Complications of Fracture

FRACTURE
Injury of the extremity (long bone) whether caused by penetrating or blunt trauma as high risk for fracture complications

COMPARTMENT SYNDROME begins with: contusion and hemorrhage within a space defined & limited by a fascia envelope produce an increased interstitial tissue pressures intracompartmental structures cannot withstand the infinite pressure introduction of excess fluid of extraneous constriction increases pressure & reduces tissue perfusion (until no O2 is available for cellular metabolism) elevated perfusion pressure occurs in response to rising intracompartmental pressure autoregulatory mechanisms are overwhelmed and a cascade of injury develops capillaries collapse when venous pressure is higher than capillary perfusion pressure blood flow to capillaries stops End result: loss of extremity, RENAL FAILURE (if condition becomes severe and left untreated), or loss of LIFE in the absence of flow, O2 delivery stops hypoxic injury causes cells to release vasoactive substances (e.g., histamines, serotonin)

nerve conduction slows, tissue pH falls due to anaerobic metabolism, surrounding tissue suffers further damage, and muscle tissue suffers necrosis, releasing myoglobin

endothelial permeability increases capillaries allow continued fluid loss, which increases tissue pressure and advances injury

Continued

FRACTURE
Injury of the extremity (long bone) whether caused by penetrating or blunt trauma as high risk for fracture complications

FAT EMBOLISM

3 Postulates:

Mechanical theory

Hormonal response

Metabolic response

after mechanical trauma pressure in long bones that have high fat content is elevated the veins within the bones are prevented from collapsing because they adhere to the bony framework fat droplets are forced into the bloodstream through the open veins

catecholamine & corticosteroid are released as response to stress act on serum lipids to mobilize tissue stores of fats that act as emboli after their release into the circulation

fat droplets arise within circulated blood as a result of metabolic response to injury stability of bodys emulsified fat (neutral triglycerides & phospholipids) is lost small fat particles coalesce and form microglobules

fat droplets/fat globules travel through arteriovenous shunts to the BRAIN

produces local ischemia and inflammation [(+) decreased cerebral blood flow] NEUROGENIC SHOCK Manifestations: mental status changes varying from headache and mild agitation to delirium and coma

fat droplets/fat globules may be dislodged in the blood vessels to the HEPATIC area local ischemia and inflammation
LIVER FAILURE

fat droplets/fat globules may be dislodged in the blood vessels to the

RENAL structure

fat droplets/fat globules may occlude

PULMONARY

circulation parenchymal damage and increased pulmonary vascular resistance edema and hemorrhage in the alveoli impairs O2 transport leading to hypoxia ABG alteration, early respiratory alkalosis then later

fat droplets/fat globules may be dislodged in the blood vessels supplying the
HEART

local ischemia and inflammation acute tubular necrosis

RENAL FAILURE Manifestation: (+) free fat in the urine (emboli are filtered by renal tubules)

MYOCARDIAL INFARCTION

ensues if severe and untreated

CARDIOGENIC SHOCK

reduced venous return reduced stroke volume decreased cardiac output

as acidosis, snowstorm infiltrate as shown by CXR

ACUTE PULMONARY EDEMA, ACUTE RESPIRATORY DISTRESS SYNDROME, and HEART FAILURE

may ensue without prompt, definitive management

Continued

FRACTURE
Injury of the extremity (long bone) whether caused by penetrating or blunt trauma as high risk for fracture complications

SHOCK

AND/OR traumatic damage to a large artery or vein that supplies due to trauma, patient may form a pseudoaneurysm (a blood hole in an artery that is a contained hematoma)

hemorrhage (both visible and nonvisible blood loss) and loss of intravascular volume into the interstitial space

gets bigger and bigger

ruptures

causes delayed hemorrhage

when initial clot lyses in about 48 hours, patient may start to bleed severely

HYPOVOLEMIC SHOCK

Continued

FRACTURE

AVASCULAR NECROSIS

REACTION TO INTERNAL FIXATION DEVICES

DELAYED COMPLICATIONS

DELAYED UNION due to fracture, especially of femoral neck disruption of blood supply bone loses its blood supply and eventually dies the devitalized bone may collapse or reabsorb Manifestations: X-rays show loss of mineralized matrix and structural collapse patient develops pain and experiences limited movement Interventions: revitalization with bone grafts, prosthetic replacement, or arthrodesis (joint fusion) due to: a. mechanical failure (inadequate insertion and stabilization) b. material failure (faulty or damaged device) c. corrosion of the device, causing local inflammation d. allergic response to the metallic alloy used e. osteoporotic remodeling adjacent to the fixation device (in w/c stress needed for bone strength is transferred to the device, causing a disuse osteoporosis) pain and decreased function as prime indicators if the device is removed, the bone needs to be protected from: refracture related to osteoporosis, altered bone structure, and trauma bone remodeling reestablishes bones structural strength associated with: a. distraction (pulling apart) of bone fragments b. systemic or local infection c. poor nutrition d. comorbidi ty (e.g., DM, autoimmu ne disease) healing does not occur at a normal rate for the location and type of fracture (+) fracture eventually heals

MALUNION

NONUNION

factors: >infection at fracture site >interposition of tissue between bone ends >inadequate immobilization or manipulation that disrupts callus formation >excessive space b/n bone fragments (bone gap) >limited bone contact >impaired blood supply resulting in AVN failure of the ends of the fractured bone to unite in a normal alignment

factors: >infection at fracture site >interposition of tissue between bone ends >inadequate immobilization or manipulation that disrupts callus formation >excessive space b/n bone fragments (bone gap) >limited bone contact >impaired blood supply resulting in AVN commonly occurs with fractures of middle third of humerus, lower third of tibia, and neck of femur in the elderly

patient complains of persistent discomfort and abnormal movement at fracture fibrocartilage or site fibrous tissue exists between bone fragments; no bone salts deposited a false joint (pseudoarthrosis) often develops at fracture site

- - FIN - Prepared by: CERIACO, Chedan Saint Louis University College of Nursing, Baguio City BSN III References: Brunner & Suddarths Textbook of Medical-Surgical Nursing-11th edition by Suzanne C. Smeltzer (et. al.) www.emedicine.com