Acute Respiratory Distress Syndrome, Fat Embolism, &

Thromboembolic Disease in the Orthopaedic Trauma Patient

Steve Morgan, MD

Objectives

Define ARDS FES Thromboembolic

Disease Understand Etiology

& Physiology of each Condition

Understand Prevention Diagnosis Treatment Outcomes

ARDS

Acute respiratory failure in the post traumatic period characterized by a decreased PaO2 and a diffuse and often massive extravasation of fluid from the pulmonary vasculature to the interstitial space of the lungs.

ARDSCommon Causes

Trauma Massive Transfusion Embolism Sepsis Aspiration Abdominal Distension

Pulmonary Edema Prolonged LOC Cardiopulmonary

Bypass Pancreatitis Major Burns

MULTIFACTORAL

ARDS Etiology

ARDS related to MSOF

Release of inflammatory mediators results in organ dysfunction

Trauma InflammatoryMediators

OrganInjury

ARDS PATHOPHYSIOLOGY

Systemic Inflammatory Mediators

Damage to Endothelial Lining

Increased Capillary Permeability

Fluid Extravasation

Alveolar Collapse Decreased Pulmonary

Compliance Ventilation Perfusion

Abnormalities Arteriolar Hypoxemia

ARDS Chest Radiograph

ARDS Chest CT Scan

ARDSPrevention

Limiting Blood Loss Decreasing Transfusion Requirements Early Fixation Of Unstable Fractures Early Prophylactic Mechanical Ventilation

ARDS Treatment

Ventilator Support Goals

Acceptable ABGs Prevent alveolar damage Facilitate healing Non-toxic FIO2 (< .60)

Research Optimal ventilator settings

ARDSOutcome

Significant Cause of Mortality Major Cause of Death in Patients with the

Lowest ISS scores 40% - 50% Mortality Rate

Mortality Rate Slowly Decreasing with Changing & Improving Therapy

Fat Embolism Syndrome(FES)

A Causative Factor In ARDS

Occurs Following A Long Bone Fracture

Characterized by: Hypoxia Mental Confusion Petechial Rash

FES

Unanticipated Respiratory Distress Diagnosis of Exclusion Often Placed in The Category of ARDS R/O other Causes of Hypoxia

Pulmonary Contusion ARDS Pneumonia

Etiology

Mechanical

Biochemical

No simple etiology

Mechanical Etiology

Fracture Liberates Fat

Intravasation - Fat Enters Venous System

Fat Causes Mechanical Obstruction

Mechanical Etiology

Systemic Fat Embolization

Patent Foramen Ovale

Pulmonary Pre-Capillary Shunts

FES To Brain On MRI

Biochemical Etiology

Chemical Mediators Released @ time of Fracture

Fat Released at Time of Fracture Fat Metabolism by Lipase releases Free

Fatty Acids Free Fatty Acids Result in Endothelial Lung

Damage

Gurd et al

FES Diagnosis

Major Criteria Hypoxemia CNS Depression Petechial Rash Pulmonary Edema

Minor Criteria Tachycardia Pyrexia Retinal Emboli Fat in Urine Fat in Sputum Thrombocytopenia Decreased Hematocrit

Gurd et al

FES Diagnosis

1 Major Criteria

4 Minor Criteria

FES Treatment

Supportive

Oxygen Therapy to maintain PaO2

Mechanical Ventilation

FES Treatment Steroids

Decrease endothelial damage 30mg/kg initial dose repeated @ 4 Hours, 1gm

dose repeated @ 8 Hours: Total 3 Doses Complications - Frequent

Infection GI

Steroid Therapy Avoided Secondary To Poor Risk Benefit Ratio

FES Prevention

Therapies Fluid Loading Hypertonic Fluid Alcohol Heparin Dextran Aspirin

Not Shown to be Effective

FES Prevention

Appropriate Splinting

Early Fracture Stabilization

Oxygen Therapy

Timing of Fracture Fixation

Early Fracture Fixation Optimal

Decreases Pulmonary Complications

Delayed Fracture Fixation Increased Pulmonary Dysfunction

Type of Fracture Fixation-Controversial-

IM Nail - Reamed vs Un-Reamed Increased Pulmonary Dysfunction With Reamed

technique Decreased with Unreamed Technique

Pape et al

IM Nail Reamed vs Plate Osteosynthesis No Difference In Pulmonary Dysfunction

Bosse et al

Effect of IM Nailing

Canal Opening Reaming Nail Insertion Unreamed Nail Insertion

All Cause Increased IM Pressure All Cause Embolic Showers On

Echocardiograms

Systemic Effects of Trauma

Injury12 hours 24 hours

PostinjuryInflammatoryResponse

Second Insult

MOF

IM Nailing As A cause of Secondary Systemic Injury

DVT Incidence

DVT occurance 60% if ISS >9.

35%-60% DVT in pelvic fracture

PE-Most common preventable cause of death in trauma.

Virchow Triad

Hypercoaguability

Tissue Thromboplastin Activated Procoagulants Decreased Fibrinolytic Activity Ineffective Heparin Clearance of Activated

Clotting Factors Catecholamine Release

Endothelial Injury

Direct Trauma to Vein @ time of Injury Compression of the Vein Secondary to

Fracture Position Vein Manipulation @ Time of Fracture

Fixation

Venous Stasis

Immobilization Hypotension Venous Occlusion

Edema Fracture Position

DVT Prevention

Goals Clinically significant events

PE Post Thrombotic syndrome

Low Complication Rate High Compliance Rate Cost Effective

DVT Prevention

Prophylaxis

Elastic Stockings Mechanical

Compression Devices

Inferior Vena Cava Filter (IVC)

Heparin Warfarin Low Molecular

Weight Heparin Aspirin

Mechanical Methods Activity Compression

Stockings Sequential

Compression Device Pedal PumpsMechanism of Action Decrease Stasis Fibrinolytic Activity

IVC Filter Indications

Anticoagulation Prohibited

High Risk Patients DVT Prior to

Necessary Surgery PE Despite

Anticoagulation

IVC Filter

Prevents Major PE Low Morbidity

96% Patent 8% Migration 4% PE

Filter insertion in the ICU

Expensive Invasive Does not treat DVT Venous Insufficiency Filter Occlusion Permanent

Advantages Disadvantage

Heparin

Heparin Potentiates Anti-Thrombin III Activity

Complex Inhibits Thrombin (IIa), IXa, Xa

Heparin effect relative short duration Reversed with Protamine Sulfate

Significant hemorrhage risk

SQ Heparin

Low Cost No Monitoring Convenient Relatively Low

Incidence of Bleeding

Insufficient Efficacy in High Risk Patients

Unpredictable Responses

Heparin Induced Thrombocytopenia

Advantages Disadvantage

Low Molecular Weight Heparin(LMWH)

Potentiates Antithrombin III Specific for Factor Xa Minimal effects on other Factors

LMWH

No Monitoring Increased Efficacy Longer 1/2 life Predictable

Response Lower risk of

thrombocytopenia

Parenteral Administration

Cost

Advantages Disadvantage

Aspirin

Inhibits cyclooxygenase Decreases Platelet Adherence

? Effectiveness in Musculoskeletal Trauma Venous clots not typically found to have

Platelet aggregates

Aspirin

Oral Administration Tolerated well In-expensive No Monitoring

? Efficacy when used alone

GI Intolerance Prolonged anti-platelet

effect

Advantages Disadvantage

Warfarin

Blocks Vit K conversion in Liver Effects Vit K Dependent Factors Effects the Extrinsic Clotting System Factor VII Effected first, Short Half Life Monitored with Pro-Time

INR 2.0-2.5 Reversed With Vitamin K or FFP

Warfarin

Effective Oral Administration Inexpensive

Requires Monitoring Difficult to Reverse Increased Bleeding

Complications in Elderly

Advantages Disadvantage

DVT screening

Physical Exam Ascending venography Duplex Ultrasonography Magnetic Resonance Venography

Physical Examination

Calf Swelling Palpable Venous Cords Calf Pain Homans Sign

All Unreliable

Ascending Contrast Venography Sensitive for detection Invasive Dye Problems

(allergies, renal) Injection Site Irritation Poor Pelvic Vein

Evaluation

Gold Standard*Invasiveness,expense make ACV a poor screening tool

Doppler/Duplex Ultrasound

Comparable to Venogram Non Invasive No Morbidity Poor Axial (i.e Pelvic)

Vein Evaluation Operator Dependent Good Screening Tool

Noninvasive, reproducible

Magnetic Resonance Venography Non Invasive Good Visualization of

Pelvic Veins Difficult in Polytrauma

Patient Excellent specificity and

sensitivity for suspected DVT

Controversial for screening

Pulmonary Embolism

ClinicalShortness of breath, agitation, confusion

Laboratory PaO2, A-a gradient

Diagnostic studiesV/Q scansPulmonary Angiogram

Ventilation Perfusion Scan

Ventilation Perfusion mismatch Results

Low probabiltity 15% False Negative

Medium Need Angiogram

High probability 15% False Positive

Screening Tool

Pulmonary Angiogram Angiographic Evaluation of

pulmonary vascular tree

Allows Placement of IVC Filter in same setting if indicated

Sensitive - Standard in PE Detection. Diagnostic

Treatment PE Anticoagulation

Filter for recurrent event despite anticoagulation

Thrombectomy Serious Acute PE Patient in extremous Large identifiable PE

Treatment DVT/PE Heparin

Bolus 10-15K units Continuous Infusion

1000Units/Hr Goal PTT 2x Control

Prevent Clot propagation and recurrent PE

Discontinue when Therapeutic on Wafarin

Warfarin INR 2.0-3.0 3-6 Month Duration Contraindicated in:

Pregnancy Liver insufficieny Poor Compliance

Prolonged Therapy may decrease recurrence rates (6 mos)

DVT/PE Outcome

No Diagnosis and Treatment 30% Mortality

Correct Diagnosis and Therapy 11% Mortality in First Hour 8% Mortality After First Hour

DVT/PE Outcome

Post Thrombotic Syndrome Valvular Incompetence Venous Stasis Edema Cutaneous Atrophy

Recurrent DVT 20% of Patients

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