Venous Thromboembolism

Pulmonary embolism (PE): Can cause catastrophic right ventricular (RV) dysrhythmias, RV failure, shock, or cardiopulmonary arrest.

PE

• Oxygen saturation and pO₂ lower than otherwise expected for the patient

• Pleuritic-type chest pain, somewhat vague in precise location but worse with deep inspiration or cough

• Dyspnea at rest or with previously easy exertion

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• Tachycardia

• Weakness, dizziness, near-syncope or syncope

• Hypotension

DVT of an extremity or the vena cava

• Asymmetric swelling (other extremities might also be swollen)

• Ache, sometimes erythema, sometimes induration, sometimes fever, sometimes pitting edema

Splanchnic venous thrombosis

• Severe abdominal pain

• If DVT of the portal system, subacute pain, sometimes with ascites

Cerebral venous thrombosis

• Headache, sometimes for days to weeks

• Seizure

• Focal deficit(s), sometimes bilateral, but loss of consciousness is rare

PE

• Anticoagulated PE patients rarely die. If the patient can safely tolerate 3 hours of full anticoagulation, give at least an intravenous (iv) heparin bolus (80 u/kg) followed by an infusion (18 u/kg/hr) while completing the diagnostic workup. Alternatively, give low molecular weight heparin.

• Assure satisfactory oxygenation.

• Support the blood pressure if needed with judicious IV crystalloid and, if necessary, norepinephrine; guided by echocardiography (see below).

• Determine if patient can be fully anticoagulated safely for several days. If not, determine if a somewhat or markedly reduced level of anticoagulation with close monitoring could be safe. If not, an IVC filter should be placed.

• Confirm diagnosis promptly.

DVT of an extremity or vena cava

• Confirm the diagnosis.

• Determine if patient can be fully anticoagulated safely for several days. If not, determine if a somewhat or markedly reduced level of anticoagulation with close monitoring could be safe. If not, an IVC filter should be placed.

• Anticoagulate.

Splanchnic venous thrombosis

• Confirm the diagnosis.

• Determine if patient can be safely fully anticoagulated for several days. If not, determine if a somewhat or markedly reduced level of anticoagulation with close monitoring could be safe.

• Promptly anticoagulate with close monitoring for bleeding.

Cerebral venous thrombosis

• Confirm the diagnosis.

• Determine if patient can be safely fully anticoagulated for several days. If not, determine if a somewhat or markedly reduced level of anticoagulation with close monitoring could be safe. Cerebral venous thrombosis does not carry an exceptional hemorrhagic risk during anticoagulant treatment, even if there is preexisting cerebral hemorrhage at diagnosis.

• Anticoagulate with iv heparin with no bolus, gradually increasing the dose to prolong the activated partial thromboplastin time (aPTT), while following clinically the patient’s central nervous system (CNS).

For all venous thromboembolic critical conditions with substantial hemorrhage risk

If there is significant hemorrhage risk, inhibit ongoing thrombosis by giving iv heparin with no bolus. Target is 18u/kg/h. Start at 5u/kg/h for high risk, 7u/kg/h for moderate to high risk, 10u/kg/h for moderate risk. Observe closely, increasing toward desired target over 72 h if no deterioration and hemorrhagic risk decreases. It may take a week or longer to reach target dose and aPTT range, but thrombogenesis will be at least partially inhibited in the meanwhile.

For critically ill patients with PE

• Supply sufficient supplementary oxygen to maintain O₂ saturation greater than 90%. Intubate if necessary.

• If hypotensive or other signs of low cardiac output, use echocardiography to evaluate cardiac chambers and inferior vena cava (IVC) diameter. Administer 0.9% normal saline until the RV diameter approximately equals that of the left ventricle (LV) by echocardiography; then add norepinephrine. Overdistension of the RV from injudicious fluid administration will compromise LV function.

• If hypotensive or in shock and no important absolute contraindication, administer 10mg rt-PA IV by bolus, then 90mg IV over 2 h. When aPTT is 2.5x laboratory normal mid-range (50 sec or lower), begin iv heparin at 18u/kg/h. For those with an absolute contraindication, consider either surgical or catheter embolectomy depending on clot location and surgical risks.

• If normotensive and no shock, can give either low-molecular-weight heparin (LMWH) subcutaneously 100u/kg q 12 h or 1mg/kg q 12 h (depends on the drug), or iv heparin 80u/kg bolus, then 18u/kg/h. If using heparin, regulate by q 4-6 h aPTT for target 2.5x laboratory normal mid-range or anti-Xa level of 0.4 to 0.8 u/mL. Some patients in this category, may have submassive PE with RV dilatation on echo. However, only those patients with submassive PE who have elevated cardiac enzymes (BNP or Troponins) are at increased risk of death (albeit still low < 4-6%). These patients may benefit from additional monitoring for high risk features or for frank deterioration to warrant use of lytic therapy. In those patients who may need lytic therapy but have a high risk of bleeding, consider low dose lytics or catheter-directed lytics, or devices that disrupt clot mechanically.

• Monitor for bleeding (hematocrit [hct] q 12 h) and, if using iv heparin, by aPTT.

• Exclude heparin-induced thrombocytopenia (HIT) if that is a possible diagnosis (recent past exposure to heparin, platelet count between 25,000 and 125,000, positive rapid antiPF4 antibody Elisa titer greater than 1.0)

• If HIT is considered possible or likely, administer fondaparinux as the anticoagulant instead, once daily subcutaneously, 5mg if weight less than 50 kg, 7.5mg if 50 to 100 kg, 10mg if greater than 100 kg. If reliable tissue perfusion is uncertain, give slow iv push instead over 5 minutes once daily.

• If anticoagulation is contraindicated, place retrievable IVC filter, gain hemostasis, and anticoagulate at least partially as soon as it is safely possible.

For extremity or vena cava DVT

• These are usually not reasons to be in the ICU, unless there is concurrent complicating serious illness (eg, hemorrhage risk, stroke, etc). Assess hemorrhage risk and if anticoagulation is acceptable, provide at an appropriate level:

  If minimal hemorrhage risk anticoagulate as #4 above for PE

  If there is significant hemorrhage risk, anticoagulate as described above for all VTE with hemorrhage risk

  If anticoagulation is fully contraindicated, place retrievable IVC filter, gain hemostasis, and anticoagulate at least partially as soon as possible.

For splanchnic venous thrombosis

• This presents as an acute abdomen. Unless contraindicated, obtain abdominal CT with iv contrast (oral contrast not necessary to make this diagnosis). Abdominal ultrasound with excellent imaging interpretation and the absence of excessive gas will also suggest the diagnosis.

For cerebral venous thrombosis

• Diagnose the intracerebral cause of pathology. If it is cerebral venous thrombosis without evidence for hemorrhage, fully anticoagulate with iv heparin bolus and drip, titrated q 4 h by aPTT. If there is evidence for hemorrhage, cautiously anticoagulate with heparin without a bolus as described above to inhibit ongoing thrombogenesis.

• Manage the airway and other aspects as in any stroke/CNS-impaired patient.

• Consider phenytoin loading or levatiracetam and ICU maintenance therapy if a seizure recurs.

PE

• A consistent history and clinical score and multi-slice computed tomography pulmonary angiogram (CT PA-gram), contrast-enhanced, confirms the diagnosis.

• A normal D-dimer is not consistent with the diagnosis in a young person but moderate to high suspicion counts more than a “normal” D-dimer. An elevated D-dimer is supportive but not specific, hence not diagnostic.

• Evidence of DVT (eg, from ultrasound) with a consistent chest syndrome confirms the diagnosis, even in the absence of a CT PA-gram.

• Radionuclide scanning: Multiple segmental or larger perfusion defects where the chest radiograph or ventilation scan is normal confirm the diagnosis. Single photon emission computed tomography (SPECT) if readily available is superior for confirming (but maybe not ruling out) PE. A completely normal perfusion scan likely excludes the diagnosis.

Extremity or caval DVT

• Failure to obliterate the venous lumen with compression ultrasound is the most reliable imaging confirmatory finding, but some clots are located in places they cannot be compressed. Duplex (B-mode plus Doppler) or color Doppler (duplex using color to distinguish centrifugal [arterial] from centripetal [venous] flow) can confirm the diagnosis. For vena caval thrombi, duplex ultrasound or contrast CT cavography or, if necessary, angiography under fluoroscopy in the radiology department or at the bedside by a radiologist with an image intensifier can confirm the diagnosis.

Splanchnic venous thrombosis (see Emergency Management)

• Contrast-enhanced abdominal CT

• Duplex ultrasound of the abdomen, focusing on vessels

Cerebral venous thrombosis

• Magnetic resonance imaging (MRI) is usually diagnostic

• MR venography is confirmatory and often done at the same time as MRI—but may not be safe if there is renal insufficiency or another contraindication to MR contrast administration

• Head CT is often done first as a screening examination but is often nondiagnostic

All venous thromboembolism

D-dimer values are usually elevated. But elevation is nonspecific, nondiagnostic and not 100% sensitive to thrombosis. The age-adjusted D-dimer (age in years x 10 in mcg/L) upper limit of normal for outpatients over 50, with a low clinical score, can help rule out DVT and PE in outpatients but is not validated for inpatients.

PE

• Cardiac troponin levels are often elevated but nonspecific. Moreover, they may remain elevated for several days.

• Brain natriuretic peptide (BNP) is often elevated in serious PE.

Cerebral venous thrombosis: See attached images (Figure 1, Figure 2, Figure 3).

Figure 1.

Figure 2.

Figure 3.

PE: If the diagnosis remains uncertain but there is little risk from anticoagulation, at least in the short term, anticoagulate with a bolus of iv heparin.

DVT: If anticoagulation has risks, wait to confirm the diagnosis. DVT is not an emergency (but PE is).

Splanchnic venous thrombosis: Urgently decide whether this is a viable diagnosis by imaging or, if necessary, at laparotomy to resect ischemic bowel.

Cerebral venous thrombosis: Obtain MRI imaging urgently.

• Pneumonia with pleurisy

• Congestive heart failure

• Pericarditis

• Acute pulmonary hypertensive crisis

PE

• Anticoagulant therapy as outlined above and specifically described below

• If there is hypotension or shock, 0.9% NS or lactated Ringer’s fluid infusion, guided by echocardiography, to assure adequate filling of the right ventricle

• Give norepinephrine iv drip to maintain perfusion while repleting (but not over-filling) the vascular space and continue if needed

• Consider thrombolytic drug infusion (see section below for dosing) if hypotension or shock and no contraindication, or an acceptable benefit-risk profile

• If therapy is failing, consider inserting retrievable inferior cava filter to prevent short-term recurrence

• Assess for refractory and overhwelming pulmonary hypertension despite other therapies by confirming small left atrial size, low left ventricular output, hypotension, and refractory arterial hypoxia despite high inspired O2 concentration. If all are present, consider pulmonary vasodilator therapy in addition to lytics and vasoactives as described below.

• For shock, if significant bleeding is a concern accompanying systemic thrombolytic drug infusion or such therapy has failed, and there is local expertise, consider for catheter-directed therapy or surgical thrombectomy

Intravenous anticoagulation is preferred in critically ill patients. Because of uncertainty regarding bioavailability and clinical efficacy after oral administration in such patients, the direct-acting oral anticoagulants are not recommended. In acute DVT or PE, we recommend initial treatment with LMWH, unfractionated heparin (UFH) or fondaparinux for at least 5 days rather than a shorter period (grade 1C); and initiation of vitamin K antagonists (VKAs) together with LMWH, UFH, or fondaparinux on the first treatment day, and discontinuation of these heparin preparations when the international normalized ratio (INR) is greater than 2.0 for at least 24 h.

Dosing recommendations

• Unfractionated heparin: 80U/kg iv bolus; 18U/kg/h iv; titrate by aPTT (see above for specific instructions on lower dosages). If administering more than 1800U/h and aPTT not in therapeutic range, titrate by anti-Xa level. For optimal/efficient titration of UFH, we recommend using a nurse driven protocol titrating heparin dose to the PTT drawn q 6 h until therapeutic and in steady state, then q/day

• Fondaparinux: SQ once daily: 5mg if less than 50kg; 7.5mg, 50 to 100 kg; 10 mg, greater than 100 kg. In critically ill patients, the primary use of fondaparinux would be for treatment of HIT with or without thrombosis.

• Enoxaparin (LMWH): SQ 1mg/kg every 12 h. For calculated creatinine clearance less than 30 mL/min, give q 24 h

• Dalteparin (LMWH): SQ 200u/kg every 24 h

• Tinzaparin (LMWH): SQ 175u/kg every 24 h

Anticoagulants administered by iv drip (indicated for HIT):

• Argatroban: 2 mcg/kg/min iv, no bolus, follow aPTT (target 1.5 to 3 x baseline value)

• Alteplase: 10mg iv bolus, then 90mg over 2 h. Start heparin after aPTT falls into therapeutic range for the lab (1.5 to 2.5 x baseline). For small patients less than 65kg and BMI less than 25, or those with some bleeding risk, consider half-dose alteplase (10mg bolus, then 40mg over 2 h)

• Steptokinase: 250,000u over 30 min, then 100,000 u/h for 24 h. Another rapid, reported, but unapproved regimen: 1.5 million u over 60 min.

• Tenecteplase: 30mg (for patients less than 60 kg) to 50mg (for patients 100 kg and above) iv bolus (add 5mg to 30mg for every 10 kg above 60 kg, eg, a patient weighing 74 kg would receive 35mg; weighing 87 kg would receive 40mg; weighing 92 kg would receive 45mg, etc).

Injected anticoagulants are all inhibitors of activated clotting factors and are superior anticoagulants to warfarin, which inhibits clotting by promoting synthesis of defective clotting factors. Thus, warfarin is never satisfactory for initial treatment in sick patients, or when rapid or certain anticoagulation is required.

Oral inhibitors of activated clotting factors (rivaroxaban, dabigatran, apixaban, edoxaban) are now marketed but for now should not be considered for treating critically ill or otherwise unstable inpatients.

For PE interfering with cardiac output and blood pressure despite iv thrombolysis (if not contraindicated), judicious volume and vasopressor infusion, consider, while hemodynamic monitoring:

To help resuscitate the right ventricle with pulmonary vasodilator therapy

• Nebulized epiprosetenol, 50 ng/kg ideal body weight/min, tapering as possible by 10 ng/kg/min q 30 min to 10 ng/kg/min as left ventricular output and oxygenation improve.

• Oral sildenafil 50mg if patient might absorb oral medication

• Inhaled iloprost 2.5 mcg. If tolerated and effective, continue every 2 h. If tolerated but insufficiently effective, give inhaled iloprost 5 mcg 2 h later and continue every 2 h (up to 9 times in 24 h) if tolerated and effective. Time interval can be increased as allowed to maintain effect while minimizing therapy. (Iloprost inhibits platelet function, therefore likely increases bleeding risk.)

• Nitric oxide therapy for now appears prohibitively expensive but if used: Inhaled nitric oxide at 5 to 20ppm to keep patient alive for anticoagulant effect and recovery

To help relieve pulmonary artery obstructing thrombus

• Consider re-treatment with thrombolytic drug (not recommended unless half-dose 50mg alteplase was used as first treatment attempt)

• Surgical embolectomy on cardiopulmonary bypass if there are experienced teams available; the author recommends this over percutaneous catheter interventions)

• Percutaneous catheter directed thrombolysis/thrombectomy if surgical embolectomy not available, contraindicated, or there is local expertise and success with catheter directed techniques

To help keep the patient alive during the critical phase of illness

Optimize all supportive therapies for hypoxemia and hypotension while minimizing risks. With proper support, the majority of patients made critically ill by PE, and critically ill patients who also suffer PE, will survive.

PE

Patients should stop deteriorating within 4 h of instituting adequate treatment, although they may not improve this quickly. If clinical deterioration continues, escalate treatment as described above.

Extremity or caval venous thrombosis

Desirable treatment response is nonprogression without hemorrhage. Over days to weeks, distal edema will remit indicating that venous obstruction has been reduced.

Splanchnic venous thrombosis

Desirable treatment response is nonprogression without hemorrhage. Since many such presentations are surgically treated abdominal catastrophes, prevention of recurrence without hemorrhage is the desired treatment response. With substantial bowel resections, reliable anticoagulation with warfarin and other oral anticoagulants is usually not possible, so injected LMWH, twice daily to start, is the best approach. Prognosis is guarded because nutrition is often a problem too.

Cerebral venous thrombosis

Nonprogression of symptoms and no hemorrhage is the desired treatment response. Headache may take days to abate. Signs of increased intracranial pressure, if present, should not worsen. Focal neurologic deficits may take weeks or months to improve.

If there is no imaging support for the diagnosis and a D-dimer level from a sensitive assay is not elevated, the diagnosis is likely incorrect.

After no longer critically ill, the patient requires injected anticoagulant (if not contraindicated) until hypoxia on usual activity is gone. Then the patient needs follow-up care by a physician experienced in the care of patients with PE or other venous thrombotic conditions.

For patients with DVT or PE secondary to a transient (reversible) risk factor, we recommend treatment with a VKA for 3 months over treatment for shorter periods.

For patients with unprovoked DVT or PE, we recommend treatment with a VKA for at least 3 months, and that all patients are then evaluated for the risk to benefits of indefinite therapy.

We recommend indefinite anticoagulant therapy for patients with a first unprovoked proximal DVT or PE and a low risk of bleeding when this is consistent with the patient’s preference (grade 1A), and for most patients with a second unprovoked DVT.

Cerebral venous thrombosis

These are rare causes of strokes. Follow-up by an experienced neurologist and life-long anticoagulation are best for most patients, along with avoidance of possibly precipitating factors (eg, oral contraceptive pills).

PE

PEs are usually multiple and bilateral. Thrombotic occlusion of pulmonary arteries may be poorly tolerated if they block a substantial portion of the pulmonary arterial tree, if the patient has preexisting hypoxemia, preexisting pulmonary artery hypertension, or preexisting cardiac vulnerability. Even small PE may push any of these preexisting conditions “over the waterfall” into inadequate tissue perfusion of a vital organ. A small thrombotic burden that lodges proximally may have greater deleterious effect than the same clot mass after it fractures and is distributed by pulsatile pulmonary artery flow into several distal branches.

Resolution of tachycardia and severe hypoxemia and relative hypotension by day 3 to 5 of injected anticoagulant treatment after PE is believed to have improved on this basis. Thrombolysis by endogenous plasmin is believed to contribute. Hence, the therapeutic goal is to support tissue oxygenation with oxygen and support cardiac output to the LV while endogenous thrombolysis, or external thrombolysis by pharmacologic (eg, alteplase) or mechanical (eg, open surgical) methods are used if circumstances warrant.

Extremity, caval splanchnic, and cerebral venous thrombosis

Inherited or acquired hypercoagulability, immobility, local injury, and local venous flow disturbance may each contribute to clot formation. Impairment of venous return can lead to distal edema and frank tissue hypoxia from venous congestion.

Venous thromboembolism

The incidence of venous thromboembolism in a large population is 1 to 2 per 1000 persons per year. But an individual’s risk depends on history as well as inherited and acquired thrombophilic conditions. Prior venous thrombosis of any site appears to be an important risk factor for recurrence, as is venous thrombosis without an apparent precipitating cause.

Immobility inside or outside the hospital is a key risk factor. The presence of circulating tissue factor, found with several cancers, deep tissue trauma, and brain injury/surgery (several PT and aPTT assays used thromboplastin derived from brain to initiate the assay) is a risk factor. Awareness of risk factors should cause physicians to have appropriate suspicion of venous thrombosis, search for it when it might be the cause of or complicating illness, and institute appropriate management, considering the risks and benefits of anticoagulant and other required treatments.

PE

Most patients with PE who survive several days in the hospital and do not have another fatal illness (eg, incurable cancer) can anticipate full recovery with adherence to appropriate treatment. Minimum treatment should be 3-6 months if a reversible risk factor was present. Otherwise, lifelong anticoagulation is recommended. Oral warfarin is started when the patient can take orally but injected therapy is continued until there is demonstrable improvement, the INR is greater than 2 for 2 days (target 2.5), and there have been 5 days of injected therapy altogether.

Re-imaging of pulmonary arteries with CTPA-gram at 6 months or other time of treatment discontinuation is recommended, if discontinuation of anticoagulation is warranted. Recurrence if anticoagulation is stopped is, however, not rare, and PE patients are at lifelong increased risk of recurrent thrombosis compared to age-matched controls who never experienced venous thromboembolism. Moreover, the incidence of symptomatic chronic thromboembolic pulmonary hypertension 2 years after a first PE is around 4%.

Extremity and caval thrombosis

Patients with antiphospholipid antibody syndrome who remain test-positive every 6 months should receive indefinite anticoagulation. For others, the presence of risk factors for thrombosis should be balanced against hemorrhagic risk to determine treatment duration beyond 3 to 6 months. Warfarin is begun orally without a loading dose when the patient can take orally and injected anticoagulant is continued for a minimum of 5 days and until 2 consecutive INRs are greater than 2 (target 2.5). Direct acting oral anticoagulants, taken without monitoring, are an alternative if affordable in the absence of active malignancy.

Ultrasound imaging of the clot site at the time of treatment cessation (if treatment is stopped) is wise to obtain the new “baseline” image, should there be recurrent symptoms. For all DVT patients as a group, the risk of recurrence is approximately 0.8-1% per month, at least up to 2 years after 6 to 24 months of treatment.

Splanchnic venous thrombosis

The prognosis is fair on continued injected anticoagulation. Anticoagulant discontinuation for other than very short peri-procedural periods for necessary procedures should not be considered unless there have been hemorrhagic complications. In that circumstance, attention should be focused on anticoagulation with reduced risk, such as with a reduced dosage of a better controllable anticoagulant.

Cerebral venous thrombosis

Limited information suggests roughly 50% of patients are independent with good function at 6 months. Good acute stroke general management, including recognition of increased intracranial pressure and visual impairment, and using effective remediation measures likely impact overall prognosis. Because impaired cerebral venous flow may persist long-term despite symptom improvement, the author recommends indefinite anticoagulation (with warfarin, for now, INR target 2.5, or with a direct acting oral anticoagulant if affordable) to prevent a new intracranial catastrophe.

Anticoagulant discontinuation for other than very short peri-procedural periods for necessary procedures should not be considered unless there have been hemorrhagic complications. In that circumstance, attention should be focused on anticoagulation with reduced risk, such as with a reduced dosage of better controllable anticoagulant.

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Attention to details of acute anticoagulation and evaluation for stability and worsening are crucial for optimal management and recovery.

Carlbom, D, Davidson, BL.. “Pulmonary embolism in the critically ill (invited review)”. Chest. vol. 132. 2007. pp. 313-324. (This reviews all aspects of management with references. Very little has changed for critically ill patients since 2007.)

Saposnik, G, Barinagarrementeria, F, Brown, RD. “Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professions from the American Heart Association/American Stroke Association”. Stroke. vol. 42. 2011. pp. 1158-92. (This comprehensive review describes available knowledge and its limitations and provides recommendations where available evidence allows them. More recent case series by interventional neuroradiologists don’t show improved outcomes.)

Harnik, iG, Brandt, LJ.. “Mesenteric venous thrombosis”. Vasc Med. vol. 15. 2010. pp. 407-18. (A recent credible instructive review of what often presents first and requires management as a surgical acute abdominal catastrophe.)

Russell, CE, Wadhera, RK, Piazza, G.. “Mesenteric venous thrombosis”. Circulation. vol. 131. 2015. pp. 1599-603. (A more recent case-based succinct review that mentions catheter directed treatment.)

Kearon, C, Akl, EA, Ornelas, J. “Antithrombotic therapy for VTE disease: Chest guideline and expert panel report”. Chest. vol. 149. 2016. pp. 315-52. (Tenth edition of the guideline across all, not only critically ill, patients. A great many weak (Grade 2) suggestions based on weak (Grade C) quality evidence mean that much presented is expert opinion rather than evidence-based consensus.)

Ingber, S, Geerts, W.. “Vena cava filters: current knowledge, uncertainties, and practical approaches”. Current Opin Hematol. vol. 16. 2009. pp. 402-6. (Still current and sober consideration of when and when not to use a vena cava filter.)

Mismetti, P, Laporte, S, Pellerin, O. “Effect of a retrievable inferior vena cava filter plus anticoagulation vs anticoagulation alone on risk of recurrent pulmonary embolism: a randomized controlled clinical trial”. JAMA. vol. 313. 2015. pp. 1627-35. (Well designed and excecuted study showing no added benefit from routine use of IVC filter added to anticoagulation.)

Hajduk, B, Tomkowski, WZ, Malek, G, Davidson, BL.. “Vena cava filter occlusion and venous thromboembolism risk in persistently anticoagulated patients: a prospective observational cohort study”. Chest. vol. 137. 2010. pp. 877-82. (Management of patients with vena cava filters that cannot or have not been retrieved. There are subsequent publications of uncontrolled series touting endovascular interventions.)

Kuo, WT, Banerjee, A, Kim, PS. “Pulmonary embolism response to fragmentation, embolectomy, and cathether thrombolysis (PERFECT). Initial results from a prospective multicenter registry”. Chest. vol. 148. 2015. pp. 667-73. (A large registry showing feasibility of catheter directed thrombolysis for acute PE.)

Meyer, G, Vicaut, E, Danays, T. “Fibrinolysis for patients with intermediate-risk pulmonary embolism”. N Engl J Med. vol. 370. 2014. pp. 1402-11. (Large clinical trial showing major, especially intracerebral bleeding offset any benefit from routine tenecteplase for acute PE with elevated troponin and/or BNP and a dilated right ventricle. Also showed mean time to deterioration was 3 days; to catch 95% of deteriorations required 5 days of observation.)

Elliott, CG.. “Fibrinolysis of pulmonary emboli—steer closer to Scylla”. N Engl J Med. vol. 370. 2014. pp. 1457-8. (Definitive, clear editorial explaining the rationale for withholding fibrinolysis unless the patient deterioriates.)

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