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Biomedical subjects

J Manny

Publications and source records attributed to J Manny.

At least 37 records · Page 2Linked to original sources
PubMed1981

Peritoneal lavage in blunt abdominal trauma.

A prospective study of an Intracath method of diagnostic peritoneal lavage was done of 100 patients with blunt abdominal trauma. Initial results in dogs confirmed the reliability and sensitivity of the technique. In patients, it proved to be 96 per cent accurate. Fifty-eight patients had true-positive results, and in 52 of these, subsequent laparotomy demonstrated significant hemoperitoneum and intra-abdominal injury. Six patients had intra-abdominal injuries of limited significance. Thirty-eight of these patients were considered to have true-negative results. In one patient, false-negative, signs of intra-abdominal bleeding later developed, and a splenectomy was performed without incidence. There were three false-positive results. These patients underwent laparotomy and recovered without a problem. The only complications noted were puncture of the urinary bladder in one patient and subcutaneous infusions of lavage fluid in two patients which were recognized during the procedure. Results of this study demonstrate the safety and reliability of the Intracath method of peritoneal lavage for patients with blunt abdominal trauma.

Abdominal Injuries↗
PubMed1980

Volume loading and vasodilators in abdominal aortic aneurysmectomy.

Preoperative infusion of volume to increase the wedge pressure will maintain stable flow and arterial pressure at the time of aortic declamping. Usually 1,500 ml of balanced salt solution given with 75 g of albumin is sufficient to accomplish this purpose. Pressor or inotropic agents are not required. In our experience 14 percent of patients will have a down-slope in the preoperative myocardial performance curves. In these persons, volume infusions should be adjusted to keep the pulmonary arterial wedge pressure on the ascending portion of the curve. The use of vasodilator agents in normotensive patients has a deleterious effect on cardiac performance.

Aged↗
PubMed1980

Structural changes in the perfused canine kidney exposed to the direct action of endotoxin.

We attempted to clarify whether structural damage or hemodynamic alterations is the primary cause of renal failure in the initial phases of endotoxic shock. Endotoxin (0.5 mg/kg) was infused directly into the renal artery and normal renal hemodynamics were maintained by cross-perfusion and controlled pressure. Direct exposure of renal parenchyma to endotoxin action was followed by changes in structure at the cellular and subcellular levels. The damage was unequally distributed and involved mainly the mitochondria and lysosomes of the distal and proximal convoluted tubules. No significant structural changes could be detected in the glomeruli or in the vascular compartment. There was no direct relationship between the degree of mitochondrial and lysosomal damage and the changes in enzymatic activity. The enzymatic systems associated with active Na transport and glycogen breakdown showed only slight alterations, while those related to energy production, hydrogen transfer and the respiratory activity of the cell were severely affected. These results indicate that structural damage in the nephron may contribute to the renal failure in the initial phase of endotoxemia.

Acid Phosphatase↗
PubMed1979

Intrapulmonary clotting and fibrinolysis during abdominal aortic aneurysm surgery.

Intravascular clotting and fibrinolysis (C and F) are events which often accompany major surgical trauma. Their role in inducing cardiopulmonary failure is debated and prompted this study of 13 patients undergoing elective AAA. Following intubation, anesthesia and pressure breathing fibrinolytic activity (FA) in arterial blood exceeded that in mixed venous blood (p < 0.001) indicating pulmonary secretion of proteolytic activity. Fibrinogen, plasminogen and fibrin degradation products (FDPs) were normal. During surgery, fibrinogen and plasminogen fell (p < 0.001) while nonplasmin mediated FA and FDPs rose (p < .001). Despite heparinization (5000 U IV) aortic clamping (avg 56 min) led to evidence of C and F within the lungs. Arterial fibrinogen was 33.2 mg/ml lower than mixed venous blood (p < 0.01) and plasminogen was 0.47 Sherry units lower (p < 0.001). Soluble fibrin monomer appeared in arterial blood (p < 0.01). At the same time nonplasmin mediated FA was consumed within the lungs (p < 0.01) and FDPs were produced (44.6 microg/ml higher in arterial blood, p < 0.001). Similar changes were noted after aortic declamping. The transient 5.3 ml/cm H(2)0 fall in dynamic compliance was unrelated to C and F. Pulmonary vascular resistance and arterial pressure were unchanged. During wound closure intrapulmonary C and F ceased. Postoperatively (6 h), the physiologic shunt of 15.1% was similar to tbe preoperative value of 13.3%. All C and F factors returned to normal except FDPs which remained elevated. An average of 0.2 U blood was given prior to aortic clamping and 3.1 U during clamping. Neither the volume nor the type of blood (7 patients received washed RBCs) influenced pulmonary C and F. The results show that pressure breathing will alter pulmonary metabolism from clearance to secretion of fibrinolytic activity. Surgery leads to systemic C and F while intrapulmonary C and F is triggered by aortic clamping despite IV heparin. Delayed functional consequences of C and F are possible. Immediate postoperative effects are not apparent.

Aorta, Abdominal↗
PubMed1979

Importance of oxygen transport in clinical medicine.

One or more of the several components of the oxygen transport system may function abnormally in critical illness. Arterial hypoxemia is an important feature of acute respiratory failure. Its prominence may obscure other limitations in oxygen availability such as low cardiac output, anemia, or an increased red cell affinity state. These several components of the oxygen transport system can be influenced by therapeutic maneuvers, but the result may not necessarily be a net benefit. For example, red blood cell transfusion therapy may correct anemia, but increase the red blood cell affinity state so as to adversely affect cardiac function. Treatment programs require consideration of the interaction of these several variables affecting oxygen transport.

Aged↗
PubMed1979

Presence of negative inotropic agents in canine plasma during positive end-expiratory pressure.

Application of positive end-expiratory pressure (PEEP) will reduce cardiac output (CO). Humoral mediation of this event by circulating negative inotropic agents was examined using a rat papillary muscle bioassay. Twenty-seven dogs were anesthetized with an iv pentobarbital infusion. Plasma was obtained before and after 30 minutes of PEEP. The plasma was oxygenated in a small (4.5-ml) papillary muscle chamber using a diffusion membrane. An average PO2 of 416 mm Hg was achieved. PEEP plasma reduced developed tension (Tpd) from 2.16 +/- 1.0 to 1.90 +/- 1.05 g (P less than 0.0001). A fall in Tpd was observed whether or not CO was maintained constant with fluid infusion. Resting tension was unchanged. The percent reduction in Tpd correlated with the fall in CO (r = 0.63, P less than 0.01) when fluid was not infused to maintain CO. Reapplication of control plasma restored Tpd. Barbiturate levels in anesthetized dogs rose from 17.3 to 19.4 microns/ml during PEEP (P less than 0.1). Addition of pentobarbital to normal plasma led to a slight decrease in Tpd only when the concentration exceeded 99 microns/ml. In three experiments on ex vivo perfused hearts, application of PEEP led to lowering of peak systolic pressure (PSP) within 5 minutes. Removal of PEEP restored PSP in a similar time. The results support the hypothesis that the decline in CO with PEEP is mediated in part by a circulating negative inotropic agent.

Acid-Base Equilibrium↗
PubMed1979

Abnormalities in organ blood flow and its distribution during positive end-expiratory pressure.

Current evidence is inconclusive regarding the possibility that positive end-expiratory pressure (PEEP) redistributes flow and may be directly responsible for systemic organ dysfunction. This study tests the hypothesis that PEEP may induce abnormalities in the distribution of cardiac output (CO). Eight anesthetized dogs were studied during (1) 0 cm H2O PEEP (Z1), (2) 15 cm H2O PEEP (P), (3) Z2, and (4) bleeding (B) to reduce the CO to the same level as P. At each of the four periods, a different 15 mu radiolabelled microsphere was injected into the left atrium. Another four dogs were used to varify that each type of microsphere had the same flow distribution. CO fell from 3.1 liters/min to 1.9 during P (P smaller than 0.01) and to 2.0 during B (P smaller than 0.01). Mean arterial pressure (MAP) declined from 102 to 83 mm Hg (P smaller than 0.01) and 86 mm Hg (P smaller than 0.01(, respectively. Left atrial pressure (LAP) rose from 5.0 to 7.9 mm Hg during P (P smaller than 0.01) and fell during B to 2.7 mm Hg. c0 and its distribution were the same during Z1 and Z2. P caused selective reductions in hepatic (52%), adrenal (25%), and bronchial (24%) blood flows (P smaller than 0.01). In contrast, total flow to these organs during B was the same as during Z. Total renal flow was unchanged by P or B, but the cortical:medullary flow ratio increased during P from 24 to 49 (P smaller than 0.01) and was unchanged by B. P induced a decrease in fundal nucosal flow as compared with Z (P smaller than 0.01). Total coronary flow fell from 100 to 64 ml/min during both P and B (P smaller than 0.01). P led to a selective fall in subendocardial flow (67 ml/min X 100 gm) as compared with B (82.5 ML/MIN X 100 gm, P smaller than 0.01) as well as in the subendocardial:subepicardial flow ratio (1.069 vs. 1.112 ml/min X 100 gm, P smaller than 0.05). It is likely that the higher left ventricular filling pressure (LAP) during P as compared with during B compressed the endocardium and induced relative ischemia. Similarly the high airway pressure during P may have impeded bronchial mucosal flow. The causes and consequences of the other P-induced variations in flow are speculative.

Animals↗
PubMed1978

The association of lung distention, PEEP and biventricular failure.

Although positive and expiratory pressure (PEEP) is known to depress the cardiac output, the mechanism remains debated. Two series of experiments were designed to explore this mechanism. In the first study, the application of 15 cm H(2)O of PEEP to nine anesthetized, ventilated dogs led to a reduction of cardiac index from (mean +/- one standard error of the mean) 2.71 L/min .m (2) +/- 0.35 to 2.19 L/min m(2) +/- 0.22 (p < .05) and a drop in mean arterial pressure (MAP) from 117 mm Hg +/- 8 to 91 mm Hg +/- 11 (p < .01). The mean net (vascular minus pleural pressure) pulmonary artery pressure (MPAP) rose from 15.3 mm Hg +/- 1.2 to 20.6 mm Hg +/- 1.8 (p < .02). The mean net central venous pressure (CVP) rose from 5.2 mm Hg +/- 0.9 to 8.4 mm Hg +/- 0.9 (p < .05) and the net pulmonary arterial wedge pressure (PAWP) rose from 6.7 mm Hg +/- 0.7 to 9.5 mm Hg +/- 0.9 (p < .01). There was a nonsignificant rise in the mean net left atrial pressure (LAP). As PEEP was raised in increments from 0 to 20 cm H(2)O, both LAP and PAWP increased. The rise in PAWP was always greater than the increase in LAP. The difference between PAWP and LAP was strongly correlated with the increase in MPAP (r = 0.98). This relationship was useful in correcting the PAWP during PEEP. The problem of cardiac depression was evaluated in a second series of eight dogs. These animals underwent complete chest wall excision to eliminate any possible direct effects of increased pleural pressure on the heart and great vessels. The absence of the chest wall permitted hyperexpansion of the lungs, particularly with positive end expiratory pressure. At 15 cm H(2)O of PEEP, the mean cardiac index fell in these animals from 2.36 L/min. m(2) +/- 0.26 to 1.47 L/min.m(2) +/- 0.18 (p < .01) and the MAP fell from 105 mm Hg +/- 16.2 to 68 mm Hg +/- 4.8 (p < .001). The CVP rose from a mean of 5.5 mm Hg +/- 0.4 to 8.3 mm Hg +/- 0.6 (p < .01) and the LAP rose from 6.3 mm Hg +/- 0.8 to 8.0 mm Hg +/- 1.1 (p < .05). The MPAP rose from 18.0 mm Hg +/- 0.6 to 23.3 mm Hg +/- 1.6 (p < .01). Comparison of Group I and II showed a significantly greater depression of the cardiac output and MAP in the open-chested animals. At the same time LAP was significantly higher. These data strongly suggest that PEEP and particularly pulmonary hyperinflation induce biventricular failure.

Animals↗
PubMed1978

Hepatic--portal venous gas in adults: etiology, pathophysiology and clinical significance.

The roentgenographic finding hepatic--portal venous gas (HPVG) has been reported extensively in the pediatric and radiology literature. The surgical implications and clinical significance have yet to be fully defined. This study reviews the 60 reported cases in the literature and adds four new cases. HPVG appears as a branching radiolucency extending to within 2 cm of the liver capsule. HPVG is associated with necrotic bowel (72%), ulcerative colitis (8%), intra abdominal abscess (6%), small bowel obstruction (3%), and gastric ulcer (3%). Mucosal damage, bowel distention and sepsis predispose to HPVG. The current mortality rate of 75% represents an improvement from previous experience. Analysis of survivors indicates that the finding of HPVG requires urgent surgical exploration except when it is observed in patients with stable ulcerative colitis.

Abscess↗