Postoperative coagulopathy in a pediatric patient after exposure to bovine topical thrombin.

Severe postoperative coagulopathy developed in a child with congenital heart disease due to a factor V inhibitor from repetitive exposure to bovine topical thrombin. This case report alerts pediatric providers to consider these inhibitors when postoperative coagulopathy occurs. Potential treatment options are reviewed.

Pericardiocentesis with extended catheter drainage: an effective therapy.

BACKGROUND: The most effective method for managing pericardial effusions has yet to be identified. This study evaluates the efficacy and safety of echocardiographic-guided placement of indwelling catheters into the pericardial space. METHODS: This study consists of a 5-year retrospective chart review of consecutive patients coded with benign or malignant pericardial effusions who presented for drainage procedures to a single surgeon at a 260-bed hospital. Complication, recurrence, and survival rates were studied. RESULTS: Between January 1996 and August 2001, a total of 29 pericardial drainage procedures were performed; eight of those also underwent talc sclerosis. Mean follow-up was 16 months. Three patients (10%) required conversion to thoracotomy; of those remaining, 25 of the 26 procedures were performed under local anesthesia with intravenous sedation. The identified etiologies for pericardial effusions were malignancy (76%), idiopathic (14%), postcoronary artery bypass grafting procedure (3%), viral pericarditis (3%), and uremia (3%). Echocardiographic features of tamponade were documented in 72%. Mean +/- SEM length of postprocedure in-hospital stay was 6.7 +/- 0.82 days. The overall complication rate was 10% (pneumothorax and cardiac injury). Recurrence rate within 30 days was 7%. Thirty-day mortality was 21%, and more than 90-day survival was 72%. CONCLUSIONS: Pericardiocentesis with extended catheter drainage is a safe treatment for management of clinically significant, malignant and benign, pericardial effusions and can be performed effectively under local anesthesia with intravenous sedation.

Ultrasound measurement of aortic diameters in rodent models of aneurysm disease.

BACKGROUND: This investigation was undertaken to evaluate transabdominal ultrasound (US) measurements of aortic diameters in rats and mice as a complementary method to video microscopy (VM), the current standard for assessing the diameter of rodent aortas. METHODS: Aortic diameters were measured in 64 rats (n = 132 sets) and 12 mice (n = 36 sets) following experimental induction of aortic aneurysms. Diameters were measured at the renal vein, midinfrarenal aorta, and aortic bifurcation. RESULTS: In the rat, anteroposterior (AP) US measurements were closely correlated with transverse VM measurements, with correlation coefficients ranging from 0.66 to 0.77 (P < 0.0001) for axial US images and 0.58 to 0.63 (P < 0.0001) for sagittal US images. In the mouse, significant correlation coefficients were 0.57 (P < 0.001) near the renal vein and 0.44 (P = 0.007) at the midinfrarenal aorta. Aortic diameters increased significantly with increasing animal age and weight (R = 0.40, P = 0.003 at the renal vein, R = 0.29, P = 0.04 in the midinfrarenal aorta, and R = 0.39, P = 0.004 at the aortic bifurcation), suggesting that weight matched rodents must be used to define aortic dimensions in treatment groups as opposed to repeated comparisons with baseline measurements in a growing rat. CONCLUSION: Noninvasive aortic US measurements throughout the course of a rodent study of aneurysmal disease provide a practical alternative to VM for the repeated determinations of aortic diameters.

Pediatric splanchnic arterial occlusive disease: clinical relevance and operative treatment.

OBJECTIVE: Splanchnic arterial occlusive disease is rare in childhood. The purpose of this study was to review the clinical relevance and operative treatment of these lesions in a unique experience from a single institution. METHODS: Seventeen children (11 boys and 6 girls) from 2 years to 17 years in age with critical narrowings of the celiac artery (CA) and superior mesenteric artery (SMA) underwent treatment at the University of Michigan from 1974 to 2000. Etiologic factors included embryologic fusion abnormalities of the fetal aortae during formation of the splanchnic arteries (n = 15), inflammatory aortoarteritis (n = 1), and radiation-induced arterial fibrosis (n = 1). Individual lesions included CA occlusions (n = 6) and stenoses (n = 7), SMA occlusions (n = 3) and stenoses (n = 11), and inferior mesenteric artery stenosis (n = 1). Fourteen children had abdominal aortic coarctations, and 15 had renal artery stenoses. Two patients had postprandial abdominal discomfort and food aversion, consistent with intestinal angina. Small stature affected five others, perhaps attributable to severe renovascular hypertension and failure to thrive. Ten children underwent intestinal revascularization, at the time of an aortoplasty or thoracoabdominal bypass for aortic coarctation (n = 7) or at the time of renal artery revascularization (n = 8). Primary splanchnic revascularization procedures included SMA-aortic implantation (n = 3), aorto-SMA and CA bypass with an internal iliac artery graft (n = 3) or a saphenous vein graft (n = 1), CA-aortic implantation at a stenotic SMA origin (n = 2), and CA and SMA intimectomy (n = 1). Secondary operations included SMA-aortic implantation (n = 2). RESULTS: All 10 children who underwent splanchnic revascularization have thrived, gained weight, and are free of abdominal pain, with follow-up periods averaging 9 years. No intestinal ischemic manifestations occurred in the seven children who did not undergo operation. CONCLUSION: Pediatric splanchnic arterial occlusive disease is a rare illness appropriately treated with operation in properly selected children.

Nitric oxide inhibition increases aortic wall matrix metalloproteinase-9 expression.

OBJECTIVE: Nitric oxide (NO) may mediate vessel wall remodeling by regulating expression of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). This study tested the hypothesis that nitric oxide synthase (NOS) inhibition in whole aortic wall causes increases in cytokine-stimulated MMP and TIMP expression. METHODS: Cultured infrarenal aortic segments from Sprague-Dawley rats were exposed to increasing concentrations (0, 0.1, 0.5, 1, and 5 mM; n = 6 per concentration) of N(G)-monomethyl-l-arginine (L-NMMA), a known inhibitor of NOS. This was in the presence of 2 ng/ml of interleukin-1beta, a known inducer of NOS, MMP, and TIMP expression. Media nitrate and nitrite (NO(x)) were measured at 72 h using the Saville method. Media MMP activity was measured using gelatin zymography. MMP-2 and -9 protein and mRNA levels were determined by Western blot and reverse transcriptase-polymerase chain reaction (RT-PCR). TIMP activity and mRNA levels were evaluated by reverse zymography and RT-PCR. Data were analyzed using ANOVA. RESULTS: Increasing concentrations of L-NMMA produced a dose-dependent decrease in NO(x) (2214 +/- 405 to 347 +/- 37 ng/mg, P < 0.001). Zymography demonstrated a dose-dependent increase in 92-kDa MMP (pro-MMP-9) activity (P < 0.001) with corresponding increases in pro-MMP-9 protein (P = 0.03) and mRNA levels (P = 0.004). While there was a dose-dependent increase in 72-kDa MMP (pro-MMP-2) activity (P = 0.001), pro-MMP-2 protein and mRNA levels were unchanged. Reverse zymography demonstrated a dose-dependent increase in 29-kDa TIMP-1 activity (P = 0.01), but there was no change in TIMP-1 mRNA levels. CONCLUSIONS: NOS inhibition in ex vivo aortic tissue causes a dose-dependent increase in MMP-9 expression and activity. It is speculated that deficiencies of NO in vivo alter MMP and TIMP homeostasis, favoring matrix degradation.