1. Ch 17. Systemic complications DEEP VENOUS THROMBOSIS

2.  Geerts et al: ~60% trauma patient  deep venous thrombosis  Diagnosis, prophylaxis, treatment

3.  silent thrombi  symptomatic deep venous thrombosis  pulmonary embolism  death from pulmonary embolism

4.  2/3 patient: die of pulmonary embolism survive < 20 minutes from the onset of symptoms  prevent

5.  incidence of death from pulmonary embolism: 1% ~ 2%  effective treatment in reducing the rate of fatal pulmonary emboli ??  no randomized prospective studies  treatment / prophylaxis

6. Vessel well damage Time of injury Venous stasis immobilization Hyper- coagulability Genetic mutation (family history Asians ↓↓ Northern Europeans ↑↑ Virchow

7.  Clinical findings: pain, swelling, tenderness: not reliable for DVT diagnosis (70% false positive)  Impedance plethysmography (IPG)( 電阻 體積描記器 ) X  Fibrinogen leg scanning X

8.  Venography: invasive, difficult to perform, more accurate for calf thrombi and nonocclusive/asymptomatic DVT  Venous doppler/ultrasonography: more accurte, available Specificity: 95% for femoral Sensitivity: 70% for calf veins Repeat/routine exam: not cost-effective

9.  D/US: for lower extremity thrombi  Pelvic thrombi: difficult to detect by D/US, CT, MRI

10. Pulmonary embolism  Transient dyspnea  Chest pain  Hemoptysis  Larger occlusive emboli  Symptoms of right side heart failure / syncope / hypotension  D.D.: pulmonary infection, musculoskeletal chest wall pain, pericarditis, esophageal spasm, anxiety

11.  Chest radiography  Electrocardiogram  Oxygenation (oximetry / gas)  70% of patient with PE: have evidence of venous thrombosis ←→ < 50% patients have PE with lower extremity D/US studies positive

12.  Pulmonary angiography: gold standard  normal pulmonary angiogram: excludes the diagnosis  normal perfusion scan: excludes PE  more specific than ventilation-perfusion scans of the lung

13.  ~1995  CT pulmonary angiogram: most frequently sensitivity and specificity: 90% for identifying central PE (main, lobar, segmental arteries)

14.  venous thromboembolism, risk of recurrence: 5% to 10% per year  prevention of the first episode with prophylactic strategies  risk of recurrent: higher among men than women (20% vs. 6%)

15. prophylaxis for preventing deep venous thrombosis Graduated stockings Pneumatic compression devices Vena caval filters Mechanical Heparin LMWH Warfarin Pentasaccharides Pharmacologic modalities

16. Mechanical prophylaxis  Graduated compression stockings / Intermittent compression devices (IPC) low patient compliance lower extremity fractures  risk of pulmonary embolism or death: X  As an adjutant to pharmacologic anticoagulation / patients who have a high risk of bleeding

17.  inferior vena cava filters: prevention of fatal pulmonary embolism in trauma patients  Indication: contraindications to anticoagulation developed venous thrombosis despite anticoagulation head injuries, multiple long bone fractures, pelvic and acetabular fractures, patients that have evidence of deep venous thrombosis before a major surgical procedure  increased risk for recurrent deep venous thrombosis  retrievable vena cava filters  anticoagulation therapy

18.  use of systemic heparinization within the first week after THR: 50% wound complication rate from hematoma formation  Contraindications to the use of pharmacologic anticoagulation: associated intracranial bleeding, spinal cord injuries, the observation of splenic injuries, any injury that has a high risk of developing recurrent bleeding

19.  intracranial injury: contraindication to the use of anticoagulation   using mechanical devices or repetitive screening to avoid worsening of the intracranial injury   vena caval filters (high risk for thromboembolism)  Removable vena caval filters: OK

20. Pharmacologic anticoagulation  mortality rate from pulmonary embolism for patients with hip fractures: 1% to 2%  after fixation of proximal femur fractures  pharmacologic prophylaxis: recommended  Fractures distal to the hip: 18% incidence of deep venous thrombosis  Factors associated with thrombi: age older than 40, a delay to surgery, prolonged operative times

21.  ideal agent: low complication rate, easy administration, low cost, and excellent bioavailability  Coumadin / LMWH: several prospective and randomized studies of deep venous thrombosis after total hip replacement: LMWH reduce the incidence of silent thrombi

22.  differing forms of prophylaxis for venous thromboembolism ?? patient's risk factors injuries surgery period of postoperative immobilization

23. OUTCOME OF CRITICAL ILLNESS ASSOCIATED WITH ORTHOPEDIC TRAUMA  short-term mortality (for example, intensive care unit, 28 day, hospital mortality)  long-term outcomes, including delayed mortality, quality of life (QOL) in survivors, and the social effects on caregivers, including family members

24. Pain  common complaint after prolonged critical illness, significantly impairing QOL  50 patients from a mixed intensive care unit (ICU) with tracheotomy for prolonged critical illness 44% of patients: pain at the highest level of severity survive the acute phase  prolonged chronic critical illness  having at least three components: injury or illness and host characteristics leading to critical illness and ICU admission ICU period of critical illness subsequent periods of post-ICU care, including hospital ward, intermediate care and rehabilitation, and outpatient care

25. ARDS  common complication of trauma and sepsis  severe and prolonged critical illness  improvement in mortality  significant impairments in physical, psychologic, and social functioning  Sepsis with ARDS QOL < trauma with ARDS  pulmonary function: improves significantly during the first 6 months illness

26. Neuromuscular weakness  more common  109 survivors identifying significant neuromuscular weakness at 12 months after ARDS  generalized weakness with global muscle wasting: 6- minute walk test, foot drop, large joint immobility, dyspnea  patients with critical illness–acquired neuromuscular weakness: 50% of ARDS survivors have not returned to work at 1 year after ICU discharge  weakness and fatigue  increase in mortality, duration of hospital and rehabilitation care, and overall health care costs  neuromuscular weakness following critical  significant and long-lasting impairments in QOL

28.  enhance neuromuscular function after severe critical illness  limiting use of neuromuscular blockade and corticosteroids  intensive insulin protocol with tight glucose control  improved neurophysiologic testing  earlier involvement of physical and occupational therapy

29.  Survivors of ARDS: Significant impairments in psychologic and social domains  Depression more than 43% of ARDS survivors 6 to 41 months after lung injury

30. Post-traumatic stress syndrome (PTSD)  related to the frequency of patients' recall of traumatic events in the ICU  9% incidence of PTSD if one or fewer traumatic events are recalled compared to 41% if two or more traumatic events are recalled  presence of delusional memories with recall of factual events  development of PTSD  delusional recall appears to be retained over time but factual recall declines over time.

31. Cognitive impairment  common after prolonged critical illness  impaired memory, attention, concentration, or decreased mental processing speed  55 consecutive survivors of ARDS (mean ICU length of stay 29 days): 78% had cognitive impairment at 1 year after ARDS

32.  brain injury during critical illness  neuropsychologic impairment ??  Reduction in cerebral blood flow, cerebral edema, and disruption in the blood–brain barrier   septic encephalopathy  systemic inflammation  endothelial and neuronal cell injury, (cellular hypoxia, and leukocyte-derived inflammatory mediator and free radical injury)

33.  Effective interventions  early psychiatric consultation for identification and treatment of depression, anxiety, and PTSD  easily miss  formal neuropsychologic testing  Identification and treatment of sleep disturbance and delirium  daily interruption of sedation may reduce the development of PTSD