Neostigmine: safe and effective treatment for acute colonic pseudo-obstruction.

BACKGROUND: Ogilvie's syndrome, or acute colonic pseudo-obstruction, is a common and relatively dangerous condition. If left untreated, it may cause ischemic necrosis and colonic perforation, with a mortality rate as high as 50 percent. Neostigmine enhances excitatory parasympathetic activity by competing with acetylcholine for attachment to acetylcholinesterase at sites of cholinergic transmission and enhancing cholinergic action. We hypothesized that neostigmine would restore peristalsis in patients with acute colonic pseudo-obstruction. METHODS: Twenty-eight patients at Fletcher Allen Health Care and The Cleveland Clinic Foundation were treated for acute colonic pseudo-obstruction with neostigmine 2.5 mg IV over 3 minutes while being monitored with telemetry. Mechanical obstruction had been excluded. RESULTS: Complete clinical resolution of large bowel distention occurred in 26 of the 28 patients. Time to pass flatus varied from 30 seconds to 10 minutes after administration of neostigmine. No adverse effects or complications were noted. Of the two patients who did not resolve, one had a sigmoid cancer that required resection and one patient died from multiorgan failure. CONCLUSION: This study supports the theory that acute colonic pseudo-obstruction is the result of excessive parasympathetic suppression rather than sympathetic overactivity. We have shown that neostigmine is a safe and effective treatment for acute colonic pseudo-obstruction.

Neurogenic pulmonary edema in fatal and nonfatal head injuries.

Impaired pulmonary function is a frequent but poorly understood complication of acute head injury (HI). A potential early contributor to the pulmonary dysfunction seen in HI patients is neurogenic pulmonary edema (NPE). We hypothesized that NPE would occur early after HI and that it would have a continuum of clinical severity depending on the severity of the HI and associated intracranial hypertension. A large autopsy data base and inpatient HI data base were used to search for cases of NPE. Patients in the autopsy data base were stratified according to injury type and whether they died at the scene or within 96 hours of injury. There were significant (p < 0.0001, analysis of variance) elevations in lung weights in patients dying at the scene and within 96 hours from HI, compared with those dying from other noncentral nervous system injuries. No other organs studied showed significant weight increases. The incidence of NPE in isolated HI patients dying at the scene was 32%. In patients with isolated HI dying within 96 hours, the incidence of NPE was 50%. We found an inverse correlation (r = 0.62; p < 0.0014) between the initial cerebral perfusion pressure and the PaO2/FIO2 ratio despite a normal-appearing chest x-ray film. We conclude that NPE occurs frequently in HI patients. The process of edema formation begins early in the clinical course and is isolated to the lung.(ABSTRACT TRUNCATED AT 250 WORDS)

Brain edema formation after brain injury, shock, and resuscitation: effects of venous and arterial pressure.

BACKGROUND: Recent work suggests that increased intracranial pressure (ICP) following brain injury and shock is related to increased central venous pressure (CVP) following resuscitation. OBJECTIVE: To analyze the relationship of intravascular pressures to edema formation and ICP in an experimental model. METHODS: In a porcine model of cryogenic brain injury and hemorrhagic shock, we studied CVP, mean arterial pressure (MAP), ICP, and cortical water content (CWC, as cortical specific gravity) at baseline (BL), 45 minutes after shock (H45), and 1, 3, 6, 12, and 24 hours (H) after resuscitation. Group 1 was the control group, group 2 brain injury only, group 3 shock only, and group 4 brain injury and shock. RESULTS: Brain injury significantly increased ICP and CWC. Mean arterial pressure significantly correlated with ICP (r = 0.54, p = 0.02) and with CWC (r = -0.48, p = 0.03) in group 4 at 24H but not in the other groups at any time period. There was no significant correlation between CVP and ICP or CWC in any group at any time interval. CONCLUSIONS: These data suggest that brain edema formation in the injured hemisphere is related to MAP and not CVP, but variability in MAP accounts for only 29% of the variability in CWC and ICP, suggesting the importance of factors other than hydrostatic pressure in determining the amount of edema and the ICP after brain injury. Previous work demonstrating the significant correlation of polymorphonuclear leukocyte infiltration with ICP (r = 0.71, p < 0.001) and with CWC (r = -0.63, p < 0.001) suggests that inflammation may be one of these factors.

Vascular complications of cardiac catheterization.

Peripheral vascular complications after cardiac catheterization constitute an increasing portion of traumatic vascular injuries. To determine the incidence of these complications and the sequelae of their treatment, we reviewed 7,690 catheterizations performed over a 40-month period. One hundred eleven vascular complications were detected (1%), 41 of which required surgical repair (0.5%). Pseudoaneurysm (10), arteriovenous fistula (4), thromboembolism (9), infection (5), and other bleeding complications (83) were all found. Significantly more complications occurred in patients who were older than 60 years of age or female (P < 0.0009). In addition, the likelihood of a vascular injury after coronary angioplasty was significantly higher than after angiography alone (3% versus 1%, P < 0.00001). Secondary local and systemic complications after surgical repair were more frequent compared with those injuries that were managed nonoperatively (32% versus 11%; P = 0.015). Vascular complications continue to be a significant problem after cardiac catheterization, especially when coronary angioplasty is performed. The sequelae of surgical repair are significant, adding to their morbidity. Periodic review of these complications may identify factors that might be modified to reduce complications.