RESUMEN
A 52-year-old man ingested 60 ml of 2 percent topical minoxidil solution resulting in severe hypotension and tachycardia. He was resuscitated with intravenously administered crystalloid solution and treated with intravenously administered dopamine, resulting in a partial hemodynamic improvement. Further treatment with intravenously administered phenylephrine infusion resulted in resolution of hypotension. The patient suffered a non-Q-wave myocardial infarction as a result of the ingestion. The toxicity of this increasingly common preparation is profound.
Asunto(s)
Minoxidil/envenenamiento , Sobredosis de Droga , Humanos , Masculino , Persona de Mediana Edad , Intoxicación/terapiaRESUMEN
In the absence of direct toxins, the majority of evidence from animal models suggests that neutrophils (PMN) are necessary for the full expression of the abnormal pulmonary permeability accompanying acute microvascular lung injury. We therefore studied the role of the PMN in the human correlate of this disease, the adult respiratory distress syndrome (ARDS), by assessing the pulmonary retention of infused autologous 111Indium-labeled PMN (PMN-In). We evaluated 79 patients, prospectively categorized as: "active" ARDS (Aa; n = 30), "active" ARDS and concurrent corticosteroid therapy (As; n = 11), "resolving" ARDS (Ar; n = 13), sepsis without pulmonary edema (S; n = 7), and cardiac pulmonary edema (C; n = 18). This clinical separation was confirmed by retrospective analysis of associated measures of hemodynamic and respiratory dysfunction. We found that both analog scintigrams (positive/negative for diffuse pulmonary PMN-In sequestration) and computer-assisted quantitative analysis in 46 patients (T 1/2 of first hour demargination and percentage of peak activity/pixel/second remaining at 17 to 20 h) showed a significant rank order decrease in the pulmonary retention of labeled PMN-In through the Groups Aa----As----S----Ar----C. Our findings recognized aspects of in vivo PMN-In behavior that implied pathophysiologic differences between groups of critically ill patients in either the PMN themselves or in PMN-pulmonary endothelial interaction. This demonstrates the possibility of abnormal in vivo PMN-endothelial interaction in ARDS by virtue of the greater pulmonary localization of PMN in active ARDS versus resolving disease, septic non-ARDS states, and cardiac pulmonary edema.(ABSTRACT TRUNCATED AT 250 WORDS)
Asunto(s)
Pulmón/fisiopatología , Neutrófilos/fisiología , Síndrome de Dificultad Respiratoria/fisiopatología , Anciano , Permeabilidad Capilar , Humanos , Indio , Persona de Mediana Edad , Neutrófilos/diagnóstico por imagen , Estudios Prospectivos , Radioisótopos , Cintigrafía , Síndrome de Dificultad Respiratoria/diagnóstico por imagenRESUMEN
To assess the concurrent influence on extravascular lung water (EVLW) content of the intravascular Starling forces, the pulmonary capillary wedge pressure (PCWP), and the colloid osmotic pressure (COP), we measured EVLW by the thermal green dye technique in 174 patients with and without radiographically defined pulmonary edema; in the former group, patients with cardiac (CPE) and noncardiac (NCPE) causes of pulmonary edema were compared (study A). In 119 patients, EVLW was again measured one to three days later (study B). Patients with CPE demonstrated a significantly lower EVLW (9.3 +/- 3.9 ml/kg) (mean +/- SD) than patients with NCPE (14.5 +/- 4.9 ml/kg; p less than 0.05), despite a higher mean PCWP in the former group (20 +/- 7 mm Hg) than in the latter (12 +/- 6 mm Hg; p less than 0.05). In patients potentially with only a hydrostatic cause of pulmonary edema in study A, regression analysis demonstrated the following: EVLW = 3.2 + 0.30 PCWP (r2 = 0.38; p less than 0.005); and in patients with NCPE, EVLW = 10.9 + 0.304 PCWP (r2 = 0.17; p less than 0.01). In study B the change (delta) in EVLW between the two studies was described as follows: delta EVLW = 0.25 + 0.173 delta PCWP (p less than 0.01) + 0.663 group NCPE (p, not significant) + 0.236 group NCPE X delta PCWP (p less than 0.01). This latter equation indicated that the EVLW content manifested a greater change with concurrent alterations in the PCWP in patients with NCPE than was found in patients with only a hydrostatic influence to EVLW formation. Therefore, NCPE is characterized by a greater measurable thermal green dye EVLW than is observed in CPE at any given PCWP, and the PCWP synergistically influences EVLW accumulation in both CPE and NCPE.
Asunto(s)
Espacio Extracelular/análisis , Pulmón/análisis , Síndrome de Dificultad Respiratoria/metabolismo , Adulto , Anciano , Presión Sanguínea , Permeabilidad Capilar , Cateterismo Cardíaco/instrumentación , Cuidados Críticos , Técnica de Dilución de Colorante , Frecuencia Cardíaca , Humanos , Pulmón/irrigación sanguínea , Persona de Mediana Edad , Edema Pulmonar/etiología , Edema Pulmonar/metabolismo , Edema Pulmonar/fisiopatología , Presión Esfenoidal Pulmonar , Síndrome de Dificultad Respiratoria/fisiopatología , Estudios Retrospectivos , Termodilución/métodosRESUMEN
We measured extravascular lung water (EVLW) by the thermal-dye technique in a broad group of critically ill patients who had either acute cardiac or noncardiac illnesses. A portable AP supine chest roentgenogram, reviewed blindly, was used to classify patients as to the presence or absence of pulmonary edema; by clinical history we categorized patients into either a cardiac or noncardiac (ie, ARDS) group. With a normal chest roentgenogram, the mean EVLW was 5.6 +/- 1.8 ml/kg, and the pulmonary capillary wedge pressure (PCWP) was 11.3 +/- 5.3 mm Hg (mean +/- SD). In contrast, patients with pulmonary edema on a cardiac basis had a mean EVLW of 10.2 +/- 3.1 ml/kg (mean PCWP, 20.5 +/- 8.2 mm Hg), while patients with clinically defined noncardiac pulmonary edema and a normal PCWP (11.6 +/- 5.7 mm Hg) had a mean EVLW of 15.8 +/- 4.6 ml/kg, significantly higher than in the cardiac group (p less than 0.001). On a severity system of 014, the EVLW increased in parallel to the severity of the chest radiologic appearance of edema in both the cardiac (r2 = .44; p less than 0.001) and noncardiac (r2 = .59; p less than 0.001) patients. This study defined a normal range of thermal-dye EVLW in critically ill patients without radiologic evidence of pulmonary edema. We further demonstrated the increased pulmonary microvascular permeability of noncardiac pulmonary edema compared with cardiac edema by the greater EVLW at normal microvascular hydrostatic pressures in the former group.