DVT and PE ========== þ PERC: PE Ruleout Criteria þ Upper Extremity DVT þ Should patients with DVT walk on it? Yes. þ Wells Criteria and Risk Factors (and Goldhaber and Stein) þ Testing for pregnant patients: þ Airline Travel as a risk factor þ Mercy DVT and PE Evaluation Guidelines þ Interpreting VQ scan results þ Detecting PE þ Sesonal Variation (in Britain) þ PE simulating MI - PEs may cause enough RV strain to cause a small MI - endocardial sloughing leads to mildly elevated troponin. þ "Minor" PE þ Thrombolysis and PE þ LMWH is as good as unfractionated - Unfractionated heparin is the traditional treatment of choice for patients presenting with submassive pulmonary embolism . However, newer low-molecular-weight heparins have been developed and tested in several clinical trials in the last 2 decades because of the many limitations of unfractionated heparin . The pharmacologic properties of the low-molecular-weight heparins allow them to be administered subcutaneously in fixed, weight-adjusted doses without need for laboratory monitoring. Different studies have recently proved their efficacy in the treatment of patients with deep vein thrombosis. Because there is good evidence that deep vein thrombosis and pulmonary embolism are 2 expressions of a single disease, the use of low-molecular-weight heparins has been extended to patients presenting with clinically stable pulmonary embolism . In particular, the results of 2 important clinical trials, the Columbus and the Th‚s‚e, have conclusively proved that the low-molecular-weight heparins are as safe and effective as unfractionated heparin . In some centers, approximately 80% of patients with deep vein thrombosis are treated at home. This suggests that carefully selected patients with clinically stable pulmonary embolism can receive home treatment with low-molecular-weight heparins. [Low-molecular-weight heparin in the treatment of pulmonary embolism. Ageno W - Semin Vasc Surg - 01-Sep-2000; 13(3): 189-93] þ Rate of bleeding with UFH is 4% þ DVT and PE association - 40-64% PE in proximal lower extremity DVT, - 12% in upper extremity DVT; - 30% of proximal leg DVT in one study had asymtomatic PE. - A DVT is found in the lower extremity of approximately 70% of patients with a proven PE. - Clots may also originate in the right heart, the pelvic veins, the upper extremities or the superficial veins of the lower extremity. Ref: Rosen's CD Rom line 20693 More on "other" sites for clot causing PE: þ Critical Points about PE - PE is extremely common and is more often than not unrecognized antemortum. - the notion that the absence of 'typical' presenting signs or symptoms has any prognostic value is a little silly -- remember, we're talking about a fatal syndrome that is clinically unsuspected until after death in more than 2/3 of patients who die from it. - warfarin is not always protective, and that starting warfarin without heparin will INCREASE thrombosis and PE. - extremely rapid clot lysis, dramatic hemodynamic improvement within minutes, and immediate angiographic or V/Q resolution is common (although unfortunately not universal) when thrombolytic therapy is used. - immediate thrombolysis is the standard of care for all hypotensive or significantly hypoxemic patients with pulmonary embolism, and for all patients whose condition will not permit them to tolerate additional embolic episodes, even in the absence of (or after the resolution of) hypotension or hypoxemia. þ High frequency of unsuspected PE (From Feied, PE, Rosen 4E) - Autopsy results have shown that up to 60% of patients dying in the hospital will have evidence of pulmonary embolism, while the diagnosis will be missed ante mortum in about 70 percent of the cases.[1] The problem is not confined to surgical patients: acute deep vein thrombosis may be demonstrated in 10% - 13% of all general medical patients placed at bedrest for a week,[2,3] in 29% - 33% of medical ICU patients,[2,4] in 20% - 26% of pulmonary disease patients kept in bed for 3 or more days,[3,5] in 27% - 33% of those admitted to a coronary care unit after myocardial infarction,[6,7] and in 48% of asymptomatic patients after coronary artery bypass graft.[8] Half or more of these patients can be shown to have suffered pulmonary embolism, even though the majority will have had none of the classic symptoms of PE.[9-12] References: - That this incidence of venous thromboembolism is clinically significant has been demonstrated beyond doubt by the demonstration of reduced mortality through prophylactic anticoagulation. For example, in a population of 1358 general medical patients admitted through the Emergency Department and randomized to receive heparin versus no heparin as prophylaxis against venous thromboembolism, heparin produced an astonishing 31.1% reduction in mortality.[13] This mortality reduction is comparable to that which has been shown for heparin prophylaxis in postoperative patients.[14] Other methods of prophylaxis have also been shown to be effective in reducing the incidence of deep vein thrombosis, pulmonary embolism, and death in the general population of hospitalized patients. References: þ Autopsy series (From Feied, PE, Rosen 4E) - Below is abstract, complete text available here: - Autopsy studies since the 1940's have consistently demonstrated that death from massive pulmonary embolism is one of the most common causes of unexpected death, and that the diagnosis is unsuspected until autopsy in approximately 80% of cases. Pulmonary embolism is second only to coronary artery disease as a cause of sudden unexpected natural death at any age,[15] and the diagnosis is especially likely to be missed in older patients: Goldhaber[16] found that the correct diagnosis of pulmonary embolism had been made in 30 percent (16 of 54) of all patients who died with massive pulmonary embolism, but in only 10 percent of those who were 70 years of age or older. Gross[17] reports that pulmonary embolism is the most commonly missed diagnosis responsible for death in the elderly institutionalized patient, being missed in 60% of cases. References: - Table collates a number of published autopsy studies, showing the total population of autopsies, the number of autopsies in which acute pulmonary embolism was noted, and the frequency with which the diagnosis of pulmonary embolism was clinically unsuspected before the autopsy. Missing data points have been left blank. A formal meta-analysis is difficult, because some authors have included all cases of PE found at autopsy, others included only acute, massive PE, and some included only PE's that were the sole immediate cause of death. Explanation is found in the comments where known. - This body of work provides convincing evidence that failure to diagnose pulmonary embolism in patients who die soon after the event is the rule in every clinical setting. Several particularly important autopsy reports are summarized below. - Pulmonary emboli were found in 18.5% of a series of consecutive autopsies in Prague, and were responsible for 11% of all deaths. 3.4% of deaths were due to PE in patients who otherwise were expected to recover from their underlying illness. 44% of patients were found to have multiple PE's of varying ages. A source of venous thrombus was found in only 55% of the cases. The frequency of missed diagnosis was 70% overall, 57% in those for whom PE was directly responsible for death, and 54% in those with an otherwise good long-term prognosis.[38] - Lower extremity venous thrombosis was noted in 40% of all hospital deaths in another series of autopsy on 1350 adults. Thrombi were located bilaterally in the calves in the majority of cases. Massive pulmonary embolism was identified in 319 of the cases (23.5%) and had caused sudden death in 7.8% of cases.[45] - A possible diagnosis of pulmonary embolism had been considered in only 49% of the 92 patients who died from autopsy-proven acute massive PE at the Mayo clinic between 1985 and 1989. Even worse, a diagnostic workup was pursued while the patient was alive in only 22% of cases. Before the autopsy, the listed cause of death was correct in only 32%. Only 60% of these patients who died from PE had dyspnea, only 17% had chest pain, and only 3% had hemoptysis. 46% of these patients had good prognoses apart from their pulmonary emboli, and the same fraction (46%) had received some (obviously inadequate) prophylaxis against venous thromboembolism.[35] - Papadakis[46] notes that at autopsy, pulmonary embolism was found to be the single most frequent unsuspected cause of death in patients who died while on a ventilator. If the unsuspected diagnosis had been made antemortum, improvement with probable survival would have been expected in 12% of the patients who died, and clinical management would have been changed substantively in 18%. - Pulmonary embolism was responsible for 20 percent of all deaths and 32% of all deaths that proceeded to autopsy in a study of patients who died on a surgical ward in Malmo, Sweden. Of all autopsy-proven pulmonary emboli, 29% were the immediate cause of death, another 27% contributed to death, and 44% were judged incidental. The diagnosis was rarely clinically apparent before death.[33] - In another surgical patient population, a favorable prognosis had been expected in 9 of 16 patients who died from autopsy-proven postoperative pulmonary thromboembolism. Four of the deaths occurred within 24 hours of surgery, another five within the first week, and the remaining seven within the next 3 weeks.[25] - There was a major missed diagnosis in 14% of patients who died while in the hospital and went to autopsy after an attempt at closed-chest cardiopulmonary resuscitation (CPR). Pulmonary embolism and bowel ischemia together accounted for 90% of these cases of missed major diagnoses.[47] - The most important lessons to be learned from a thorough survey of the autopsy literature are general ones. DVT and PE are much more common than is usually realized. Most patients with DVT will develop PE, and the majority of cases will be clinically unrecognized. Untreated, approximately 1/3 of patients with pulmonary embolism will die from a future embolic episode. This is true whether the initial embolism is small or large. Most patients who die from pulmonary embolism have not had any diagnostic workup nor prophylaxis for the disease, even when classic signs and symptoms are documented in the chart. Appropriate diagnostic and therapeutic management is most often withheld even when the potential diagnosis of pulmonary embolism has been explicitly considered and documented in the chart. References: þ Natural History of PE - The issue of the natural history of untreated PE has been raised. I pointed to a recent short-term (3 month) analysis of a subgroup of the PIOPED study which documented mortality in 1/20 untreated patients. I noted Craig's recent citation of a 1960 study which was discontinued after randomizing 35 patients because of clear benefit of antocoagulation. Tintinalli (3rd ed) mentions a study involving 516 patients. The subgroup that was anticoagulated had a 92% survival and 16% recurrence rate compared to the group in whom anticoagulation was contraindicated (42% survival and 55% recurrence). No citation is given. Admittedly these two groups may not have been comparable in all respects. --H Louzon, M.D. þ Incidence of PE in the ED - One study showed a very high incidence (21%) of pulmonary embolism in patients presenting to the ED with chest pain (1). These emboli were documented either at autopsy or by pulmonary angiography. [Hull RD, Raskob GE, Carter CJ, Coates G, Gill GJ, Sackett DL, Hirsh J, Thompson M. Pulmonary embolism in outpatients with pleuritic chest pain. Arch Intern Med 1988 Apr;148(4):838-44.] Abstract: þ PIOPED Study, Famous and important: [PIOPED Investigators. Value of the ventilation/perfusion scan in acute pulmonary embolism: Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). JAMA 1990;263(2):2753-2759.] Random sampling of 933 of 1493 patients, prospective. 931 had VQ and 755 had angiograms. 33% of the 755 (251) had PE. Almost all had high, intermediate or low probability, but so did most without PE (sensitivity 98%, specificity 10%.) Of 116 with high-probability scans and definitive angiograms, 102 (88%) had PE, but only a minority with PE had high probability scans (sensitivity 41%, specificity 97%). Of 322 with intermediate-probability scans and definitive angiograms, 105 (33%) had PE. Follow up and angiograms together suggest PE in 12% of those with low probability scans. þ Previous PE - Comment in PIOPED study: previous PE may cause scarring that may be mistaken for acute PE. þ Management Sequence: - Thrombolysis in general - Thrombolysis in PE: þ Craig Feied's Treatise on DVT and PE: þ Epidemiology of DVT and PE - up to 2.5 million a year DVTs in US; 25% will also have PE. DVT === þ risk stratification for potential DVT: - treatment for CA in past 6 months - immobilization in bed or cast - previous DVT or PE - swollen leg - swollen calf more than 3 cm compared with other side - pitting edema - evidence of collateral circulation (John Michael, MD FRCPC FAAEM Ottawa Civic Hospital) þ Virchow's Triad: (predisposing factors for developing a deep venous thrombosis; Rosen's CD Rom line 20692) - venostasis - hypercoagulability and - vessel wall inflammation. þ 15-30% of calf DVT propagate proximally. þ Many believe that DVT occurs in multiple veins at about the same time, not starting distally and proceeding proximally. þ Negative contrast venogram = only 1-1.5% risk of true DVT in the six months following. þ IPG: must have significant thrombus, may be confused by pelvic mass compression, poor study. þ Tests for DVT - Virchow described triad of risks: stasis, hyercoagulable state, venous damage þ Anticoagulation --------------------------------------------------------------------------- Pretest Venous Clinical Doppler Probability Results Rx --------------------------------------------------------------------------- Low (5% Normal No Rx have DVT) Abnormal Venogram Moderate (35% Normal Serial Dopplers have DVT) Abnormal Treat as DVT High (85% Normal Venogram have DVT) Abnormal Treat as DVT [Scientific American Medicine 5/96] --------------------------------------------------------------------------- >How do you manage your calf DVT's then? Do you admit and heparinize, or >send home? Do you have a good reference for me to show my group regarding [calf DVT]? > Personally, I now treat calf DVT as follows: Below the trifurcation and not in the anterior tibial vein, I use the european approach: put them in 30-40 mm Hg gradient compression hose, start BID subQ lovenox, which is fully anticoagulating but doesn't prolong the PTT, and follow closely as outpatient. In the popliteal and anterior tibial segments, which are basically a straight-shot continuation of the femoral vein, I treat as for more proximal DVT. Craig Feied, MD