Outpatient management of intra-corporeal left ventricular assist device system in children: a multi-center experience.

Little is known about the outcomes of children supported on intracorporeal left ventricular assist device (HVAD), and the feasibility of outpatient management. All centers with pediatric patients discharged from the hospital on the device were identified using company database. A total of 14 centers were contacted, with 9 centers, contributing data retrospectively. From 2011 to 2013, 12 pediatric patients (7 females), mean aged 11.9 ± 2.3 years (range 8-15), mean weight 43 ± 19 kg (range 18-81), mean body surface area 1.3 ± 0.3 m(2) (range 0.76-1.96) were identified. Diagnosis included: dilated cardiomyopathy (CMP) (n = 5), noncompaction CMP (n = 4), toxic CMP (n = 2) and viral CMP (n = 1). Indications for support were permanent support (n = 1), bridge to recovery (n = 1) and bridge to transplantation (n = 10). Prior to HVAD implantation, all patients received intravenous inotropes and two patients were on temporary mechanical support. Overall mortality was 0%. Mean duration of inpatient and outpatient support were 56 (range: 19-95 days) and 290 days (range: 42-790), respectively. Mean readmission rate was 0.02 per patient month (2.1 per patient). No adverse events involving emergency department occurred. Eight children resumed local schooling. Home discharge of children supported on HVAD is feasible and safe. School integration can be achieved. There is wide center variability to discharge practice for children.

The role of left ventricular reconstruction for cardiogenic shock.

Left ventricular remodeling after myocardial infarction is recognized as an early adaptive mechanism that later results in adverse physiologic changes. Surgical therapy for this condition includes exclusion of nonfunctional segments of ventricular wall and restoration of more normal ventricular geometry. The Dor procedure, or endoventricular patch plasty, is recognized as an excellent means of accomplishing this goal. Most series in regard to the Dor procedure report results in patients who electively come to surgery after developing global ventricular distension after an area of akinesia or dyskinesia. We report a small series of 6 patients who presented with acute myocardial infarction and who developed cardiogenic shock after ventricular dilation. Each patient underwent emergent revascularization and left ventricular reconstruction using the Dor technique. A seventh patient with akenesia, but without preoperative shock, required the Dor procedure to wean from cardiopulmonary bypass. There were no in-hospital deaths, and follow-up showed good outcomes. In certain select acute subsets (large anterior myocardial infarction, cardiogenic shock, and ventricular dilation), immediate revascularization and restoration of left ventricular size improves outcomes by changing left ventricular shape and thereby pre-empting remodeling and restoring blood flow to ischemic myocardium.

Retrograde venous perfusion with hypothermic saline and adenosine for protection of the ischemic spinal cord.

PURPOSE: Spinal cord injury and the resultant postoperative paraplegia are devastating complications of thoracic aortic surgery, for which no widely accepted protective interventions exist. We hypothesized that retrograde venous perfusion-cooling of the spinal cord with a hypothermic saline and adenosine solution would protect it from ischemic injury caused by thoracic aortic occlusion. METHODS: Adult domestic swine of either sex (weight range, 20 to 30 kg) were intubated and ventilated. A left thoracotomy was performed. The accessory hemiazygous vein was divided, and a catheter was inserted distally. The aorta was clamped at the left subclavian artery. The venous catheter was not used in the animals in the control group (n = 7); in the animals in the experimental group (n = 7), a cold (4 degrees C) saline and adenosine solution was infused into the accessory hemiazygous vein. After 30 minutes, the clamp and catheter were removed, and the chest was closed. A blinded observer evaluated the animals' hind-leg motor activity 24 hours later. The Tarlov scale was used: 0, complete paralysis; 1, minimal movement; 2, stands with assistance; 3, stands alone; 4, weak walk; 5, normal gait. The animals' rectal temperatures were measured at the end of the experiment, and blood pressure was measured throughout. Two other groups were studied to assess the effect of the intervention on spinal cord temperature. RESULTS: The animals in the control group had a mean Tarlov score of 1.7 +/- 0.6; the animals in the experimental group had a mean Tarlov score of 4.9 +/- 0.1 (P <.01). The animals in the experimental group had a significantly greater drop in spinal cord temperature than those in the control group (4. 05 +/- 0.6 degrees C vs 0.58 +/- 0.12 degrees C; P <.01). No significant difference in rectal temperatures was found, nor did any arrhythmias or hypotensive episodes occur in either group. Perfusion of the spinal cord was confirmed with angiography by using this approach. CONCLUSION: Retrograde venous perfusion-cooling of the spinal cord with a hypothermic saline and adenosine solution protects the cord from ischemic injury caused by clamping of the thoracic aorta.

Early carotid endarterectomy after stroke.

The authors sought to determine if patients with stroke and a high-grade carotid stenosis benefited from a delay before carotid endarterectomy. A retrospective study of 45 patients undergoing carotid endarterectomy after stroke is presented. The patients were divided into two groups: group I (early group, n = 20), composed of patients who had carotid endarterectomy less than 6 weeks after stroke, and group II (late group, n = 25), comprised of patients who had carotid endarterectomy more than 6 weeks after stroke. As assessed by cerebral angiography, 100% of patients in group I and 64% of patients in group II had carotid artery stenoses > 76% (P < 0.001). The median interval from stroke to carotid endarterectomy was 14 days in group I and 129 days in group II. There was no mortality in either group. No patients in either group demonstrated any neurological deterioration. The authors conclude that, in select patients, carotid endarterectomy may be done safely less than 6 weeks after stroke in order to avoid new events or carotid occlusion while awaiting surgery.

Intensive care is cost-effective in carotid endarterectomy.

The purpose of this study was to analyze the utilization, cost profile, and predictors of intensive care unit (ICU) services after carotid endarterectomy. A retrospective medical record review of all patients undergoing isolated carotid endarterectomy by a vascular surgery service at one university hospital during a 12-month period was performed. Eighty-four patients undergoing 91 carotid endarterectomies were identified for review. All carotid endarterectomy patients at the authors' institution were routinely admitted to an ICU postoperatively. Sixty-five of the 91 patients (71.4%) required ICU interventions, the majority of which were intravenous antihypertensive therapy. There were no deaths in the group. There was one non-fatal stroke (1.1%), and one non-fatal myocardial infarction (1.1%). There were three reoperations (3.3%): two for hematoma and one for a change in neurological status. One patient required reintubation. Five of the six major adverse events after carotid endarterectomy occurred within 12 hours postoperatively. No preoperative factors predicted a significant risk for complications following carotid endarterectomy. There is no reliable predictor that carotid endarterectomy patients will require postoperative interventions or develop adverse outcomes. Mandatory intensive care immediately after carotid endarterectomy upholds high safety standards, avoids the uncertainty of preoperative ICU planning, and avoids the high cost of a recovery room stay to determine the need for intensive care. In addition, costs may be further reduced as the ICU length of stay may be decreased if there are no necessary interventions or complications after 12 hours of intensive care.

Spinal cord protection during aortic cross-clamping using retrograde venous perfusion.

BACKGROUND: Paraplegia remains a devastating complication following thoracic aortic operation. We hypothesized that retrograde perfusion of the spinal cord with a hypothermic, adenosine-enhanced solution would provide protection during periods of ischemia due to temporary aortic occlusion. METHODS: In a rabbit model, a 45-minute period of spinal cord ischemia was produced by clamping the abdominal aorta and vena cava just below the left renal vessels and at their bifurcations. Four groups (n = 8/group) were studied: control, warm saline, cold saline, and cold saline with adenosine infusion. In the experimental groups, saline or saline plus adenosine was infused into the isolated cavae throughout the ischemic period. Clamps were removed and the animals to recovered for 24 hours before blinded neurological evaluation. RESULTS: Tarlov scores (0 = paraplegia, 1 = slight movement, 2 = sits with assistance, 3 = sits alone, 4 = weak hop, 5 = normal hop) were (mean +/- standard error of the mean): control, 0.50 +/- 0.50; warm saline, 1.63 +/- 0.56; cold saline, 3.38 +/- 0.26; and cold saline plus adenosine, 4.25 +/- 0.16 (analysis of variance for all four groups, p < 0.00001). Post-hoc contrast analysis showed that cold saline plus adenosine was superior to the other three groups (p < 0.0001). CONCLUSION: Retrograde venous perfusion of the spinal cord with hypothermic saline and adenosine provides functional protection against surgical ischemia and reperfusion.

Reduced neutrophil infiltration protects against lung reperfusion injury after transplantation.

BACKGROUND: There is evidence that lung ischemia reperfusion injury is a result of the activation of components of the inflammatory cascade. However, the role of neutrophils in lung reperfusion injury continues to be a source of controversy. METHODS: Using an isolated, whole blood-perfused, ventilated rabbit lung model, we sought to characterize the pattern of reperfusion injury and investigate the contribution of neutrophils to this injury. Donor rabbits underwent lung harvest after pulmonary arterial prostaglandin E1 injection and Euro-Collins preservation solution flush. Group I lungs (n = 8) were immediately reperfused without ischemic storage. Group II lungs (n = 8) were stored for 18 h at 4 degrees C before reperfusion. Group III lungs (n = 10) underwent 18 h of ischemic storage and were reperfused with whole blood that was first passed through a leukocyte-depleting filter. All lungs were reperfused for 2 h. RESULTS: Arterial oxygenation in group III progressively improved, and was significantly higher than that of group II after 2 h of reperfusion (272.58+/-58.97 vs 53.58+/-5.34 mm Hg, p = 0.01). Both pulmonary artery pressure and pulmonary vascular resistance were significantly reduced in group III when compared with group II (27.85+/-1.45 vs 44.15+/-4.77 mm Hg, p = 0.002; and 30,867+/-2,323 vs 52,775+/-6,386 dynes x sec x cm(-5), p = 0.003, respectively). Microvascular permeability in group III lungs was reduced to 73.98+/-6.15 compared with 117.16+/-12.78 ng Evans blue dye/g tissue in group II (p = 0.005). Group III myeloperoxidase activity was 56.92+/-6.31 deltaOD/g/min compared with 102.84+/-10.41 delta0d/g/min in group II (p = 0.002). CONCLUSIONS: Leukocyte depletion of the blood reperfusate protects against microvascular permeability and significantly improves pulmonary graft function. The neutrophil plays a major role in amplifying lung injury later during reperfusion, and this lung ischemia reperfusion injury may be reversed through the interruption of the inflammatory cascade and the interference with neutrophil infiltration.

Preservation of intercostal arteries during thoracoabdominal aortic aneurysm surgery: a retrospective study.

OBJECTIVE: The purpose of this article was to examine the influence of reimplantation of patent intercostal and lumbar arteries on the incidence of postoperative paraplegia/paraparesis in patients undergoing clamp-and-sew surgical repair of thoracoabdominal aortic aneurysms. METHODS: Data from January 1987 through December 1997 were retrospectively collected on 132 patients. Ninety-one patients in group I underwent aneurysm repairs before January 1995 and did not undergo intercostal artery reimplantation. Group II included the more recent 41 patients who had vessels between the eighth thoracic intercostal and the second lumbar arteries reimplanted to the graft or preserved at the aortic anastomoses. RESULTS: The operative mortality rate was 13.2% (12/91) in group I and 4.9% (2/41) in group II (P =.22). The incidence of postoperative paraplegia was significantly lower in the more recent cohort of patients (8.8% [8/91] in group I vs 0% [0/41] in group II, P =.05). The overall rate of spinal cord dysfunction was lowered from 9.9% (9/91) in group I to 2.4% (1/41) in group II (P =.17). However, a multivariable logistic regression analysis identified only aneurysm extent (Crawford type I and type II) as a predictor of less postoperative spinal cord injury (P =.08). The average aortic crossclamp time in group I was 30.3 +/- 11.5 (SD) minutes, and the time of aortic occlusion in group II was not significantly prolonged, with an average crossclamp time of 31.0 +/- 21.0 (SD) minutes (P =. 88). CONCLUSIONS: An aggressive approach to maintain intercostal artery patency during clamp-and-sew repair of thoracoabdominal aortic aneurysms may effectively lower the incidence of spinal cord injury without prolonging aortic crossclamp time.

Does a focal neurologic deficit contraindicate operation in a patient with endocarditis?

BACKGROUND: As many as 40% of patients with left-sided bacterial endocarditis will sustain a neurologic insult. The importance of a neurologic change as an indication or a contraindication for valve replacement remains controversial. METHODS: We performed a retrospective analysis of the records of 33 patients admitted to the University of Virginia Health Sciences Center between January 1, 1978, and June 30, 1996, with a diagnosis of endocarditis and a neurologic change. RESULTS: All 33 patients had echocardiographic or pathologic evidence of left-sided endocarditis; 23 were seen with focal neurologic findings and had a mortality rate of 22% (5 of 23), and 10 patients were seen with nonfocal, diffuse encephalopathy and had a mortality rate of 60% (6 of 10) (p<0.05). Of the 33 patients, 14 underwent operation and 19 were treated medically. The mortality rate was 21.4% (3 of 14) in the surgical group and 42.1% (8 of 19) in the medical group (p = not significant). In 71% (10 of 14) of the surgical patients, the operation was done within 1 week of the neurologic event. Additional neurologic deterioration occurred in 18.2% (2 of 11) of survivors in the surgical group and 9.1% (1 of 11) in the medical group (p = not significant). CONCLUSIONS: Choosing therapy for a patient with endocarditis and a neurologic change remains a difficult challenge. Initial findings of nonfocal, global dysfunction on examination are a predictor of a poor outcome. By comparing surgical and medical groups derived from the same series of patients, it is clear that patients with bacterial endocarditis and central nervous system changes face substantial mortality regardless of intervention. However, these data demonstrate that when compared with a similar group of medical patients, surgical patients who require and receive operation early in the course of their illness do comparatively well. Improving outcomes by delaying surgical intervention may serve to "select out" hardier patients but will lead to the death of patients who might benefit from such intervention.

Simultaneous coronary artery bypass grafting and abdominal aneurysm repair decreases stay and costs.

BACKGROUND: Patients with large (> or = 5.0 cm) abdominal aortic aneurysms (AAA) frequently have marked associated coronary artery disease. We hypothesized that a single operation for coronary artery bypass grafting (CABG)/AAA would provide equivalent, if not improved, patient care while decreasing postoperative length of stay and hospital costs compared with staged procedures. METHODS: Eleven patients to date have undergone a combined procedure at our institution. Ten underwent CABG followed by AAA repair, whereas one patient received an aortic valve replacement before aneurysm repair. We performed a retrospective analysis comparing the postoperative length of stay and hospital costs for this single procedure to a combined cohort of 20 randomly selected patients who either received AAA repair (n = 10) or standard CABG (n = 10) during the same time period. RESULTS: No operative mortality has been reported. There were no episodes of neurologic deficit or cardiac complication after these procedures. The postoperative length of stay was significantly decreased for the CABG/AAA group compared with the combined postoperative length of stay for the AAA plus CABG group (7.44+/-0.88 days versus 14.10+/-2.00; p = 0.012). Total hospital costs were also significantly decreased for the CABG/AAA group compared with total hospital costs for the AAA plus CABG group ($22,941+/-$1,933 versus $34,076+/-$2,534; p = 0.003). CONCLUSIONS: A single operation for coronary revascularization and AAA repair is safe and effective. Simultaneous CABG and AAA repair substantially decreases postoperative length of stay and hospital costs while avoiding possible interim aneurysm rupture and repeat anesthesia.

Inhibition of inducible nitric oxide synthase after myocardial ischemia increases coronary flow.

BACKGROUND: The role of nitric oxide synthase in myocardial ischemia-reperfusion injury is complex. Our hypothesis was that inducible nitric oxide synthase has a role in the regulation of coronary flow after ischemia. METHODS: Four groups of isolated blood-perfused rabbit hearts underwent sequential periods of perfusion, ischemia, and reperfusion (20, 30, and 20 minutes). Two groups underwent 40 minutes of perfusion. Ischemic groups received saline vehicle, N omega-nitro-L-arginine methyl ester (L-NAME) or the highly specific inducible nitric oxide synthase inhibitor 1400W in low or high doses during reperfusion. Two nonischemic groups were treated with saline vehicle or 1400W during the last 20 minutes of perfusion. Left ventricular developed pressure and coronary flow were measured after each perfusion period. Ventricular levels of myeloperoxidase and cyclic guanosine monophosphate were measured at the end of the second perfusion period. RESULTS: Coronary flow was significantly increased in both 1400W groups versus L-NAME (p < 0.001) and in high-dose 1400W versus control (p < 0.001). Coronary flow was not significantly different between the nonischemic groups. Left ventricular developed pressure was not significantly different among the ischemic groups or between the two nonischemic groups. There were no differences in cyclic guanosine monophosphate levels in any of the ischemic hearts. Myeloperoxidase levels were significantly elevated in L-NAME versus high-dose 1400W, nonischemic 1400W, and nonischemic saline groups (p < 0.02). CONCLUSIONS: Highly selective inhibition of inducible nitric oxide synthase results in increased coronary flow after ischemia but not after continuous perfusion. This occurs with decreased neutrophil accumulation and a trend toward increased contractility without elevation of cyclic guanosine monophosphate levels.

Preservation with 8-bromo-cyclic GMP improves pulmonary function after prolonged ischemia.

BACKGROUND: Cyclic guanosine monophosphate (cGMP) is a potent second messenger for the nitric oxide pathway in the pulmonary vasculature. Increased cytosolic cGMP levels elicit pulmonary vasodilatation resulting in decreased pulmonary vascular resistance and maximized pulmonary function after ischemia-reperfusion injury. We hypothesized that the addition of a membrane-permeable cGMP analogue (8-bromo-cGMP) to a Euro-Collins (EC) preservation solution would ameliorate pulmonary reperfusion injury better than prostaglandin E1 injection alone after prolonged hypothermic ischemia. METHODS: All lungs from New Zealand White rabbits (weight, 3 to 3.5 kg) were harvested en bloc, flushed with EC solution, and reperfused with whole blood for 30 minutes. Group 1 lungs (immediate control) were immediately reperfused. Group 2 lungs (control) were stored inflated at 4 degrees C for 18 hours before reperfusion. Groups 3 and 4 lungs were flushed with EC solution containing 200 micromol/L 8-bromo-cGMP and stored at 4 degrees C for 18 and 30 hours, respectively. Fresh, nonrecirculated venous blood was used to determine single-pass pulmonary venous-arterial oxygen gradients at 10-minute intervals. Assays for cGMP, cyclic adenosine monophosphate, nitric oxide synthase activity, and myeloperoxidase were performed on all lung tissue samples. Wet to dry weight ratios were determined after 2 weeks of passive desiccation. RESULTS: Oxygenation (venous-arterial oxygen gradient), pulmonary artery pressure, pulmonary vascular resistance, and edema formation were significantly improved in groups 3 and 4 (addition of 8-bromo-cGMP to EC plus 18 or 30 hours of hypothermic ischemia). Hypothermic storage (groups 2, 3, and 4) decreased both nitric oxide synthase activity and myeloperoxidase levels compared with immediate reperfusion (group 1). CONCLUSIONS: These results suggest that the addition of a membrane-permeable cGMP analogue to an EC pulmonary flush solution improves pulmonary function after prolonged storage compared with EC and prostaglandin (E1) preservation alone. The finding of myeloperoxidase reduced levels after hypothermic storage and subsequent reperfusion may suggest a more important role for pulmonary hemodynamic control in mitigating pulmonary reperfusion injury.

Acellular low-potassium dextran preserves pulmonary function after 48 hours of ischemia.

BACKGROUND: We previously have shown that extracellular preservation solutions provide superior pulmonary protection after 18 hours of cold ischemia at 4 degrees C in an isolated, whole-blood-perfused, rabbit lung model. We also reported that the addition of 20% whole blood to a low-potassium dextran solution (BLPD) conferred no discernible advantage over low-potassium dextran (LPD) alone in this same model. Our current study was aimed at documenting the importance of blood in buffering extracellular preservation solutions during 24 to 48 hours of hypothermic ischemia. METHODS: We studied three groups of lungs using an isolated, whole-blood-perfused, ventilated, rabbit lung model. Lungs were flushed with Euro-Collins, LPD, or BLPD solution, and then were reperfused after 24, 36, or 48 hours of hypothermic storage at 4 degrees C. Continuous measurements of pulmonary artery pressure, pulmonary vascular resistance, left atrial pressure, tidal volume, and dynamic airway compliance were obtained. Fresh, non-recirculated venous blood was used to determine single-pass pulmonary venous-to-arterial O2 gradients. RESULTS: The 24-hour Euro-Collins group could not be completed because of immediate reperfusion failure. The 36-hour LPD group oxygenated significantly better than the 36-hour BLPD group (363.3 +/- 65.1 versus 145.3 +/- 40.3 mm Hg, respectively; p = 0.015). The 48-hour LPD group also experienced significant improvements in oxygenation when compared with the 48-hour BLPD group (pulmonary venous-arterial O2 difference of 239.4 +/- 48.4 versus 70.7 +/- 19.5 mm Hg, respectively; p = 0.012). The 48-hour LPD group also displayed significant improvements in pulmonary artery pressure (34.72 +/- 0.96 versus 55.52 +/- 7.37 mm Hg, respectively; p = 0.031) and pulmonary vascular resistance (39,737 +/- 1,291 versus 67,594 +/- 9,467 dynes.s.cm-5, respectively; p = 0.027) when compared with the 48-hour BLPD group. There were no significant differences between the three LPD groups. CONCLUSIONS: Extracellular solutions provide improved pulmonary preservation in an isolated rabbit lung model after 48 hours of cold ischemia. The addition of blood to extracellular preservation solutions diminishes pulmonary function when combined with ischemic periods of 36 to 48 hours.

An experimental model for laparoscopic common bile duct exploration.

The development of an effective and reliable technique for laparoscopic common bile duct exploration has been limited by the technical difficulty of the procedure and the lack of a suitable animal model with a bile duct diameter large enough to accommodate the fiberoptic choledochoscope and other instruments used for stone extraction. Short-term bile duct ligation in the dog provides a simple and reproducible animal model that enables the surgeon to gain experience with laparoscopic common bile duct exploration in a laboratory setting. This model will enable the surgeon to develop the technical skills necessary to perform laparoscopic common bile duct exploration. In addition, the model may facilitate the development and refinement of new techniques and instruments that will facilitate laparoscopic common bile duct exploration in the clinical setting.