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PubMed1987

Injuries to the abdominal vascular system: how much does aggressive resuscitation and prelaparotomy thoracotomy really help?

The records of 154 patients with 254 abdominal vascular injuries seen over 5 years (1980 to 1985) were reviewed. The overall mortality rate (MR) was 46%. This included 100% (5/5) for blunt injuries, 49% (59/119) for gunshot wounds, and 23% (7/30) for stab wounds. The most common venous injuries and the MRs were: inferior vena cava, 59% (33/56) and iliac veins, 65% (10/16). The most common arterial injuries and the MRs were: aorta, 68% (15/22), iliac artery, 57% (12/21), and superior mesenteric artery, 67% (8/12). Of 84 patients who presented to the emergency department (ED) with a blood pressure (BP) less than 70 mm Hg, 60 (71%) died, and of 64 patients with four or more associated injuries, 41 (64%) died. Failure to reduce the duration of shock, amount of bleeding, or severity of hypotension before surgery is highly lethal. Of the 42 patients who had shock for more than 30 minutes, 38 (90%) died. Of the 93 patients who received more than 10 U of blood in the ED and operating room (OR) 60 (64%) died. Of the 60 patients presenting to the OR with a systolic BP less than 70 mm Hg, 52 (87%) died. Prelaparotomy cross-clamping of the thoracic aorta for persistent shock is controversial. However, of the 26 patients with this procedure, 12 responded with a sustained increase in systolic BP greater than 90 with five (42%) survivors. Of the 14 no responders, none survived. Of 17 patients with persistent shock without a prelaparotomy thoracotomy, only one (6%) survived. In the high-risk group (admission systolic BP less than 70 mm Hg and four or more associated injuries), if shock was kept to less than 30 minutes and bleeding to 10 U of blood or less, the MR was reduced from 92% (24/26) to 0% (0/12). In patients presenting to the OR with a BP less than 70, a prelaparotomy cross-clamping of the aorta should be considered. In those patients not responding, prolonged surgical efforts are futile.

Abdominal Injuries↗
PubMed2004

Hypoxia and hypoxia-inducible factor-1 target genes in central nervous system radiation injury: a role for vascular endothelial growth factor.

PURPOSE: Microvascular permeability changes and loss of blood-brain barrier integrity are important features of central nervous system (CNS) radiation injury. Expression of vascular endothelial growth factor (VEGF), an important determinant of microvascular permeability, was examined to assess its role in CNS radiation damage. Because hypoxia mediates VEGF up-regulation through hypoxia-inducible factor-1alpha (HIF1alpha) induction, we studied the relationships of hypoxia, HIF1alpha expression, and expression of VEGF in this damage pathway. EXPERIMENTAL DESIGN: Expression of HIF1alpha, VEGF, and another hypoxia-responsive gene, glucose transporter-1, was assessed in the irradiated rat spinal cord using immunohistochemistry and in situ hybridization. Hypoxic areas were identified using the nitroimidazole 2-(2-nitro-1H-imidazole-L-yl)-N-(2,2,3,3,3,-pentafluoropropyl) acetamide. To determine the causal importance of VEGF expression in radiation myelopathy, we studied the response of transgenic mice with greater (VEGF-A(hi/+)), reduced (VEGF-A(lo/+)), and wild-type VEGF activity to thoracolumbar irradiation. RESULTS: In rat spinal cord, the number of cells expressing HIF1alpha and VEGF increased rapidly from 16 to 20 weeks after radiation, before white matter necrosis and forelimb paralysis. A steep dose response was observed in expression of HIF1alpha and VEGF. HIF1alpha and VEGF expressing cells were identified as astrocytes. Hypoxia was present in regions where up-regulation of VEGF and glucose transporter-1 and increased permeability was observed. VEGF-A(lo/+) mice had a longer latency to development of hindlimb weakness and paralysis compared with wild-type or VEGF-A(hi/+) mice. CONCLUSIONS: VEGF expression appears to play an important role in CNS radiation injury. This focuses attention on VEGF and other genes induced in response to hypoxia as targets for therapy to reduce or prevent CNS radiation damage.

Animals↗