Confession and Some Lessons The PISA-PED study

Confession and Some Lessons The PISA-PED study

radio logic, and physiologic dat a. Th e pr esen ce of deep venous thrombosis or other causes of emboli should be rigorously sou ght. Fin ally, wher e...

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radio logic, and physiologic dat a. Th e pr esen ce of deep venous thrombosis or other causes of emboli should be rigorously sou ght. Fin ally, wher e PE is confirmed it is imp ortant to rep eat th e lung scan once anti coagulation is complet ed . Clea rly, even with succes sful the rapy, some Vio.mismatch de fects occasionally do not resolve, and a follow-up lung scan pro vides a useful baselin e to monitor future events. Th e frequ ency of th is message in e mine ntly quot able articles is lacking.

[amshed B. Bommyi, AID, Institu te of Nuclear Medicine, Middlesex Hospital, London, England R EFERENCES

I PIOPED Investigators. Value of the ventilation-perfusion scan in acute pulmonary embolism: results of the Prospective Investigation of Pulmonary Embolism Diagnosis (PIO PE D) . JAMA 1990; 263:2753-59 2 Morrell NW , Nijran KS, Jones BJ, et al, Th e underestimation of segmental defect size in radionuclide lung scanning. J Nucl Med 1993; 34:370-74

To the Edit or: Th ere is, in fact, considerable skill and judgem ent required in distin guishing a mod er ate size mismatched segmental perfusion defect (25% to 75% of a segment ) from a large size mismatched segm e ntal perfusion defect (> 75% of a segmen t). As Dr. Bom anji indicates, Morrell and associates IJ Nucl Med 1993; 34:370-74 ) showe d th at experie nced rea ders of radionucl ide lung scans often under estimated and occas ional ly overestim ated the size of segm ental perfusion defects. In view of thi s, we reevaluated the interpretation s of ventilation/pe rfusion lung scans fro m Prospective In vestigation of Pul monary Embolism Diagnosis (PIO P E D) on th e basis of th e number of mismatched perfusion defects, irrespec tive of whether such defects wer e mod erate or large segmental defect s. We defin ed th ese defects as, "mismatche d vascular defects".' We showed that the pred ictive value of the cumulative number of mismatch ed mod erate size mismatched segme ntal perfusi on defects was th e same as that of mism atch ed large seg mental perfusion defects.' This suggested that the diagnostic value of mismat ch ed moderate size segme ntal defects is the same as mism atch ed large segm ental defects. We concluded that the number of mismatched vascular defects is as powerful for the assessme nt of ventilat ion/ perfusion lung scans as the number of mismat ch ed segme ntal equivalent perfusion defects (where one segmental equivalent perfusion defect is defined as one large mismat ched segmental perfusion defect or two mod erate size mismatched perfusi on defects). Th e number of mismatched vascular defects is easier to interpret and permits a mor e objec tive evaluation.' We provided , ther efore, a sche me th at does not require the sizing of mismat ched perfusion defects. We agree with D r. Bomanji th at it is imp ort ant to rep ort the lung scan afte r integ rating the clinical data. We showed that stratification according to th e presence or absen ce of prior cardiopulmonary disease pe rmitt ed a more acc ura te assessment of both groups when ventilatio n/perfusion lun g scans we re interpreted on the basis of eithe r mismatched seg mental equivalent perfusion defects,2 or mismatched vascular defects, 1 the latt er not req uiring sizing of th e perfusion defects. Pati ents with no prior cardiopulmonary disease req uired fewer mismatch ed perfusion defect s to indicate a high predictive value of pu lmon ary e mbolism th an pati ents who had pri or cardio pulmo nary dise ase . 1•2 We showed th at the addition of clinical assessme nt to stratification according to prior cardi opulmonary disease furthe r optimizes

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th e interp retation of ventilation/p erfu sion lung scans, irrespe ctive of wheth er the lu ng scans wer e read on the basis of mism atch ed vascular defects or on the basis of mismatch ed segme ntal equivalent d efects.3 Regarding repeat lun g scans once anticoagulation has been complete d, ther e is not uni form agree ment on this point. Th e Urokin ase Pul monary Embolism T rial showed that pro min ent residual scan defects (2:: 10% residu al defect ) rem ained in 16% of patients at the end of I year." Such residual de fects might readily be interpret ed as high probability for p ulmon ary embolism if rep eat lu ng scans wer e ob taine d in the absence of a baselin e lung scan. In PIOPED there was a statistically significant loss of specificity in the high prob ability ve ntilation perfu sion sean diagnosis for pati ents with histories of prior pulmonary c mbohsm/' Th ese d ata suggest a need to obtain a new ba selin e pe rfusion lung scan in patients with ve nous th romboembolism when treatm ent is concluded. The costeffective ness of this, however , has not been established. Th e issue is bein g discussed by a group of physicians at th e American Co llege of C hest Physicians, and hop efully the opinions will be publish ed soon . Regarding th e PISA-PED study (CHEST 1995 ; 107[supp l]:33S38S) we agree that their criteria for interpretation of perfusion scans avoided the problem of sizing of perfusi on defects . However , their interpret ations ofthe perfusion scans gave uncert ain results. Among patients in whom the perfusion lung scan was read as "not co mpatible with pu lmonary embo lism," 5 of 27 (18.5%) had pulmonary e mbolism. Even wh en clinical assessment was "unlikely" and the per fusion lun g scan was "not co mpatible with pulmonary embolism," thi s concordant com bination showed pulmonary e mbolism in 2 of 17 (12%). We continue to believe th at PIOPED5 served an extre me ly useful purpose in gathe ring car efu lly docu ment ed data. Co ntinuing analysis of the PIOPED data has shown ways in which interp retation of the ventilation/perfusion scan can be improved l -3.6 and such investigations are still in p rogress.

Paul D. Stein, MD, FCCI', Henru Ford Heart and Vascular Institut e, Detroit; and Alexander Gottschalk, MD , FCCP, Michigan State University, East Lans ing Rer!rint requests: Dr. Stein, Medical Director, Levine Health Enhacement Center, New Center Pavilion, Room 1107, 2921 W est Grand Blvd, Detroit, MI 48202-2691 R EFERENCES

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Stein PD, H enry JW, Gotts chalk A. Mismatched vascular defects : an easy alternati ve to mismat ched segmental equivalent defects for the interpretation of ventilation/perfusion lung scans in pu lmonary e mbolism. Chest 1993; 104:1468-72 Stein PD , Gottsc halk A, Hen ry JW, et a1. Stratification ofpatients acco rding to prior cardiopulmonary disease and probability assessme nt based upon the number of mismatched segme ntal equivalent pe rfusion defects: approaches to strengthen the diagnostic value of ventilation/perfusion lung scans in acute pulmonary e mbolism. Ch est 1993; 104:1461-67 Stein PD, Hen ry JW, Gottschalk A. Th e addition of clinical assessment to stratification accor ding to prior cardiopulmonary disease furth er optimi zes the interpretation of ventilation/perfusion lung scans in pulmonary embolism. C hest 1993 ; 104: 1472-76 A Natio nal Coope rative Study. Th e urokinase pulmonary embolism trial: perfusion lung scanning. Circulation 1973; 47(suppl 2):11-46-11-59 PlOPED Investigators. Value of the ventilation-perfu sion scan in acute pulmonary embolism: results of the Prosp ective Investigation of Pulm onary Embolism Diagnosis (PIOPE D). JAMA 1990; 263:27.53-59 Communications to the Editor

6 Gottschalk A, Sostman H D , Cole man RE , et al. Ventilation-perfusion scintigraphy in the PIOPED study. Part II . Evaluation of the scintigra phic criteria and interpretations. J Nucl Med 1993; 34:1119-26

Heliox Therapy for Acute Vocal Cord Dysfunction To the Editor: At the Natio na l Jewish Center for Im mu nology and Respiratory Med icine, app roximately 10% of the patients referred for inp atient evaluation for refractory asthma have vocal cord dysfun ction without any evide nce of asth ma. An addition al 30% are diagno sed as having both vocal cor d dysfun ction and asthma .' Based on thi s data, we would have expecte d a significant number of patients treated by Kass and Castriotta , as described in th eir article published in th e March 1995 issue (CHEST 1995; 107:757-60), to have had vocal cord dysfun ction . While potentially of som e value in the tr eatment of asth ma, heliox is particularly efficacious in the treatm ent of an acut e episode of vocal cord disease, whi ch frequently masquerades as severe asth ma unresponsive to standa rd th erapy. It is thus surpri sing th at th is disease entity was not aggressively looked for by Kass and Cas triotta. It is equally surp rising that it was not mentioned in the follow-up editorial by Madi son and Irwin (CHEST 1995; 107:597-98). We sugge st the pati ents presented in the study by Kass and Castriotta under go rh inola ryngoscopy wh en symptomatic or th at this test be performed whe n asym ptomatic in conjunctio n with a challe nge test looking for parad oxical motion of the vocal cords ,

Colin Reisner, MD , and Lam) Barish, MD ; Division of Allergy and Clinical l mmunologg, National [euiisl: Center f or Im mun ology and Bespiratoru Medicine, Denver R EFERENCE

1 Newma n KB, Dubester SN. Vocal cord dysfunction : masquerader of asthma. Se min Respir Med 1994; 15:161-67

To the Editor: Drs. Reisner and Borish raise the interestin g possibility that som e of the patients we treated with heliox might have had acute vocal cord dysfun ction. Th ey quote th e expe rience at th e National Jewish Center for Immunology and Respirato ry Medi cine where there is an approximate 40% incid ence of vocal cord dysfun ction in patients referred for refractory asthma . 1 Seven of our 12 pati ents underwent endotrache al intu ba tion. If they had had vocal cord dysfun ction , their "asthma" should have disappeared with the endotr ache al intubation. In our stu dy seve re airways ob struc tio n continued to be a p robl em afte r intu bation. All of ou r patients also had acute hypercapn ia, which has not shown to be associated with vocal cord dysfunction du ring an episode of wheezing and dyspn ea.2•3 Although it does not pr eclude vocal cord dysfun ction , none of our pati ents had stridor or pr ed ominantly anterior inspiratory wh eezing, whi ch are common physical findin gs in voc-al cord dysfun ction . Our patients were dr awn from an urban popul ation for whom th e hospital was th e traditional primary caregive r. Th e incidence of acute vocal cord dysfunction in a nonrefer ral urban population is not

known . Th e high incide nce ofvocal cord dysfun ct ion at the National [ewish Ce nte r cannot be extrapolated to our pati ent population. In add ition , our patients did not have chro nic refract ory asth ma. We suspect th at this patient population is substantially differ ent from those patients refe rred to th e Natio nal Jewish Ce nter for refractory asth ma. Although heliox may also be an e ffective tr eat ment for vocal cord dysfunct ion, th ere was no evide nce to support th e diagnosis in our patients. Physical findings of diffu se exp iratory wheeze without inspiratory wheeze or strido r, hyper cap nia with acute respiratory acidos is, failure to imp rove with e ndotrac heal intu batio n, and th e patient p rofiles of th e study popul ation are indicative of acute sever e asth ma.

Jonath an E. Kass, MD, FCCP , Division of Pulmonary and Critical Care Medicine, Cooper Hospital/University Medical Center, Robert W ood [ohns on School of Medicine Camden , Camden, New Jersey; and Richard J. Castriotta , MD , FCCP, Pulmonaru Section, Mount Sinai Hospital, University of Connecticu t School of Medicin e, Hartford, Connecticut R EFERENCES

Newm an KB, Dubester SN. Vocal cord dysfunction: masquerader of asthma. Semin Respir C rit Care Med 1994; 15:161-67 2 C hristopher KL, Wood RP II, Eckert RC, et al. Vocal-cord dysfunction presenting as asthma. N E ngl J Med 1983; 308:1566 70 3 Gold man J, Muer s M. Vocal cord dysfunction and wheezing. Thorax 199 1; 46:401-04

Stridor From Edema of the Arytenoids, Epiglottis, and Vocal Cords After Use of Free-Base Cocaine To the Editor: We have read with great interest th e art icle by Haim and colleagu es in the January 1995 issue (CHEST 1995; 107:233-40 ) in which th e authors reviewed the various respiratory eons equences of free-b ase cocaine inhalation. We wish to rep ort a case of a young wom an with recurrent episodes of stridor from free-base cocaineinduced upper airway ede ma. A 45-year-old woman pr esen ted to ou r e me rgency department with dyspnea, dysph agia, hoarsen ess, and sore throat. She had previous mult iple visits to the e me rgency department for similar probl em s. Each tim e she was tr eated with inhal ed bronchodilators and sho rt co urses of oral corti coster oid s. Because of chronic cornplaints, she was re ferred to an ear, nose, and throat physician . H er direct Imyngoseopi c examination less than 24 h before her current visit was normal. She had no Significant medi cal illnesses and was taking no medi cation s. She ad mitted to using injectable and nasal coca ine in th e past, but d eni ed any othe r drug use in the past few yea rs. Initial examination revealed inspi ratory and expiratory stridor and the use of accessory respirat ory mu scles. Th er e was minimal imp rove me nt in her sympto ms in spite of nebulized bronchodilator s. C hest roen tgenogra ms showed no infiltrates. However, a subglottic stenosis was visua lized on her neck radiographs. On broncho scopy, the aryten oid s, intraaryt enoid space, epiglottis, and false and tru e vocal cords were markedly ede matous. She CHEST 1 108/ 51 NOVEMBER, 1995

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