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CHEST edilOr~~~E Are Modifications Necessary in the Performance of Pulmonary Angiograms?
The confirmation of the diagnosis of pulmonary embolism is often an arduous, complex and expensive chore. As the sensitivity and specificity of studies have been refined, it appears that a negative radioisotope perfusion study is about 99 percent specific as an exclusionary study for pulmonary embolism.1.2 However, to establish a positive diagnosis, the selective pulmonary angiogram has been considered the most specific test for demonstrating pulmonary emboli. 3.4 Due to recent reports of false negative pulmonary angiograms (see page 139) a reappraisal of pulmonary angiographic methodology seems appropriate.5.6 It has been shown that normal individuals have normal lung scans. 7.S Therefore, an abnormal lung scan indicates lung pathology, but not necessarily pulmonary infarction. ~ Kipper et al lO studied patients with suspected pulmonary emboli and normal lung scans who remained untreated. Since none developed findings of pulmonary embolization, they concluded that the probability of a false negative lung scan was low. In that study, withholding anticoagulant treatment after a normal lung scan was not associated with morbidity or mortality; therefore, if pulmonary emboli are too small to be resolved by a perfusion scan, they are of no clinical significance. In another study of 180 consecutive patients undergoing pulmonary angiography, 167 had positive lung scans but were untreated because of negative angiographic results. 11 None died of pulmonary embolization during a six-month follow-up period. This study demonstrated that a negative angiogram is reliable when the angiography is carefully performed. These investigators used selective left and right pulmonary artery injections, sequentially filming each lung in at least two views. Superselective angiograms utilizing magnification angiography were recorded from those lung segments in which the perfusion scan indicated potential obstruction. Techniques as comprehensive as this can demonstrate emboli or vessel cut off as small as 0.5 mm, whereas in a selective main
88 I NUMBER 1 I JULY, 1985
pulmonary artery injection resolution is limited to 2 mm. 12•13 Furthermore, these new techniques obviated the need for using soft criteria such as blood flow slowing and oligemia, which are very subjective and unreliable. 14 The role of cineangiographic techniques in the detection of pulmonary embolus is as yet undefined. However, most cardiac catheterization laboratories are equipped with high resolution cineangiographic equipment with varying magnification potentials. Although visualization oflarge areas of a pulmonary field may not be possible, it is possible to obtain angiograms of smaller areas with a high degree of resolution. 15 If high resolution cineangiography is capable of resolving branch vessels of coronary arteries, it should be suitable for resolving pulmonary vessels as well. Superselective pulmonary artery injections of small volumes of angiographic contrast material into areas of the lung which have demonstrated perfusion defects by radionuclide scans can provide angiograms of high resolution. The dynamic nature of the study helps resolve lesions that would be considered suspicious by static filming techniques. Furthermore, respiratory movement, which is undesirable in static filming techniques, is helpful in separating overlying vessels in cine recordings. 16.17 The minimum goal in angiographic studies should be defined. Is it to detect all emboli or only those with clinical importance? The latter is probably more realistic. Although conventional cut film techniques have proven reliable, new methodology may be helpful or superior. us Patients with negative perfusion scans need not undergo pulmonary angiography because there is little likelihood of significant embolism. 17 Patients with positive perfusion scans are potential candidates for anticoagulant therapy. Since anticoagulant therapy is associated with high morbidity and some mortality, a definitive diagnosis should be made whenever possible. This probably can be done most efficiently by superselective pulmonary cineangiograms in the heart catheterization laboratory. This also provides an opportunity for measuring pulmonary pressure, cardiac output and pulmonary vascular resistances. Superselective cineangiographic pulmonary angiography has not undergone critical comparative studies with current nonselective static film techCHEST I 88 I 1 I JULY. 1985
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niques. Such studies are indicated. LeRoi Price, M.D.; and Maroin Dunn, M.D., F.C.C.P. Kansas City, Kansas Cardiovascular Division, Department of Medicine, University of Kansas School of Medicine. Reprint requests: Dr. Dunn, University of Kansas Medical Center Hospital, 116 E Bldg, 39th and Raisoow, Kansas City, KS 66103
REFERENCES
1 Sostman HD, Rapoport S, Glickman MG, Gottschalk A. Problems in noninvasive imaging of pulmonary embolism. Radiol North Am 1983; 21:759-74 2 Wagner HN, Strauss HW Radioactive tracers in the differential diagnosis of pulmonary embolism. Prog Cardiovasc Dis 1975; 17:271-82 3 Dalen JE, Brooks HL, Jonson LW, Meister SG, Szucs MM, Dexter L. Pulmonary angiography in acute pulmonary embolism: Indications, techniques, and results in 367 patients. Am Heart J 1971; 81:175-85 4 HuB RD, Hinh}, Carter CJ, Jay RM, Dodd PE, Ockelford PA, et ale Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983; 98:891-99 5 Bell WR, Simon TL. A comparative analysis of pulmonary perfusion scans with pulmonary angiograms. Am Heart J 1976;
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92:700-06 6 Sostman HD, Ravin CE, Sullivan DC, Mills SR, Glickman MG, Dortman GS. Use of pulmonary angiography for suspected pulmonary embolism: Influence of scintigraphic diagnosis. AJR 1982; 139:673-77 7 Fedullo PF, Moser KM, Hartman Ml: Ashburn WL. Patterns of pulmonary perfusion scans in normal subjects. Am Rev Respir Dis 1983; 127:776-79 8 Wallace JM, Moser KM, Hartman Ml: Ashburn WL. Patterns of pulmonary perfusion scans in normal subjects. Am Rev Respir Dis 1981; 124:480-83 9 Goldhaber SZ, Hennekens CH, Evans DA, Newton EC, Godleski JJ. Factors associated with correct antemortem diagnosis of major pulmonary embolism. Am J Med 1982; 73:822-26 10 Kipper MS, Moser KM, Kortman KE, Ashburn WL. Long term follow-up of patients with suspected pulmonary embolism and a normal lung scan. Chest 1982; 82:411-15 11 Novelline RA, Baltarowich OH, Athanasoulis CA, Waltman AC, Greenfield AJ, McKusick KA. The clinical course ofpatients with suspected pulmonary embolism and a negative pulmonary arteriogram. Radiology 1978; 126:561-67 12 Boolcstein JJ. Segmental arteriography in pulmonary embolism. Radiology 1969; 93:1007-12 13 McIntyre KM, Sasahara AA, Sharma G~ Pulmonary thromboembolism: Current concepts. Adv Intern Med 1972; 18:199-218 14 Boolcstein JJ, Silver TM. The angiographic differential diagnosis of acute pulmonary embolism. Radiology 1974; 110:25-33 15 Grossman W Cardiac catheterization and angiography. Philadelphia: Lea & Febiger, 1980 16 Meister SG, Brooks HL, Szucs MM, Dexter L. Pulmonary cineangiography in acute embolism. Am Heart J 1972; 84:33-7 17 Cheely R, McCartney WH, Perry JR, Delany OJ, Bustad L, Wynia VH, et ale The role ofnoninvasive tests versus pulmonary angiography in the diagnosis ofpulmonary embolism. Am J Med 1981; 70:17-22 18 Ferris E, Smith ~ Lim ~ Whittle J, Bon B, Angtuaco L Radionuclide-guided balloon cineangiography: An adjunct to pulmonary arteriography. Am Heart J 1984; 108:539-42
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Nutritional Support Whether or Not Some Is Good, More Is Not Better
I ntional a recent editorial, I challenged the use of nutrisupport of patients on respirators. As of this l
writing, no prospective randomized controlled trial (PRCf) has yet assessed the efficacy of parenteral or enteral feeding. Nonetheless, these therapies continue to be used, not without associated morbidity. In this issue of Chest, (see page 141) Drs. Dark, Pingleton, and Kerby have provided more information concerning the complication of nutritional support of most interest to pulmonary physicians, that of excessive CO2 production. In 1979 Burke et al, 2 and Askanazi and coworkers3 in the next yeat; described patients who produced increased amounts ofCO2 while receiving carbohydratebased total parenteral nutrition (TPN). Although patients without overt lung disease did not develop CO2 retention, three patients of Covelli et aI" did; two of them had underlying chronic obstructive lung disease and the third bilateral empyemas. We now learn of two patients with the adult respiratory distress syndrome who also became hypercapnic as a consequence of nutritional support. As Dark and coinvestigators report, the excess CO2 production is due to the oversupply of carbohydrate calories; those which are not immediately burned are converted to fat with an associated release of CO2 • Although the reports cited above deal with patients on TPN, presumably the same phenomenon would occur with enteral nutrition. The patients described by Dark et al did not develop hypercapnia while on mechanical respiration, even in the face ofthe extra CO2 load. Unfortunately, what the machine could do, nature could not; when weaning was attempted, CO2 retention appeared. It was only after the caloric infusion was reduced that the respirator could be detached. For such patients, the crucial issue is determining how many calories are really required. When I was a fledgling in the area of nutritional support in the early 19708, the premise seemed to be that if some was good, more just had to be better; it was not at all unusual for patients to be receiving 4,000-5,000 calories per day. For some time n~ we have recognized that "hyper"-alimentation increases body weight by increasing body water and fat. 6-8 From more recent studies we are beginning to realize that the actual energy requirements of hospitalized patients, even the critically ill, are usually more on the order of 2,000 calories per day.9-li The two patients reported by Dark et al were initially begun on daily regimens containing over 4,000