Correção dos distúrbios do equilíbrio ácido-básico na infância / Treatment of the acid-base disorders in childhood

Este artigo tem por objetivo abordar os aspectos mais relevantes da correção dos distúrbios ácido-básicos na infância. São abordados inicialmente alguns parâmetros úteis para a análise das gasometrias e interpretação dos distúrbios ácido-básicos. Ressalta-se a importância de buscar o diagnóstico etiológico do distúrbio ácido- básico através da análise dos dados clínicos e laboratoriais. São também discutidas a importância do cálculo do intervalo aniônico para indicar o mecanismo do distúrbio e orientar o tratamento, bem como a utilização do gradiente alvéolo-arterial de oxigênio para avaliar a hematose. Na segunda parte deste trabalho, aborda- se mais especificamente a correção dos distúrbios ácido-básicos, com ênfase na acidose metabólica por ser a alteração mais frequentemente observada na infância. São comentadas as indicações, os riscos e a forma de utilização do bicarbonato de sódio para correção das acidoses metabólicas. A seguir, é discutido de forma resumida o tratamento das alcaloses metabólicas, priorizando a correção das alcaloses cloreto-sensíveis por serem mais usualmente vistas em pediatria. Finalmente, são feitos comentários gerais sobre o tratamento dos distúrbios primariamente respiratórios - acidose e alcalose respiratória.

The aim of this paper is to establish some guidelines for the treatment of acid-base disorders in childhood. First, some useful guidelines for the blood gas analysis and the interpretation of acid-base disturbances are discussed. The etiology of the acid-base disorders must be investigated through clinical history and laboratorial features. The determination of the cause of the disarrangement is essential for an appropriate treatment. The use of anion gap calculation to define the mechanism of metabolic alterations is emphasized. The importance of the measurement of the alveolar-arterial gradient is also discussed, mostly related to respiratory diseases. In the second part of this paper, the treatment of each acid-base disturbance is reported in separate parts. Metabolic acidosis is more extensively discussed since it is the commonest acid-base disorder observed in children. The risks, indications and different forms of bicarbonate administration to correct the metabolic acidosis are descrised. The guidelines for the treatment of metabolic alkalosis are also summarized. The metabolic alkalosis is divided in two subtypes: chloride-sensitive and chloride-resistant disarrangement. Since the chloride-sensitive metabolic alkalosis is more frequent in childhood, it is more extensively discussed in this article than chloride-resistant disorders. Finally, general aspects about the treatment of the respiratory disturbances - acidosis and alkalosis — are briefly included.

Systemic acidosis associated with diamox [abstract]

Glaucoma is an optic neuropathy defined by the presence of characteristic morphological alterations to the optic nerve head and suggestive visual field abnormalities. The aetiology of primary open angel glaucoma remains elusive but intraocular pressure is presumably the most important risk factor in all forms of glaucoma. In addition, the intraocular pressure remains the only modifiable risk factor, and current glaucoma therapy focusses on addressing the variable. A variety of drugs is available to reduce the intraocular pressure and they work by reducing aqueous production, increasing aqueous overflow or both. Although generally safe, these medications can be associated with local and systemic side effects. Topical beta blockers and systemic carbonic anhydrase inhibitors are notable for their effects on multiple organ systems and their potential for severe toxity. As with most medications, their safe use requires knowledge of the patient's health status, an awareness of specific contraindications to their use, sensitivity to the effects of ageing on drug metabolism, familarity with drugs which may cause adverse interaction and due diligence in the detection of insidious long-term effects. An illustrative case of marked acid-base imbalance associated with carbonic anhydrase inhibitor use is presented. (AU)

[Cardiopulmonary resuscitation: acid-base alterations and alkalizing therapy]. / Resucitación cardiopulmonar: alteraciones ácido-base y tratamiento alcalinizante.

It is generally believed that metabolic acidosis prevails during cardiac arrest. However, recent experimental and clinical studies have demonstrated that respiratory acidosis in mixed venous blood and respiratory alkalosis in arterial blood with only minor increases in lactic acid characterize the early acid-base changes that follow cardiac arrest and cardiopulmonary resuscitation (CPR). While continued CO2 production with critical reduction in systemic perfusion explains the accumulation of CO2 in the venous side, the reduction of pulmonary blood flow with maintenance of constant minute ventilation explains the decreases in expired CO2 and therefore arterial PCO2. In the heart, marked increases in CO2 tension and lactic acid are associated with dramatic decreases in myocardial pH with consequent depression of contractile function. Administration of sodium bicarbonate, however, neither increases resuscitability nor improves long term outcome. Moreover, adverse effects stemming from increases in plasma osmolality, increases in hemoglobin-O2 affinity, induction of alkalemia and generation of CO2 are potentially deleterious for myocardial and cerebral function. Consequently, the American Heart Association has recently discouraged the routine administration of bicarbonate during the initial 10 minutes of CPR in which interventions with proven efficacy such as artificial ventilation, precordial compression, electric defibrillation and epinephrine administration take place. Alternative experimental buffer therapy with agents that consume CO2 have also failed to alter the outcome of cardiac arrest.