Surgical treatment for acute massive pulmonary embolism

A recent paper reminds us that surgery is an option in the management of massive pulmonary embolism(1), to be considered in the patient for whom thrombolysis has failed or is contraindicated. Good outcomes were produced when surgery was performed in a centre capable of cardiopulmonary bypass (6% 30-day postoperative mortality), but is surgery an option when these facilities are unavailable?

The “venous inflow occlusion” technique involves clamping the venae cavae prior to removing clot directly from the pulmonary artery and its branches after median sternotomy, and can be performed in any hospital with surgical facilities. Under normothermic conditions, speed is of the essence once cardiac arrest occurs, since the irreversible anoxic cerebral injury will occur after just a few minutes.

Clarke and Abrams wrote in the Lancet in 1972(2):

Our use of venous inflow-occlusion has given results which compare well with those obtained with extracorporeal circulation. 50% of our patients survived. All patients who had emboli removed without an episode of ventricular asystole survived surgery. Late deaths in 3 patients were from causes unrelated to pulmonary embolism, and from a further massive pulmonary embolus a week later. The technique has been applied with equal success in a major hospital fully equipped for cardiac surgery and in hospitals where resident and nursing staff had no experience of either thoracic or cardiac surgery. The simplicity and speed of the method has enabled the obstructed right ventricle to be relieved within thirty minutes of the onset of symptoms. The interval between induction of anaesthesia and the skin incision should be kept as short as possible, and drugs to maintain the blood pressure should be given. The period between skin incision and the restoration of the circulation has, with practice, been reduced to ten minutes.

But this clearly still requires surgical expertise and facilities. Emergency physicians can open the chest to deal with penetrating trauma. Could an ED thoracotomy facilitate clot removal from the pulmonary artery?

In 1969, a lady in her 50s arrested on the ward after an operation to remove a mass via a left lateral thoractomy. Pulmonary embolism was suspected and her thoracotomy wound was re-opened and the pulmonary artery incised, resulting in the removal of large amounts of clot. Return of spontaneous circulation resulted after a brief period of internal cardiac massage. Her case was written up decades later, in 1998(3):

The patient recovered rapidly and left the hospital on the 21st day without signs of cerebral damage. This patient is now 86 years old, mentally normal, living alone, and doing her own housekeeping. She remembers the hospital stay and the past years as worth living

Some patients may be considered too high risk for surgery and in some centres Extracorporeal Membrane Oxygenation (ECMO) is an option. It has been used both as life support pending surgery(4), or as an alternative to surgery to allow heparinisation to be used(5,6).

In summary, some patients with massive pulmonary embolism may benefit from surgery (contraindication to ‘lysis or failed ‘lysis). Getting them to surgery alive, or operating on them during cardiac arrest, is a challenge. Ideally they would undergo embolectomy under cardopulmonary bypass in the operating room, or could be placed on ECMO in the ED prior to going to the OR. If they present to a centre without these facilities, then the venous inflow occlusion technique could be used in the OR without bypass. Just rarely a patient may present in extremis with PE to an ED without these options. If that patient has major contraindications to thrombolysis, would an ED thoracotomy be something you would entertain?

I have done several thoracotomies for penetrating trauma but never for PE. I do not pretend to know how, and cannot find a case report of ED thoracotomy for pulmonary embolism in the literature. I’m therefore NOT recommending it. However, I would love to know people’s views on its feasibility. A possible approach could be summarised as:

Massive pulmonary embolism fascinates me, because it’s seen in the ‘talk and die’ patient. It is a single, treatable pathology that if diagnosed and treated appropriately truly makes the difference between life and death. When medicine presents us with an opportunity ‘on a plate’ like that to save a life, we need to be prepared. I have had great saves with this diagnosis and sadly have seen disastrous failures to act. When the time comes, we need to ask: ‘have we explored all options?’.

1. Surgical treatment of acute pulmonary embolism–a 12-year retrospective analysis.
Scand Cardiovasc J. 2012 Jun;46(3):172-6. Epub 2012 Mar 27.
Click for abstract

2. Pulmonary embolectomy with venous inflow-occlusion.
The Lancet 1972;1(7754):767–769
Click for abstract

3. Left Anterior Thoracotomy for Pulmonary Embolectomy With 29-Year Follow-up
The Annals of Thoracic Surgery 1998, 66(4):1420-1421
Click for abstract

4.ECMO treatment saved life of a young woman with acute pulmonary embolism
Lakartidningen 2004, 101(44):3420-3421
Click for abstract

5. Extracorporeal membrane oxygenator for pulmonary embolism.
The Annals of Thoracic Surgery 1997, 64(3):883-884 Free full text

6. Peripheral Extracorporeal Membrane Oxygenation: Comprehensive Therapy for High-Risk Massive Pulmonary Embolism
Ann Thorac Surg 2012;94:104–8
Click for abstract

Echocardiography in Pulmonary Embolism

I had great fun joining in a Google Hangout with the Ultrasound Podcast guys and some real masters of emergency/critical care ultrasound. You can watch it here:

Thrombolytic Therapy in Unstable Patients with PE

Most of us would give strong consideration to giving thrombolytics to patients with massive pulmonary embolism (PE), which is in keeping with many guidelines. Some physicians remain reluctant to do so, often citing the lack of good evidence. It is true that large scale RCTs have not been done in this population. The authors of this recent retrospective study state:

There are no definitive trials that prove the value of thrombolytic therapy in unstable patients with pulmonary embolism. It is extremely remote that a randomized controlled trial will be performed in the future. We therefore analyzed the database of the Nationwide Inpatient Sample to test the hypothesis that thrombolytic therapy reduces case fatality rate in unstable patients with acute pulmonary embolism.

They demonstrate a striking difference in mortality when thrombolysis is given to unstable patients with PE, which is further reduced with the addition of a vena cava filter. ‘Unstable’ was defined as having a listed code for shock or ventilator dependence.

Associated comorbid conditions were more often present in those who did not receive thrombolytic therapy than in those who did. However in their discussion the authors add:

Although unstable patients who received thrombolytic therapy had fewer comorbid conditions than those who did not, this would not explain the difference in case fatality rate because unstable patients with a primary diagnosis of pulmonary embolism and none of the comorbid conditions…also showed a lower case fatality rate with thrombolytic therapy. Therefore, differences in comorbid conditions in this group were eliminated as a possible cause of the lower case fatality rate in unstable patients who received thrombolytic therapy.

They round off their conclusion with:

Despite the marked reduction of case fatality rate with thrombolytic therapy in unstable patients, only 30% of unstable patients received it, and the proportion receiving thrombolytic therapy is diminishing. On the basis of these data, thrombolytic therapy in combination with a vena cava filter in unstable patients with acute pulmonary embolism seems indicated.

Many thanks to Dr Daniel Horner for highlighting this paper.

BACKGROUND: Data are sparse and inconsistent regarding whether thrombolytic therapy reduces case fatality rate in unstable patients with acute pulmonary embolism. We tested the hypothesis that thrombolytic therapy reduces case fatality rate in such patients.

METHODS: In-hospital all-cause case fatality rate according to treatment was determined in unstable patients with pulmonary embolism who were discharged from short-stay hospitals throughout the United States from 1999 to 2008 by using data from the Nationwide Inpatient Sample. Unstable patients were in shock or ventilator dependent.

RESULTS: Among unstable patients with pulmonary embolism, 21,390 of 72,230 (30%) received thrombolytic therapy. In-hospital all-cause case fatality rate in unstable patients with thrombolytic therapy was 3105 of 21,390 (15%) versus 23,820 of 50,840 (47%) without thrombolytic therapy (P< .0001). All-cause case fatality rate in unstable patients with thrombolytic therapy plus a vena cava filter was 505 of 6630 (7.6%) versus 4260 of 12,850 (33%) with a filter alone (P<.0001). Case fatality rate attributable to pulmonary embolism in unstable patients was 820 of 9810 (8.4%) with thrombolytic therapy versus 1080 of 2600 (42%) with no thrombolytic therapy (P<.0001). Case fatality rate attributable to pulmonary embolism in unstable patients with thrombolytic therapy plus vena cava filter was 70 of 2590 (2.7%) versus 160 of 600 (27%) with a filter alone (P<.0001).

CONCLUSION: In-hospital all-cause case fatality rate and case fatality rate attributable to pulmonary embolism in unstable patients was lower in those who received thrombolytic therapy. Thrombolytic therapy resulted in a lower case fatality rate than using vena cava filters alone, and the combination resulted in an even lower case fatality rate. Thrombolytic therapy in combination with a vena cava filter in unstable patients with acute pulmonary embolism seems indicated.

Thrombolytic Therapy in Unstable Patients with Acute Pulmonary Embolism: Saves Lives but Underused
Am J Med. 2012 May;125(5):465-70

Clotbusting wisdom on tap – your questions answered

The prevention and management of venous thromboembolic disease is a huge topic, which generates questions for emergency, critical care, and acute physicians during many shifts:

• How long should someone requiring cardioversion for atrial fibrillation be anticoagulated for?
• How should I provide thromboprophylaxis for this intubated patient?
• This patient with submassive pulmonary embolism isn’t hypotensive yet. Can I thrombolyse them? Can I?
• There’s a large superficial vein thrombosis in that limb – is anticoagulation indicated?
• This asymptomatic patient on warfarin has an INR of 9.0 – should I reverse them?
• Do I need to add Vitamin K if I’ve reversed warfarin with prothrombin complex concentrate?

The answers to these – and many, many more – questions are provided in one of the most comprehensive guidelines I’ve ever come across. I can see myself clicking on the link below in future when on duty in the ED.

Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines
Chest. 2012 Feb;141(2 Suppl) Full Text

Enoxaparin in acute medical patients

A large multinational study challenges the practice of routine thromboprophylaxis for hospitalised acutely ill medical patients. Enoxaparin plus graduated compression stockings did not reduce 30 day mortality compared with stockings alone. There was no significant difference in the rates of major bleeding.

Background Although thromboprophylaxis reduces the incidence of venous thromboembolism in acutely ill medical patients, an associated reduction in the rate of death from any cause has not been shown.

Methods We conducted a double-blind, placebo-controlled, randomized trial to assess the effect of subcutaneous enoxaparin (40 mg daily) as compared with placebo — both administered for 10±4 days in patients who were wearing elastic stockings with graduated compression — on the rate of death from any cause among hospitalized, acutely ill medical patients at participating sites in China, India, Korea, Malaysia, Mexico, the Philippines, and Tunisia. Inclusion criteria were an age of at least 40 years and hospitalization for acute decompensated heart failure, severe systemic infection with at least one risk factor for venous thromboembolism, or active cancer. The primary efficacy outcome was the rate of death from any cause at 30 days after randomization. The primary safety outcome was the rate of major bleeding during and up to 48 hours after the treatment period.

Results A total of 8307 patients were randomly assigned to receive enoxaparin plus elastic stockings with graduated compression (4171 patients) or placebo plus elastic stockings with graduated compression (4136 patients) and were included in the intention-to-treat population. The rate of death from any cause at day 30 was 4.9% in the enoxaparin group as compared with 4.8% in the placebo group (risk ratio, 1.0; 95% confidence interval [CI], 0.8 to 1.2; P=0.83). The rate of major bleeding was 0.4% in the enoxaparin group and 0.3% in the placebo group (risk ratio, 1.4; 95% CI, 0.7 to 3.1; P=0.35).

Conclusions The use of enoxaparin plus elastic stockings with graduated compression, as compared with elastic stockings with graduated compression alone, was not associated with a reduction in the rate of death from any cause among hospitalized, acutely ill medical patients. (Funded by Sanofi; LIFENOX ClinicalTrials.gov number, NCT00622648.)

Low-Molecular-Weight Heparin and Mortality in Acutely Ill Medical Patients
N Engl J Med 2011; 365:2463-2472

ACEP policy on PE

The American College of Emergency Physicians has revised its 2003 clinical policy on pulmonary embolism.

 

Among the areas considered is the the role of thrombolytic medication. The policy provides the following recommendations to this question:

What are the indications for thrombolytic therapy in patients with PE?

Level B recommendations

Administer thrombolytic therapy in hemodynamically unstable patients with confirmed PE for whom the benefits of treatment outweigh the risks of life-threatening bleeding complications.*

*In centers with the capability for surgical or mechanical thrombectomy, procedural intervention may be used as an alternative therapy.

Level C recommendations

(1) Consider thrombolytic therapy in hemodynamically unstable patients with a high clinical suspicion for PE for whom the diagnosis of PE cannot be confirmed in a timely manner.

(2) At this time, there is insufficient evidence to make any recommendations regarding use of thrombolytics in any subgroup of hemodynamically stable patients. Thrombolytics have been demonstrated to result in faster improvements in right ventricular function and pulmonary perfusion, but these benefits have not translated to improvements in mortality.

The document contains a detailed appraisal of the literature to date on benefits and harms from thrombolysis. Of interest is the Pulmonary Embolism Severity Index (PESI) – a scoring system that appears to reliably predict mortality and thus has the potential to assist physicians in making risk-benefit decisions when considering administration of thrombolytics. The full text of the policy, which covers far more than just thrombolysis, can be found by following the link below.

Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Suspected Pulmonary Embolism
Annals of Emergency Medicine 2011 June 57(6):628-652 – Free Full Text

Thrombolysis in submassive PE – still equipoise?

The AHA has produced a comprehensive guideline on venous thromboembolic disease. Here are some excerpts pertaining to resuscitation room decision making, particularly: ‘should I thrombolyse this patient?’

Definition for massive PE: Acute PE with sustained hypotension (systolic blood pressure <90 mm Hg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or left ventricular [LV] dysfunction), pulselessness, or persistent profound bradycardia (heart rate <40 bpm with signs or symptoms of shock).

Definition for submassive PE: Acute PE without systemic hypotension (systolic blood pressure ≥90 mm Hg) but with either RV dysfunction or myocardial necrosis.
RV dysfunction means the presence of at least 1 of the following:

• RV dilation (apical 4-chamber RV diameter divided by LV diameter >0.9) or RV systolic dysfunction on echocardiography
• RV dilation (4-chamber RV diameter divided by LV diameter >0.9) on CT
• Elevation of BNP (>90 pg/mL)
• Elevation of N-terminal pro-BNP (>500 pg/mL); or
• Electrocardiographic changes (new complete or incomplete right bundle-branch block, anteroseptal ST elevation or depression, or anteroseptal T-wave inversion)

Myocardial necrosis is defined as either of the following:

• Elevation of troponin I (>0.4 ng/mL) or
  Elevation of troponin T (>0.1 ng/mL)

Odds ratio for short-term mortality for RV dysfunction on echocardiography = 2.53 (95% CI 1.17 to 5.50).

Troponin elevations had an odds ratio for mortality of 5.90 (95% CI 2.68 to 12.95).

Definition for low risk PE: those with normal RV function and no elevations in biomarkers with short-term mortality rates approaching ≈ 1%

Recommendations for Initial Anticoagulation for Acute PE

• Therapeutic anticoagulation with subcutaneous LMWH, intravenous or subcutaneous UFH with monitoring, unmonitored weight-based subcutaneous UFH, or subcutaneous fondaparinux should be given to patients with objectively confirmed PE and no contraindications to anticoagulation (Class I; Level of Evidence A).
• Therapeutic anticoagulation during the diagnostic workup should be given to patients with intermediate or high clinical probability of PE and no contraindications to anticoagulation (Class I; Level of Evidence C).

 

Patients treated with a fibrinolytic agent have faster restoration of lung perfusion. At 24 hours, patients treated with heparin have no substantial improvement in pulmonary blood flow, whereas patients treated with adjunctive fibrinolysis manifest a 30% to 35% reduction in total perfusion defect. However, by 7 days, blood flow improves similarly (≈65% to 70% reduction in total defect).

Thirteen placebo-controlled randomized trials of fibrinolysis for acute PE have been published, but only a subset evaluated massive PE specifically.
When Wan et al restricted their analysis to those trials with massive PE, they identified a significant reduction in recurrent PE or death from 19.0% with heparin alone to 9.4% with fibrinolysis (odds ratio 0.45, 95% CI 0.22 to 0.90).

Data from registries indicate that the short-term mortality rate directly attributable to submassive PE treated with heparin anticoagulation is probably < 3.0%. The implication is that even if adjunctive fibrinolytic therapy has extremely high efficacy, for example, a 30% relative reduction in mortality, the effect size on mortality due to submassive PE is probably < 1%. Thus, secondary adverse outcomes such as persistent RV dysfunction, chronic thromboembolic pulmonary hypertension, and impaired quality of life represent appropriate surrogate goals of treatment.

Data suggest that compared with heparin alone, heparin plus fibrinolysis yields a significant favorable change in right ventricular systolic pressure and pulmonary arterial pressure incident between the time of diagnosis and follow-up. Patients with low-risk PE have an unfavorable risk-benefit ratio with fibrinolysis. Patients with PE that causes hypotension probably do benefit from fibrinolysis. Management of submassive PE crosses the zone of equipoise, requiring the clinician to use clinical judgment.

An algorithm is proposed:

Two criteria can be used to assist in determining whether a patient is more likely to benefit from fibrinolysis: (1) Evidence of present or developing circulatory or respiratory insufficiency; or (2) evidence of moderate to severe RV injury.

Evidence of circulatory failure includes any episode of hypotension or a persistent shock index (heart rate in beats per minute divided by systolic blood pressure in millimeters of mercury) >1

The definition of respiratory insufficiency may include hypoxemia, defined as a pulse oximetry reading < 95% when the patient is breathing room air and clinical judgment that the patient appears to be in respiratory distress. Alternatively, respiratory distress can be quantified by the numeric Borg score, which assesses the severity of dyspnea from 0 to 10 (0=no dyspnea and 10=sensation of choking to death).

Evidence of moderate to severe RV injury may be derived from Doppler echocardiography that demonstrates any degree of RV hypokinesis, McConnell’s sign (a distinct regional pattern of RV dysfunction with akinesis of the mid free wall but normal motion at the apex), interventricular septal shift or bowing, or an estimated RVSP > 40 mm Hg.

Biomarker evidence of moderate to severe RV injury includes major elevation of troponin measurement or brain natriuretic peptides.

Two trials are currently ongoing that aim to assess effect of thrombolysis on patients with submassive PE: PEITHO and TOPCOAT

Recommendations for Fibrinolysis for Acute PE

• Fibrinolysis is reasonable for patients with massive acute PE and acceptable risk of bleeding complications (Class IIa; Level of Evidence B).
• Fibrinolysis may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory insufficiency, severe RV dysfunction, or major myocardial necrosis) and low risk of bleeding complications (Class IIb; Level of Evidence C).
• Fibrinolysis is not recommended for patients with low-risk PE (Class III; Level of Evidence B) or submassive acute PE with minor RV dysfunction, minor myocardial necrosis, and no clinical worsening (Class III; Level of Evidence B).
• Fibrinolysis is not recommended for undifferentiated cardiac arrest (Class III; Level of Evidence B).

Recommendations for Catheter Embolectomy and Fragmentation

• Depending on local expertise, either catheter embolectomy and fragmentation or surgical embolectomy is reasonable for patients with massive PE and contraindications to fibrinolysis (Class IIa; Level of Evidence C).
• Catheter embolectomy and fragmentation or surgical embolectomy is reasonable for patients with massive PE who remain unstable after receiving fibrinolysis (Class IIa; Level of Evidence C).
• For patients with massive PE who cannot receive fibrinolysis or who remain unstable after fibrinolysis, it is reasonable to consider transfer to an institution experienced in either catheter embolectomy or surgical embolectomy if these procedures are not available locally and safe transfer can be achieved (Class IIa; Level of Evidence C).
• Either catheter embolectomy or surgical embolectomy may be considered for patients with submassive acute PE judged to have clinical evidence of adverse prognosis (new hemodynamic instability, worsening respiratory failure, severe RV dysfunction, or major myocardial necrosis) (Class IIb; Level of Evidence C).
• Catheter embolectomy and surgical thrombectomy are not recommended for patients with low-risk PE or submassive acute PE with minor RV dysfunction, minor myocardial necrosis, and no clinical worsening (Class III; Level of Evidence C).

 

Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension
Circulation. 2011 Apr 26;123(16):1788-1830 (Free Full Text)

Thrombolysis for PE after limb surgery

A patient develops shock and dyspnoea on the orthopaedic ward after a total knee replacement and massive pulmonary embolism is confirmed radiologically. Would you give a fibrinolytic or is it contraindicated? Harry Wright and colleagues did, but before giving 50 mg of intravenous rtPA they applied a tourniquet (Cryocuff) to the limb to limit the proportion of the systemic thrombolytic agent that would reach the site of the surgery. The tourniquet was inflated just before the infusion and was left on for one hour. There was some oozing of blood from the postoperative wound, which settled with bandage compression. The authors state that the inflation time of one hour was sufficient for the thrombolytic agent to be largely eliminated from the circulation, since alteplase has a plasma half-life of less than five minutes, although some plasminogen activator activity does persist for up to four hours.

The patient was well at three month follow up. They suggest:

Given the success in this case, we believe that major limb surgery no longer represents a contraindication to thrombolysis.

Thrombolysis for postoperative pulmonary embolism: limiting the risk of haemorrhage
Thorax. 2011 May;66(5):452

CVT guideline

Thanks to neuro-icu.com for highlighting this one: The American Heart Association and American Stroke Association have produced guidelines for the diagnosis and management of cerebral venous thrombosis. Here is a summary of their recommendations. The full text of the guidelines is available via the link at the bottom.

Routine Blood Work

• In patients with suspected CVT, routine blood studies consisting of a complete blood count, chemistry panel, prothrombin time, and activated partial thromboplastin time should be performed (Class I; Level of Evidence C).
• Screening for potential prothrombotic conditions that may predispose a person to CVT (eg, use of contraceptives, underlying inflammatory disease, infectious process) is recommended in the initial clinical assessment (specific recommendations for testing for thrombophilia are found in the long-term management section of this document) (Class I; Level of Evidence C).
• A normal D-dimer level according to a sensitive immunoassay or rapid enzyme-linked immunosorbent assay (ELISA) may be considered to help identify patients with low probability of CVT (Class IIb; Level of Evidence B). If there is a strong clinical suspicion of CVT, a normal D-dimer level should not preclude further evaluation.

Common Pitfalls in the Diagnosis of CVT

• In patients with lobar ICH of otherwise unclear origin or with cerebral infarction that crosses typical arterial boundaries, imaging of the cerebral venous system should be performed (Class I; Level of Evidence C).
• In patients with the clinical features of idiopathic intracranial hypertension, imaging of the cerebral venous system is recommended to exclude CVT (Class I; Level of Evidence C).
• In patients with headache associated with atypical features, imaging of the cerebral venous system is reasonable to exclude CVT (Class IIa; Level of Evidence C).

Imaging in the Diagnosis of CVT

• Although a plain CT or MRI is useful in the initial evaluation of patients with suspected CVT, a negative plain CT or MRI does not rule out CVT. A venographic study (either CTV or MRV) should be performed in suspected CVT if the plain CT or MRI is negative or to define the extent of CVT if the plain CT or MRI suggests CVT (Class I; Level of Evidence C).
• An early follow-up CTV or MRV is recommended in CVT patients with persistent or evolving symptoms despite medical treatment or with symptoms suggestive of propagation of thrombus (Class I; Level of Evidence C).
• In patients with previous CVT who present with recurrent symptoms suggestive of CVT, repeat CTV or MRV is recommended (Class I; Level of Evidence C).
• Gradient echo T2 susceptibility-weighted images combined with magnetic resonance can be useful to improve the accuracy of CVT diagnosis (Class IIa; Level of Evidence B).
• Catheter cerebral angiography can be useful in patients with inconclusive CTV or MRV in whom a clinical suspicion for CVT remains high (Class IIa; Level of Evidence C).
• A follow-up CTV or MRV at 3 to 6 months after diagnosis is reasonable to assess for recanalization of the occluded cortical vein/sinuses in stable patients (Class IIa; Level of Evidence C).

Management and Treatment

• Patients with CVT and a suspected bacterial infection should receive appropriate antibiotics and surgical drainage of purulent collections of infectious sources associated with CVT when appropriate (Class I; Level of Evidence C).
• In patients with CVT and increased intracranial pressure, monitoring for progressive visual loss is recommended, and when this is observed, increased intracranial pressure should be treated urgently (Class I; Level of Evidence C).
• In patients with CVT and a single seizure with parenchymal lesions, early initiation of antiepileptic drugs for a defined duration is recommended to prevent further seizures (Class I; Level of Evidence B).
• In patients with CVT and a single seizure without parenchymal lesions, early initiation of antiepileptic drugs for a defined duration is probably recommended to prevent further seizures (Class IIa; Level of Evidence C).
• In the absence of seizures, the routine use of antiepileptic drugs in patients with CVT is not recommended (Class III; Level of Evidence C).
• For patients with CVT, initial anticoagulation with adjusted-dose UFH or weight-based LMWH in full anticoagulant doses is reasonable, followed by vitamin K antagonists, regardless of the presence of ICH (Class IIa; Level of Evidence B).
• Admission to a stroke unit is reasonable for treatment and for prevention of clinical complications of patients with CVT (Class IIa; Level of Evidence C).
• In patients with CVT and increased intracranial pressure, it is reasonable to initiate treatment with acetazolamide. Other therapies (lumbar puncture, optic nerve decompression, or shunts) can be effective if there is progressive visual loss. (Class IIa; Level of Evidence C).
• Endovascular intervention may be considered if deterioration occurs despite intensive anticoagulation treatment (Class IIb; Level of Evidence C). In patients with neurological deterioration due to severe mass effect or intracranial hemorrhage causing intractable intracranial hypertension, decompressive hemicraniectomy may be considered (Class IIb; Level of Evidence C).
• For patients with CVT, steroid medications are not recommended, even in the presence of parenchymal brain lesions on CT/MRI, unless needed for another underlying disease (Class III; Level of Evidence B).

Long-Term Management and Recurrence of CVT

• Testing for prothrombotic conditions, including protein C, protein S, antithrombin deficiency, antiphospholipid syndrome, prothrombin G20210A mutation, and factor V Leiden, can be beneficial for the management of patients with CVT. Testing for protein C, protein S, and antithrombin deficiency is generally indicated 2 to 4 weeks after completion of anticoagulation. There is a very limited value of testing in the acute setting or in patients taking warfarin. (Class IIa; Level of Evidence B).
• In patients with provoked CVT (associated with a transient risk factor), vitamin K antagonists may be continued for 3 to 6 months, with a target INR of 2.0 to 3.0 (Table 3) (Class IIb; Level of Evidence C).
• In patients with unprovoked CVT, vitamin K antagonists may be continued for 6 to 12 months, with a target INR of 2.0 to 3.0 (Class IIb; Level of Evidence C).
• For patients with recurrent CVT, VTE after CVT, or first CVT with severe thrombophilia (ie, homozygous prothrombin G20210A; homozygous factor V Leiden; deficiencies of protein C, protein S, or antithrombin; combined thrombophilia defects; or antiphospholipid syndrome), indefinite anticoagulation may be considered, with a target INR of 2.0 to 3.0 (Class IIb; Level of Evidence C).
• Consultation with a physician with expertise in thrombosis may be considered to assist in the pro- thrombotic testing and care of patients with CVT (Class IIb; Level of Evidence C).

Management of Late Complications (Other Than Recurrent VTE)

• In patients with a history of CVT who complain of new, persisting, or severe headache, evaluation for CVT recurrence and intracranial hypertension should be considered (Class I; Level of Evidence C)

CVT in pregnancy

• For women with CVT during pregnancy, LMWH in full anticoagulant doses should be continued throughout pregnancy, and LMWH or vitamin K antagonist with a target INR of 2.0 to 3.0 should be continued for at least 6 weeks postpartum (for a total minimum duration of therapy of 6 months) (Class I; Level of Evidence C).
• It is reasonable to advise women with a history of CVT that future pregnancy is not contraindicated. Further investigations regarding the underlying cause and a formal consultation with a hematologist and/or maternal fetal medicine specialist are reasonable. (Class IIa; Level of Evidence B).
• It is reasonable to treat acute CVT during pregnancy with full-dose LMWH rather than UFH (Class IIa; Level of Evidence C).
• For women with a history of CVT, prophylaxis with LMWH during future pregnancies and the postpartum period is probably recommended (Class IIa; Level of Evidence C).

Children

• Supportive measures for children with CVT should include appropriate hydration, control of epileptic seizures, and treatment of elevated intracranial pressure (Class I; Level of Evidence C).
• Given the potential for visual loss owing to severe or long-standing increased intracranial pressure in children with CVT, periodic assessments of the visual fields and visual acuity should be performed, and appropriate measures to control elevated intracranial pressure and its complications should be instituted (Class I; Level of Evidence C).
• In all pediatric patients, if initial anticoagulation treatment is withheld, repeat neuroimaging including venous imaging in the first week after diagnosis is recommended to monitor for propagation of the initial thrombus or new infarcts or hemorrhage (Class I; Level of Evidence C).
• In children with acute CVT diagnosed beyond the first 28 days of life, it is reasonable to treat with full-dose LMWH even in the presence of intracra- nial hemorrhage (Class IIa; Level of Evidence C).
• In children with acute CVT diagnosed beyond the first 28 days of life, it is reasonable to continue LMWH or oral vitamin K antagonists for 3 to 6 months (Class IIa; Level of Evidence C).
• In all pediatric patients with acute CVT, if initial anticoagulation is started, it is reasonable to perform a head CT or MRI scan in the initial week after treatment to monitor for additional hemor- rhage (Class IIa; Level of Evidence C).
• Children with CVT may benefit from thrombophilia testing to identify underlying coagulation defects, some of which could affect the risk of subsequent rethromboses and influence therapeutic decisions (Class IIb; Level of Evidence B).
• Children with CVT may benefit from investigation for underlying infections with blood cultures and sinus radiographs (Class IIb; Level of Evidence B).
• In neonates with acute CVT, treatment with LMWH or UFH may be considered (Class IIb; Level of Evidence B).
• Given the frequency of epileptic seizures in children with an acute CVT, continuous electroencephalography monitoring may be considered for individuals who are unconscious or mechanically ventilated (Class IIb; Level of Evidence C).
• In neonates with acute CVT, continuation of LMWH for 6 weeks to 3 months may be considered (Class IIb; Level of Evidence C).
• The usefulness and safety of endovascular intervention are uncertain in pediatric patients, and its use may only be considered in carefully selected patients with progressive neurological deterioration despite intensive and therapeutic levels of anticoagulant treatment (Class IIb; Level of Evidence C).

Diagnosis and Management of Cerebral Venous Thrombosis: A Statement for Healthcare Professionals From the American Heart Association/American Stroke Association
Stroke. 2011 Feb 3. [Epub ahead of print] Full Text

ED US for DVT

Made a radiologist go red with rage recently? If not, you could try showing them this paper¹ in this month’s Annals of Emergency Medicine that describes accurate emergency physician ultrasound diagnosis of deep vein thrombosis after just ten minutes training!
ED patients with a suspected lower extremity deep venous thrombosis were assessed using a bedside 2-point compression technique by emergency physicians using a portable US machine and all patients subsequently underwent duplex ultrasonography performed by the Department of Radiology.

The emergency physicians had a 10-minute training session before enrolling patients

The techinque involved 2 specific points: the common femoral and popliteal vessels, with subsequent compression of the common femoral and popliteal veins. The study result was considered positive for proximal lower extremity deep venous thrombosis if either vein was incompressible or a thrombus was visualised.

A total of 47 physicians performed 199 2-point compression ultrasonographic examinations in the ED.
There were 45 proximal lower extremity deep venous thromboses observed on Department of Radiology evaluation, all correctly identified by ED 2-point compression ultrasonography. The 153 patients without proximal lower extremity deep venous thrombosis all had a negative ED compression ultrasonographic result. One patient with a negative Department of Radiology ultrasonographic result was found to have decreased compression of the popliteal vein on ED compression ultrasonography, giving a single false-positive result, yet repeated ultrasonography by the Department of Radiology 1 week later showed a popliteal deep venous thrombosis. The sensitivity and specificity of ED 2-point compression ultrasonography for deep venous thrombosis were 100% (95% confidence interval 92% to 100%) and 99% (95% confidence interval 96% to 100%), respectively.

These figures may appear to fail the ‘sniff test’, ie. seem too good to be true. Not surprisingly Annals acknowledge this by providing an accompanying editorial² by emergency ultrasound heavyweight Michael Blaivas, MD, who is healthily skeptical of such a minimal training program but is overwhelmingly supportive of the principle. Dr Blaivas also provides a fantastic summary of the existing evidence base on ED ultrasound for DVT. To me he hits the nail on the head when with a philosophical point on the practice of EM: ‘One common challenge proponents of any new application or procedure face in emergency medicine is overcoming the inertia of comfort with the status quo.’ Spot on, Dr B.

1. Compression Ultrasonography of the Lower Extremity With Portable Vascular Ultrasonography Can Accurately Detect Deep Venous Thrombosis in the Emergency Department
Annals of Emergency Medicine 2010;56(6):601-10

2. Point-of-Care Ultrasonographic Deep Venous Thrombosis Evaluation After Just Ten Minutes’ Training: Is This Offer Too Good to Be True?
Annals of Emergency Medicine 2010;56(6):611-3

The guys at ‘EM Live’ have a short video on how to do DVT ultrasound:

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