Jonah Manny

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.

A review of 561 cases of cecal volvulus that were published between 1959 and 1989 along with 7 new cases, was performed to characterize the clinical and laboratory profile and to evaluate the various surgical options in treating this life-threatening condition. The age and sex distribution of these patients have changed over the years and shifted toward older patients (mean, 53 years) and female predominance (female:male ratio, 1.4:1). The clinical presentation was usually of distal closed-loop small bowel obstruction. Forty-six percent of the plain abdominal radiographs were suspected for cecal volvulus, but only 17 percent were diagnostic. Barium enema had a high rate of accuracy (88 percent) and was associated with minimal complications. True volvulus was 6 times more common than bascule, and gangrenous cecum was found in 20 percent of cases. Detorsion alone and cecopexy had almost similar complications, mortality, and recurrence rates (15, 10, and 13 percent, respectively), whereas, resection, which was performed primarily for gangrenous cecum, had higher rates. However, the highest rates of complications (52 percent), mortality (22 percent), and recurrence (14 percent) were noticed after cecostomy. These data suggest that resection should be reserved for patients with necrotic cecum and that detorsion is sufficient for patients with viable cecum. Cecostomy should be abandoned.

We studied the relationship between oxygen consumption (Vo2) and cardiac output in 17 hemodynamically stable, septic and eight nonseptic ICU patients. Each received 300 ml of fresh-frozen plasma or 25% albumin with up to 500 ml of crystalloids, in addition to regular maintenance fluids; this treatment increased pulmonary wedge pressure (WP) by 3 to 4 mm Hg. Measurements were performed before and after approximately 5 h of volume loading. Because cardiac index (CI) decreased as WP increased in four septic and three nonseptic patients, we grouped the data according to the state of flow instead of the recording time sequence. From low to high flows, mean CI increased in septic patients and nonseptic patients. Oxygen delivery (Do2) increased in septic and nonseptic patients. Vo2 remained unchanged in nonseptic patients, while it increased in septic patients. Accordingly, arteriovenous oxygen difference narrowed in nonseptic patients from 4.46 +/- 1.62 to 3.59 +/- 1.21 ml/dl (p less than .05) but did not change in septic patients. In the septic group, the difference in CI between high and low flows was significantly (p less than .05) greater in survivors than in nonsurvivors. We conclude that the septic state is accompanied by a peripheral oxygen deficit, which can be partially reversed by maintaining an above-normal CI and Do2.

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.