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Pulmonary Embolism



Incidence: 3rd leading cause of acute death / 1 in 1000 / 150,000 to 200,000 deaths/year in the United States / males > females / increased age, most occur < 1 month after delivery / probably underdiagnosed by 170,000/yr

Recurrence: 5% recurrence if DVT (even treated; 10% recur if initial PE)

Mechanisms: Virchow’s Triad: local trauma, hypercoagulable state, venous stasis / small clot causes disproportional increase in pulmonary MAP due to vasoconstriction from inflammatory mediators (serotonin, thromboxane, PAF) and vagus nerve / saddle embolus (massive) / paradoxical embolism (R to L shunt)

Pathology: pulmonary hypertension, hypoxia, RVF, mortality

Presentation: 5-10% present with normal O2 saturation and Aa gradient / some hemoptysis (usually not massive) / massive PE causes tachycardia, loud P2, RHF signs, pulsus paradoxus / chest pain and hemoptysis usually takes a few hours to develop

Symptoms: dyspnea (80%), pleuritic pain (70%), apprehension (60%), cough (50%), hemoptysis (30%), diaphoresis (40%), syncope (10%, > elderly)

Physical findings: tachypnea (90%), rales (60%), accentuated P2 (50%), tachycardia (40%), mild fever (40%), phlebitis (30%), cyanosis (20%), right-sided S3 (large emboli with acute pulmonary hypertension)

Causes: DVT, air (usually iatrogenic), cholesterol, tumor, amniotic fluid (mimics sepsis), foreign body (arthroplasty cement, talc) / 40% trauma/surgery, 40% idiopathic/undiagnosed, 20% genetic predisposition, 10% heart disease (e.g. arrhythmias) / 10-20% hypercoagulable state (factor V Leiden most common) / 10% will have malignancy [more] (lung, pancreas, stomach, colon > prostate, ovary, other > gallbladder, breast, kidney)

Risk factors: surgery/trauma, obesity / oral contraceptives, pregnancy, post-partum / cancer or cancer-chemotherapy / immobilization / central venous catheter / diabetic ketoacidosis

Differential Diagnosis: MI (75% of PE misdiagnosed as MI), unstable angina, pneumonia, bronchitis, COPD exacerbation, CHF, asthma, pericarditis, primary pulmonary hypertension, rib fracture, pneumothorax, costochondritis, musculoskeletal pain, anxiety

Work-up: [algorithm]

  • EKG: sinus tachycardia, new-onset Afib/flutter, non-specific ST changes are most common finding / classical finding (S1Q3T3): I deep S, III Q wave, inverted T III / V1-4 inverted T waves (only 15%) [pic]

  • CXR: r/o pneumothorax et al / Westermark’s oligemia (15%) [pic] / raised hemi-diaphragm / pleural-based parenchymal radiodensity with rounded profile toward hilus (Hampton’s lump or hump) / pleural effusion (transudate or exudates) / Palla sign (enlargement of right descending pulmonary artery)

  • ABG on RA (expect respiratory alkalosis, PaO2 < 80 / PaCO2 < 30)

  • VQ scan: [pic] [pic2] [normal: stop / high: treat / low-intermediate (up to 40% have PE) / most PE have moderate to low probability VQ scans / often want to go directly to CT for 2 reasons 1) pre-existing lung disease usually causes non-informative study 2) CT is much faster to get (especially during off-hours) / T-99 [pic] / 60% of COPD patients have indeterminate scans

  • CT angiogram [pic]: better for central pulmonary arteries, not peripheral / not so good for diagnosing sub-segmental PE / Note: if not PE, CT reveals the alternate diagnosis > 30% of cases / some choose pulmonary angiogram 1st if patient’s renal function only allows one test / false negatives (patient hemodynamics, motion artifact, oblique running arteries, note: interlobar artery in r. lung not well seen) / false positives (hilar, bronchopulmonary lymph nodes, artifacts, reduced pulmonary perfusion) / Note: differing opinions (obstruction, PE, etc.) is the rule if reviewed by > 1 radiologist, you’ll see

  • Pulmonary angiogram [pic]: gold standard / 1% morbidity/mortality of test / rarely done unless equivocal or negative VQ/CT and high suspicion for PE

  • Ultrasound: looking for DVT in lower extremities (most come from pelvis however) / more than ½ will have leg vein clot (sensitivity is high if study done properly), which means ⅓ will have no DVT

  • Echocardiogram: may see RV dilation/strain/failure (which is leading cause of death from PE, and which may provide support for use of thrombolytics) / depressed RV function with apical sparing is McConnell’s sign (does not always mean PE) / this is an adjuvant test used to determine RV function (and may also provide alternative explanations for patient’s symptoms) but is NOT a diagnostic test for PE

  • D-dimers: if lab does proper assay, can have 90% sensitivity with lower specificity (cannot rule in, but does have high negative predictive value)

Prevention: any medical or surgical patient at high risk for venous thrombosis (older than 40, limited mobility, one risk factor; there are many [NEJM]) should receive sc heparin 5000 U bid/tid or sc Lovenox 30 mg qd or Fragmin / for high bleeding risk, compression stockings or (better) pneumatic compression device

Treatment'>Treatment: [annals][annals]

  • Anticoagulation (heparin or LMWH then coumadin as soon as PTT is therapeutic, same day with LMWH) / 5% overall recurrence rate / 2% overall risk of major bleed / Duration: 6 months if risk-factor associated, indefinite if no identifiable risk-factors. [annals] / recent studies suggest once-daily LMWH may be as good as twice-daily (2009) and measure factor-Xa levels (best way to ensure therapeutic and safe range (esp. with renal insufficiency)

  • Thrombolysis – controversial when to use. [NEJM] says use alteplase + heparin when concern for RV failure is high. [NEJM] / accepted risk of ICH about 3%

  • Thrombectomy – for pts who have RHF and cannot tolerate or fail thrombolysis

  • IVC filters (vena cava interruption) with known DVT’s, poor cardiopulmonary reserve, PE in spite of anti-coagulation or contraindications to anti-coagulation (recent CVA or CNS surgery, CNS malignancy, GI bleed) / many complications of filters (overall 10-20%) [pic]

Note: expect rapid changes here with onslaught of new methods of anti-coagulation (11/00)
Lemierre’s syndrome
Classical organisms: fusobacterium, Prevotela, Peptostreptococcus, Eikenella

involvement of posterior compartment of the lateral pharyngeal space, bacteremia, septic IJ thrombophlebitis



Contiguous spread: carotid artery rupture, hoarseness, CN IX – XII involvement, Horner’s syndrome

Septic embolization: pulmonary, suppurative arthritis, osteomyelitis, abscesses, skin lesions, hepatic abscesses +/- cholestasis

Diagnosis: CT/MRI/ultrasound, high degree of clinical suspicion



Treatment:

  • prolonged IV antibiotics against anaerobes / 1st metronidazole, 2nd clindamycin, chloramphenicol (often produce B-lactamases)

  • surgical ligation or IJ excision may be necessary

  • some feel heparin is useful




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