Liver cell membrane alterations during hemorrhagic shock in the rat.
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Animals↗
Biomedical subjects
R L Holliday
Publications and source records attributed to R L Holliday.
Anatomic and cardiopulmonary responses to trauma with associated blunt chest injury.
Myocardial dysfunction may result from severe trauma. Therefore, left (LV) and right ventricular (RV) function were prospectively assessed by ECG-gated blood pool radionuclide (RN) angiography in 25 consecutive patients who had sustained severe trauma including blunt chest injuries. Focal abnormalities of RV and LV wall motion were defined in 17 patients; 12, RV; two, LV; and three, biventricular. In two patients traumatic tricuspid insufficiency was also demonstrated, and subsequently verified by contrast angiography. Other means to detect myocardial contusion (enzymatic, electrocardiographic, and Tc-99m pyrophosphate scintigraphy) proved to be insensitive when compared to RN angiography. Two of the five deaths in the group were attributed to refractory arrhythmias. Surgical or post-mortem evidence of traumatic myocardial injury was obtained in five instances when RN angiography indicated contusion. Of the 13 patients available for followup examinations, 11 showed complete or partial resolution of the abnormality and two were unchanged. Comprehensive cardiopulmonary monitoring revealed an inverse relationship between right ventricular ejection fraction (RVEF) and pulmonary vascular resistance (PVR) (R2 = 0.42; p < 0.01) and between the PVR and left ventricular ejection fraction (LVEF) (R2 = 0.48; p < 0.01) and left ventricular end-diastolic volume (LVEDV) (R2 = 0.69; p < 0.01). Further, as right ventricular end-diastolic volume (RVEDV) was increased in trauma, left ventricular function and compliance were reduced. In blunt chest trauma RV contusion occurs more frequently than previously recognized and positive RN angiography constitutes prima facie evidence of direct myocardial injury. Further, LV function remains preload dependent, but may be depressed by elevated PVR impeding the blood flow from RV to LV and/or decreases in LV compliance.
Adolescent↗
Pulmonary microvascular clearance of radiotracers in human cardiac and noncardiac pulmonary edema.
We examined the integrity of the alveolocapillary membrane in human cardiac (hydrostatic) (group 1) and noncardiac (permeability) (group 2) edema by measuring the clearance of two intravenously administered radiotracers from the blood to suctioned bronchoalveolar secretions (BAS), representing pulmonary edema fluid, and compared the clearances to simultaneously measured pulmonary capillary wedge pressure (PCWP) and colloid osmotic pressure (COP), representing the intravascular Starling forces, Pmv and pimv. 111In-labeled diethylenetriamine pentaacetic acid (DTPA), mol wt 504, a hydrophilic radiotracer that equilibrates with extracellular water, and 125I-labeled human serum albumin (HSA), mol we 69,000, were injected intravenously. Samples of blood and BAS were then collected hourly for 405 h, and clearances were calculated. We found the clearance of both radiotracers to be greater in group 2 than in group 1 patients, despite a low mean PCWP-COP gradient, indicating greater alveolocapillary membrane permeability membrane in noncardiac, than in cardiac edema. Furthermore, 111In-DTPA clearance was linearly correlated with the PCWP-COP gradient in both groups (group 1, R2 = 0.726, P less than 0.001; group 2, R2 = 0.879, p less than 0.001 as was the clearance of 125I-HSA in group 2 (R2 = 0.35, P less than 0.027). Clinically, the data suggest that in cardiac and noncardiac pulmonary edema the transmicrovascular flux of small and large solutes may be favorably influenced by therapeutic alterations aimed at widening the intravascular PCWP-COP gradient. However, the greater permeability of the alveolocapillary membrane in noncardiac edema would prohibit any major resolution of edema by simple therapeutic alterations of this gradient.
Capillary Permeability↗
Alveolo-capillary permeability in human septic ARDS. Effect of high-dose corticosteroid therapy.
High-dose corticosteroid therapy has been advocated as adjunctive therapy in the adult respiratory distress syndrome (ARDS). We evaluated the effect of pharmacologic doses of corticosteroid (methylprednisolone and dexamethasone) on alveolo-capillary permeability in human septic ARDS by examining the change in appearance of intravenously administered iodine 131 (131I) human serum albumin (I-HSA) into broncho-alveolar secretions, before and after corticosteroid administration. Of 19 patients examined, in 14 (group 1) the clearance of I-HSA was reduced by corticosteroid (pre, .204 +/- .08 ml;/hr; post, .096 +/- .01 ml/hr; P less than .001), while in five (group 2) it was unaffected (pre, .23 +/- .02 ml/hr; post, .215 +/- .01 ml/hr; P=NS). Group 2 patients were more severely ill than group 1 patients in that their mean intrapulmonary shunt fractions and mean pulmonary artery pressures were higher. We conclude that high-dose corticosteroid therapy may reduce alveolo-capillary permeability in human septic ARDS if used early in the course of the illness.
Bronchi↗
Necrotizing anaerobic infections.
Severe necrotizing anaerobic infections carry a high mortality. From a retrospective review of 17 cases of gas gangrene, necrotizing fasciitis and nonclostridial myonecrosis seen at the Victoria and University hospitals in London, Ontario, between Jan. 1, 1975 and Dec. 31, 1977, the most common antecedent was found to be minor trauma. Location of the infection varied; the scrotum and perineum were most commonly involved. Local findings were most frequently edema, skin tenderness and induration. Mixed infections predominated with a pure growth of Clostridium sp. occurring in only three cases. The overall mortality was 29%. The mainstay of treatment after initial administration of fluids followed by broad-spectrum antibiotics is early aggressive surgical debridement of all necrotic tissue.
Anaerobiosis↗
Total exchangeable potassium in patients receiving total parenteral nutrition.
Total exchangeable potassium (Ke) measurements were done on 13 patients who received total parenteral nutrition (TPN) at 25% dextrose and 2.5% amino acids (AA) (a hypertonic dextrose solution) by central vein, and 12 patients who received TPN as 10% dextrose, 10% fat emulsion (Intralipid), and 2.5% AA with lipid supplying about 60% of the nonprotein calories. There were 13 patients with benign diseases, three with carcinoma resected for cure, four with sepsis, three with severe burns, and two receiving chemotherapy for cancer. All but four of the septic and three of the burned patients had lost more than 10% of their normal body weight. A tracer dose of 150 to 300 microCi of K42 was injected intravenously during the first few days of the TPN therapy and a 48-hour urine collection and 24-, 36-, and 48-hour urine spot samples were obtained. Measurement of Ke was repeated after 7, 14, or 21 days of TPN therapy. Calories per kilogram per day, delta K per day, and percent delta K per day were determined for each patient and the data entered into a Textronics graphics computer for selection of curves of best fit. Similar curves of calories per kilogram per day versus delta K per day were obtained for the central and peripheral TPN groups. Intercepts where the body cell mass was maintained were at 32 calories/kg/day for the central TPN group and 34 calories/kd/day for the peripheral TPN group. Patients in both groups received a minimum of 0.6 gm protein/kg/day and the majority received from 0.8 to 1.2 gm protein/kg/day. Protein intake correlated with delta K per kilogram per day in the central but not the peripheral TPN group. We conclude that in nonseptic malnourished patients, an Intralipid calorie is as efficient as a dextrose calorie and that delta K is related to caloric rather than protein intake. None of the septic or burned patients maintained his body cell mass. However, they all received less than 30 calories/kg/day for a number of reasons.
Amino Acids↗
Monitoring the critically ill surgical patient.
Critically ill surgical patients account for approximately half the patients in an active multidisciplinary critical care unit. Hypovolemia and sepsis are common in such patients and affect a number of organ systems. Monitoring these systems provides therapeutically relevant information that may decrease morbidity and improve patient survival. Circulatory hemodynamics may be assessed by direct measurement of the arterial blood pressure, central venous and pulmonary artery pressure monitoring and cardiac output determination; the data thus obtained are valuable in guiding fluid replacement in the hypovolemic individual. The respiratory status may be assessed by bedside spirometry and measurement of arterial blood gas tensions to gauge pulmonary function and the need for assisted ventilation. Renal dysfunction is common in such patients; careful analysis of both urine and blood may identify prerenal as opposed to renal and postrenal factors. Monitoring of the gastrointestinal tract, especially for hemorrhage, is important. Finally, careful attention to nutritional status and provision of adequate protein and energy intake by mouth or by vein is a vital component of the optimal care of these patients.
Blood Volume↗
Pathogenesis of pulmonary edema associated with the adult respiratory distress syndrome.
Pulmonary edema is common cause of acute respiratory failure and can be seen in not only cardiac but also noncardiac diseases. The pathophysiologic mechanism for the development of acute pulmonary edema in any clinical situation can usually be explained alterations in the forces governing the transvascular flux of fluid in the pulmonary microvasculature, according to the Starling equation. "Cardiac" pulmonary edema is primarily due to an increase in the capillary hydrostatic pressure of sufficient magnitude to overcome the forces maintaining fluid within the vessel and the ability of the lymphatics to drain the transudated fluid. On the other hand, pulmonary edema occurring in association with noncardiac disease (e.g., sepsis, aspiration or shock) is secondary to an increase in the permeability of the pulmonary microvasculature and is referred to as noncardiogenic pulmonary edema or the adult respiratory distress syndrome. This article examines the mechanisms for the development of pulmonary edema and discusses the differences between the cardiac and noncardiac types.
Animals↗
Wedged balloon catheter angiography in the critical care unit.
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Blood Pressure↗
Documentation of pulmonary capillary permeability in the adult respiratory distress syndrome accompanying human sepsis.
Current evidence suggests that pulmonary edema accompanying human sepsis may result either from changes in the serum oncotic and hydrostatic pressures or an increase in the permeability of the pulmonary microvasculature. In this study, we compared the "clearance" of injected 131I-labeled human serum albumin from blood to bronchoalveolar secretions in intubated patients with pulmonary edema secondary to sepsis or myocardial infarction. A significantly increased mean +/- SE clearance of the radionuclide was seen in patients with sepsis (0.34 +/- 0.03 ml per hour) compared to those with myocardial infarction (0.043 +/- 0.008 ml per hour) (P less than 0.001), although both groups had similar degrees of edema on chest radiographs. Because the patients with sepsis had no severe decrease in serum oncotic pressure (18.4 +/- 5.0 mm Hg) or evidence of left heart failure, as determined by the pulmonary wedge pressure (11.0 +/- 6.8 mm Hg), we concluded that the genesis of the pulmonary edema in sepsis was due to an increase in pulmonary microvascular permeability, as measured by the increased clearance of 131I-labeled human serum albumin.
Adult↗
Predictive value for survival of lymphocytes and polymorphonuclear leukocytes in patients with sepsis.
To study their value in predicting prognosis, tests were performed on peripheral blood lymphomononuclear cells and polymorphonuclear leukocytes in 34 critically ill patients with sepsis. Intially, the number of lymphomononuclear cells was reduced by 32% compared with healthy control subjects and was 42% lower in those who died than in survivors. The values remained low in those who died. The numbers of T and B cells, determined by rosette formation using sheep and mouse erythrocytes, did not change during the period of observation. Intially, K cell activity was decreased by 48% compared with normal activity. In those younger than 65 years, K cell activity was 68% lower in patients who later died than in survivors. It returned to normal at 20 to 30 days and decreased in those who died. Polymorphonuclear leukocyte adherence was decreased by 50% compared with healthy control subjects and tended to be lower in those who died. Chemotactic migration of polymorphonuclear leukocytes and intracellular killing of Staphylococcus aureus and Pseudomonas aeruginosa were not impaired. It was concluded that the lymphomononuclear cell count, K cell activity and adherence of polymorphonuclear leukocytes were decreased in patients with sepsis and that the values were useful in predicting prognosis.
Adolescent↗
Femoral arteriovenous amino acid differences in septic patients.
Femoral arteriovenous differences and flux of amino acids across the leg were measured in seven septic patients and compared with those of six nonseptic patients on days 1 and 3 following major surgery. The septic patients were seriously ill and judged clinically to be catabolic. The postoperative patients, although not septic, were expected to have a maximal catabolic response to operation during the first 3 days after operation. Both groups had increased release of phenylalanine from the leg, an index of muscle proteolysis. Septic patients had decreased femoral arteriovenous differences (--20 vs --74 and --60 mumoles/liter) and decreased flux (34 vs 169 and 128 nm/100 gm of calf muscle) of the branched-chain amino acids as compared with the nonseptic postoperative patients on days 1 and 3. The arterial plasmal levels of the branched-chain amino acids and alanine were not different, but phenylalanine was elevated in the septic patients (88 vs 49 and 55 mumoles/liter). The insulin:glucagon molar ratio was lower in the septic patients (2.4 vs 4.4 and 5.5). These findings suggest that in the catabolism of sepsis there is greater oxidation of branched-chain amino acids in muscle than in the catabolism associated with uncomplicated surgery.
Abscess↗
Plasma catecholamine levels and pulmonary dysfunction in sepsis.
In a retrospective analysis of 18 patients with sepsis and adult respiratory distress syndrome, we found that high plasma epinephrine and noradrenalin levels were associated with severe defects in oxygenation that accompany this disease. The result of previous experimental work support the concept that high plasma catecholamine levels augment already existing defects in the ventilation to perfusion ratio and increases the measured intrapulmonary shunt fraction. The results of this study do not, however, delineate whether or not the relationship between high circulating plasma catecholamine levels and severe adult respiratory distress syndrome is causal or simply a measurement of two indexes which reflect the severity of the underlying disease process.
Epinephrine↗
The Trendelenburg position: hemodynamic effects in hypotensive and normotensive patients.
The effect of the Trendelenburg position on systemic and pulmonary hemodynamics in critically ill patients is not generally appreciated. This study examined the hemodynamoc effect of 15-20 degrees head-down tilt in 61 normotensive and 15 hypotensive patients with acute cardiac illness or sepsis. In normotensive patients, the head-down tilt increased the preload of both right and left ventricles, increased cardiac output slightly, decreased systemic vascular resistance, and did not change the mean arterial pressure. This effect was probably mediated by baroreceptor stimulation. In hypotensive patients, the Trendelenburg position did not increase preload, slightly increased afterload, and decreased cardiac output. This study failed to document any beneficial hemodynamic effect of the Trendelenburg position in critically ill normo- or hypotensive patients.
Adult↗
Hypophosphatemia associated with coma.
In three cases of severe hypophosphatemia profound coma was associated. Although the occurrence of hypophosphatemia appeared to coincide with a high rate of intravenous administration of glucose and water, two of the three patients had liver disease and the other had hypothermia. In two instances the neurologic status improved with intravenous phosphate therapy. These case reports emphasize the importance of early recognition and treatment of profound hypophosphatemia in critically ill patients.
Adult↗
Pulmonary hypertension in sepsis: measurement by the pulmonary arterial diastolic-pulmonary wedge pressure gradient and the influence of passive and active factors.
To examine the relative roles of passive factors (flow; filling pressures of left side of heart) and active factors (acidosis; arterial unsaturation) in the genesis of pulmonary hypertension when associated with sepsis, 37 patients with sepsis and 24 patients without sepsis were examined. Pulmonary hypertension was measured by the pulmonary arterial diastolic-pulmonary wedge pressure gradient (PAd-PWP gradient) and correlated reasonably with a standard formula for calculated resistance ([PA--PWP]/CI, where PA is mean pulmonary artery pressure and CI is cardiac index). In 22 of 37 patients, sepsis was associated with a significant degree of resistance to flow in the pulmonary circulation, as measured by the PAd-PWP gradient: and the higher the PAd--PWP gradient, the greater the likelihood of early death. None of the examined passive or active factors appeared to be adequate to explain pulmonary hypertension when present. By the use of previously derived formulae to estimate the compliance of the elastic pulmonary arteries, factors affecting this part of the pulmonary microcirculation could not be held accountable for apparent pulmonary hypertension. Therefore, the presence of pulmonary hypertension in sepis appears to be an active, rather than a passive, phenomenon and unrelated to arterial oxygen saturation or acid-base imbalance. Although the exact cause is unknown, pulmonary hypertension in sepis is associated with a high mortality and may be clinically followed by measurement of the PAd-PWP gradient.
Bacterial Infections↗
Altered gluconeogenesis in sepsis.
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Alanine↗
Ionized hypocalcemia in critically ill patients with sepsis.
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Bacterial Infections↗