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Biomedical subjects

J E Rinaldo

Publications and source records attributed to J E Rinaldo.

48 records · Page 3Linked to original sources
PubMed1983

Adult respiratory distress syndrome following intrapleural instillation of talc.

After intrapleural instillation of talc for sclerosis of malignant pleural effusions, dyspnea occurred in three patients, progressed gradually over 72 hours, and culminated in acute respiratory failure characterized by bilateral diffuse pulmonary infiltrates with normal pulmonary artery occlusion pressures. Two patients recovered and one died. The chronological similarity of the sequence of fever, dyspnea, and respiratory failure in the absence of documented infection or other conditions that predispose to the adult respiratory distress syndrome (ARDS) suggests that intrapleural talc may have induced the syndrome in these patients through unknown mechanisms. This experience emphasizes that other agents are preferable for initial attempts to promote pleural symphysis in the palliation of recurrent malignant effusions. When talc is used in patients who are unresponsive to tetracycline, we suggest clinical monitoring for respiratory compromise for 72 hours after the procedure.

Adult↗
PubMed1982

Mapping of human local pulmonary ventilation by xenon enhanced computed tomography.

Functional maps of local pulmonary ventilation are derived from serial computed tomographic images acquired prior to and during a short period of inhalation of subanesthetic xenon/oxygen gas mixtures. Preliminary results from human studies yield quantitative maps of local ventilation rates with excellent anatomic specificity demonstrating nonuniformities in the distribution of ventilation in normal and abnormal human lungs.

Adult↗
PubMed1982

Ischemic necrosis of both lower extremities as a result of the microembolism syndrome complicating the adult respiratory distress syndrome caused by Escherichia coli pneumonia and septicemia.

Extensive gangrene of both lower extremities necessitating bilateral above-the-knee amputations complicated the adult respiratory distress syndrome (ARDS) caused by Escherichia coli pneumonia and septicemia in a 52-yr-old man. Concurrent with the evolution of tissue necrosis, peripheral blood leukocyte and platelet counts fell, and pulmonary vascular resistance increased. Adequacy of the cardiac output was confirmed by repeated thermodilution cardiac output measurements, and major vascular occlusion was excluded surgically. Fibrin degradation products and thrombocytopenia were present, but the other usual criteria for disseminated intravascular coagulation were absent. Small vessel thrombosis by fibrin and leukocytes was observed histologically in the amputated extremities. These findings suggest that gangrene was due to the "microembolism syndrome"--diffuse small vessel occlusion by fibrin thrombi complicating ARDS. This unusual complication of ARDS may occur without abnormalities suggestive of diffuse intravascular coagulation in routine laboratory tests of blood coagulation. It should be suspected and treated promptly to avoid severe disability in survivors.

Escherichia coli Infections↗
PubMed1982

Massive hemoptysis and tension pneumothorax following pulmonary artery catheterization.

We report a case of massive hemoptysis and bilateral tension pneumothorax immediately following placement of a fiberoptic pulmonary artery catheter. We postulate air entry into a traumatic communication caused by the catheter, traversing a parenchymal artery, the contiguous airspace and the interstitial space. Dissection of air through the perivascular sheath and into tissue planes of the thorax and abdomen followed. This sequence was rapidly fatal. Tension pneumothorax should be considered if dynamic respiratory system compliance remains poor despite aggressive evacuation of blood from the trachea of a patient with a recently inserted balloon-type catheter.

Catheterization↗
PubMed1980

Oxygen therapy, oxygen therapy in medical patients hospitalized outside of the intensive care unit.

The administration of O2-enriched breathing mixtures to acutely ill patients is based on the premise that this form of treatment can overcome the known deleterious effects of tissue hypoxia. Therapeutic practices are founded on a knowledge of the physiology of oxygenation in normal and diseased persons and on knowledge of pulmonary O2 toxicity rather than on demonstrated alterations in disease outcome. The arterial PO2 (Pao2), when markedly diminished, indicates O2 deprivation of tissues, especially in unstable or acute states. However, th Pao2 may show little or no abnormality in states with sharply diminished generalized or regional systemic blood flow. Despite these shortcomings, the Pao2 remains a useful guide for initiating and monitoring O2 therapy in many circumstances. To minimize pulmonary O2 toxicity, the concentration of O2 chosen should be the lowest dose that will correct hypoxemia; 40% O2 is not known to be clinically toxic even after prolonged administration, but toxicity increases progressively above this value. In hypoxemic eucapnic patients, Pao2 of 60 mm Hg represents a reasonable value for treatable hypoxemia, but it is often rational to treat unstable patients with higher Pao2 values, especially if the alveolar-arterial Po2 difference is abnormally wide; 40% O2 represents a reasonable initial dose, with adjustments made on the basis of serial Pao2 measurements. When hypercapnia accompanies hypoxemia, O2 is often not given for Pao2 values greater than 50 mm Hg, and controlled low-dose O2 (24 to 30%) should be used to correct hypoxemia partially while preserving an element of hypoxemic ventilatory drive. In states of low blood flow, high O2 concentrations should be used to maximize the amount of O2 dissolved in plasma, and the duration of therapy should be as brief as possible to minimize O2 toxicity.

Carbon Dioxide↗
PubMed1975

Active chloride secretion by in vitro guinea-pig seminal vesicle and its possible relation to vesicular function in vivo.

1. The guinea-pig seminal vesicle in vivo is characterized by a transmural electrical potential difference of approximately 11 mV with the lumen electrically negative with respect to the interstitial fluid. The concentrations of Na, Cl and K in the vesicular fluid are 13, 15, and 0-4 mM, respectively. 2. When mounted as a flat sheet in a short-circuit apparatus, guinea-pig seminal vesicles initially undergo a decline in the transmural electrical potential difference and short-circuit current ('low phase') followed by a spontaneous increase in these parameters ('high phase'). 3. During the low phase, net C1 movements across the tissue do not differ significantly from zero, and there is a small 'residual' current that is unaccounted for. 4. During the high phase, there is a significant active C1 secretion into the mucosal solution, not detectable net movement of Na and an unaccounted for or 'residual' current that is equal to that found in the low phase. 5. Theophylline, dibutyryl-3'-5' cyclic adenosinemonophosphate,prostaglandin E1 and prostaglandin F2alpha markedly stimulate the transmural electrical potential difference and short-circuit current during the low phase, but have no effect when added to the bathing solution during the high phase. 6. Diffusion potentials determined across in vitro seminal vesicles suggest that the spontaneous transmural electrical potential difference in vivo may be attributable to the large ionic asymmetries between the vesicular fluid and the plasma. 7. It is postulated that two phases are involved in the elaboration of seminal vesicular fluid. The initial phase, following emptying of the vesicle, is characterized by the secretion of electrolytes, organic molecules and water. Active C1 secretion presumably regulated by intracellular cyclic adenosinemonophosphate and/or prostaglandins may be the driving force for this initial secretion of electrolytes. Following this secretory phase, electrolytes and water are reabsorbed, thereby concentrating the organic components in the vesicular reservoir.

Animals↗
PubMed1975

Effects of unilateral sodium replacement on sugar transport across in vitro rabbit ileum.

The effects of unilateral sodium replacement with either choline or mannitol on passive and active 3-O-methyl-D-glucose (3-MG) absorption by in vitro rabbit ileum were examined. The results indicate that the predominant factor influencing 3-MG absorption is the presence of sodium in the mucosal bathing solution. Replacement of sodium in the mucosal solution alone markedly inhibits passive and essentially abolishes active 3-MG absorption regardless of the presence or absence of sodium in the serosal bathing solution. The presence or absence of sodium in the serosal solution does not affect transmural 3-MG transport regardless of the sodium concentration in the mucosal solution. Further, when sodium is replaced in the mucosal solution alone, the bidirectional transmural fluxes of 3-MG do not differ markedly from those of D-mannitol, a solute whose transport is probably attributable to simple diffusion. The present findings together with those of previous studies (15, 16) are consistent with the notion that replacement of sodium in the mucosal solution alone essentially abolishes transcellular 3-MG transport and that the remaining transepithelial fluxes are largely due to diffusion through the paracellular or shunt pathway. The relation of these findings to in vivo and in vitro studies in which perfusion of a segment of small intestine with a Na-free solution disclosed little or no inhibition of sugar absorption is discussed.

Animals↗