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)

Intoxicación por ácido acetilsalicílico, fisiopatología y manejo / Physiopathology and management of acetylsalicylic acid intoxication

Acetylsalicylic acid (ASA) intoxication is potentially lethal. After ingestion, AAS is rapidly transformed into salicylic acid that dissociates into an hydrogen ion plus salicylate. Salicylate is the main form of AAS in the body and produces multiple alterations. Initially, the stimulation of the ventilatory center promotes a respiratory alkalosis. Then, the mitochondrial dysfunction induced by salicylate, will generate a progressive metabolic acidosis due to the accumulation of ketoacids, lactic acid and dicarboxylic acids among others. Another alterations include hydro electrolytic disorders, gastrointestinal lesions, neurological involvement, ototoxicity and coagulopathy. The correct handling of acetylsalicylic acid intoxication requires an thorough knowledge of its pharmacokinetics and pharmacodynamics. Treatment consists in life support measures, gastric lavage, activated charcoal and urinary alkalization to promote the excretion of salicylates. In some occasions, it will be necessary to start renal replacement therapy as soon as possible.

Acute but not chronic metabolic acidosis potentiates the acetylcholine-induced reduction in blood pressure: an endothelium-dependent effect

Metabolic acidosis has profound effects on vascular tone. This study investigated the in vivo effects of acute metabolic acidosis (AMA) and chronic metabolic acidosis (CMA) on hemodynamic parameters and endothelial function. CMA was induced by ad libitum intake of 1% NH4Cl for 7 days, and AMA was induced by a 3-h infusion of 6 M NH4Cl (1 mL/kg, diluted 1:10). Phenylephrine (Phe) and acetylcholine (Ach) dose-response curves were performed by venous infusion with simultaneous venous and arterial blood pressure monitoring. Plasma nitrite/nitrate (NOx) was measured by chemiluminescence. The CMA group had a blood pH of 7.15±0.03, which was associated with reduced bicarbonate (13.8±0.98 mmol/L) and no change in the partial pressure of arterial carbon dioxide (PaCO2). The AMA group had a pH of 7.20±0.01, which was associated with decreases in bicarbonate (10.8±0.54 mmol/L) and PaCO2 (47.8±2.54 to 23.2±0.74 mmHg) and accompanied by hyperventilation. Phe or ACh infusion did not affect arterial or venous blood pressure in the CMA group. However, the ACh infusion decreased the arterial blood pressure (ΔBP: -28.0±2.35 mm Hg [AMA] to -4.5±2.89 mmHg [control]) in the AMA group. Plasma NOx was normal after CMA but increased after AMA (25.3±0.88 to 31.3±0.54 μM). These results indicate that AMA, but not CMA, potentiated the Ach-induced decrease in blood pressure and led to an increase in plasma NOx, reinforcing the effect of pH imbalance on vascular tone and blood pressure control.

Oxidative response of neutrophils to platelet-activating factor is altered during acute ruminal acidosis induced by oligofructose in heifers

Reactive oxygen species (ROS) production is one of the main mechanisms used to kill microbes during innate immune response. D-lactic acid, which is augmented during acute ruminal acidosis, reduces platelet activating factor (PAF)-induced ROS production and L-selectin shedding in bovine neutrophils in vitro. This study was conducted to investigate whether acute ruminal acidosis induced by acute oligofructose overload in heifers interferes with ROS production and L-selectin shedding in blood neutrophils. Blood neutrophils and plasma were obtained by jugular venipuncture, while ruminal samples were collected using rumenocentesis. Lactic acid from plasma and ruminal samples was measured by HPLC. PAF-induced ROS production and L-selectin shedding were measured in vitro in bovine neutrophils by a luminol chemiluminescence assay and flow cytometry, respectively. A significant increase in ruminal and plasma lactic acid was recorded in these animals. Specifically, a decrease in PAF-induced ROS production was observed 8 h after oligofructose overload, and this was sustained until 48 h post oligofructose overload. A reduction in PAF-induced L-selectin shedding was observed at 16 h and 32 h post oligofructose overload. Overall, the results indicated that neutrophil PAF responses were altered in heifers with ruminal acidosis, suggesting a potential dysfunction of the innate immune response.

Ifosfamide-induced Fanconi syndrome with diabetes insipidus

Ifosfamide-induced Fanconi syndrome is a rare complication that typically occurs in young patients due to a cumulative dose of ifosfamide > 40-60 g/m2, a reduction in kidney mass, or concurrent cisplatin treatment. It is usually characterized by severe and fatal progression accompanied by type II proximal renal tubular dysfunction, as evidenced by glycosuria, proteinuria, electrolyte loss, and metabolic acidosis. Diabetes insipidus is also a rare complication of ifosfamide-induced renal disease. We herein describe a case involving a 61-year-old man who developed ifosfamide-induced Fanconi syndrome accompanied by diabetes insipidus only a few days after the first round of chemotherapy. He had no known risk factors. In addition, we briefly review the mechanisms and possible therapeutic options for this condition based on other cases in the literature. Patients who receive ifosfamide must be closely monitored for renal impairment to avoid this rare but fatal complication.

Transdermal methyl alcohol intoxication cause of pain relief / Intoxicación transdérmica con alcohol metílico tratando de aliviar un dolor

A 60-year old female patient was found comatosed at home and taken to the hospital's Emergency Department by her relatives. It was learnt that she wrapped her knees with spirit-impregnated cotton pad for pain for one week. On physical examination, only a colour change of purple violet on her knees was noted. Metabolic acidosis with increased anion gap was detected by arterial blood analysis. The patient underwent haemodialysis. She was discharged from the hospital with no complaints, alert and rational following five days of follow-up treatment, with the diagnosis of methyl alcohol poisoning.

Una paciente de 60 años de edad fue hallada en estado comatoso en su casa, y trasladada por sus familiares al departamento de emergencias del hospital. Se supo que la paciente había sentido dolor en sus rodillas, y las cubrió con almohadillas de algodón impregnadas de metanol por espacio de una semana. Al realizarse el examen físico, sólo se observó un cambio de color violeta púrpura en sus rodillas. El análisis de sangre arterial reveló acidosis metabólica con hiato iónico elevado. A la paciente se le practicó una hemodiálisis. Fue dada de alta del hospital sin dolencias, consciente, y en su sano juicio, luego de cinco días de seguimiento de su tratamiento, tras de haber sido diagnosticada con envenamiento por alcohol metílico.

Reported survival with severe mixed acidosis and hyperlactemia after toluene poisoning

Lactic acidosis is a recognized complication of the inhalant abuse such as toluene, especially in patients with renal insufficiency. We report a case of severe metabolic acidosis and hyperlactemia due to toluene sniffing. The favorable outcome, despite extremely poor clinical symptoms, signs, laboratory and radiological findings, was unexpected. Specific aspects of the clinical course are addressed. Toluene sniffing should be considered in evaluating sever metabolic acidosis. Favorable outcome could be achieved with early diagnosis and proper interventions

Advancement of methanol poisoning mechanism research / 法医学杂志

The methanol poisoning by oral intake or skin contact occurs occasionally, which may have serious consequences including blindness and/or death. Methanol and its metabolites, formaldehyde and formic acid, are associated with metabolic acidosis, visual dysfunction and neurological symptoms. At present, the mechanism of methanol poisoning primarily focuses on the cell hypoxia, the alteration of structure and biological activity induced by free radical and lactic acid. Meanwhile, methanol poisoning causes changes in the balance between the production of free radicals and antioxidant capacity and in the proteases-protease inhibitors system, which lead to a series of disturbances.

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”.

Isoniazid Toxicity Presenting As Status Epilepticus and Severe Metabolic Acidosis.

Isoniazid (INH) is an integral component of treatment of tuberculosis. An acute overdose is potentially fatal and is characterized by the clinical triad of repetitive seizures unresponsive to the usual anticonvulsants, metabolic acidosis with a high anion gap and coma. The diagnosis of INH overdose should be considered in any patient who presents to emergency medical services (EMS) with the triad. We report a patient presenting with multiple generalised tonic clonic (GTC) convulsions with severe metabolic acidosis as a manifestation of INH toxicity. ©

Accidental isoniazid poisoning--a report.

Eight patients who had taken accidental overdose of Isoniazid were followed in relation to its clinical manifestations, EEG changes and management. All cases survived without any residual effect.

Ethylene glycol poisoning following ingestion of brake fluid / Envenenamiento con glicol de etileno tras la ingestión de líquido de frenos

A 32-year old male, with a history of depression and previous suicide attempts, was brought to hospital comatose after ingestion of brake fluid. He developed severe metabolic acidosis with an increased anion gap, hypotension, seizures and mild renal impairment. He required intensive care treatment for ventilatory and inotropic support. The clinical features, diagnosis and treatment of this unusual poison are discussed.

Un sujeto masculino de 32 años de edad, con una historia de depresión y previos intentos de suicidio, fue llevado en estado comatoso al hospital, luego de haber ingerido líquido de freno. El paciente desarrolló una acidosis metabólica severa con aumento del gap aniónico, hipertensión, convulsiones, e insuficiencia renal moderada. Requirió tratamiento mediante cuidados intensivos con apoyo ventilatorio e inotrópico. El trabajo analiza las características clínicas, el diagnóstico y el tratamiento de este envenenamiento inusual.

Predisposition to metabolic acidosis induced by topiramate

RATIONALE: Metabolic acidosis induced by topiramate is a well documented but infrequent adverse event. The objective was to demonstrate the lowering of carbon dioxide serum levels, which is usually asymptomatic but may facilitate the occurrence of metabolic acidosis in patients using topiramate. METHODS: We evaluated, prospectively, the carbon dioxide serum levels of 18 patients seen at the epilepsy clinic of our university hospital, before and 3 months after introducing topiramate. RESULTS: Five patients were female and 13 were male, age ranging from 2 to 16 years old (mean=9.3). Carbon dioxide mean serum levels were 25 and 21.2 mmol/L (normal = 22 to 30), before and 3 months after introducing topiramate, respectively. Dose ranged from 2.08 to 11.76 mg/kg/day (mean=6.7mg/kg/day). Adverse events were anorexia, nausea and somnolence. CONCLUSION: We conclude that the lowering of carbon dioxide serum levels induced by topiramate is mostly asymptomatic, but may facilitate the occurrence of metabolic acidosis. Since patients in use of topiramate have refractory epilepsy, they may need epilepsy surgery, and must be carefully monitored for the risk of metabolic acidosis during surgery

Acidosis metabólica inducida por metanol administrado por vía cutánea en un niño de 9 meses de edad / Metabolic acidosis induced by methanol administered per cutaneous acoute in a 9 month infant

Se presenta el caso de un niño de 9 meses de edad con intoxicación accidental por metanol. El paciente desarrolló las siguientes alteraciones clínicas y bioquímicas: Hiperventilación, convulsiones, acidosis metabólica y aumento del anion gap. Fue tratado con infusión de bicarbonato, ventilación mecánica y etanol. Se revisa la fisiopatología, diagnóstico y tratamiento de esta intoxicación

Metabolic acidosis induced by cetrimide-chlorhexidine solution in hydatid cyst surgery.

A patient with a large hydatid cyst of the left lobe of the liver developed metabolic acidosis following rather liberal use of cetrimide-chlorhexidine solution as a scolicidal agent. The progress and management of this complication are described in the patient is being reported.

Toxicity of exposed aluminium phosphide.

Poisoning by the partially or fully exposed compound of aluminium phosphide (ALP) is becoming common, Fifty patients with history of ingestion of ALP either in the form of broken tablets or granular powder were included in this study for analysis of systemic effects and outcome. Forty patients (Gr. I) consumed broken or granular form of tablets. Ten patients (Gr. II) consumed only powder form of tablets from an old container. 30 patients in group-I developed mild hypotension (BP 80-90 mm Hg). 4 patients (10%) developed ECG changes and mild metabolic acidosis. One patient died constituting 2.5% mortality rate. The patients of group-II neither developed any systemic effects nor showed any mortality. The aim of the study is to differentiate these cases from patients who consume active, fresh compound where mortality rate will be much higher.