Unrecognized Emboli to the Lungs with Subsequent Cor Pulmonale

Owen, William R.; Thomas, W.A.; Castleman, Benjamin; Bland, Edward F.

doi:10.1056/nejm195312032492302

Cited by 164 publications

(24 citation statements)

References 25 publications

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“…This has also been reported by Owen et al (1953) and Smith et al (1964). After the first clinical episode there may be a period of days or weeks when treatment can be instituted if the diagnosis can only be made.…”

Section: Discussionsupporting

confidence: 58%

Massive pulmonary embolism in healthy people.

Fleming¹,

Bailey²

1966

BMJ

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Early Chronic Bronchitis MEDICAL JOURNAL nor therapy had any effect on the rate of decline of F.E.V. or on the volume or purulence of sputum specimens.We wish to record our appreciation to Pfizer Limited for their generous supply of oxytetracycline and indistinguishable dummy tablets, and for their willing cooperation in the analysis of numerous blood and urine samples for oxytetracycline, both before and during the trial ; and to Messrs. Parke Davis and Co. for their supply of chloramphenicol, sulphamethoxypyridazine, and penicillin capsules. Murphy (1963), and by the fact that three of our own severe but fortunately non-fatal cases were also doctors' wives in whom there was considerable delay in diagnosis. This failure is mirrored in a number of otherwise excellent monographs and conference proceedings on the pulmonary circulation, and even one on pulmonary embolic disease, which have nothing whatever to say on fatal pulmonary embolism in healthy persons.The frequency with which we made this clinical diagnosis led us to wonder if there were not a number of such patients who died either before diagnosis was made or before treatment could be effectively instituted (Fleming, 1962). This led to the present study of fatal cases, and of cases diagnosed and treated in life.* Consultant Cardiologist, East Anglian Regional Hospi:al Board and Addenbrooke's Hospital, Cambridge. Of the nine cases of sudden death outside hospital eight were women, and all but one had a recorded complaint of some dyspnoea or chest discomfort preceding death. The 23-year-old patient was five months pregnant, and had been treated for venous thrombosis three and a half weeks previously.In all cases either a large embolus straddled the pulmonary artery bifurcation or both main pulmonary arteries were blocked

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Section: Discussionsupporting

confidence: 58%

Massive pulmonary embolism in healthy people.

Fleming¹,

Bailey²

1966

BMJ

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“…In our study, the diseases that mimicked PE and brought to erroneous diagnoses were most frequently dys pnea of unknown origin, left heart failure and pneumonia. Owing to the lack of diagnosis, PE was not treated in pa tients of this series, and the absence of early antithrom botic treatment, as reported in other studies [14,[19][20][21], possibly led to CTPH. This points to the mandatory need of raising promptly and accurately the suspicion of pulmo nary embolism in the presence of compatible symptoms and signs in order to avoid that most patients are not de tected.…”

Section: Discussionmentioning

confidence: 80%

From Not Detected Pulmonary Embolism to Diagnosis of Chronic Thromboembolic Pulmonary Hypertension: A Retrospective Study

Palla

Formichi²,

Santolicandro³

et al. 1993

Respiration

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The past and present clinical history of 13 patients with hemodynamic and angiographic diagnosis of chronic thromboembolic pulmonary hypertension (CTPH) was reviewed in order to investigate the reasons for failure of resolution of acute pulmonary embolism (PE) and findings useful for diagnosis of CTPH. All patients had chest radiograph, ECG, arterial blood gas analysis and pulmonary perfusion scintigraphy performed. Clinical assessment demonstrated that no patient had diagnosis and treatment of the several retrospectively identified episodes of PE (from 1 to 8); the lack of diagnosis was due to underestimation of symptoms and signs such as dyspnea (85%), pleuritic chest pain (31%) or phlebitis (46%) that were present months or years earlier. Alternative diagnoses erroneously made were dyspnea of unknown origin (5 cases), left heart failure (4 instances) and pneumonia (2 cases). Once CTPH has developed, chronic dyspnea (92%) and substernal chest pain (100%) are almost always present: chest radiograph and ECG show signs of chronic hypertension such as enlargement of hila (100%), right heart sections (77%), azygos vein (46%) and P pulmonale (67%), T inversion on right precordial leads (75%), S-T segment depression (75%), respectively. Perfusion scintigraphy shows severe perfusion impairment (55.7% of the total vascular bed) paralleled by severe hypoxia (standard PaO₂ = 49 ± 14.1 mm Hg). In conclusion, patients with PE who develop CTPH are not diagnosed and thus untreated because clinical symptoms and signs of acute PE have not been recognized. If CTPH develops, clinical assessment (including simple and noninvasive techniques such as chest radiograph, ECG and blood gas analysis) may show a quite characteristic pattern useful for diagnosis.

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“…The case of a 6-months-old boy was described by Goodale and Thomas (1954). However, it is well known that small pulmonary emboli to the arteriolar bed can produce progressive cor pulmonale (Owen et al, 1953), while the findings of Evans et al (1957) suggest that thrombosis may well occur as a secondary phenomenon. Dexter (1957) considered that all patients with pulmonary hypertension of undetermined cause should be regarded as having recurrent pulmonary emboli, and we believe this to be true for the great majority.…”

Section: Discussionmentioning

confidence: 99%

“…In idiopathic hypertension the prognosis is uniformly bad, and this is also true for thrombo-embolic pulmonary hypertension, for once symptoms develop the course is usually unfavourable (Owen et al, 1953). A few patients with established thrombo-embolism have recovered, however.…”

Section: Prognosis and Incidence Of Obliterative Pulmonary Hypertensionmentioning

confidence: 99%