It is obstruction of pulmonary vessels .OBSTRUCTION can be- Thrombotic –blood clot. Non-thrombotic : Fat, Air,Tumour , Amnioticfluid. Clot may be – Primary -formed in the pulmonary vesselsitself. secondary-Thrombosis of peripheral veins, embolization to pulmonary vessels.
PE is one of the three major cardiovascular causes ofdeath, along with MI and stroke. Among survivors Chronic thromboembolic pulmonaryhypertension (2-4 %)is often disabling and causesbreathlessness and Postphlebitic syndrome (also known aspostthrombotic syndrome or chronic venousinsufficiency ) causes the venous valves of the leg tobecome incompetent and exude interstitial fluid. Ptscomplain of chronic ankle or calf swelling and legaching, especially after prolonged standing. In itsmost severe form, it causes skin ulceration, especiallyin the medial malleolus of the leg.
Hypercoagubility-MalignancyNonmalignant thrombophiliaPregnancyPostpartum status (<4wk)Estrogen/ OCP’sGenetic mutations (FactorV Leiden,prothrombin gene,}Protein C & S, anti-thrombin deficiency)Venous StatisBedrest > 24 hrRecent cast or external fixatorLong-distance travel or prolong automobile travelVenous InjuryRecent surgery requiring endotracheal intubationRecent trauma (especially the lower extremities and pelvis)
About one-half of patients with pelvic veinthrombosis or proximal leg DVT developPE, which is often asymptomatic. Isolated calf vein thrombi pose a much lowerrisk of PE but are the most common source ofparadoxical embolism. upper limb venous thrombosis rarelyembolise and cause PE.
"the Great Masquerader" If a pt with pneumonia or CCF fails to responddespite standard medical treatment think ofthe possible coexistence of PE.
With Infarction Dyspnea,Hemoptysis,Pleutitic Pain,Friction Rub,Fever,Brochospasm.
WithHemodynamicImpairmentAngina,Tachycardia,P++, Gallop,JVP++,Hypotension,Cyanosis,SyncopeThis meansobstruction of30-50% ofpulmonaryvascular bed
Mc symptom of DVT is leg cramps. Mc symptom of PE is unexplained SOB. MC sign of PE is tachypnea.
The initial task is to decide on the clinicallikelihood of the disorder. For this we have various scores likewells,geneva etc
Clinical Signs and Symptoms of DVT?(Calf tenderness, swelling >3cm, errythema, pittingedema affected leg only)+3PE Is #1 Diagnosis, or Equally Likely +3Heart Rate > 100 +1.5Immobilization at least 3 days, or Surgery in thePrevious 4 weeks+1.5Previous, objectively diagnosed PE or DVT? +1.5Hemoptysis +1Malignancy w/ Rx within 6 mo, or palliative? +1>6: High Risk2 to 6: Moderate Risk2 or less: LowAdapted with permission fromWells PS, Anderson DR, Rodger M, GinsbergJS, Kearon C, Gent M, et al. Derivation of a simpleclinical model to categorize patients probability of pulmonary embolism: increasing the models utility with the SimpliRED d-dimer.Thromb Haemost 2000;83:416-20.
The sensitivity is >80% for DVT and >95%for PE. a useful "rule out" test. More than 95% of patients with a normal(<500 ng/mL) d-dimer do not have PE. It is not specific. Levels increase in patientswith MI, pneumonia, sepsis, cancer, and thepostoperative state and those in the2nd or3rd trimester of pregnancy. .
A normal or nearly normal chest x-ray oftenoccurs in PE. Others -1. focal oligemia (Westermarks sign),2. a peripheral wedged-shaped density abovethe diaphragm (Hamptons hump)3. an enlarged right descending pulmonaryartery (Pallas sign
ECG 2 Most Common finding on EKG:▪ Nonspecific ST-segment andT-wave changes▪ SinusTachycardia Historical abnormality suggestive of PE▪ S1Q3T3▪ Right ventricular strain▪ New incomplete RBBB
CTchest with IVcontrast is the principal imaging test for thediagnosis of PE The CT scan also obtains excellent images of the RV and LV andcan be used for risk stratification along with its use as a diagnostictool. In patients with PE, RV enlargement on chest CT indicates anincreased likelihood of death within the next 30 days comparedwith PE patients who have normal RV size on chest CT. When imaging is continued below the chest to the knee, pelvicand proximal leg DVT also can be diagnosed by CT scanning. In patients without PE, the lung parenchymal images mayestablish alternative diagnoses not apparent on chest x-ray suchas pneumonia, emphysema, pulmonary fibrosis, pulmonarymass, and aortic pathology.
Lung Scanning(V/Q scan) Lung scanning has become a second-linediagnostic test for PE, used mostly forpatients who cannot tolerate intravenouscontrast. A high-probability scan for PE is defined asone that indicates two or more segmentalperfusion defects in the presence of normalventilation.
Findings loss of vein compressibility. homogeneous and has low echogenicitythrombus can be found . Loss of normal respiratory variation .
A normal venous USG does not rule out DVT . It helps to rule out other DD.
Main role is to rule out PE mimics. The best-known indirect sign of PE onTTE isMcConnells sign: hypokinesis of the RV freewall with normal motion of the RV apex.
Resustiation is important mainly in pts with massiveembolism.1. Respiratory support- intubation and oxygen1. Hemodynamic support- For patients with massive PE and hypotension, oneshould administer 500 mL of normal saline. Additional fluid should be infused with extremecaution. Dopamine and dobutamine are first-line inotropicagents for treatment of PE-related shock.
PRIMARYTHERAPY –1.Clot dissolution with thrombolysis2.Removal of PE by embolectomySECONDARY PREVENTION-1.Anticoagulation with heparin and warfarin2.Placement of IVC filters
Parenteral - 1. IV or SC UFH2.LMWH(enoxaparin )3. fondaparinux These are the ones recommended by ACCP Oral - 1.warfarin2. rivaroxaban3. dabigatran
If patient is having proven or suspected HITuse a direct thrombin inhibitor likeargatroban,lepirudin,or bivalirudin
ACCP suggests LMWH or fondaparinuxinstead of UFH EXCEPTION – Pt in whom SC absorption is inadequate Pts who are being considered forthrombolytic therapy
Better subcutaneous bioavailability. Longer and more consistentmonoexponential t1/2 once daily dose. Since aPTT is not prolonged no need of labmonitoring . Incidence of HIT is less
Once the diagnosis is confirmed ,begin t/twith parenteral form and also start oral formon the same day or next day. Continue the parenteral form for atleast 5days ( even if INR reaches 2 earlier) or untilthe INR is atleast 2 for 24 hrs or more
Both the parenteral and oral forms are startedsimultaneously because Warfarin takes 5-7 days to achieve atherapeutic effect . If warfarin is initiated as a montherapy duringan acute thrombotic illness, paradoxicalexacerbation of hypercoagulability canincrease the likelihood of thrombosis ratherthan prevent it.
For UFH Initial bolus 80units/kg followed by 18/kg/hriebolus of 5000-10000 units followed byinfusion of 1000-1500 units /hr.
strating dose of warfarin is 10 mg daily for 2days then dose by INR Target INR is 2.5 range is 2-3 (this applies toall the pts including those at high risk APLASwith previous arterial or venous thrombosis)
In people with stable INR can be recheckedas infrequently as once every 3 months . INR can be allowed to fluctuate upto 0.5below or above therapeutic range withoutany change in dose – just recheck INR in 1-2weeks.
INR upto 10 with no evidence of bleeding –donot give vitamin k or plasma products .Justhold warfarin and recheck INR infrequently. For INR greater than 10 without evidence ofgive oral vitamin k. For pts with major bleeding at any dose, rapidly reverse the coagulopathy usingfactor 4 prothrombin complex [ NOT FFP]andvitamin k 5-10 mg IV slow injection.
ACCP suggests using once daily dosing ratherthan twice daily dosing
Drug t1/2 Duration ofactionLoadingdoseMaintainance doseADRWARFARINSODIUM36-48 Hr 3-6 days 10-15 mg 2-10 mg Alopecia,dermatitis,diarrhoeaACENOCOUMAROL(ACITROM)18-24 hr 2-3 days 8-12 mg 2-8 mg Oral ulcers,gitdistrurbance,dermatitis,urticaria,alopecia
warfarin can be stopped abruptly oncetreatment period is over no need to taper it.
INDICATIONS: The only FDA-approved indication is massivePE. For patients with preserved systolic BP andsubmassive PE with moderate or severe RVdysfunction,ACCP recommendindividualisation of treatment.
Absolute Contraindications toThrombolysis Active or recent internal bleeding History Hemorrhagic Stroke Intracranial Neoplasm Recent cranial surgery or head trauma
100 mg of RtPA administered as a continuousperipheral intravenous infusion over 2 hours. Patients appear to respond to fibrinolysis forup to 14 days after the PE has occurred
Rapidly reverses right heart failure and may resultin a lower rate of death and recurrent PE by (1) dissolving much of the anatomicallyobstructing pulmonary arterial thrombus, (2) preventing the continued release ofserotonin and other neurohumoral factors thatexacerbatePAH (3) lysing much of the source of the thrombus inthe pelvic or deep leg veins, thereby decreasingthe likelihood of recurrent PE.
Indications –(1) active bleeding that precludesanticoagulation(2) recurrent venous thrombosis despiteintensive anticoagulation.
Follow up at about 6 weeks with a repeatecho to determine whether pulmonaryarterial pressure has normalized. consider for pulmonarythromboendarterectomy if persistant. The mortality rate is approximately 5% withthis operation.
For post phelibitic syndrome there is noeffective medical management.
ACCP guide linesFor acutely ill hospitalised medical pts at lowrisk of thrombosis ACCP recommends againstthe use of prophylaxsis.Pts at moderate to high risk but who are notbleeding or at high risk of bleeding should begiven either LMWH or UFH or fondaparinux.
For pts who are bleeding or at risk of bleedinguse leg compression devices only. Pts are considered to be at high risk ofbleeding if they meet any of the followingcriteria active gatrodeodenal ulcer Bleeding in 3 months prior to admission Platelet count <50,000
Or if they had multiple risk factors forbleeding of lesser predictive strengthlike age>84 yrs,severe renal failure , hepatic failurewith INR > 1.5 , male ,current cancer, ICUadmission.
Harrison -18 th edition ACCP guidelines Fishmans Pulmonary Diseases and Disorders Crofton and Douglass Respiratory Diseases(Wiley, 2000)