Analytical calculation and acid-base analysis for detection of mixed disorders in critical care medicine.

Aim: The purpose of the study was to validate the systematic six-step arterial blood gas (ABG) analysis in critically ill patients to diagnose mixed ABG disorders. Materials and method: The study was conducted in the ICU of a tertiary care hospital (between 1 June and 30 September, 2007) for 4 months. A total of 560 ABG samples were evaluated from 183 patients. 50 samples were randomly picked and evaluated by single step, quick look method and six-step approaches for detecting mixed ABG disorders. Results: Single, quick and six-step methods when applied on same data, revealed higher number of mixed disorders with systematic six-step approach. Quick-step method revealed only 48% mixed disorders while six-step analysis confirmed 62% having mixed disorders, from the samples which initially appeared to be single disorder. Metabolic acidosis with respiratory acidosis (26%) was the commonest disorder. Metabolic acidosis with respiratory alkalosis (20%), respiratory alkalosis with metabolic alkalosis (6%), metabolic alkalosis with respiratory acidosis (4%), metabolic acidosis with NGMA (4%) and metabolic acidosis with metabolic alkalosis (2%) were the other mixed disorders seen. Conclusion: Mixed disorders as suspected on clinical grounds can only be validated after complete analysis by six-step approach in critically ill patients. pH, PaCO2, and HCO3 – allow determination of primary disorder, but it is only the inequality between predicted and actual compensatory response for simple acid-base disorders which reveals a mixed disorder.

Failure to thrive, can this be Bartter's syndrome?

A case series of four children, of different age groups, having complaints of polyuria and failure to thrive. These cases include two infants, a toddler and a child and investigations revealed that they had hyponatremia, hypokalemia, hyperchloremia and metabolic alkalosis, leading to a diagnosis of Bartters syndrome. Two of the patients also had hypomagnesemia. All the children were put on treatment for Bartter's Syndrome, and they responded well but unfortunately one of them was lost to follow-up

Cloreto e status hidroeletrolítico e ácido-básico: importância clínica da determinação laboratorial / Chloride and hydroelectrolytic and acid base status: clinical importance of laboratorial determination

Apesar de o cloreto ser um exame amplamente disponível e solicitado em instituições de saúde, a maior pane dos médicos crê ser difícil interpretar seus resultados, estabelecer correlações com outros parâmetros laboratoriais associados e tomar decisões terapêuticas baseadas no mesmo. Devido à complexidade de sua homeostase e à intrincada correlação com o status hidroeletrolítico e ácido-básico, poucos médicos se sentem efetivamente aptos a aproveitar a valiosa informação clínica que ele pode revelar. Isto é agravado pela rarefeita bibliografia objetiva sobre o tema. Os autores desta revisão não foram capazes de encontrar nenhum capítulo especificamente dedicado ao cloreto nos principais livros-texto de Fisiologia, Clínica Médica e Nefrologia, disponíveis, à exceção de três revisões bibliográficas no Medline. Não obstante, tentamos organizar a informação tão claramente quanto possível, com o objetivo de tornar o cloreto uma ferramenta útil aos nossos colegas profissionais de saúde.

Even though chloride is a widely available and requested test in health institutions, most part of physicians find it difficult to interpret its results, establish correlations with other laboratory linked parameters and take therapeutic decisions based on it. Due to the complexity of its homeostatic balance and intrincated correlation to hydroelectrolytic and acid base status, few doctors feel actually able to fully profit from the valuable clinical information it can unfold. This is aggravated by the scarce objective bibliography on the issue. The authors of this review were not able to find any chapters specifically dedicated to chloride on major Physiology, Internal Medicine and Nephrology textbooks, but only three reviews on Medline. Nevertheless, we managed to organize the information as clearly as possible with the aim of making chloride test an useful tool to our fellow health professionals.

Severe hypertension and hypokalemia as first clinical manifestations in ectopic Cushing's syndrome / Hipertensão grave e hipocalemia como primeiras manifestações clínicas em casos de síndrome de Cushing ectópica

Ectopic ACTH production occurs in about 10 percent of all cases of Cushing's syndrome, and about 25 percent of cases of ACTH-dependent Cushing's syndrome. Diverse tumor types are able to produce ACTH ectopically, including small cell lung carcinoma. Ectopic ACTH secretion by malignant neoplasm has been reported to have earlier and more aggressive metabolic effects. We report a 59-year-old male patient with severe hypertension, metabolic alkalosis and hypokalemia as the first clinical manifestations of an ACTH-secreting small cell lung carcinoma, although the typical phenotypic features of Cushing's syndrome were not present. Ectopic Cushing's syndrome should always be ruled out in patients with severe hypertension and hypokalemia.

A produção de ACTH ectópico ocorre em aproximadamente 10 por cento dos casos de síndrome de Cushing, e em aproximadamente 25 por cento dos casos de síndrome de Cushing dependentes de ACTH. Diversos tipos de tumores são capazes de produzir ACTH ectopicamente, incluindo carcinoma pulmonar de células pequenas. Relatórios indicam que a secreção de ACTH ectópico por neoplasma maligno causa efeitos metabólicos prematuros e mais agressivos. Apresentamos um paciente, 59 anos, com hipertensão grave, alcalose metabólica e hipocalemia, tendo estas como as primeiras manifestações clínicas de um carcinoma pulmonar de células pequenas com secreção de ACTH, embora as características fenótipas típicas da síndrome de Cushing não estavam presentes. A síndrome de Cushing ectópica deveria ser excluída sempre em pacientes com hipertensão grave e hipocalemia.

Diagnosis and management of metabolic alkalosis.

Elevated pH and elevated plasma bicarbonate level above normal characterise metabolic alkalosis. When bicarbonate is elevated pCO2 must also be elevated to maintain pH to its normal range. Therefore with metabolic alkalosis, the compensation is to decrease alveolar ventilation, and increase pCO2. The causes of metabolic alkalosis are gastro-intestinal hydrogen and chloride loss and due to renal cause. For metabolic alkalosis to continue both generation and maintenance of high levels of bicarbonate are necessary. The diagnosis of metabolic alkalosis is established by noting pH, serum bicarbonate (elevated) and pCO2 (compensatory) elevation. To establish the causes it is necessary to determine intravascular volume, supine and standing blood pressure and renin angiotension alolosterone axis. In chloride responsive alkalosis in which the conditions are extracellular volume depletion, hypokalaemia and hypochloraemia correction of intravascular volume with sodium chloride is needed. In severe metabolic alkalosis of any cause dilute hydrochloric acid (0.1 N HCl) may be infused intravenously but haemolysis may be a complication. In emergency situation with severe hypokalaemia dialysis with higher K+, Cl- and low HCO3- bath will be appropriate.

Memorias del V curso internacional: avances en enfermedad diarreíca y desequilibrio hidroelectrolítico, 5 / Memories of the V international course: advances in diarrheic disease and hydroelectrolitical unbalance

La alcalosis metabólica es un aumento primario del bicarbonato del plasma que se produce por una ruptura de la alineación bicarbonato/presión de anhídrido carbónico con disminución en las concentraciones de hidrogeniones y aumento del pH del plasma. Se caracteriza por presentar el pH, el bicarbonato del plasma y la presión de anhídrido carbónico elevados en sangre arterial acompañada, normalmente, de hipokalemia e hipocloremia. Las causas que provocan la alcalosis metabólica se clasifican en cuatro grupos: 1. Por administración contínua de alimentos. 2. Por la respuesta de la alcalosis hacia los cloruros. 3. Por resistencia de la alcalosis hacia los cloruros y 4. Otras causas diferentes de los grupos anteriores pero que producen alcalosis metabólica. El cuadro clínico que presenta el paciente se caracteriza por la presencia de vómitos abundantes, generalmente en lactantes, con ausencia de bilis y acompañados de respiraciones lentas y superficiales, en ocasiones se presentan crisis de apnea o tambien el paciente manifiesta debilidad y decaimiento con calambres, pudiendo, además, mostrar signos clínicos de tetania. Además hay irritabilidad y signos de hipotasemia. Para el diagnóstico de la alcalosis metabolica además de la observación del vómito, se realizan estudios de: Gasometría, ionograma, pH en la orina y determinación de cloro y potasio en la orina. El método clínico para determinar el tratamiento consiste en detrminar primero la causa

Alcalosis metabólica en fibrosis quística del páncreas / Metabolic alkalosis in cystic fibrosis of the pancreas

Un varón que había sufrido bronconeumonía 45 días después de nacer, ingresó al hospital a los 3 meses de edad por dificultad respiratoria, cianosis, deshidratación moderada, alcalosis metabólica, hiponatremia, hipocloremia, hipokalemia, excreción urinaria reducida de sodio y cloro y elevada de potasio. Sus funciones renales eran normales y en las radiografías de tórax se observaba evidencia de imágenes intersticiales de condensación y múltiples atelectasias segmentarias. La actividad de renina plasmática era de 30 ng/mL x h (n= 1 a 2,5 ng/mL x h) y la eliminación de cloro y sodio en el sudor estaban aumentadas a -x 62,6 y -x 83,9 mEq/L, respectivamente, respaldando el diagnóstico de fibrosis quística. La alcalosis metabólica es poco común. En ausencia de causas iatrogénicas debe sugerir hiperaldosteronismo, síndrome de Bartter y fibrosis quística