Experimental comparison of percutaneous vena caval devices: titanium Greenfield filter versus bird's nest filter.

A venous embolism model with autogenous thrombus was used for comparison of the functional properties of two new vena caval devices: a titanium Greenfield filter and the bird's nest filter. All nine Greenfield filters were correctly placed in the inferior vena cava and produced significant clot lysis of 81.3% +/- 16.3% (p less than 0.001, paired t test). Difficulty was encountered in affixing the hooks of the bird's nest device into the vein wall and resulted in two filters not being inserted and two filters being placed too proximally. One set of hooked wires of another bird's nest device migrated to the right atrium despite correct insertion. Eight bird's nest devices allowed clot lysis of 83.4% +/- 17.7% (p less than 0.001), paired t test) but thrombus size was increased in one case. The Greenfield and bird's nest filters have comparable effects on trapped emboli, but the bird's nest filter may be susceptible to thrombosis and occlusion under certain circumstances. The pre-shaped hooked wires of the bird's nest device may be difficult to insert and may allow proximal migration after a large thrombus was trapped.

The acridine orange fluorochrome microassay: a new technique for quantitation of neutrophil function in burned patients.

A new assay for determination of neutrophil bacterial killing and phagocytosis is presented. The acridine orange (AO) fluorochrome microassay is a simple, reliable technique for assessing polymorphonuclear (PMN) function. It requires small amounts of blood and provides a rapid and reproducible quantitation of neutrophil activity. Using this technique, bacterial killing and phagocytosis were assessed in a group of five severely burned patients admitted to the Medical College of Virginia Burn Unit. All patients studied demonstrated a significant decrease in bacterial killing at some point during their clinical course. The AO assay was found to be a reliable and effective means of quantitating PMN bacterial phagocytosis and killing in this group of burned patients.

Experimental superior vena caval placement of the Greenfield filter.

Pulmonary embolism (PE) from sources superior to the right atrium has been documented in several reports, but mechanical device protection has not been advised because of the morbidity associated with occlusion of the superior vena cava (SVC). Mechanical protection must maintain caval patency, protect against recurrent PE, and be safe. Since the Greenfield filter has fulfilled these criteria when placed in the inferior vena cava (IVC), we tested its suitability for use in the SVC in 11 dogs. Thrombus was harvested from phenolized segments of infrarenal vena cava and embolized into filters positioned in the SVC through the jugular or brachiocephalic vein under fluoroscopic guidance. Central venous pressure (CVP) was monitored before and after embolization. The dogs were allowed to recover and were followed up with monthly vena caval contrast studies and CVP measurements. After 3 months the animals were put to death and autopsies performed to determine the size of any residual thrombus and to examine the pulmonary arteries for signs of PE. Ten dogs had correct placement of the filter in the SVC; there were no perforations and no episodes of PE. CVP rose slightly after embolization into the filter but caval patency was maintained in all animals. Resolution of filter-entrapped thrombi occurred in all animals (mean initial weight = 1.02 gm, mean final weights = 0.11 gm, p less than 0.05). In the eleventh animal the filter was discharged high, with one leg perforating the brachiocephalic vein. No hemorrhage or distal embolism occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

Cimetidine therapy for burn shock: a quantitative assessment.

Optimal cardiac output (CO) resuscitation for severely burned guinea pigs is obtained with intravenous volumes of lactated Ringer's (LR) calculated at 4 cc/kg/%burn/24 hr. When one half this volume of LR is given (2 cc/kg/%burn/24 hr) CO is significantly (p less than 0.05) reduced at 2, 4, and 8 hours after injury. When early postburn cimetidine therapy (0.5 hours after injury) is added to only 1 cc/kg/%burn/24 hr LR, CO is significantly elevated for the same time periods and is not significantly different from CO values of LR at 4 cc/kg/%burn/24 hr for the first 24 hours after injury. However, postburn cimetidine therapy delayed until 1 hour after burn injury did not improve CO compared to treatment with LR at 2 cc/kg/%burn/24 hr. These observations suggest that early postburn cimetidine therapy administered within 1/2-hour of severe scald injury will result in significant CO improvement while simultaneously reducing resuscitative fluid volume requirements by as much as 70% for the first 24 hours after injury.

Prevention of free radical-induced myocardial reperfusion injury with allopurinol.

Growing evidence supports the concept that oxygen free radicals are an important cause of myocardial ischemic and reperfusion injury. This study was designed to determine if toxic oxygen metabolites may exacerbate ischemic injury upon reoxygenation. Left ventricular function was studied in a group of seven dogs receiving intermittent, 4 degrees C, hyperosmolar, hyperkalemic (KCI 25 mEq/L) saline cardioplegic solution. This group was compared to a group (n = 7) receiving a hyperkalemic (KCI 25 mEq/L) cardioplegic solution designed to scavenge superoxide anion and hydroxyl radical: superoxide dismutase (3,000 U/ml) and mannitol (325 mOsm/L). A third group of five animals received allopurinol pretreatment (50 mg/kg/day) for 72 hours and hyperkalemic saline cardioplegic solution. After 60 minutes of ischemia (10 degrees to 15 degrees C) and 45 minutes of reperfusion, left ventricular mechanical function was better in the groups receiving free radical scavengers and allopurinol pretreatment than in the group receiving only hyperkalemic saline cardioplegic solution. Free radical scavengers preserved myocardial function in this model of hypothermic global ischemia and reperfusion. Our data support the concept that injury occurs primarily during reperfusion with the generation of oxygen free radicals via the hypoxanthine-xanthine oxidase reaction. Allopurinol has potential clinical application in the prevention of reperfusion injury.

Inhibition of surgically induced ischemia/reperfusion injury by oxygen free radical scavengers.

Recent experimental work implicates oxygen free radicals as mediators of ischemia/reperfusion injury. A simple cardioplegic solution was designed to scavenge superoxide anion and hydroxyl free radical with superoxide dismutase (10 micrograms/ml), mannitol (325 mOsm/L), and KCl 25 mEq/L (FRS). Hemodynamic and subcellular functions were studied in seven in situ canine models of hypothermic global ischemia receiving FRS, compared to a group (n = 7) receiving hyperosmolar, hyperkalemic saline (HSK) and to a standard model of topical hypothermia (TH, n = 5). Following 60 minutes of ischemia (10 degrees to 15 degrees C), hearts were reperfused and rewarmed. After 45 minutes of reperfusion, left ventricular peak systolic pressure (LVPSP), developed pressure (LVDP), dP/dt max, -dP/dt max, compliance, and elastic stiffness constant (K) were improved in the FRS group and not significantly different from control. Sarcoplasmic reticulum (SR) calcium transport in the FRS group was significantly improved (control = 1.077 +/- 0.022, TH = 0.754 +/- 0.018, HSK = 0.725 +/- 0.05, and FRS = 0.966 +/- 0.05 mumol/mg-min). Calcium adenosine triphosphatase (ATPase) activity did not differ significantly from control at pH 7.0. In this model of hypothermic global ischemia and reperfusion, free radical scavengers provide significant protection of mechanical and subcellular function. These findings support the hypothesis that oxygen free radicals are important mediators of myocardial ischemia and reperfusion injury.

Comparison of Greenfield filter and vena caval ligation for experimental septic thromboembolism.

Septic thromboembolism resulting from the placement of infected autologous thrombi was studied in three groups of ten dogs each following vena caval ligation (VCL) or Greenfield filter (GF) placement with or without antibiotic treatment. All the dogs that did not receive antibiotic therapy died, and the shortest survival time was after acute VCL. Dogs with GF and with delayed embolism after VCL survived significantly longer than did the control animals. Antibiotic therapy consisting of ampicillin and clindamycin resulted in survival except for one control dog with lung abscess. Cultures of the GF and contained thrombus were negative after 2 weeks. However, after VCL, two died of sepsis and two survivors had caval abscess. In a group of six dogs with VCL and delayed embolism, there were four deaths from sepsis and one survivor found to have a caval abscess. To test secondary infection of a trapped thrombus, in 12 dogs with GF and a sterile thrombus we created an extremity abscess with a fecally contaminated sponge, which resulted in death from sepsis in six animals within 3 days. Surgical drainage and antibiotic treatment of the remaining six resulted in survival in five dogs. Cultures of filters and emboli showed heavy contamination in the untreated animals and in one treated dog that died within 24 hours. The remainder had sterile filters and emboli. The presence of sepsis does not preclude use of the Greenfield filter, which is well tolerated in the face of septic embolism and allows sterilization with antibiotic treatment. Prophylactic antibiotic therapy seems advisable for any patient with a filter during a procedure that may produce bacteremia.

Operative removal of misplaced Greenfield vena caval filters.

Operative retrieval has not been necessary in our experience, though interest has been expressed by other surgeons. Specifically, during removal the hooks of the filter may become attached to adjacent structures, making manipulation and eventual extraction difficult. Because the occasion for late removal of a misplaced filter may arise, we have developed this method using readily available materials. We anticipate that this technique will be most useful for removal of filters that have been in place for more than 7 days. A method to retrieve filters in place less than 1 week has already been reported [4]. We have found the technique quite satisfactory in experimental animals.

Mechanisms of burn shock protection after severe scald injury by cold-water treatment.

Following a 3-second subxiphoid immersion of shaved, unresuscitated guinea pigs in 100 degrees C water, cardiac output (CO), mean systemic blood pressure (BP), total peripheral resistance (TPR), hematocrit (HCT), serum histamine (SH), and serum lactate (SL) were measured in untreated and cold-water treated animals up to 24 hours after injury. Animals receiving cold-water treatment (CWT) were immersed in 15 degrees C water for 15 minutes immediately after scald injury. CWT significantly (p less than 0.05) reduced SH and SL for up to 8 and 24 hours, respectively, after injury compared to untreated injured animals. HCT of CWT animals remained significantly lower than that of untreated animals for the first 8 hours after injury. However, CWT-animal HCT was not significantly different from control-animal HCT for this same period. CWT-animal BP was significantly greater than untreated-animal BP for the first 8 hours after injury. CWT- and untreated-animal TPR progressively rose after injury; however, at 24 hours after injury CWT-animal TPR was significantly reduced to 87% +/- 18.0 of preinjury values while untreated-animal TPR was maximally elevated to 170% +/- 10.0 of preinjury values. At 4 hours after injury CO of both untreated and SWT animals was significantly depressed at 56% +/- 3.0 and 50% +/- 10.0 of preinjury values, respectively. However, by 24 hours after injury untreated-animal CO remained depressed at 52% +/- 3.0 while CWT-animal CO was significantly improved at 92% +/- 19.0 of preinjury values. These studies document a beneficial hemodynamic response of severely burned animals after CWT and further verify the phenomenon of cold inhibition of burn wound tissue histamine release after severe scald injury. A correlation between decreased serum histamine and lactate levels and improved cardiovascular function following severe scald injury and CWT is also suggested.

Hemodynamics and renal function following experimental suprarenal vena caval occlusion.

In this study, the cardiovascular and renal effects of acute suprarenal caval occlusion were investigated in dogs. Marked hemodynamic effects were noted, with an immediate 60 per cent reduction in cardiac output and a 26 per cent drop in mean systemic arterial pressure. In spite of these, there was only a transient disturbance of renal function which had resolved both biochemically and structurally by the end of two weeks. The relevance of these findings to acute occlusion above the renal veins in humans has been reviewed, and we conclude that the Greenfield filter may be inserted in the suprarenal vena cava when indicated with little likelihood of an increase in mortality from recurrent embolism.

Clinical results of suprarenal placement of the Greenfield vena cava filter.

Twelve patients have had Greenfield vena cava filter placement above the renal veins since 1975. The indication for placement was most commonly contraindication to anticoagulation or recurrent pulmonary embolism during treatment. The follow-up consisted of physical examination, isotope phlebography-lung scan, venous Doppler evaluation, serum specimen evaluation of renal function, and abdominal roentgenograms. The follow-up averaged 16.9 +/- 6.2 months (range 5 weeks to 58 months) in 10 patients. Five patients died after filter insertion, but no death was attributable to filter placement or recurrent embolism. Renal function was unchanged in all patients. Recurrent embolism was documented postoperatively in one patient. Migration of the filter was not observed. The vena cava was demonstrated to be patent in all patients. Two patients had evidence of embolus trapped in the filter.

Retrieval of the Greenfield vena caval filter.

A retrieval device has been developed that allows removal of misplaced Greenfield vena caval filters. The technique was evaluated in 15 dogs in which filters were placed in the vena cava, iliac vein, or right atrium. Retrieval was possible in seven of nine dogs up to 7 days after insertion. After 7 days, retrieval was not possible because of fixation of the device. Retrieval was not possible in dogs with a jugular vein too small to accept the retrieval unit. The case of one patient in whom the filter was dislodged at the tricuspid valve is reported herein. This experience confirms that retrieval can be accomplished without significant risk.

Oxygen toxicity in normal and anoxic ventilated perfused canine lungs.

Oxygen toxicity was studied in 26 canine isolated, perfused lung lobes which included nine control lobes, 13 lungs ventilated with FIO2 1.0 for 4 hours, and four lobes ventilated with FIN2 1.0 for 1 hour prior to 4 hours of FIO2 1.0 to evaluate the postulated protective effect of anoxia. A significant increase in wet weight was seen in the O2 ventilated lungs which did not alter pulmonary capillary isogravimetric pressure (PCI), alveolar-arterial oxygen gradient, or pulmonary vascular resistance. In contrast, preliminary N2 ventilation resulted in a significant increase in PCI and greater weight gain while pulmonary vascular resistance was reduced. Pulmonary compliance was reduced minimally in all groups. Anoxic ventilation not only failed to protect the isolated canine lung from presumed increased capillary permeability of oxygen toxicity, but seemed to contribute to the formation of interstitial pulmonary edema.