Introduction: Surge capacity for optimization of access to hospital beds is a limiting factor in response to catastrophic events. Medical facilities, communication tools, manpower, and resource reserves exist to respond to these events. However, these factors may not be optimally functioning to generate an effective and efficient surge response. The objective was to improve the function of these factors.

Methods: Regional healthcare facilities and supporting local emergency response agencies developed a coalition (the Healthcare Facilities Partnership of South Central Pennsylvania; HCFPSCPA) to increase regional surge capacity and emergency preparedness for healthcare facilities. The coalition focused on 6 objectives: (1) increase awareness of capabilities and assets, (2) develop and pilot test advanced planning and exercising of plans in the region, (3) augment written medical mutual aid agreements, (4) develop and strengthen partnership relationships, (5) ensure National Incident Management System compliance, and (6) develop and test a plan for effective utilization of volunteer healthcare professionals.

Results: In comparison to baseline measurements, the coalition improved existing areas covered under all 6 objectives documented during a 24-month evaluation period. Enhanced communicationsbetween the hospital coalition, and real-time exercises, were used to provide evidence of improved preparedness for putative mass casualty incidents.

Conclusion: The HCFP-SCPA successfully increased preparedness and surge capacity through a partnership of regional healthcare facilities and emergency response agencies. [West J Emerg Med. 2012;13(5):445–452.]

In multiple sclerosis, in which brain tissue becomes permeable to blood proteins, extravascular fibrin deposition correlates with sites of inflammatory demyelination and axonal damage. To examine the role of fibrin in neuroinflammatory demyelination, we depleted fibrin in two tumor necrosis factor transgenic mouse models of multiple sclerosis, transgenic lines TgK21 and Tg6074. In a genetic analysis, we crossed TgK21 mice into a fibrin-deficient background. TgK21fib(-/-) mice had decreased inflammation and expression of major histocompatibility complex class I antigens, reduced demyelination, and a lengthened lifespan compared with TgK21 mice. In a pharmacologic analysis, fibrin depletion, by using the snake venom ancrod, in Tg6074 mice also delayed the onset of inflammatory demyelination. Overall, these results indicate that fibrin regulates the inflammatory response in neuroinflammatory diseases. Design of therapeutic strategies based on fibrin depletion could potentially benefit the clinical course of demyelinating diseases such as multiple sclerosis.