Compartment Syndrome Causes & Pathophysiology - Everything You Need To Know - Dr. Nabil Ebraheim скачать в хорошем качестве

Compartment Syndrome Causes & Pathophysiology - Everything You Need To Know - Dr. Nabil Ebraheim

Educational video describing the causes and pathophysiology of compartment syndrome. my new book about compartment syndrome https://www.amazon.com/dp/B0C51X2CWB?... Increased pressure to 30 mmHg OR WITHIN 30 mmHg of diastolic blood pressure will lead to impending compartment syndrome. If the elevated pressure is not relieved within 6-8 hours, irreversible damage to the contents of the compartment will occur. Initiating event: force edema-hemorraheg accumulation-elevated compartment pressure venous obstruction- further elevation of compartment pressure- arteriolar pressure is exceeded- loss of capillary exchange- muscle ischemia/infarction nerve damage- irreversible damage to content of the compartment, tissue ischemia and necrosis. Blood flow reduction theory The reduction of blood flow occurs due to obstruction of the small vessels. This will lead to ischemia, necrosis, irreversible damage to the limb and possible systemic conditions resulting from traumatic rhabdomyolysis and reperfusion injury. Resting compartment pressure is higher in children than in adults. Muscle and nerve changes •Within the first 3-4 hours of compartment syndrome, muscular changes are still reversible. •After 6 hours, there is clear muscle damage that varies. •After 8 hours of established compartment syndrome, irreversible changes have occurred to the muscles. •Within the first 2 hours, there is loss of nerve conduction. •After 4 hours, neuropraxia develops. The nerve survive, but no longer transmit impulses. •After 8 hours, there is total axontemesis and secondary scar. If compartment syndorme progresses to this stage, irreversible changes occur to the nerves. P and ischemia There is general relationship between the perfusion pressure gradient (P) and ischemic muscle damage. At 20 mmHg below diastolic blood pressure, blood flow is reduced but phosphocreatine stores are unaffected, allowing the muscle to survive up to 8 hours. Once pressure reaches a P of 10 mmHg, however both local blood flow and phosphocreatinine stores disappear, csuing severe necrosis. Muscle fiber types: muscle vulnerability to ischemia varies according to the muscle type •Type I: red slow twitch fibers. More vulnerable to ischemia as they depend on oxidative metabolism of triglycerides e.g muscles of the anterior compartment. •Type II: white fast-twitch fibers. Less vulnerable to ischemia as they depend on anaerobic metablosim e.g gastrocnemius muscle. Reperfusion injury It occurs after reestablishment of the blood flow to ischemic tissues following fasciotomy. There will be more swelling of the muscles due to inflammatory response that results from the release of the break down product of the injured muscles. This will lead to damage of vascular endothelium, increased vascular permeability and swelling. Become a friend on facebook:   / drebraheim   Follow me on twitter: https://twitter.com/#!/DrEbraheim_UTMC