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Objective and Importance: Effective treatment for unclippable giant vertebrobasilar aneurysms remains unclear. We present the first reported case of a giant vertebrobasilar aneurysm being successfully treated with trapping of the aneurysm and internal carotid artery to basilar artery bypass with a saphenous vein graft that was performed with the patient under hypothermic circulatory arrest., Clinical Presentation: A 15-year-old female patient with a history of probable subarachnoid hemorrhage and chronic headaches presented with a relatively acute exacerbation of her headache, nausea, vomiting, and weakness. Imaging studies revealed a 4 x 4 x 3-cm vertebrobasilar aneurysm, supplied by an angiographically dominant right vertebral artery and causing significant brain stem compression., Intervention: Initially, a petrosal approach with a hearing-preserving partial labyrinthectomy was used to perform a right external carotid artery to posterior cerebral artery bypass with saphenous vein. Delayed occlusion of the right vertebral artery with an intraluminal balloon was planned; however, intraoperative angiography revealed poor graft flow, presumably because of the small size of the posterior cerebral artery. Postoperative graft occlusion was anticipated. During this same time interval, the patient deteriorated neurologically. Brain imaging failed to reveal evidence of cerebral infarction. The patient underwent subsequent surgery. After a total petrosectomy, the aneurysm was trapped, an aneurysmectomy was performed, and, with the patient under deep hypothermic circulatory arrest, a new interposition saphenous vein graft was inserted between the internal carotid and basilar arteries. Excellent flow was observed angiographically. At her 4-month follow-up examination, the patient had improved to near baseline., Conclusion: We present a technically challenging but safe and definitive treatment option for an unclippable giant vertebrobasilar aneurysm. Using cranial base approaches and hypothermic circulatory arrest techniques, aneurysmal trapping and successful bypass grafting directly into the basilar artery was performed.

1-deamino-8-D-Arginine vasopressin (DDAVP) shortens the bleeding time in some patients with platelet dysfunction and decreases blood loss in some cardiopulmonary bypass patients. We studied platelet membrane glycoproteins in patients with von Willebrand disease (vWD), disorders of platelet function, and in cardiopulmonary bypass patients after infusion of 0.3 microgram/kg of DDAVP. Platelets from 8 cardiopulmonary bypass patients, receiving DDAVP immediately after surgery, were compared to those of 14 patients not receiving DDAVP. We also studied 12 patients with vWD, and 8 patients with platelet dysfunction receiving DDAVP. Fixed platelets, stained with monoclonal fluorescein (FITC)-labeled antibodies directed against GPIb (CD42b antigen), GPIb/IX, GPIIb/IIIa (CD41a antigen), CD63 antigen (a platelet activation protein), and P-selectin (CD62 antigen) were studied by flow cytometry. Binding of CD42b monoclonal antibody (MoAb) and anti-GPIb/IX to platelets from both groups of bypass patients increased during the 18-20 hr after surgery, but the group receiving DDAVP showed the greater increase (P = 0.032). Platelets from patients receiving DDAVP for vWD or for platelet dysfunction, had increases in CD42b MoAb and anti-GPIb/IX binding (P < 0.01) that coincided with shortening of their bleeding time. No changes were seen in binding of other antibodies. When platelets from normal donors were incubated with DDAVP for 20 hr, there were increases in platelet surface CD42b MoAb binding, while immunogold-stained transmission electron micrographs of permeabilized platelets demonstrated decreases in cytoplasmic CD42b MoAb binding. DDAVP increases platelet membrane GPIb expression in a variety of patients and may account for improvement in hemostasis seen in some studies. Redistribution of GPIb from the cytoplasm to the membrane may account for this increased expression.

Six weeks after aortic aneurysm repair, computed tomography (CT) showed mediastinal gas where absorbable gelatin sponge (Gelfoam) was used. A leukocyte scan labeled with indium 111, however, was normal and surgical exploration showed no infection. Sterile gas collections may be seen following absorbable gelatin sponge use many weeks after surgery and 111In-labeled leukocyte scanning may be a useful differential test.

The value of repeating diagnostic peritoneal lavage (DPL) when initial results are indeterminate or negative has not been defined. From January 1974 to June 1980, 1884 patients underwent DPL. Ninety-six had repeat DPL. Eighty-eight (4.7%) patients with indeterminate initial DPL results had repeat DPL. Results were true positive in 20, false positive in non, false negative in three, and true negative in 64 patients. If results for all 88 patients had initially been considered positive and all had undergone operation, the additional yield would have been low, three patients (3.4%); 64 patients would have undergone unnecessary laparotomy. If all 88 results had been considered negative, 20 patients (23%) with intra-abdominal injuries would have been diagnosed late or not at all. Eight patients with initial negative DPL but with persistent abdominal pain underwent repeat DPL. Results were true positive in three, false negative in one, and true negative in four. Repeat lavage has an accuracy of 95.8%, sensitivity of 85.2%, and specificity of 100%; with repeat lavage, DPL overall has high accuracy (98.4%), sensitivity (94.2%), and specificity (99.7%). Repeat lavage can be helpful in evaluating patients with initial negative lavage but with persistent abdominal pain. Repeat lavage is also indicated when initial results are indeterminate.

From January 1974 through July 1979, 1,588 patients underwent diagnostic peritoneal lavage. The test had an accuracy of 98.6%, sensitivity of 94.3%, and specificity of 99.8%. It was true positive in 21.9%, false positive in 0.1%, false negative in 1.3%, and true negative in 76.6%. Fifty-nine patients from the true-positive group had grossly equivocal tests, but had positive lavage results based on quantitative cell count. Thus without cell count the test would have a sensitivity of 78.3%, accuracy of 94.8%, and specificity of 99.8. Eight patients had positive lavage based on WBC count but negative RBC count; all of these patients had bowel injuries. Measurement of lavage fluid amylase resulted in minimal or no improvement in the accuracy (0.06%), sensitivity (0.3%), or specificity (0.0%). Five of six patients with positive amylase levels but grossly negative tests had concomitant positive WBC count. The added cost of the amylase measurement is estimated to be $154,472. Peritoneal lavage has high accuracy, sensitivity, and specificity. Cell counts significantly improve sensitivity. Patients with a grossly equivocal test but with a positive cell count should undergo laparotomy. The lavage-fluid amylase measurement is costly and is of insignificantly yield.

The criteria for declaring the results of a diagnostic peritoneal lavage (DPL) positive have been controversial. Lowered cell count criteria result in increased sensitivity, decreased specificity, and altered accuracy. Consecutive lavages on 105 patients with penetrating trauma (PT) to the lower chest and abdomen (48 gunshot wounds and 57 stab wounds) and 1812 patients with blunt abdominal trauma (BT) were studied. Varied cell count criteria were analyzed. The best criteria for BT were as follows: positive, lavage fluid red blood cells (LRBCs) greater than 100,000/mm3 or lavage fluid white blood cells (LWBCs) greater than 500/mm3; indeterminate, LRBCs 50,000/mm3 to 100,000/mm3 or LWBCs 100 to 500/mm3; and negative, LRBCs less than 50,000/mm3 and LWBCs less than 100/mm3. Based on these criteria the accuracy of the test was 99.1%. The highest accuracy would be achieved for PT if the criteria were as follows: positive, LRBCs greater than 50,000/mm3 or LWBCs greater than 500/mm3; indeterminate, LRBCs 25,000 to 50,000/mm3 or LWBCs 100 to 500/mm3; negative, LRBCs less than 25,000/mm3 and LWBCs less than 100/mm3. Based on these criteria the accuracy of the test for PT would range from 96.2% (101 of 105) to 98.1% (103 of 105), depending on the results of repeat lavage for two patients with indeterminate initial lavages. The standard lavage criteria were the best for BT and achieved the highest accuracy. However, the LRBC criteria should be lowered for PT.

Loss of myocardial adenosine triphosphate (ATP) during ischemia can result in decreased cardiac function. Postischemic ATP levels remain low, and the reason for this is poorly understood. Previous attempts to enhance ATP recovery after ischemia have been only partially successful. To determine the long-term dynamics of ATP recovery and evaluate the effect of providing ATP precursors, we devised a method of obtaining sequential ventricular biopsies in dogs after 20 minutes of normothermic global ischemia on cardiopulmonary bypass. Our kinetic data show adenine (A) is metabolically favored over adenosine to regenerate ATP levels when adequate ribose (R) is present to produce phosphoribosylpyrophosphate. Therefore A (20 mM) plus R (80 mM) or saline (NS) was infused (1.0 ml X min-1) into the right atrium of dogs for 48 hours after ischemia. During A infusion myocardial tissue A was 0.19 +/- 0.07 nmol X mg-1, arterial A was 18.3 +/- 1.3 microM, coronary sinus A was 11.0 +/- 1.6 microM, and extraction of A by the myocardium was 38% +/- 10%. We found that while the decrease in ATP levels during ischemia was at least 50% in both groups, the postischemic ATP recovery rate in A/R dogs was more than eightfold greater than de novo synthesis (2.8 +/- 0.59 versus 0.34 +/- 0.06 nmoles X mg-1 X day). ATP levels in NS dogs were only 54% +/- 8% of preischemic values by 48 hours and required 9.9 +/- 1.4 days for full recovery. Recovery in A/R dogs required 1.2 +/- 0.2 days. Our results reveal that ATP recovery after a significant ischemic insult is slow, precursor availability is an important limiting factor in ATP recovery, and recovery time can be greatly shortened with precursor infusion even when started after the ischemic insult.

Myocardial ATP levels remain depressed following significant periods of ischemia (Isc) despite reperfusion (Rpf). Neither the rate of in vivo ATP return following global Isc nor the factors which influence recovery have been defined. In order to determine the time course to complete the return of ATP levels and evaluate methods of enhancing recovery of ATP levels, we have devised a chronic canine model of global Isc. In this model serial ventricular biopsies can be taken in the awake animal over several days without reoperation which allows an investigation of the recovery of the myocardium following a uniform global insult to be performed. Recovery of ATP levels has been shown to depend, at least in part, on the availability of precursors and the activity of the ATP regenerating enzymes. Because complete recovery of ATP levels takes days, short term (hours) models have limitations. Previous attempts at enhancing ATP recovery following Isc have been only partially successful because either the degree of depression was not great or the period of observation was short, resulting in incomplete return. To identify the best precursor choice, we previously measured the activity of the AMP regenerating enzymes, adenosine kinase (AdK) (adenosine----AMP) and adenine phosphoribosyl transferase (APRT) (adenine----AMP). Because APRT activity was 20 fold higher than AdK with similar Km values for substrates, it appeared that adenine (A) is preferred to adenosine for AMP regeneration in the dog's myocardium. The formation of 5-phosphoribosyl 1-pyrophosphate (PRPP) may also be rate limiting and, therefore, the effect of ribose (R) on ATP recovery was also evaluated. Recovery of ATP levels was assessed in three groups: (1) normal saline (NS), (2) A (20 mM) in normal saline (A/NS) or (3) A with R (80 mM) in normal saline (A/R) were infused (1.0 ml/min) into the right atrium of dogs for 48 hours following Isc. In all groups, ATP levels fell to between 46-60% of pre-Isc levels during Isc. In the NS dogs, ATP levels continued to fall slightly to 46% pre-Isc levels during the first four hours of Rpf after Isc. By 24 hours no appreciable recovery had occurred and the measured ATP was only 51% of the pre-Isc value. Even by seven days, ATP had not returned fully, and by extrapolation, complete recovery required 9.9 +/- 1.4 days. Treated dogs showed, however, that ATP recovery could be significantly enhanced.(ABSTRACT TRUNCATED AT 400 WORDS)

The manner in which the left ventricle responds to an acute volume overload has not been well defined. Left ventricular performance was studied in six chronically instrumented resting awake dogs in the control state and serially after creation of a large abdominal aortocaval shunt. Ultrasonic transducers measured minor and major axis diameters and equatorial wall thickness. Left ventricular pressure was obtained with micromanometers. Cardiac contractility was evaluated by the load-independent contractility index, EMAXsc (slope of the normalized end-systolic equatorial midwall circumferential stress-equatorial midwall circumference relationship). By 1 week postshunt, the dog had clinical signs of congestive heart failure (ascites, dyspnea, limb edema); although systolic aortic pressure remained stable, heart rate, end-diastolic volume, pulse pressure (systolic minus diastolic pressure), cardiac output, minute work and dp/dtmax were significantly increased. At 1 week the calculated left ventricular mass was increased by 10.1% +/- 4.0% above control. EMAXsc was significantly increased immediately after shunting but returned to control at 1 day and was less than control at 1 week. Thus adaptation of the left ventricle to acute volume overload is characterized by use of inotropic, chronotropic, and Starling reserves. However, chronic volume overload is characterized by decreased inotropic state and an apparent increase in hemodynamic performance (dp/dtmax, cardiac output, minute work), which appears to be maintained by an increase in cardiac mass and by chronotropic and Starling reserves.

Although left ventricular (LV) function appears altered by severe hemorrhagic shock (HS), the mechanisms of this dysfunction have been difficult to characterize. Depression in the LV function curve could be caused by altered diastolic or systolic function. It has been difficult to assess the systolic function, but the use of the rate and load independent index of contractility, Emax (the slope of the end-systolic pressure-dimension relationship), offers a new approach to the quantification of systolic mechanical performance. Emax and the LV diastolic pressure-strain relationship were measured in 15 chronically instrumented dogs by sonomicrometric and micromanometric techniques. Gradual LV unloading was obtained from transient vena caval occlusion. After control study, each dog underwent 2 hours of HS (mean aortic pressure 40 mm Hg), followed by reinfusion of all shed blood. Upon reinfusion, Emax was not decreased; however, all dogs had a significant decrease in LV compliance. During the next 4 days, the LV compliance of the eight survivors progressively returned toward control, while Emax remained stable. All seven nonsurvivors demonstrated progressive loss of LV compliance, and Emax was significant decreased prior to death. Cardiac contractility appeared improved immediately after shock, but a consistent decrease in compliance was observed. Reversal of abnormal diastolic function was demonstrated in all survivors and progressive depression in all nonsurvivors. Depression in systolic function was observed only in nonsurvivors immediately prior to death.

The management of children's tumors has changed significantly in the past several years. New techniques and combined surgical, chemotherapeutic, and radiation approaches are responsible for improved survival in most instances. Cooperation of the surgeon with the specialists in separate disciplines is imperative to continued advancements in neoplastic disease of childhood.

Using the load independent contractility index, end-systolic pressure-volume ratio (Emax), contractility of the hypertrophied left ventricle (LV) from three different models was evaluated in conscious, resting dogs. The experimental animals included 12 dogs with perinephritic hypertension (HYP) (aortic diastolic pressure 130 +/- 5 mm Hg), 12 dogs who underwent aortic banding (AOB) at 6 to 8 weeks of age (resting aortic gradient 110 +/- 15 mm Hg), and 12 dogs with chronic fluid overload from aortocaval fistula (ACF). These were compared with 12 normal dogs (CTL). LV dimension and pressure were measured with ultrasonic tranducers and micromanometers. All three models resulted in hypertrophy with significant (P less than 0.01) increase in LV weight-to-body weight ratio (6.3 +/- 0.4, 8.4 +/- 0.5, 6.3 +/- 0.4, respectively, vs 4.4 +/- 0.1 g/kg). Cardiac output (6908 +/- 740 vs 2424 +/- 276 ml/min) and end-diastolic volume (118 +/- 11 vs 50 +/- 4 ml) were significantly (P less than 0.01) increased in AOB (18 +/- 1 vs 9 +/- 2 mm Hg). dp/dtmax was not significantly different among all groups. Emax (CTL = 5.3 +/- 0.4 mm Hg/ml) was not significantly changed in HYP (9.5 +/- 2.1) but was significantly (P less than 0.01) increased in AOB (14.1 +/- 2.6), and significantly (P less than 0.01) depressed in ACF (2.4 +/- .03). Thus, LV hypertrophy from systemic hypertension (HYP) or proximal aortic hypertension (AOB) is, at least initially, associated with preservation of contractility and normal hemodynamic performance.(ABSTRACT TRUNCATED AT 250 WORDS)

The end-systolic pressure-volume (ESPV) ratio (Emax) has recently been accepted as a valid cardiac contractility index. However, in vivo, it is difficult to define end systole (ES) precisely. This study was designed to analyze the effects of eight different ES definitions on Emax. Nine chronically instrumented dogs were studied prior to and during the sequential infusions of phenylephrine (0.2 mg/min), epinephrine (2.0 micrograms/min), and dobutamine (10 micrograms/kg/min). Left ventricular (LV) dimensions and pressure were measured with sonomicrometers and micromanometer. ES was defined at peak LV pressure (PLVP), end-ejection, dp/dt min, 10, 20, 30 msec before dp/dt min, minimum volume before dp/dt min, and left-upper-corner of pressure volume loop (LUC). Although ESPV relationship from each definition was linear (mean r 0.89 +/- 0.3, range 0.76 to 0.99) and sensitive to inotropic changes, the Emax's were not all the same. The r was highest with LUC (mean 0.94 +/- .02, range 0.90 to 0.99) and lowest with PLVP (mean 0.85 +/- 0.03, range 0.76 to 0.92). Emax from PLVP was least sensitive to epinephrine and dobutamine infusions. Thus, in order to compare different values of Emax, the definition of ES must be precise and consistent. Although all the above eight definitions of ES appeared to produce reasonable ESPV relationship, PLVP appeared to be the worst while LUC appeared to be the best ES definition for determining Emax.

The characteristics of left ventricular (LV) function in the nonimmunosuppressed heterotopic heart transplant (TX) with less than 3 hr of cold preservation, were studied in 12 awake chronically instrumented dogs prior to TX (control), 1-12 hr post TX (P1), 12-24 hr post TX (P2), and 24-48 hr post TX (P3). Micromanometers measured LV transmural pressure and ultrasonic transducers measured ventricular dimension in order to allow calculations of myocardial mechanical properties. Immediately after transplant (P1) there was significant (P less than 0.05) depression noted in both diastolic function and systolic function (peak LV pressure, 137 +/- 5 vs 80 +/- 10 mm Hg; dp/dtmax, 2642 +/- 170 vs 1038 +/- 98 mm Hg/sec; maximum velocity of minor axis shortening, 4.46 +/- 0.50 vs 2.41 +/- 0.56; and Emax, 6.5 +/- 1.2 vs 2.0 +/- 1.4 mm Hg/ml). However, the contractility reserve (studied in six dogs) as estimated by postextrasystolic potentiation ratio was maintained (1.41 +/- 0.07 vs 1.37 +/- 0.15), suggesting reversibility of the depressed function. Over the next 2 days the diastolic function and the systolic function (at P3: 109 +/- 6 mm Hg, 1842 +/- 450 mm Hg/sec, 5.54 +/- 0.77 cm/sec, and 4.5 +/- 1.3 mm Hg/ml, respectively) gradually improved toward control. Microscopic examination of the autopsied hearts did not show significant evidence of rejection. Thus, the early depression of function in the heart TX appeared to be the result of ischemia from preservation and surgical trauma.(ABSTRACT TRUNCATED AT 250 WORDS)