ORTHOPAEDIC COMPLICATIONS

ORTHOPAEDIC COMPLICATIONS
In this session, we will review the high risk orthopaedic complications associated with musculoskeletal injury or that may occur following elective orthopaedic surgery.

Objectives Identify the primary risk factors for orthopaedic complications Discuss the signs/symptoms of orthopaedic complications Describe common treatment for the primary orthopaedic complications Develop a nursing plan of care for specific orthopaedic complications The objectives for this session are: To identify the primary risk factors for orthopaedic complications. To discuss the signs/symptoms of orthopaedic complications. To describe common treatment for the primary orthopaedic complications. To develop a nursing plan of care for specific orthopaedic complications.

Potential Complications
Low Risk Acute Confusion Constipation Impaired Skin Integrity High Risk DVT/PE Compartment Syndrome Fat Emboli Syndrome Hemorrhage Wound/Surgical Site Infection Delayed/Nonunion Per the th edition of the Core Curriculum, there are both low and high risk potential complications for the orthopaedic patient. Low risk complications include acute confusion, constipation and impaired skin integrity. As these are basic complications common to many injured and hospitalized patients, we will not discuss them here. A review can be found in the Core Curriculum for your reference. Rather for the purpose of this session, our focus will be on the High Risk potential complications of: DVT/PE Compartment Syndrome Fat Emboli Syndrome (FES) Hemorrhage Wound or Surgical Site Infection (SSI) Delayed/Nonunion.

Question # 1 DVT prevention requires the nurse to educate the patient on anticoagulant therapy to be alert for : 1. Headache 2. Epistaxis 3. Nausea 4. Chest pain Question # 1. DVT prevention requires the nurse to educate the patient on anticoagulant therapy to be alert for : 1. Headache 2. Epistaxis 3. Nausea 4. Chest pain

Question # 1 DVT prevention requires the nurse to educate the patient on anticoagulant therapy to be alert for : 2. Epistaxis Rationale: The high vascularity of the nose, combined with its susceptibility to trauma (e.g. sneezing, nose blowing) makes it a frequent region for hemorrhage. The other symptoms are usually not associated with anticoagulant therapy.

Venous Thromboembolic Conditions
Virchow’s Triad Endothelial injury Hypercoagulable state Venostasis The first high risk and a major high risk complication for many immobilized or surgical patients is venous stasis. Venous thromboembolic conditions occur based on the triad described by Rudolph Virchow in the 19th century. Virchow’s Triad consists of: Endothelial injury Hypercoagulable state Venostasis.

Deep Vein Thrombosis (DVT)
Formation of fibrin leads to development of a thrombus (fibrin clot) Clinical symptoms appear when thrombus is large enough to impede blood flow in a large vessel Deep Vein Thrombosis (DVT) is well known to nurses. DVT occurs when : Formation of fibrin leads to development of a thrombus (fibrin clot) Clinical symptoms appear when thrombus is large enough to impede the blood flow in a large vessel.

Pulmonary Embolism (PE)
When venous thrombosis or part of a thrombus dislodges from its primary site, it becomes an embolus Embolus can enter pulmonary circulation and perfusion distal to the embolus can be partially or completely occluded Pulmonary Embolism (PE) occurs : When venous thrombosis or part of a thrombus dislodges from its primary site, it becomes an embolus. Embolus can enter pulmonary circulation and perfusion distal to the embolus can be partially or completely occluded.

DVT & PE: Risk Factors Patient related Increasing age Malignancy
Varicose veins Obesity Trauma Prior DVT/PE CHF/CVA Pregnancy Deficiencies in clotting cascade Oral contraceptives The risk factors for DVT and PE include: Increasing age Malignancy Varicose veins Obesity Trauma Prior DVT/PE CHF/CVA Pregnancy Deficiencies in clotting cascade Oral contraceptives

DVT & PE: Risk Factors (continued)
Procedure related Pelvic, hip or leg surgery/ fracture fixation Surgery > 30 minutes Postop immobilization Postop infection Re-operations Additional DVT/PE risk factors can be procedure related such as: Pelvic, hip or leg surgery/fracture fixation Surgery greater than 30 minutes Postoperative immobilization Postoperative infection Re-operation (ex. revisions of THA)

DVT & PE: Risk Factors (continued)
Anesthesia related General anesthesia Nurses are also familiar with the established fact that general anesthesia is a predisposing factor to DVT/PE occurrence.

DVT: Clinical Manifestations
Unilateral swelling of thigh/lower leg Erythema Warmth Tenderness Palpable, tender venous cord in popliteal space Discomfort in leg The clinical manifestations of DVT include: Unilateral swelling of the thigh/lower leg Erythema Warmth Tenderness Palpable, tender venous cord in the popliteal space Discomfort in the leg

DVT: Diagnostics Contrast venography Doppler ultrasonography
Magnetic Resonance Imaging (MRI) Radionuclide venography The most common diagnostics utilized in the diagnosis of DVT are: Contrast venography Doppler ultrasonography Magnetic resonance Imaging (MRI) Radionuclide venography.

PE: Clinical Manifestations
Dyspnea Chest pain Palpitations Apprehension Confusion Anxiety Restlessness Cough Hemoptysis Diaphoresis Syncope Distended neck veins Clinical manifestations of a PE can be observed in patients with any of these presenting symptoms: Dyspnea Chest pain Palpitations Apprehension Confusion Anxiety Restlessness Cough Hemoptpysis Diaphoresis Snycope Distended neck veins

PE: Diagnostics Arterial blood gas (ABG) Chest x-ray (CXR)
Electrocardiogram (EKG) Ventilation-perfusion scan (VQ scan) Pulmonary angiography CT scan PE diagnostics include: ABGs (arterial blood gases) CXR (chest x-ray) EKG (electrocardiogram) VQ scans (ventilation-perfusion scan) Pulmonary angiography CT scan.

DVT & PE: Prevention External pneumatic compression and graduated compression stockings Early ambulation and range of motion Elevation of lower extremities Prevention of DVT and PE are paramount in the nursing plan of care. The most important interventions to be performed or monitored by nurses include: The use of external pneumatic compression devices in conjunction with graduated compression stockings. Early ambulation and range of motion of patients Elevation of lower extremities to reduce edema.

DVT & PE: Prevention (cont.)
Prophylactic inferior vena cava filter Anticoagulation Heparin LMWH (low molecular weight heparin) Warfarin (Coumadin) Continued from previous slide: Prevention of DVT and PE are paramount in the nursing plan of care. The most important interventions to be performed or monitored by nurses include: The administration of anticoagulation Heparin LMWH (low molecular weight heparin) Fragmin Lovenox/Enoxaprin Aggrenox Warfarin (Coumadin).

DVT & PE: Interventions
Full dose anticoagulation with heparin/warfarin (target INR 2-3) Oxygen therapy for PE Thrombolytic therapy urokinase, streptokinase Surgical embolectomy Inferior vena cava filter If a DVT or PE in suspected, common interventions which may be utilized include: Full dose anticoagulation with Heparin/Warfarin, with a target INR of 2-3 Oxygen therapy for PE Thrombolytic therapy of Urokinase/Streptokinase Surgical embolectomy Inferior vena cava filter.

Question # 2 4. Progressive pain on PROM and elevated ESR & WBC
The nurse uses critical thinking to assess an impending compartment syndrome as indicated by which of the following patient presentations? 1. Progressive pain on PROM, paresthesia and diminished pulse 2. Progressive pain on AROM, shiny skin and pulselessness 3. Progressive pain on AROM, increased tissue pressure and edema 4. Progressive pain on PROM and elevated ESR & WBC Question # 2 The nurse uses critical thinking to assess an impending compartment syndrome as indicated by which of the following patient presentations? 1. Progressive pain on PROM, paresthesia and diminished pulse 2. Progressive pain on AROM, shiny skin and pulselessness 3. Progressive pain on AROM, increased tissue pressure and edema 4. Progressive pain on PROM, petechiae and hematoma

Question # 2 The nurse uses critical thinking to assess an impending compartment syndrome as indicated by which of the following patient presentations? 1. Progressive pain on PROM, paresthesia and diminished pulse Question # 2 The nurse uses critical thinking to assess an impending compartment syndrome as indicated by which of the following patient presentations? Progressive pain on PROM, paresthesia and diminished pulse Remember the 5 P’s: Pain on passive stretch, i.e. PROM (passive range of motion) Pallor Pulselessness Paresthesia Paralysis

Compartment Syndrome Compromised circulation and function of tissues within a specific area due to progressive pressure within a confined space Acute, chronic or crush Our next high risk complication is Compartment Syndrome. Compartment Syndrome is defined as compromised circulation and function of tissues within a specific area due to progressive pressure within a confined space. Compartment Syndrome can be either acute, chronic or crush in nature. The human body has 46 anatomic compartments, 38 of those located in the extremities.

Compartment Syndrome: Pathophysiology
Tissue swelling Compression of vessels and nerves Histamine release Capillary dilation Increase in capillary permeability Increased edema Decreased perfusion Increased lactic acid Increased blood flow The pathophysiology of compartment syndrome begins with tissue swelling. This edema leads to compression of vessel and nerves and stimulates the release of histamine. With the increasing pressure in the compartment, capillary dilation results in increased capillary permeability and increasing edema. As compartment syndrome progresses, the decreased perfusion and edema creates an increase in lactic acid and an increased blood flow. This then establishes a cyclic mechanism for the pathophysiology to continually progress this severe and potentially limb-threatening complication.

Compartment Syndrome: Risk Factors
External compression forces Tight cast Tight dressing Prolonged compression Crush injuries Internal factors Bleeding Significant swelling/edema Exertional Compartment Syndrome can be the result of external or internal compression forces. Some examples of external compression forces include: Tight cast Tight dressings (also consider pneumatic anti-shock garments-PASG used during prehospital care) Prolonged compression (also consider prolonged tourniquet times) Crush injuries Venomous snack bites may also result in compartment syndrome. . Some examples of internal factors are: Bleeding (be aware of anticoagulant therapy; hemophilia) Significant swelling/edema (burns) Exertional.

Compartment Syndrome: Risk Factors (continued)
Miscellaneous Acute trauma Fracture Infection Skin traction Tibial nailing Exercise Insensate extremity Additional risk factors for Compartment Syndrome include: Acute trauma Fracture Infection Skin traction Tibial nailing Exercise Insensate extremity.

Compartment Syndrome: Clinical Manifestations
Early signs Increasing pain Pain with passive stretch of muscles Paresthesia Late signs Delayed capillary refill Pale extremity Loss of pulse Paralysis Early signs of Compartment Syndrome can be manifested by: Increasing pain Pain with passive stretch of muscles Paresthesia. Late manifestations of Compartment Syndrome include: Delayed capillary refill Pale extremity Loss of palpable pulse Paralysis.

Compartment Syndrome: 5 Ps
Pain on passive stretch Pallor Pulselessness Paresthesia Paralysis The hallmark of assessing neurovascular status in relation to determining the complication of Compartment Syndrome is through determining the 5 Ps. Pain on passive stretch – Most orthopaedic surgeons state this is the fundamental and most important change to be assessed by the nurse! Pallor – any change in the color of the extremity Pulselessness – A Doppler must be available to use on patients who will undoubtedly have edema following trauma, burns, etc. Paresthesia – should the patient begin to describe this change in sensation, it is imperative to begin intervention; remember this is a limb-threatening complication. Paralysis – We have not done our job as the nurse if this occurs.

Compartment Syndrome: Monitoring
If compartment syndrome is not recognized and pressure is not relieved, muscle damage will be irreversible after 4-6 hours of ischemia, and nerve damage will be irreversible after hours of ischemia. (Janzing et al., 1996) Through the use of a Wick catheter (or a rigged up CVP monitoring device into the muscle compartment if a compartment monitoring device is unavailable), compartment pressures can be monitored on individuals deemed at high risk. Normal compartment pressure is less than 10 mmHG. Per Janzing (1996), if compartment syndrome is not recognized and pressure is not relieved, muscle damage will be irreversible after 4-6 hours of ischemia, and nerve damage will be irreversible after hours of ischemia.

Neurovascular Assessment
Peripheral vascular assessment Color pale/white, pink, dusky, cyanotic, mottled Temperature cool/cold, warm, hot Capillary refill normal < 3 seconds Peripheral pulses distal to injury, bilateral non-palpable: doppler Edema pitting To monitor the 5Ps, the nurse must have a thorough knowledge of neurovascular assessment. The basic components of the peripheral vascular assessment are: Color: pale/white, pink, dusky, cyanotic, mottled Temperature: cool/cold, warm, hot Capillary refill: normal < 3 seconds (say or think capillary refill and that is sufficient time for blanching to occur) Peripheral pulses: distal to the injury, bilaterally, if non-palpable use a Doppler Edema: pitting.

Neurovascular Assessment
Peripheral neurologic assessment Sensation Motor function Both elements evaluate: Upper extremity: radial, median and ulnar nerves Lower extremity: tibial, peroneal, femoral and sciatic nerves The peripheral neurologic assessment incorporates: Sensation Motor function Both elements evaluate Upper Extremity: radial, median and ulnar nerves Lower Extremity: tibial, peroneal, femoral and sciatic nerves.

Compartment Syndrome: Diagnostics
Muscle damage indicated by: Myoglobin in urine Elevated CPK, LDH and SGOT Intracompartmental pressure monitor Pressures of mmHG a concern Diagnosis of Compartment Syndrome is ascertained by monitoring intracompartment pressures, where a pressure of mmHG is of imminent concern as tissue necrosis begins due to poor perfusion. Also monitored is the amount of muscle damage being done which can be measured by the release of myoglobin in the urine. Lab work of CPK, LDH and SGOT also are indicative of muscle damage and can be utilized in the diagnostic process.

Compartment Syndrome: Prevention
Early recognition is key to preventing or minimizing negative outcome Astute nursing intervention to identify pathologic pain in the presence of good pain control (epidural, PCA) The key to Compartment Syndrome is prevention. Early recognition is paramount to prevention or to the minimization of negative outcomes of this complication. Astute nursing interventions to identify the pathologic pain in the presence of good pain management with PCAs, epidurals, etc. is the hallmark of sound critical thinking by the nurse.

Compartment Syndrome: Interventions
Relieve pressure source Remove constrictive dressing Bivalve cast Initiate pain management Elevate extremity at heart level Ongoing neurovascular assessments Fasciotomy if indicated The ongoing progression of a Compartment Syndrome can be halted by numerous interventions, or at least slowed until the need for further intervention is determined. It is important not to use cryotherapy (ice) as the vasoconstriction will further reduce distal perfusion which is already compromised. The most imperative initial intervention is to Relieve the pressure source Remove constrictive dressing Bivalve casts Additional nursing interventions are: Initiate pain management Elevate extremity at heart level – NOT ABOVE Continue ongoing neurovascular assessments Surgical fasciotomy may be indicated to treat progressing Compartment Syndrome. Significant wound care will be subsequently required.

Question # 3 Which nursing assessment finding might suggest the presence of a fat embolism? Ecchymosis Hematoma Petechiae Edema Question # 3 Which nursing assessment finding might suggest the presence of a fat embolism?

Question # 3 Which nursing assessment finding might suggest the presence of a fat embolism? 3. Petechiae Question # 3 Petechiae of skin and mucosa (appear above the nipple line and may or may not blanch, does NOT blanch on approximately 50 % of patients with FES)

Fat Emboli Syndrome (FES)
Mechanical blockage of blood vessels by circulating fat particles Occurs following long bone fracture, pelvic fracture and total hip arthroplasty FES or Fat Emboli Syndrome is our next high risk potential complication. FES is a mechanical blockage of the blood vessels in the lungs caused by circulating fat particles. FES occurs and should be assessed for following long bone fractures, pelvic fracture and total hip arthorplasty.

FES: Pathophysiology Mechanical theory Biochemical theory
Injured adipose tissue and/or disruption of intramedullary compartment releases fat into the blood stream Biochemical theory Fatty acids cause endothelial damage; fatty acids and fats lead to platelet aggregation and fat globule formation There are two theories as to the pathophysiology of FES. The Biochemical theory correlates that fatty acids cause endothelial damage to the lung tissue. The fatty acids combine with fats creating an environment where platelet aggregation can occur and thus fat globule formation begins. The Mechanical theory is based upon injury to both adipose tissue and/or disruption of the intramedullary canal of fractured bones. The environment where intramedullary fat (from bone marrow) and the lack of integrity of the vascular system, affords the opportunity for fat globules to enter the circulation and thus travel to the pulmonary bed.

FES: Clinical Manifestations
Signs and symptoms can appear hours post injury Change in mental status Increased respiratory distress Petechiae of skin & mucosa (appear above nipple line and blanch) FES can often be confused with a PE as the clinical manifestations are very similar. FES is to be suspected when symptoms appear hours following the traumatic injury or THA, These symptoms can include: Change in mental status (restless, confused, anxious, agitated) Increased respiratory distress Petechiae of skin and mucosa (appear above the nipple line and may or may not blanch, does NOT blanch on approximately 50 % of patients with FES)

FES: Diagnostics No specific labs
Fat globules may be detected in blood, urine or sputum PO2 drops to < 50 mmHG CXR with diffuse “snowstorm” effect VQ scan to r/o PE Diagnostics for FES are minimal, as there are very few definitive exams. With no specific labs for definitive diagnosis, the few available diagnostic aids are: Fat globules may be detected in blood, urine or sputum; however these fat globules are not always found PO2 level drops below 50% CXR will show a diffuse “snowstorm” effect – that is the pulmonary bed will appear like a snowstorm due to the multiple fat globules lodged in the pulmonary bed VQ scan should be performed to rule out PE

FES: Interventions Early recognition to prevent morbidity and mortality Minimize movement of long bone fractures Respiratory support Intubation Ventilator management ICU monitoring Interventions for suspected or diagnosed FES focus on respiratory support. Early recognition of FES is paramount to prevent morbidity and mortality. Minimizing movement of long bone fractures during care reduces the risk For patients in need of respiratory support the options may include: Intubation Ventilator management ICU monitoring FES has a 5-15 % mortality.

Question 4A Which indicators are BEST for diagnosing hemorrhage
A) Blood in urine/stool B) Labs (cbc, coagulation studies) C) Radiographic studies

Hemorrhage/Postoperative Bleeding
Etiology Trauma/surgery Slipped ligature Anticoagulation or coagulation disorder Erosion of blood vessel by foreign body or tumor Infection Our next high risk complication is postoperative bleeding or hemorrhage, which is defined as abnormal and excessive loss of blood related to internal or external bleeding. Causes of hemorrhage can arise from: Trauma/surgery Slipped ligature Anticoagulation or coagulation disorder Erosion of blood vessel by foreign body or tumor Infection.

Hemorrhage: Risk Factors
Patient-related Coagulation disorders Low platelet count Excessive coagulation Tumor growth Injury-related Fracture or foreign body interrupts blood vessel Procedure-related Risk factors for hemorrhage can be patient-related, injury-related or procedure related. As you see on this slide, patient-related risk factors consider coagulation disorders, low platelet count, excessive coagulation and tumor growth. Injury-related risk factors focus on a fracture or foreign body that interrupts a blood vessel.

Hemorrhage: Clinical Manifestations
Dizziness Weakness Anxiety Restlessness Confusion Tachycardia Lowered BP Rapid, shallow respirations Pallor Cold, clammy skin Abnormal drainage from wounds or drains Decreased urine output The clinical manifestations of hemorrhage include: Dizziness Weakness Anxiety Restlessness Confusion Tachycardia Hypotension Rapid, shallow respirations Pallor Cold, clammy skin Abnormal drainage from wounds or drains Decreased urine output.

Hemorrhage: Diagnostics
CBC Coagulation studies Urine and stool for blood Radiographic studies To diagnose hemorrhage, lab values are the best clinical indicator. CBC, coagulation studies, urine (dipstick) and stool (occult hematest) samples for microscopic blood loss, and the use of radiology studies to determine the integrity of vascular structures are healthcare standards.

Hemorrhage: Interventions
Direct pressure Surgical intervention as indicated Use of autologous or synthetic clotting material Vitamin K or clotting replacement factors Volume replacement and blood transfusion as necessary Iron supplementation Interventions during hemorrhage are based upon the intensity of the situation. Direct pressure may be necessary in the pre-hospital, ED and OR setting. Use of direct pressure is first line defense in any situation where bleeding is out of control. Surgical intervention may be required to control hemorrhage. Autologous or synthetic clotting factors can be used to augment and stabilize patients. Vitamin K or clotting replacement factors may help to reverse anticoagulation conditions. Volume replacement and blood transfusions may be indicated to sustain life. Includes intraoperative blood salvage and autotransfusions. Once patients are stabilized iron supplementation to correct anemias should be considered.

Question # 4 To prevent nosocomial wound/surgical site infection, the most important intervention the nurse should perform is: 1. Thorough handwashing 2. Aseptic technique with dressing changes 3. Administration of antibiotic 4. Monitoring BP and glucose levels Question # 4 To prevent nosocomial wound/surgical site infection, the most important intervention the nurse should perform is: 1. Thorough handwashing 2. Aseptic technique with dressing changes 3. Administration of antibiotic 4. Monitoring BP and glucose levels

Question # 4 To prevent nosocomial wound/surgical site infection, the most important intervention the nurse should perform is: 1. Thorough handwashing Question # 4 To prevent nosocomial wound/surgical site infection, the most important intervention the nurse should perform is: 1. Thorough handwashing It is imperative that the nurse use thorough handwashing in addition to the other listed nursing activities. Handwashing is the principal mode of breaking the transmission cycle of nosocomial infections.

Wound and Surgical Site Infection (SSI)
Nosocomial surgical site infections occur within 30 days after the operative procedure (within 1 year if an implant is in place) and can involve skin, subcutaneous tissue, deep soft tissues, or actual organs manipulated during the operative procedure. (CDC) Wound and SSI or Surgical Site Infection is the next high risk potential complication for our review. According to the Center for Disease Control (CDC), nosocomial surgical site infections occur within 30 days after the operative procedure or within 1 year if an implant is in place, and can involve skin, subcutaneous tissue, deep soft tissues, or actual organs manipulated during the operative procedure.

Wound/SSI: Risk Factors
Patient characteristics Advanced age Obesity/malnutrition Hypovolemia Diabetes Rheumatoid arthritis Steroid use/NSAID use/chemotherapy Tobacco use Substance abuse Risk factors for wounds/SSI include the following patient characteristics: Advanced age Obesity or malnutrition Hypovolemia Diabetes Rheumatoid arthritis Steroid use/NSAID use/chemotherapy Tobacco use Substance abuse Most of these risk factors are associated with problems with healing related to chronic conditions.

Wound/SSI: Intrinsic Risk Factors
Injury characteristics Bone displacement, comminution Periosteal stripping Involvement of more than one bone Vascular injury Significant soft tissue injury Open fracture/foreign body/contamination In musculoskeletal injury there are a few specific intrinsic risk factors related to wounds or SSI. These include: The amount of bone displacement or comminution at the time of the injury. The amount of periosteal stripping at the fracture site. The number of fractures, with more fractures requiring more healing time. The extent of vascular injuries which could reduce blood supply to a healing area. The amount of significant soft tissue injury and thus severe contusions in a wound/SSI area. The most significant factor: the number of open fractures and the amount of foreign body or wound contamination that occurred at the time of initial injury.

Wound/SSI: Extrinsic Risk Factors
Preoperative Inadequate immobilization of fractured bone Preoperative shave > 1 day prior to surgery Duration of preoperative hospitalization Intraoperative Hair removal Positive intraop contamination Irrigation, drains, packing Primary/secondary closures Type and length of procedure Surgeon expertise Glove punctures As healthcare professionals, the extrinsic risk factors in the pre-intra-and post operative periods are within our control and significantly impact the formation of wound/SSI infections. Preoperative risk factors: Inadequate immobilization of fractured bone Preoperative shave > 1 day prior to surgery Duration of preoperative hospitalization (this may be due to other systemic traumatic injuries) Intraoperative risk factors: Hair removal Positive intraop contamination Irrigation, drains, packing Primary/secondary closure Type and length of procedure Surgeon expertise Glove punctures

Wound/SSI: Extrinsic Risk Factors
Postoperative Cold room (vasoconstriction) Insufficient fluid replacement Hypertension Inadequate analgesia Compromised blood perfusion Low oxygenation Postoperative risk factors include: Cold room (vasoconstriction) – always in the OR and PACU Insufficient fluid replacement Hypertension Inadequate analgesia Compromised blood perfusion Low oxygenation

Wound/SSI: Clinical Manifestations
Increased pain Fever or chills Malodor from incision or wound Edema Increased temperature around incision or wound Erythema around wound or incision Purulent exudate, poor wound healing Elevated WBC, ESR, C-reactive protein Wound/SSI are manifested in the clinical setting by: Increased pain Fever or chills Malodor from the incision or wound Erythema around the wound or incision Edema Increased temperature around the incision or wound Purulent exudate Poor wound healing Elevated WBC, ESR, C-reactive protein

Wound/SSI: Prevention
Preoperative Control hypertension and blood sugar Minimize unnecessary movement of fractures Treat existing infections Replenish nutritional deficits Prevent vasoconstriction Intraoperative Antimicrobial prophylaxis Strict aseptic technique Meticulous tissue debridement Stabilize fractures Avoid vasoconstriction Gently handling of soft tissue Wound closure without excessive tension Prevention of wound/SSI complications can be aided in the preoperative period by: Controlling hypertension and blood sugar levels Minimizing unnecessary movement of fractures Treating existing infections aggressively Replenishing nutritional deficits Preventing vasoconstriction occurrence. Intraoperative prevention is aided by: Antimicrobial prophylaxis Strict adherence to aseptic technique Meticulous tissue debridement Stabilization of fractures Avoiding vasoconstriction Gently handling soft tissue Wound closure without excessive traction/tension.

Wound/SSI: Prevention
Postoperative Provide adequate analgesia Avoid vasoconstriction Control BP and BS Provide for adequate nutrition Aseptic dressing changes Microbial therapy Thorough handwashing Post-operative wound/SSI prevention is aided by: Provision of adequate analgesia Avoidance of vasoconstriction Controlling blood pressure and blood sugar levels Providing adequate nutrition Adherence to aseptic dressing changes Administering microbial therapy Thorough handwashing

Wound/SSI: Interventions
Wound care Systemic antibiotics Adequate perfusion Adequate oxygenation Optimal nutritional intake If a wound or surgical site infection does occur, the most commonly employed treatment interventions are: Meticulous wound care, including extensive debridement and wound irrigation Administration of systemic antibiotics Maintenance of adequate perfusion Maintenance of adequate oxygenation Maintaining optimal nutritional intake.

Question #5 A fracture that isn’t healing is considered to be a non union (as opposed to a delayed union) fracture after how long? 6-12 weeks 8-14 weeks 16-24 weeks 28-36 weeks

Delayed Union/Nonunion
Delayed union is a continuation of or increase in bone pain and tenderness beyond a reasonable healing period; healing is slowed but not completely stopped Nonunion occurs when fracture healing has not taken place 4-6 months after the fracture occurs and spontaneous healing is unlikely (Morris, 2001) The final high risk potential complication is also related to healing of fractures. Delayed union is defined as a continuation of or an increase in bone pain and tenderness beyond a reasonable healing period. In delayed union, healing is slowed but not completely stopped. Non union is defined when fracture healing has not taken place 4-6 months after the fracture occurred and spontaneous healing is unlikely.

Delayed Union/Nonunion
Pathophysiology Infection Inadequate fracture immobilization Inadequate blood supply to fracture site Diagnostics Serial x-rays CT scans MRI The pathophysiology for delayed union/nonunion can be attributed to: Infection Inadequate fracture immobilization Inadequate blood supply to the fracture site. The basic diagnostics utilized are: Serial x-rays (to ascertain callus formation) CT scans MRI

Delayed Union/Nonunion: Interventions
Bone grafting Internal fixation External fixation Electrical bone stimulation The primary interventions to aid in delayed union or nonunion are: Bone grafting – often taken from the iliac crest Internal fixation – especially if casting was the primary intervention for fracture fixation External fixation – dependent upon muscle loss and infection at the site; vascular supply must be intact Electrical bone stimulation – to prompt bone healing