Prepartum anionic diet induces hyperchloremic acidosis in high-producing dairy cows without preventing subclinical hypocalcemia / Dieta aniônica pré-parto provoca acidose hiperclorêmica em vacas leiteiras de alta produção mas não evita a hipocalcemia subclínica

In this study we evaluated the effects of the prepartum anionic diet on the electrolyte balance and calcemia of high producing dairy cows in the first days of lactation, and investigated the impact on the frequency of subclinical hypocalcemia (SCH). Sixty healthy Holstein cows, producing 30 kg of milk/day, handled in intensive system (compost barn), were distributed in groups (n=15) according to lactation order: first, second, third, and fourth to sixth. In the last three weeks before calving they received a diet with negative DCAD (-6mEq/100g DM) and high chloride content. After calving, they received a diet with positive DCAD (18mEq/100g DM). Urine pH was measured before calving. Serum Na+, Cl-, K+, and total Ca concentrations, and the strong ion difference (SID3) were determined in samples taken soon after calving (0h), 24, 48, 72 and 96h after. The frequencies of SCH were determined considering the critical value of 2.125mmol/L (8.5mg/dL). Two-way repeated measures ANOVA and chi-square test were used for comparisons. The cows eliminated acidic urine before calving. Na+, K+, Cl-, and SID3 values did not differ between groups. Na+ and K+ did not vary between days; Cl- was elevated at calving and decreased until 72h; and SID3 was reduced at calving and increased up to 48h. The Ca levels were reduced until 24h and increased up to 72h. Cows of third and fourth to sixth lactations presented lower values up to 24h. SCH was observed in almost half of the cows (43.3% to 55%) until 48h. The maintenance of hypocalcemia for three or more consecutive days occurred in 53.3% of third and fourth to sixth lactations cows. Ingestion of a high chloride prepartum anionic diet led to hyperchloremic acidosis and this imbalance was reversed on the second postpartum day. The induced effects on electrolyte and acid-base balances were not able to prevent the occurrence of SCH in the first days of lactation.(AU)

Os objetivos do estudo foram avaliar os efeitos que a dieta aniônica pré-parto provoca sobre o equilíbrio eletrolítico e sobre a calcemia de vacas leiteiras de alta produção nos primeiros dias de lactação, e verificar o impacto sobre a frequência da hipocalcemia subclínica (HSC). Sessenta fêmeas hígidas HPB, com produção de 30 kg de leite/dia, manejadas em sistema intensivo (compost barn), foram distribuídas por grupos (n=15) de acordo com a ordem de lactação: primeira, segunda, terceira e quarta a sexta. Nas três semanas pré-parto receberam dieta com DCAD negativa (-6mEq/100g MS) e teor de cloreto elevado. Após o parto receberam dieta com DCAD positiva (18mEq/100g MS). O pH da urina foi mensurado antes do parto. As concentrações séricas de Na+, Cl-, K+ e Ca total e a diferença de íons fortes (SID3) foram determinadas em amostras colhidas ao parto (0h), 24, 48, 72 e 96h após. As frequências de HSC foram determinadas considerando-se o valor crítico de 2,125mmol/L (8,5mg/dL). ANOVA de medidas repetidas e teste de qui-quadrado foram empregados para as comparações. As vacas eliminavam urina ácida antes do parto. Os valores de Na+, K+, Cl- e SID3 não diferiram entre os grupos. Na+ e K+ não variaram entre os dias; Cl- era elevado ao parto e diminuiu até 72h; e SID3 era reduzida ao parto e aumentou até 48h. A calcemia era reduzida até 24h e se elevou até 72h. Vacas de terceira e de quarta a sexta lactações apresentaram valores mais baixos até 24h. A HSC foi observada em quase metade das vacas (43,3% a 55%) até 48h. A manutenção de hipocalcemia por três ou mais dias seguidos ocorreu em 53,3% das vacas de terceira e de quarta a sexta lactações. A ingestão de dieta aniônica pré-parto com alto teor de cloreto provocou acidose hiperclorêmica e este desequilíbrio se reverteu no segundo dia pós-parto. Os efeitos induzidos sobre os equilíbrios eletrolítico e ácido base não foram capazes de prevenir a ocorrência de HSC nos primeiros dias da lactação.(AU)

Experimental protocol for metabolic acidosis induction by intravenous administration of hydrochloric acid in sheep / Protocolo de indução experimental de acidose metabólica por administração intravenosa de ácido clorídrico em ovinos

The aim of this study was to assess the magnitude and duration of blood and urine changes and the side effects of hyperchloremic acidosis induced by the intravenous administration of hydrochloric acid in sheep. Five healthy, crossbred adult ewes, with a mean body weight of 44±2.9kg were used. The hydrochloric acid solution was administered intravenously at a rate of 25mL/kg/h for 4 hours continuously. Venous blood and urine samples were collected and pH values, blood carbon dioxide partial pressure, bicarbonate, base excess, strong ion difference, anion gap, total concentration of nonvolatile buffers, creatinine, plasma L-lactate, plasma and urine sodium, potassium, and chloride were determined. The experimental protocol induced severe hyperchloremic acidosis at the end of the infusion, with a decreased plasma strong ion difference. The fractional excretion of sodium and chloride remained increased during 4 hours after the infusion. Aciduria was observed at approximately 24 hours. Twenty-four hours after the infusion, the animals showed mild and compensated metabolic acidosis. This protocol was effective in inducing severe and long-lasting hyperchloremic acidosis and did not cause serious side effects. Therefore, this protocol can be used safely in adult sheep for studies on the treatment of this condition.(AU)

O objetivo deste estudo foi avaliar a magnitude e a duração das alterações sanguíneas e urinárias, bem como os efeitos colaterais da acidose hiperclorêmica induzida por administração intravenosa de ácido clorídrico, em ovinos. Foram utilizadas cinco ovelhas mestiças, adultas, sadias, com peso médio de 44±2,9kg. A solução de ácido clorídrico foi administrada por via intravenosa, na velocidade de 25mL/kg/h, totalizando quatro horas de administração contínua. Amostras de sangue venoso e de urina foram colhidas, e determinaram-se os valores de pH, pressão parcial de dióxido de carbono, bicarbonato, excesso de bases, diferença dos íons fortes, ânion-gap, creatinina, lactato L, sódio, potássio e cloro. O protocolo de indução experimental foi capaz de induzir acidose hiperclorêmica grave ao término da infusão, com diminuição da diferença dos íons fortes plasmáticos. Houve aumento da excreção fracionada de sódio e cloro por até quatro horas após o término da infusão. A acidúria foi observada por cerca de 24 horas. Após 24 horas do início da infusão, os animais apresentaram acidose metabólica leve e compensada. Esse protocolo foi eficaz na indução da acidose hiperclorêmica grave e duradoura e não causou efeitos colaterais. Conclui-se que o protocolo pode ser usado com segurança em ovelhas adultas, para estudos sobre tratamento dessa condição.(AU)

A prospective, randomized, comparison study on effect of perioperative use of chloride liberal intravenous fluids versus chloride restricted intravenous fluids on postoperative acute kidney injury in patients undergoing off-pump coronary artery bypass grafting surgeries

Context and Aims: Off-pump coronary artery bypass graft (OPCABG) is a form of CABG surgery. It is performed without the use of cardiopulmonary bypass machine as a surgical treatment for coronary heart disease. Acute kidney injury (AKI) is one of the common postoperative complications of OPCABG. Previous studies suggest important differences related to intravenous fluid (IVF) chloride content and renal function. We hypothesize that perioperative use of chloride restricted IVFs may decrease incidence and severity of postoperative AKI in patients undergoing OPCABG. Methods: Six hundred patients were randomly divided into two groups of 300 each. In Group A (n = 300), chloride liberal IVFs, namely, hydroxyethyl starch (130/0.4) in 0.9% normal saline (Voluven), 0.9% normal saline, and Ringer's lactate were used for perioperative fluid management. In Group B (n = 300), chloride-restricted IVFs, namely, hydroxyethyl starch (130/0.4) in balanced colloid solution (Volulyte) and balanced salt crystalloid solution (PlasmaLyte A), were used for perioperative fluid management. Serum creatinine values were taken preoperatively, postoperatively at 24 h and at 48 h. Postoperative AKI was determined by AKI network (AKIN) criteria. Results: In Group A, 9.2% patients and in Group B 4.6% patients developed Stage-I AKI determined by AKIN criteria which was statistically significant (P < 0.05). Conclusion: Perioperative use of chloride restricted IVF was found to decrease incidence of postoperative AKI. The use of chloride liberal IVF was associated with hyperchloremic metabolic acidosis.

Cloro, el ion olvidado y su relación con el suero fisiológico / The forgotten ion Cl

Chloride is the anion of highest concentration in the extracellular fluid, it contributes between 100 to 300 mosm/L to the tonicity of plasma[1], and its plasma concentration is frequently reported in the different services as part of the general evaluation of plasma electrolytes. However, chloremia is often not taken into account beyond its role in the acid-base calculation. In the last times, chloride has begun to take importance by diverse reports where it would be associated to dyschloremias and in particular the hyperchloremic acidosis with harmful effects in the organism[2]. On the other hand, we have normal saline, which is massively used worldwide[3]. With a composition characterized by supra-physiological levels of chloride[4], being the main cause of hyperchloremic acidosis[5]. The objective of this review is to show the importance of chloride in different systems of the body, its relationship with normal saline and in turn the relationship of this one with the potential deleterious effects of hyperchloremic acidosis.

El cloro es el anión de mayor concentración en el líquido extracelular, aporta entre 100 a 300 mosm/L a la tonicidad del plasma[1], su concentración plasmática es frecuentemente informada en los distintos servicios como parte de la evaluación general de los electrolitos plasmáticos. Sin embargo, la cloremia muchas veces no es tomada en cuenta más allá de su rol en el cálculo ácido-base. En el último tiempo, el cloro ha comenzado a tomar importancia por diversos reportes donde se asociaría a las discloremias y en particular la acidosis hiperclorémica con efectos dañinos en el organismo[2]. Por otra parte, tenemos el suero fisiológico, el cual es masivamente usado a nivel mundial[3]. Con una composición caracterizada por niveles supra fisiológicos de cloro[4], siendo el principal causante de la acidosis hiperclorémica[5]. El objetivo de esta revisión es mostrar la importancia que cumple el cloro en distintos sistemas del organismo, su relación con el suero fisiológico y a su vez la relación de este, con los potenciales efectos deletéreos de la acidosis hiperclorémica.

Acidosis metabólica hiperclorémica en Terapia Intensiva / Metabolic acidosis hyperchloremia in Therapy Intensive

El síndrome de respuesta inflamatoria sistémica responde actualmente a múltiples causas y su tratamiento tiene implicancias pronósticas. Uno de los pilares es la reanimación precoz con fluidos con el fin de restablecer las variables macro y microhemodinámicas determinantes del desarrollo de la hipoperfusión tisular. En este sentido, la persistencia de hipoxia tisular contribuye al desarrollo del síndrome de disfunción orgánica múltiple, principal causa de muerte en los pacientes críticos. Recientemente, ha surgido un interés creciente en los efectos de la acidosis metabólica hiperclorémica debido al uso exagerado de soluciones no balanceadas y la elevada prevalencia de acidosis dilucional en este grupo de pacientes. Existe evidencia experimental y clínica que demuestra los efectos nocivos del exceso de Cl­ incrementando citocinas proinflamatorias y modificando la circulación renal. De modo que, en la siguiente revisión, mi objetivo es revisar la fisiología del anión Cl­ y las evidencia experimental y clínica relevante a la fecha.(AU)

The presence of inflammatory response syndrome is due to several etiologies and its treatment has prognosis implications. The treatment key is early resuscitation with fluids to improve macro and microhemodynamic variables because they are the main determinants of tissue hypoperfusion development. In this sense, tissue hypoxia persistence causes multiorgan disfunction syndrome and it is the main cause of mortality in critically ill patients. Recently, an increased interest has emerged in the effect of hyperchloremic metabolic acidosis due to the excessive use of non-balanced solutions and the high prevalence of dilutional acidosis in this patient group. There is experimental and clinical evidence related to the deleterous effects of chloride excess in critically ill patients. Hyperchloremic metabolic acidosis increases pro-inflammatory citokines modifying the renal circulation. The aim of this review is to refresh the chloride physiology and the present relevant experimental and clinical evidence.(AU)

Acidosis hiperclorémica: mito y realidad / Hyperchloremic acidosis

La acidosis metabólica es una alteración ácido-base frecuentemente observada en pacientes críticos. Aunque en situaciones extremas este desorden en sí mismo es amenazante para la vida, la presencia de una acidosis metabólica leve no siempre es nociva y puede ser un reflejo de la adaptación fisiológica del organismo a la injuria aguda. Diferentes autores han documentado el desarrollo de acidosis metabólica hiperclorémica asociada al aporte de grandes cantidades de solución salina 0,9 por ciento. Algunos consideran que se trata de una condición benigna y autolimitada, mientras otros sostienen que la acidosis hiperclorémica puede deteriorar la perfusión renal y esplácnica, sin embargo su relevancia clínica real es aún incierta. En un afán de evitar la aparición de acidosis hiperclorémica y sus potenciales efectos adversos, se han desarrollado cristaloides y coloides en formulaciones modificadas para que se asemejen más a la composición del plasma. En este artículo de revisión analizaremo slos mecanismos de producción de la acidosis metabólica hiperclorémica en base al abordaje físico-químico de Stewart; la evidencia existente sobre el impacto de este trastorno sobre las variables de desenlace de los pacientes críticos, y el rol clínico de las nuevas “soluciones balanceadas”.

Metabolic acidosis is an acid-base alteration frequently observed in critically ill patients. Even in extreme situations this disorder in itself is life threatening, the presence of a mild metabolic acidosis is not always harmful and may be the result of physiological adaptation of the organism to acute injury. Several authors have documented the development of hyperchloremic metabolic acidosis associated with the infusion of large amounts of 0.9 percent normal saline. Some consider this to be a benign and transient, while others argue that hyperchloremic acidosis can impair renal and splanchnic perfusion, but her real clinical relevance remains uncertain. In an effort to prevent the development of hyperchloremic acidosis and its potential adverse effects have been development formulations of crystalloid and colloid modified to more closely resemble the composition of the plasma. In this review article will discuss the mechanism of production of hyperchloremic metabolic acidosis by the physicochemical approach Stewart, the existing evidence on the impact of this disorder on the outcome variables in critically ill patients, and clinical role of new “balanced solutions”.

Serum Electrolyte and Acid Base Composition in Patients with Graded Degrees of Chronic Renal Failure

One hundred sixty-three patients with graded degrees of uncomplicated stable chronic renal failure were studied to investigate the quantitative relationship between serum acid-base and electrolyte composition and serum creatinine level. Even in patients with a mild degree of renal failure, the serum total carbon dioxide (tCO2) content was reduced significantly. Progressive decrements in tCO2 were noted in the more severe degrees of renal failure with the reciprocal relationship between tCO2 and serum creatinine concentration. Depending upon the degree of chronic renal failure, the type of metabolic acidosis was different. In patients with a moderate degree of renal failure, hyperchloremic acidosis was noted with anion gap remaining normal. As the renal failure progressed to a more severe degree, this pattern of hyperchloremic acidosis changed to anion gap acidosis with a normal serum chloride level. The highest anion gap was 25 mEq/L in the patient with serum creatinine concentration 24.7mg/dL.