo

Acidosis láctica / Lactic acidosis

Se conoce que el ácido láctico es un producto terminal del metabolismo anaeróbico de la glucosa, que, en condiciones normales, los niveles séricos alcanzan las 2 mEq/L o menos. La mayor parte del lactato se elimina de forma muy eficaz por el hígado y se utiliza en la gluconeogénesis o para obtener energía. Si se producen incrementos considerables de las cifras de lactato sérico con disminución del metabolismo de conversión de lactato a piruvato se instala un cuadro de acidosis metabólica, a menudo grave, que puede llevar al paciente a la muerte. Desde el punto de vista clínico se debe sospechar ante un paciente con acidosis metabólica no bien explicada y anión Gap elevado, el cual se encuentra por encima de 25-30 mEq/L, aún en presencia de insuficiencia renal, de cetoacidosis o de la ingestión de un tóxico. La prevención de la hipoxia hística desempeña un papel importantísimo y en este sentido todas las medidas que contribuyen a garantizar una buena perfusión hística. Se señala la importancia del control adecuado de la diabetes mellitus, la selección más adecuada de hipoglicemiantes, el aporte de tiamina en los pacientes de riesgo, entre otras medidas