Search

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.

After lung surgery, some patients complain of unexplained increased dyspnoea associated with hypoxaemia. This clinical presentation may be due to an interatrial right-to-left shunt despite normal right heart pressure. Some of these patients show postural dependency of hypoxaemia, whereas others do not. In this article, the pathogenesis and mechanisms involved in this post-surgical complication are discussed, and the techniques used for confirmation and localisation of shunt are reported. An invasive technique, such as right heart catheterisation with angiography, was often used in the past as the diagnostic procedure for the visualisation of interatrial shunt. As to noninvasive techniques, a perfusion lung scan may be used as the first approach as it may detect the effect of the right-to-left shunt by visualising an extrapulmonary distribution of the radioactive tracer. The 100% oxygen breathing test could also be used to quantify the amount of right-to-left shunt. Particular emphasis is given to newer imaging modalities, such as transoesophageal echocardiography, which is minimally invasive but highly sensitive in clearly visualising the atrial septum anatomy. Finally, the approach to closure of the foramen ovale or atrial septal defect is discussed. Open thoracotomy was the traditional approach in the past. Percutaneous closure has now become the most used and effective technique for the repair of the interatrial anatomical malformation.

To assess the value of perfusion lung scan in the diagnosis of pulmonary embolism, we prospectively evaluated 890 consecutive patients with suspected pulmonary embolism. Prior to lung scanning, each patient was assigned a clinical probability of pulmonary embolism (very likely, possible, unlikely). Perfusion scans were independently classified as follows: (1) normal, (2) near-normal, (3) abnormal compatible with pulmonary embolism (PE+: single or multiple wedge-shaped perfusion defects), or (4) abnormal not compatible with pulmonary embolism (PE-: perfusion defects other than wedge-shaped). The study design required pulmonary angiography and clinical and scintigraphic follow-up in all patients with abnormal scans. Of 890 scans, 220 were classified as normal/or near-normal and 670 as abnormal. A definitive diagnosis was established in 563 (84%) patients with abnormal scans. The overall prevalence of pulmonary embolism was 39%. Most patients with angiographically proven pulmonary embolism had PE+ scans (sensitivity: 92%). Conversely, most patients without emboli on angiography had PE- scans (specificity: 87%). A PE+ scan associated with a very likely or possible clinical presentation of pulmonary embolism had positive predictive values of 99 and 92%, respectively. A PE- scan paired with an unlikely clinical presentation had a negative predictive value of 97%. Clinical assessment combined with perfusion-scan evaluation established or excluded pulmonary embolism in the majority of patients with abnormal scans. Our data indicate that accurate diagnosis of pulmonary embolism is possible by perfusion scanning alone, without ventilation imaging. Combining perfusion scanning with clinical assessment helps to restrict the need for angiography to a minority of patients with suspected pulmonary embolism.

Present evidence suggests that venous thromboembolism is the third most common acute cardiovascular disease after cardiac ischemic syndromes and stroke. The frequency of the diagnosis of pulmonary embolism (PE) at a given hospital greatly increases if a referral unit for PE is set up in the hospital. Pulmonary embolism is characterized by a continuous spectrum of severity, from 2 to 3 to 15 to 16 embolized pulmonary segments (over a total of 19). Morbidity from PE increases with age and male sex (males/females ratio: 1.24). In only a minority (10%) of patients with PE and/or deep-vein thrombosis (DVT), primary deficiencies of coagulation-inhibiting proteins have been shown. Primary abnormalities of the fibrinolytic system seem even more rare. On the basis of the clinical conditions preceding the embolic episode, patients may be divided into different groups: apparently primary or idiopathic PE (40%), surgery or trauma (43%), heart disease (12%), neoplastic disease (4%), and systemic disease (1%). Patients with apparently primary or idiopathic PE often develop subsequent clinically overt cancer (9.1%), whereas surgery or trauma patients rarely do (1.4%). Furthermore, the former exhibit a significantly shorter survival than the latter mostly for causes of death that reflect increased predisposition to thrombogenesis. Thus, as for DVT, it is convenient to consider a primary or idiopathic form also for PE.

Pulmonary embolism (PE) is a frequent necroscopic finding in neurosurgical patients and this contrasts with the difficult diagnosis of it when the patient is still alive. Such a lack of diagnosis has promoted numerous studies into deep-vein thrombosis (DVT) which is, in most cases, the cause of pulmonary embolism. However, a prophylaxis of DVT cannot be indiscriminately carried out in neurosurgical patients because it is not without potential risks. For this reason we considered it useful to investigate whether among the risk factors for DVT there were any particularly responsible for the development of PE in neurosurgical patients. Our case study was carried out retrospectively on 144 patients hospitalised in the Neurosurgical Institute of Pisa University suspected of PE. In 88 of the cases the suspicion had been confirmed by perfusion lung scanning; in 56, on the other hand, it had been excluded. These two groups of patients resulted homogeneous for sex, age, blood group, and for the presence of any risk factors of cardiovascular diseases. An important difference between the two groups was the pathology which had motivated their hospitalisation; in fact, 50% of the patients with PE were affected by neoplastic pathologies of the CNS, against 28% of the others. The anamenestic evidence of previous neoplastic pathology in different sites of the CNS was much more frequent in patients who had developed PE. As far as the other risk factors we examined are concerned, it resulted that only 12.5% of the patients with PE had presented clinical signs or symptoms of phlebitis.(ABSTRACT TRUNCATED AT 250 WORDS)

Seven hundred fifty four consecutive cases of pulmonary embolism, diagnosed between 1969 and 1982 at S. Chiara Hospital in Pisa, were examined in order to assess the causes and the rate of the early mortality. Full documentation was not obtained in 47 cases (6.2%) and they were excluded from the study; 81 (11.4%) of the remaining 707 died within 30 days of diagnosis, and in 56.8% of them pulmonary embolism was the primary cause of death. The survival rate was 90.6% in patients with apparently primary pulmonary embolism, 89.8% in post surgical cases, 81.5% in cardiac patients and 75% in patients affected by neoplasm. Twenty five per cent of patients were not treated during the acute phase, because the diagnosis was made more than one month after the onset of symptoms or because the fear of bleeding precluded anticoagulant treatment. The incidence of fatal haemorrhage during treatment was 0.5% overall, and 0.4% in surgical patients. Mortality was 9.2% in patients who received treatment, versus 25.2% in untreated patients. Sixteen fatal recurrent embolisms occurred after the end of treatment: 11 were observed in patients not treated with oral anticoagulants. Routine autoptic examinations, performed in 44.4% of the cases, often demonstrated both recent and organized emboli, especially in cardiac patients. Recurrence of pulmonary embolism may account for both the severity of clinical patterns and the high mortality rate in the early phase of treatment.

Dissolution of pulmonary emboli with heparin and urokinase is ascribed, respectively, to anticoagulation and fibrinolysis. Since truly independent assessment of these effects in man is lacking, we administered each drug alone. Fibrinogen and plasminogen plasma levels and the resolution of pulmonary emboli were measured in three randomized groups of 10 patients each: groups A and C infused with small repeated doses of urokinase and a large single dose of urokinase, respectively, and group B who received heparin. After 6 h of treatment, fibrinogen fell in all the groups, while, after 12 h, remained equally reduced in groups A and B and declined further in group C. Plasminogen behaved similarly. Up to 60 h, statistical analysis showed that these effects were related to timing and amounts of urokinase and heparin infusion. These observations suggest that heparin may induce a lytic state. As to signs of pulmonary emboli resolution, no differences between groups were found in lung perfusion and gas exchange recovery at any time (from 1 day to 1 year) and in pulmonary artery pressure reduction at 1 week. The greater angiographic and scintigraphic recovery observed with urokinase, versus heparin alone, after 1 day of treatment in the Urokinase Pulmonary Embolism Trial may be ascribed to a synergistic effect with urokinase of heparin administered during the diagnostic work-out. The indications of heparin and urokinase should be evaluated in the light of these results.

To assess the effect of left heart disease on pulmonary blood flow distribution, we measured mean pulmonary arterial and wedge pressures, cardiac output, pulmonary vascular resistance, pulmonary blood volume, and arterial oxygen tension before and after treatment in 13 patients with longstanding ischemic heart failure and pulmonary edema. Pulmonary edema was evaluated by a radiographic score, and regional lung perfusion was quantified on a lung scan by the upper to lower third ratio (U:L ratio) of pulmonary blood flow per unit of lung volume. In all cases, redistribution of lung perfusion toward the apical regions was observed; this pattern was not affected by treatment. After treatment, pulmonary vascular pressures, resistance, and edema were reduced, while pulmonary blood volume did not change. At this time, pulmonary vascular resistance showed a positive correlation with the U:L ratio (r = 0.78; P less than 0.01), whereas no correlation was observed between U:L ratio and wedge pressure, pulmonary edema, or arterial oxygen tension. Hence, redistribution of pulmonary blood flow, in these patients, reflects chronic structural vascular changes prevailing in the dependent lung regions.

To provide clinical diagnostic criteria for pulmonary embolism (PE), we evaluated 750 consecutive patients with suspected PE who were enrolled in the Prospective Investigative Study of Acute Pulmonary Embolism Diagnosis (PISA-PED). Prior to perfusion lung scanning, patients were examined independently by six pulmonologists according to a standardized diagnostic protocol. Study design required pulmonary angiography in all patients with abnormal scans. Patients are reported as two distinct groups: a first group of 500, whose data were analyzed to derive a clinical diagnostic algorithm for PE, and a second group of 250 in whom the diagnostic algorithm was validated. PE was diagnosed by angiography in 202 (40%) of the 500 patients in the first group. A diagnostic algorithm was developed that includes the identification of three symptoms (sudden onset dyspnea, chest pain, and fainting) and their association with one or more of the following abnormalities: electrocardiographic signs of right ventricular overload, radiographic signs of oligemia, amputation of hilar artery, and pulmonary consolidations compatible with infarction. The above three symptoms (singly or in some combination) were associated with at least one of the above electrocardiographic and radiographic abnormalities in 164 (81%) of 202 patients with confirmed PE and in only 22 (7%) of 298 patients without PE. The rate of correct clinical classification was 88% (440/500). In the validation group of 250 patients the prevalence of PE was 42% (104/250). In this group, the sensitivity and specificity of the clinical diagnostic algorithm for PE were 84% (95% CI: 77 to 91%) and 95% (95% CI: 91 to 99%), respectively. The rate of correct clinical classification was 90% (225/250). Combining clinical estimates of PE, derived from the diagnostic algorithm, with independent interpretation of perfusion lung scans helps restrict the need for angiography to a minority of patients with suspected PE.