Failure to rescue the elderly: a superior quality metric for trauma centers.

BACKGROUND: Trauma centers require reliable metrics to better compare the quality of care delivered. We compared mortality after a reported complication, termed failure to rescue (FTR), and FTR in the elderly (age >65 years) (FTRE) to determine which is a superior metric to assess quality of care delivered by trauma centers. METHODS: This was a retrospective review of the National Trauma Databank (NTDB) research data sets 2010 and 2011. Patients ≥16 years admitted to centers reporting ≥80% of AIS and/or ≥ 20% of comorbidities with > 200 subjects in the NTDB were selected. Centers were classified based on the rate of FTR and FTRE (<5 vs. 5-14 vs. ≥15%). The primary outcome was adjusted mortality for each group of trauma centers based on FTR and FTRE classifications. RESULTS: The overall mean ± SD FTR rate was 7.2 ± 5.2% and FTRE was 10.4 ± 7.9%. The adjusted odds ratio (AOR) for mortality was not different when centers with FTR <5% were compared to those with FTR of 5-14 or ≥15%. In contrast, a stepwise increase in FTRE predicted a significantly higher mortality when centers with FTRE 5% were compared to those with 5-14% (AOR: 1.05, p = 0.031) and ≥15% (AOR: 1.13, p < 0.001). Similarly, stepwise increase in FTRE predicted higher adjusted mortality for severely and critically injured patients, whereas FTR did not. CONCLUSIONS AND RELEVANCE: Higher FTRE predicts increased adjusted mortality better than FTR after trauma and should, therefore, be considered an important metric when comparing quality care delivered by trauma centers.

Loss of endothelial barrier function requires neutrophil adhesion.

BACKGROUND: The inflammatory response is characterized by cytokine-induced up-regulation of endothelial adhesion molecules followed by polymorphonuclear neutrophil (PMN) adhesion and breakdown of tight junctions between cells. The purpose of this investigation was to determine whether PMN adhesion is an essential element in the alteration of endothelial permeability or whether cytokines alone can produce this change. METHODS: Human umbilical vein endothelial cells (HUVECs) were exposed to formylated met-leu-phe-activated PMNs. In a second series of experiments, PMNs were contained in a microporous membrane that allowed passage of secreted cytokines but not cells. Permeability was quantified by using transendothelial electrical resistance (TEER, ohm.cm2,) whereas expressions of two cell adhesion molecules (endothelial leukocyte adhesion molecule-1 [ELAM-1] and intercellular adhesion molecule-1 [ICAM-1]) were measured by flow cytometry (% shift). Cytokine production was monitored with enzyme-linked immunosorbant assays (picograms per milliliter). RESULTS: Stimulated PMNs secreted comparable amounts of cytokines whether allowed access to HUVECs or trapped in a microporous membrane (interleukin-1 alpha, 5.88 +/- 2.38 versus 3.65 +/- 1.84 pg/ml; tumor necrosis factor-alpha, 10.27 +/- 3.21 versus 6.61 +/- 1.82 pg/ml). Up-regulation of ELAM-1 and ICAM-1 was observed whether PMNs were free or restricted (52.97% +/- 2.14% versus 75.32% +/- 4.19% and 71.66% +/- 7.37% versus 73.66% +/- 4.32%, respectively). TEER was unchanged in controls and when PMNs were membrane restricted. In contrast, TEER decreased precipitously (51% +/- 5.9% of control, p < 0.05) if PMNs were allowed access to HUVECs. CONCLUSIONS: Cytokine secretion by PMNs is independent of endothelial contact and is sufficient to upregulate adhesion molecules. However, PMN adhesion is essential for the loss of endothelial barrier function, which leads to diapedesis of activated PMNs and eventual tissue injury.

Prolonged hypoxia alters endothelial barrier function.

BACKGROUND: It is well recognized that hypoxia/reoxygenation and exposure to inflammatory mediators such as cytokines and neutrophils alter the barrier function of the vascular endothelium. The experiments we conducted tested whether hypoxia alone could produce changes in permeability and whether a prolonged period of hypoxia alters the surface expression of cell adhesion molecules. METHODS: Endothelial cells were cultured from human umbilical vein endothelial cells (HUVECs). Hypoxia was created by isolating the cells in a chamber through which 1% 02, 5% CO2, and 94% N2 were insufflated (30 min at 1/min). Oxygen tension was measured through oxygen-quenching phosphorescence. Hypoxia was maintained for 24 hours. Changes in endothelial permeability were measured by transendothelial electrical resistance (TEER). Endothelial leukocyte adhesion molecule 1 (ELAM-1) and intercellular adhesion molecule 1 (ICAM-1) expression were assessed by flow cytometry (mean +/ standard error of the mean [SEM]. RESULTS: Exposure of endothelial cells to hypoxia resulted in increased permeability between 6 and 24 hours, with the greatest decrease in TEER at 18 hours (63% +/ 3%; P < .05). Prolonged hypoxia produced no change in the surface expression of ELAM-1 or ICAM-1. CONCLUSIONS: Hypoxia alone produced a significant reversible alteration in endothelial permeability. However, this change was observed only under severe hypoxic conditions (eg, below 20 mm Hg); higher oxygen tensions (25 and 35 mm Hg) had no significant effect. Unlike observations made after cytokine exposure, hypoxic breakdown of endothelial barrier function was unassociated with up-regulation of either ELAM-1 or ICAM-1.

Cytokine-induced increases in endothelial permeability occur after adhesion molecule expression.

BACKGROUND: Transmigration of neutrophils (PMNs) through endothelial cell tight junctions is a critical stage in the tissue injury of ischemia-reperfusion (I/R). Although cytokines are released in I/R, it is unclear whether cytokines directly increase permeability or this phenomenon requires both expression of cell adhesion molecules and PMN adhesion-activation. METHODS: We exposed confluent monolayers of human umbilical vein endothelial cells to physiologic concentrations of interleukin-1 (10 pg/ml) and tumor necrosis factor-alpha (10 pg/ml) in the absence of PMNs. Tight junction permeability was quantified with both transendothelial electrical resistance and albumin flux, whereas expression of endothelial-leukocyte adhesion molecule-1 was measured by flow cytometry (t test p < 0.05). RESULTS: Stimulation with tumor necrosis factor-alpha or interleukin-1 produced maximal transendothelial electrical resistance decreases at 12 hours with return to baseline at 24 hours. Increases in albumin flux began at 6 hours, with maximum effects at 24 hours. These changes occurred soon after maximal expression of endothelial-leukocyte adhesion molecule-1 at 4 hours. CONCLUSIONS: Cytokines induced increases in both cell adhesion molecule expression and endothelial permeability. This sequence of events is consistent with direct cytokine effects on cytoarchitecture, because it occurred without the adhesion-activation of PMNs.

Serum proteins facilitate neutrophil induction of endothelial leukocyte adhesion molecule 1.

BACKGROUND: Although the individual actions of neutrophils and serum proteins such as complement in acute inflammation are well characterized, less is known about their effects in combination. We investigated the combined effects of neutrophil contact and active serum proteins on the expression of endothelial leukocyte adhesion molecule 1 (ELAM-1). METHODS: Confluent monolayers of human umbilical vein endothelial cells were incubated with neutrophils in the presence and absence of fresh human serum. Flow cytometry was used to assess expression of endothelial intercellular adhesion molecule 1 (ICAM-1) and ELAM-1. In addition, neutrophils were retained in a semipermeable insert, which allowed their secretions to contact the endothelium but restricted neutrophil-endothelial contact. RESULTS: ELAM-1 expression was significantly increased on the cells coincubated with neutrophils and fresh human serum (25.8%; p < 0.001). There was no significant change in ELAM-1 expression on endothelial cells incubated with fresh human serum alone (3.9%; p > 0.01) or in those incubated with neutrophils and heat-inactivated serum (9.3%; p > 0.01). In the absence of neutrophil contact, ELAM-1 expression was increased only in the presence of fresh human serum (9.6%; p < 0.05). CONCLUSIONS: These findings suggest that serum proteins may potentiate the volume or potency of neutrophil-derived diffusable mediators of ELAM-1 expression. These effects are eliminated with the heat inactivation of serum proteins, implicating a heat sensitive mediator such as the complement cascade.

Selective intra-arterial tolazoline infusion in peripheral arterial trauma.

Intra-arterial tolazoline has been used as an adjunct for angiographers and has been investigated for application in certain peripheral vascular disorders secondary to its potent activity as a vasodilator. We have had experience with three cases in which severe peripheral arterial trauma had resulted in nonviable extremities in spite of both orthopedic manipulation and vascular reconstruction. Continuous infusions of intra-arterial tolazoline were begun with marked improvement in blood flow in all extremities and resultant viability in all three within 48 hours. All three of these extremities, although severely traumatized, had one patent vessel distal to the popliteal trifurcation which was patent and which insured at least some flow to the distal extremity. Canine experiments were performed which demonstrated that intra-arterial tolazoline increased distal limb blood flow but did not moderate muscle surface hydrogen ion increase. These experiments confirm that the most important effect of the drug is in opening of precapillary arteriovenous shunts in the skin which increase total blood flow in medium and large size blood vessels in the injured limb. Major systemic effects of the drug were not observed when used in these specified concentrations and when monitored carefully by nursing personnel. We therefore feel that infusion of tolazoline can be used in specified cases of peripheral arterial trauma when both orthopedic and vascular reconstruction have not restored adequate blood flow to the traumatized extremity.

Effect of nitroglycerin and aortic occlusion on myocardial blood flow.

To better characterize the cardiac and peripheral effects of nitroglycerin during aortic occlusion, we measured myocardial blood flow in 43 normal and pentobarbital (PB)-depressed dogs (groups I to VII). PB was continuously infused in groups IV to VII to maintain reduced cardiac output and contractility. In groups VI and VII nitroglycerin was administered at 2 micrograms/kg/min. Sequential injections of radioactive microspheres (10 micrometers) and hemodynamic measurements were performed during 2-hour occlusions of the infrarenal aorta. The hearts were divided into endocardium, midmyocardium, and epicardium; total and regional blood flows and the ratio of endocardial to epicardial blood flow (endo/epi) were calculated. The results (mean +/- SEM) were subjected to analysis of variance. Normal dogs that underwent aortic occlusion had predictable increases in peripheral vascular resistance. Coronary vascular resistance fell (P less than 0.05) and endo/epi ratios were maintained above 1. Following PB administration, the myocardial blood flow uniformly fell (1.08 +/- 0.34 to 0.55 +/-0.09 ml/min/gm, P less than 0.001), and the animals not treated with nitroglycerin demonstrated decreased endo/epi ratios (1.11 +/- 0-.07 to 0.83 +/- 0.08, P less than 0.001). Although nitroglycerin did not prevent decreases in total myocardial blood flow, endo/epi ratios were maintained above 1 in treated animals (group VI, 1.04 +/- 0.08; group VII, 1.18 +/- 0.17). Furthermore, the increases in left ventricular end diastolic pressure in the untreated animals were significantly greater than those in animals receiving nitroglycerin (P less than 0.01). Despite severe cardiac depression, nitroglycerin maintained normal transmural distribution favoring the endocardium. Since coronary and peripheral vascular resistances were not altered, this benefit most probably reflects decreased ventricular wall tension secondary to preload reduction.

Arterial disruption and remodeling following balloon dilatation.

We studied immediate and long-term alterations in human atherosclerotic arteries subjected to balloon dilatation. Pathologic material included vessels obtained at amputation or autopsy that had been previously dilated in vivo and cadaver vessels dilated under physiologic pressure and temperature. All vessels were pressure-perfusion fixed, and morphologic observations were correlated with sequential angiograms obtained in 36 patients. Balloon dilatation resulted in disruption of both the plaque and the artery wall, with separation of the plaque from the tunica media, rupture of the tunica media, and stretching of the tunica adventitia to increase lumen cross-sectional area. The intimal plaque protruded into the lumen, accounting for the angiographic appearance of local flaps and dissection channels. Remodeling occurred by readherence of the intimal flaps with little change in plaque volume. Achievement of a sufficient radius of curvature may be necessary to achieve long-term patency. Restenosis may occur because of insufficient dilatation but may also result from extention of dissection channels into nondilated segments of the artery.

Angioplasty does not affect subsequent operative renal artery revascularization.

BACKGROUND: Although increased application of percutaneous renal artery angioplasty and stenting has facilitated nonoperative renal revascularization, patient outcomes after failed angioplasty are not established. METHODS: Renal artery revascularization was performed in 31 patients (38 arteries) from 1993 to 1999. Twenty patients underwent primary surgical repair, and 11 patients underwent secondary reconstruction after angioplasty (n = 7) or angioplasty and stenting (n = 4). Before operation, all patients had severe hypertension (blood pressure 166+/-5.2/92 +/- 2.7 mm Hg) that required an average of 3.0 +/- 0.2 medications for control. In addition, 12 patients (primary 45% vs secondary 27%; P = NS) had evidence of renal insufficiency (creatinine > or =1.7 mg/dL). RESULTS: There was no difference between primary and secondary procedures in the length of hospital stay (12+/- 1.4 vs. 12+/-3.2 days; P = NS), major morbidity (10% vs. 18%; P = NS) or perioperative mortality (overall mortality 2 of 31; primary 5% vs secondary 9%; P = NS). The majority of patients demonstrated improvement or cure of hypertension (primary 94% vs secondary 90%; P = NS) and stable or decreased creatinine (primary 74% vs secondary 82%; P = not significant). Overall survival (mean follow-up 22+/-3.5 months) was 89%+/-5.7%. CONCLUSIONS: Although this surgical series does not address the true outcomes of renal artery angioplasty, the results suggest that renal artery angioplasty does not prejudice subsequent surgical outcomes in patients who are carefully followed after angioplasty.

Selective infusion of streptokinase for arterial thrombosis.

We have treated 13 patients with limb-threatening ischemia caused by acute arterial thrombosis with selective arterial infusion of streptokinase. The indications for thrombolytic therapy included medical contraindication to surgery, surgically inaccessible thrombi, arterial thrombosis following percutaneous transluminal angioplasty, and thrombosed distal arterial bypass. Patients were evaluated with arteriography, Doppler segmental arterial pressure studies, and coagulation profile. Objective evidence of complete or partial thrombolysis was demonstrated in 11 of the 13 patients (85%). Treatment after thrombolytic therapy included percutaneous transluminal angioplasty in six patients and distal bypass in two patients. Of five patients who had received no additional treatment, three required amputation. Overall limb salvage was achieved in 10 of the 13 patients. The most serious complications were puncture site bleeding in five patients, acute renal failure in one patient, and retroperitoneal hemorrhage in another patient. Bleeding was more frequent in patients with decreased serum fibrinogen levels. Although lysis of acute arterial thrombi can be achieved, thrombolytic therapy alone will allow limb salvage in only a few patients. Selective thrombolytic therapy with streptokinase must be used with caution and is associated with serious complications.

Predicting cerebral ischemia during carotid endarterectomy.

We reviewed 86 consecutive patients undergoing elective carotid endarterectomy to determine whether preoperative clinical and angiographic data could be used to predict the risk of intraoperative cerebral ischemia during carotid occlusion. Electroencephalographic (EEG) monitoring with on-line Berg-Fourier transformation was carried out in all patients. A total of 32 patients (37.2%) underwent intraoperative shunting. Of these, 13 had no EEG changes but underwent shunting because of the surgeon's preference, while 19 patients underwent shunting because of EEG changes consistent with cerebral ischemia. There was one permanent (1.2%) and one transient (1.2%) neurologic deficit. Angiographic findings, clinical histories, and intraoperative EEGs were retrospectively reviewed to determine which risk factors best predicted the occurrence of intraoperative cerebral ischemia. Stroke within six weeks increased the risk of intraoperative cerebral ischemia 20-fold. Intracranial disease and contralateral carotid stenosis increased the risk of ischemia 17-fold and 16-fold, respectively. Statistical summation of all risk factors yielded a probability equation for EEG change that accurately quantitated pre-operative risk. Prospective application of this probability equation may simplify operative decision making if EEG monitoring is not available.

Renal artery dissections.

Renal artery dissections encountered in 15 patients, aged 3 to 75 years, were categorized as to pathogenesis (blunt abdominal trauma, catheter injury, and spontaneous). Blunt traumatic dissections (seven patients) were characterized by hypertension, gross hematuria, and pain. Catheter-induced dissections (four patients) were asymptomatic, although two exhibited accelerated hypertension. Spontaneous dissections (four patients) were all associated with preexistent arterial disease. Symptoms in these patients were uncommon, despite accelerated hypertension in three cases. Intravenous pyelography lacked specific diagnostic value for renal artery dissections. Early arteriographic examination proved essential in diagnosis and surgical treatment. Criteria for operative intervention included existence of technically correctable dissections causing (1) hemodynamically significant occlusions of the main or major segmental renal arteries, (2) documented renovascular hypertension, or (3) significant deterioration of renal function.

Implications of precancerous rectal biopsy in patients with inflammatory bowel disease.

Sixty-five patients with an initial diagnosis of ulcerative colitis who underwent total proctocolectomy between 1955 and 1973 were studied retrospectively. Rectal mucosa in each patient was examined microscopically for the presence or absence of "precancerous" alterations as described by Morson and Pang. Histologic examination was made with no knowledge of concomitant colon carcinoma or the patients' clinical courses. Three of ten patients with precancerous rectal mucosa had invasive colon carcinoma, while none of the 55 patients without such changes had colon cancer (P less than .05, Fischer exact test). The duration of disease was significantly greater in those patients with rectal precancer (P less than .05). Reexamination changed the pathologic diagnosis in 15 patients from ulcerative colitis to granulomatous or "mixed" colitis. Two of three invasive cancers occurred in the reclassified group. Results support previous contentions that careful histologic evaluation of rectal biopsy specimens from individuals with inflammatory bowel disease may better define that population of patients with an increased risk of colonic carcinoma.

Appendicitis and aortofemoral graft infection.

A 59-year-old man who underwent successful aortofemoral bypass had acute appendicitis at an indeterminate time in the postoperative period. Thirteen months later, a pulsatile groin mass developed. After a complicated course, it was found that infection from appendicitis had extended to the body of the graft. This unusual cause of graft infection reaffirms the importance of careful closure of the retroperitoneum over an aortic anastomosis and suggests a relationship of other intra-abdominal inflammatory processes to graft infection.

Arterial fibrodysplasia. Histopathologic character and current etiologic concepts.

Arterial fibrodysplasia affected 196 patients (172 females, 24 males) harboring a total of 316 diseased vessels. Renal artery lesions were documented in 152 adult and 25 pediatric patients. Superior mesenteric, celiac, common hepatic, and external iliac arteries were occasionally involved. Intimal fibroplasia and medial hyperplasia are uncommon types of arterial dysplasia. Medical fibroplasia represents a continum of disease, including pathologic processes heretofore categorized as subadventital or perimedial fibroplasia. A previously unrecognized form of perimedial dysplasia, characterized by dense accumulations of elastic tissue about the periphery of the media, is reported as a distinct pathologic entity. Hormonal influences, traction-stretch stresses, and peculiarities in distribution of vasa vasorum in vessels affected by dysplastic processes may be prerequisite to the evolution of arterial fibrodysplasia.

Cimetidine vs antacid in prophylaxis for stress ulceration.

Seven-seven critically ill patients were prospectively randomized into four groups to compare antacids and various doses of cimetidine in the neutralization of gastric acid for preventing complications of stress ulcers. Gastric pH was monitored hourly, basing the efficacy of neutralization on preselected pH values for each study group. Cimetidine provided adequate neutralization in 14 (23%) of 61 patients. Gastric acid in all 16 patients treated with antacids was adequately neutralized. Stress bleeding occurred in three (5%) patients treated with cimetidine and in no patient treated with antacids. Reversible thrombocytopenia developed in six (26%) of 23 patients treated with 2,400 mg/day of cimetidine. Hourly monitoring of gastric pH is a mandatory component in the prevention of stress bleeding. Antacid is the preferred agent for gastric acid neutralization because it is more effective, safer, and less expensive.

Saphenous vein interposition grafts in the microsurgical treatment of cerebral ischemia.

Saphenous vein interposition grafts of varying lengths have been used in 25 extracranial-intracranial bypasses since 1974. Indications for operation included transient ischemic episodes (13 cases), prophylactic augmentation of middle cerebral artery (MCA) collateral flow prior to surgical treatment of intracranial aneurysm (four), and traumatic occlusion of cervical or intracranial internal carotid arteries (eight). Vein grafts to cortical branches of MCA originated from superficial temporal or occipital arteries in ten cases, common or external carotid arteries in ten, and subclavian or innominate vessels in five. Twenty-one patients have been followed up for a minimum of 12 months. Immediate patency rate was 84%; one late graft occlusion decreased overall patency to 80%. There was one operative mortality. Early technical problems, including donor-recipient size disparity, anastomotic distortion, and inappropriate graft routing, have been overcome by the use of 2-mm veins, the avoidance of hydrostatic dilation, and the construction of retroauricular tunnels. It is reasonable to assume that long-term patency of these reconstructions will parallel that of extracranial-intracranial bypasses using autologous arteries.

Limb salvage in poor-risk patients using transluminal angioplasty.

We performed percutaneous transluminal angioplasty (PTA) in 97 limbs of 86 patients with end-stage occlusive disease in whom vascular reconstruction was not possible. Most patients required dilation of long-segment occlusions and/or multiple lesions. Angiographic appearance was improved in 87 limbs of 78 patients (90%). Ankle-brachial pressure index increased from 0.40 +/- 0.03 to 0.64 +/- 0.03, and increased more than 0.15 in 63% of the limbs. Major amputation was required in 19 of the 87 limbs (22%) following PTA. The incidence of restenosis was 19% at three months, 42% at six months, and 57% at one year. Repeated PTA successfully maintained vascular patency in ten limbs, and four patients have since had successful distal bypass. Two limbs that initially improved needed amputation four to 19 months after dilatation. Follow-up ranged from one to 45 months; overall limb salvage rate was 76%. Thus PTA can enhance limb salvage in poor-risk patients with end-stage disease.

Current results of surgical therapy for chronic mesenteric ischemia.

BACKGROUND: Although recognition of chronic mesenteric ischemia has increased in recent years, this disorder has continued to present diagnostic and therapeutic challenges. OBJECTIVE: To examine the modern results of surgical revascularization for chronic mesenteric ischemia. DESIGN: Retrospective review. SETTING: University medical center. PATIENTS: The management of 24 consecutive patients (mean +/- SEM age, 58 +/- 3 years; 5 men, 19 women) who were undergoing surgical treatment of chronic mesenteric ischemia between 1986 and 1996 was reviewed. INTERVENTION: Surgical mesenteric revascularization. MAIN OUTCOME MEASURES: Postoperative course, long-term graft patency rate, and long-term symptom-free survival rate. RESULTS: The most frequent presenting symptoms were postprandial abdominal pain (18 patients [75%]) and weight loss (14 patients [58%]). Less specific complaints included nausea and vomiting (8 patients [33%]), diarrhea (7 patients [29%]), and constipation (4 patients [17%]). Atherosclerotic risk factors were common, including tobacco use (20 patients [83%]), coronary artery disease (10 patients [42%]), and hypertension (10 patients [42%]). The cause was identified as atherosclerosis in 21 patients, median arcuate ligament compression in 2 patients who were monozygotic twins, and Takayasu arteritis in 1 patient. Lesions were localized to all 3 major visceral vessels (celiac artery, superior mesenteric artery [SMA], and inferior mesenteric artery) in 8 patients, celiac artery and SMA in 13, SMA alone in 2, and SMA and inferior mesenteric artery in 1. Seventeen patients underwent antegrade reconstructions from the supraceliac aorta to the SMA and/or celiac artery; 7 patients underwent revascularization by use of a retrograde bypass that originated from the infrarenal aorta or a prosthetic graft. There were no perioperative deaths although 1 patient died in the hospital 6 weeks after early graft failure and sepsis (overall in-hospital mortality, 4%). Follow-up ranged from 3 months to 10 years (median, 2.4 years). The mean +/- SEM 5-year primary graft patency rate, as objectively documented by use of contrast angiography or duplex scanning in 19 of 24 patients, was 78% +/- 11%. Primary failure was documented in 3 patients (at 3 weeks, 5 months, and 7 months). Two patients required a thrombectomy; 1 of these patients subsequently died of an intestinal infarction. The mean +/- SEM 5-year survival rate by use of life-table analysis was 71% +/- 11%. No patient with a patent graft experienced a symptomatic recurrence. CONCLUSIONS: Chronic mesenteric ischemia is usually a manifestation of advanced systemic atherosclerosis. Symptoms almost always reflect midgut ischemia in the distribution of the SMA. An antegrade bypass from the supraceliac aorta can be performed with acceptable operative morbidity and is currently the preferred reconstructive technique. Surgical revascularization affords long-term symptom-free survival in a majority of patients with chronic mesenteric ischemia.

Endothelial response to venous injury.

This investigation characterized venous endothelial healing after surgical manipulation. Procedures were performed on jugular and femoral veins in 21 mongrel dogs without systemic anticoagulation. Veins were harvested at varying intervals and vessel structure evaluated with light, transmission, and scanning electron microscopy. Veins that were mobilized or stripped of adventitia demonstrated 25% to 50% endothelial loss at one hour. Endothelial damage was rapidly repaired with complete healing observed in some veins at 48 hours. Tourniquets and clamps resulted in prominent medial and endothelial injury at occlusion sites. Eighteen of 24 transected veins remained patent for the study period. Endothelial healing was unaffected by tension at anastomoses. These observations confirm that venous endothelium receives nutrition by luminal diffusion. The healing process of venous anastomoses is characterized by an early fibrin sleeve sealing the anastomotic site; endothelial bridging of defects can be noticeably delayed by excessive fibrin deposition.