PULMONARY  EMBOLISM

Etiology:

  1. Stasis: DVT, Immobilization ( formed 2ry to cast, long-distance airplane travel, taxi/bus driver, etc.), Polycythemia, SC, Burns, Pregnancy, Obesity,
     
  2. Cardiac: Arrhythmia, CHF, Cardiomyopathy, Indwelling Central Line.
     
  3. Hypercoagulability: BCP (estrogen based), Malignancy, ­ homocystine, ¯ protein C or S
     
  4. Trauma: Postoperative state,  Leg trauma,
     
  5. Prior PE or DVT, ¯ protein C or S, LES (antiphospholipid).
     
  6. Fat embolism (2ry to liposuction or bone fracture).

NOTE !!! Pts encountered in clinical practice may have IVC filter "umbrella". This only  prevents PE from DVT of lower extremity  or pelvic area, but not from PE 2ry to other hypercoagulability states. In addition,  the filter is considered itself  prothrombogenic, and  microthrombi may form around the filter and cause small  PE.

S & S:

  1. Dyspnea, Pleuritic Chest pain, (may be present 3-4 days prior to diagnosis) , Tachypnea,
     
  2. Cough,  Anxiety, Rales (50%), Tachycardia (40 - 50%), Low grade fever (40%)
     
  3. DVT in about 30% of cases,

LABS:

  1. ABG:
      1. pCO2 ¯ , pH ­ , pO2 is <75% ( but 15-20% can have >80%),
         
      2. A-a gradient: Simple formula to calculate A-a gradient is  140-(Po2+Pco2) =10 - 15 mmHg  (see below). The A-a gradient must be adjusted to age  if pt is > 65 years old.  After the age of  60-65 PaO2 drops by 1mmHg for every year.  The following  formula  is 10+(age/10) and this value is added to the PaO2. In other words if pt is 80 y.o. and his PaO2 is 70, when adjusted to the age his PaO2 is  88 and thus not hypoximic.
              
  2. EKG: most commonly  NSSTT changes, tachycardia. S1Q3T3 (i.e. R sided strain) occurs in 25-30% of cases only
     
  3. CXray: most commonly is abnormal with non specific findings such as atelectasis, effusion, elevated hemidiaphragm, Hampton's hump (consolidation distally 2ry to infarction, wedge shape), Westermark's sign (obstruction of pulmonary artery with consequent decreased perfusion  distally).
     
  4. Positive D-dimers  30-40% specific. Negative D-dimers are 90% sensitive in excluding  PE and posite DVT/PE were witnessed in presence of negative D-dimers. Both depend on the methods (ELISA vs. latex, whole blood vs. plasma) used by hospital lab.

DX:

    1. A-a gradient = [(713) x (FiO2)] – [PaCO2 x 1.25] - PaO2.  Normal is 10 to 15 mmHg. The A-a gradient must be adjusted toage if pt is > 65 years.  After  the age of  60-65, PaO2 drops by about 1mmHg for every year.
       
    2. V/Q scan. High  probability V/Q is essentially diagnostic, and medium probability V/Q is  diagnostic if  there are other S & S that could create a high clinical suspicion of  PE (O2 SAT <95%, DVT, SOB,  >A-a gradient, Tachycardia, Tachypnea).  If medium probability V/Q is not accompanied by S&S but pt has risk factors, Pulmonary Angio is the next step for dx.  Patients  with low probability V/Q have 10% chance of having PE, and patients  with normal V/Q still have as much as a 5% chance of having PE. Risk factors, S & S and proper F/U must be taken into account in these categories of patients.
       
    3. Spiral CT. This rules out only life threatening large PE but cannot r/o PE to small vascular bed.  Negative CT should be regarded similarly to a "low" probability V/Q and pt should be  treated on the basis of clinical exam  and clinical suspicion.
       
    4. ECHO. Patients unstable to leave the monitored bed would benefit from bedside ECHO. Clear signs of R ventricular failure may suffice for the dx of PE in proper setting, i.e. in pt with clinical evidence of PE. In addition it also helps to r/o other entities causing hypotension such as MI, Aortic Dissection, Tamponade. 
       
    5. Venous Doppler. When positive in the presence of  pulmonary S & S and  the presence of  "low -to-medium probability" V/Q, Heparin treatment for PE is indicated.
       
    6. Angiogram. Indicated when:
       
      • V/Q is low-mod probability and DVT study is negative, yet pt has high clinical suspicion based on S&S and/or  risk factors. 
      • Patient is High risk for bleed if put empirically  on anticoagulants.

Note! Recurrent  PE may occur despite good anticoagulation.

Treatment:

  1. O2
     
  2. Heparin dose is 5000 - 10,000 U bolus followed by 25,000 U in 250 D5W @ 10 - 15cc/hr  (or 17U / kg / hr). Peak effect in 20-60 min and T1/2 0.5-2.5 hr.
     
  3. Enoxaparin (Lovenox) is used more frequently nowadays. Administered SQ. No PT, PTT monitoring is needed. Peak effect occurs after 3-5 hrs. Is eliminated renally, and RF prolongs T1/2, yet dose adjustment is not needed. Usual T1/2 is 12 hrs. Can be given in pregnancy.  If reversal is needed Protamine is given; and 1 mg Protamine reverses 1 mg of Enaxaparin. The dose for  treatment of acute PE is 1.5 mg/kg qd or 1 mg/kg SQ bid x at least 5 days, with  warfarin started on day 2 (while Lovenox is continued until PT is therapeutic for 5 consecutive days). 
     
  4. Thrombolytics used only when documented PE causes  hemodynamic compromise.
     
  5. Embolectomy.

 

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