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Complications of Fracture
 begins with: contusion and hemorrhagewithin a space defined & limited by afascia envelope produce an increasedinterstitial tissue pressuresintracompartmental structures cannotwithstand the infinite pressureintroduction of excess fluid of extraneousconstriction increases pressure & reducestissue perfusion (until no O2 is available for cellular metabolism)elevated perfusion pressure occurs inresponse to rising intracompartmental pressureautoregulatory mechanisms are overwhelmedand a cascade of injury developscapillaries collapse when venous pressureis higher than capillary perfusion pressure blood flow to capillaries stopsEnd result: loss of extremity,
RENAL FAILURE
(if condition becomes severe and left untreated), or loss of LIFEin the absence of flow, O2 delivery stopshypoxic injury causes cells to release vasoactivesubstances (e.g., histamines, serotonin)nerve conduction slows, tissue pH fallsdue to anaerobic metabolism, surroundingtissue suffers further damage, and muscletissue suffers necrosis, releasing myoglobinendothelial permeability increasescapillaries allow continued fluid loss,which increases tissue pressure and advances injury
 
FRACTURE
Injury of the extremity (long bone) whether caused by penetrating or blunt trauma ashigh risk for fracturecomplicationsCOMPARTMENTSYNDROME
 
Continued…
after mechanical trauma pressurein long bones that have high fatcontent is elevatedthe veins within the bones are prevented from collapsing becausethey adhere to the bony framework fat droplets are forced into the bloodstream through the open veinscatecholamine & corticosteroid arereleased as response to stressact on serum lipids to mobilizetissue stores of fats that act asemboli after their release into thecirculation
 
fat droplets arise within circulated blood as a result of metabolicresponse to injurystability of body’s emulsified fat(neutral triglycerides & phospholipids) is lostsmall fat particles coalesce andform microglobulesfat droplets/fatglobules travelthrougharteriovenous shuntsto the
BRAIN produces localischemia andinflammation [(+)decreased cerebral blood flow]
NEUROGENICSHOCK 
Manifestations:
mental statuschangesvarying fromheadache andmild agitationto deliriumand coma
fat droplets/fatglobules may bedislodged in the blood vessels to the
HEPATIC
arealocal ischemia andinflammation
LIVER FAILURE
ensues if severe anduntreatedfat droplets/fatglobules may bedislodged in the blood vessels to the
RENAL structure
local ischemia andinflammationacute tubular necrosis
RENAL FAILURE
Manifestation:
(+) free fat inthe urine(emboli arefiltered byrenal tubules)
fat droplets/fatglobules mayocclude
PULMONARY
circulation parenchymaldamage andincreased pulmonary vascular resistanceedema andhemorrhage in thealveoliimpairs O2 transportleading to hypoxiaABG alteration,early respiratoryalkalosis then later fat droplets/fatglobules may bedislodged in the blood vesselssupplying the
HEART
MYOCARDIALINFARCTIONCARDIOGENICSHOCK 
reduced venousreturnreduced strokevolumedecreased cardiacoutput
FRACTURE
Injury of the extremity (long bone)whether caused by penetrating or  blunt trauma as high risk for fracturecomplications
FAT EMBOLISM3 Postulates:Mechanical theoryHormonal responseMetabolic response
 
as acidosis,“snowstorminfiltrate” as shown by CXR 
ACUTEPULMONARYEDEMA, ACUTERESPIRATORYDISTRESSSYNDROME, andHEART FAILURE
may ensue without prompt, definitivemanagement
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