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In acute pulmonary embolism, patients free from circulatory failure usually present a blood gas pattern consistent with respiratory alkalosis. We investigated whether the appearance of arterial base deficit in these patients indicates disease severity and diagnostic delay. Twenty-four consecutive patients with pulmonary embolism were retrospectively evaluated. Twelve patients had arterial base excess > or =0 mmol/L (Group 1), and 12 patients arterial base deficit <0 mmol/L (Group 2). No patient showed signs of circulatory failure. Group 1 was characterized by a mean base excess of 2.2 +/- 1.7 mmol/L, while in Group 2, the mean base deficit was -1.9 +/- 0.7 mmol/L (p < 0.0001). At 1 week since the embolism, 11 patients of Group 1 and 6 of Group 2 received a PE diagnosis (p < 0.05). The vascular obstruction index was more severe in Group 2 than in Group 1 (48 +/- 12 vs. 36 +/- 17%, respectively, p < 0.05). In Group 2, the PaCO(2) was lower (33 +/- 3 vs. 36 +/- 5 mmHg, respectively, p < 0.05), the arterial pH was decreased (7.442 +/- 0.035 vs. 7.472 +/- 0.050, respectively, p = 0.097), the Pv(50) was lower (28.3 +/- 1.7 vs. 29.8 +/- 1.6 mmHg, respectively, p < 0.05), the aHCO(3) (-) was lower (22.5 +/- 0.7 vs. 26.1 +/- 1.6 mmol/L, respectively; p < 0.0001), while between the Groups, O(2) delivery, O(2) mixed venous saturation, and O(2) extraction ratio were equivalent. Despite no signs of circulatory failure, an arterial Base deficit develops in patients with respiratory alkalosis subsequent to more severe pulmonary vascular obstruction. Diagnostic delay favors a base deficit. Depending on the degree of hypocapnia, there may be limitation of peripheral O(2) uptake despite adequate O(2) availability. Progressive bicarbonate deficit suggests an increased risk for underlying conditions such as cardio-respiratory disorders or cancer, and requires close control and treatment.

Pulmonary embolism remains a challenging diagnostic problem. We developed a simple diagnostic strategy based on combination of assessment of the pretest probability with perfusion lung scan results to reduce the need for pulmonary angiography. We studied 390 consecutive patients (78% in-patients) with suspected pulmonary embolism. The pretest probability was rated low (<10%), intermediate (>10%, < or =50%), moderately high (>50%, < or =90%) or high (>90%) according to a structured clinical model. Perfusion lung scans were independently assigned to one of four categories: normal; near-normal; abnormal, suggestive of pulmonary embolism (wedge-shaped perfusion defects); abnormal, not suggestive of pulmonary embolism (perfusion defects other than wedge shaped). Pulmonary embolism was diagnosed in patients with abnormal scans suggestive of pulmonary embolism and moderately high or high pretest probability. Patients with normal or near-normal scans and those with abnormal scans not suggestive of pulmonary embolism and low pretest probability were deemed not to have pulmonary embolism. All other patients were allocated to pulmonary angiography. Patients in whom pulmonary embolism was excluded were left untreated. All patients were followed up for 1 year. Pulmonary embolism was diagnosed non-invasively in 132 patients (34%), and excluded in 191 (49%). Pulmonary angiography was required in 67 patients (17%). The prevalence of pulmonary embolism was 41% ( n=160). Patients in whom pulmonary embolism was excluded had a thrombo-embolic risk of 0.4% (95% confidence interval: 0.0%-2.8%). Our strategy permitted a non-invasive diagnosis or exclusion of pulmonary embolism in 83% of the cases (95% confidence interval: 79%-86%), and appeared to be safe.

Purpose: Echocardiography is advocated by some as a useful diagnostic test for patients with suspected pulmonary embolism (PE), but its diagnostic accuracy is unknown. The present study was undertaken to determine prospectively the sensitivity and specificity of transthoracic echocardiography in the diagnosis of PE., Subjects and Methods: We examined 110 consecutive patients with suspected PE. The study protocol included assessment of clinical probability, echocardiography, and perfusion lung scanning. Pulmonary angiography was performed in all patients with abnormal scans. As echocardiographic criteria to diagnose acute PE, we used the presence of any two of the following: right ventricular (RV) hypokinesis, RV end-diastolic diameter >27 mm (without RV wall hypertrophy), or tricuspid regurgitation velocity >2.7 m/sec. Clinical estimates of PE served as pretest probabilities in calculating, after echocardiography, the posttest probabilities of PE., Results: Pulmonary angiography confirmed PE in 43 (39%) of 110 patients. Echocardiographic diagnostic criteria for PE yielded a sensitivity of 56% and a specificity of 90%. For pretest probabilities of 10%, 50%, and 90%, the posttest probabilities of PE conditioned by a positive echocardiogram were 38%, 85%, and 98%, respectively. The posttest probabilities of PE conditioned by a negative echocardiogram were 5%, 33%, and 81%, respectively., Conclusions: In unselected patients with suspected PE, transthoracic echocardiography fails to identify some 50% of patients with angiographically proven PE. Although echocardiographic findings of RV strain, paired with a high clinical likelihood, support a diagnosis of PE, the transthoracic echocardiography has to have a better sensitivity to be used as a screening test to rule out PE.

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.

Pulmonary embolism (PE) remains a challenging diagnostic problem because it mimics other cardiopulmonary disorders. Pulmonary angiography is still the reference standard for diagnosing PE but it is costly, invasive and not readily available. Non-invasive diagnostic strategies have therefore been developed to forego pulmonary angiography in patients suspected of having PE. Ventilation/perfusion lung scanning is, at present, the most widely used non-invasive diagnostic test for PE. A high probability ventilation/perfusion scan (segmental or greater perfusion defects with normal ventilation) warrants the institution of anticoagulant therapy especially when paired with high clinical suspicion of PE. Yet, only a minority of patients with confirmed PE have high probability ventilation/perfusion scans. Ventilation/perfusion abnormalities other than those of the high probability scan should be regarded as non-diagnostic. Under these circumstances, documentation of deep vein thrombosis by non-invasive leg testing warrants anticoagulation without the need for angiography. However, a single negative venous study result does not permit to rule out PE in patients with non-diagnostic ventilation/perfusion scans. Results of a recent prospective study indicate that accurate diagnosis or exclusion of PE is possible with perfusion lung scanning alone (without ventilation imaging). Combining perfusion lung scanning with clinical assessment helps to restrict the need for angiography to a minority of patients with suspected PE.

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.

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.

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)

Starting from 1969, the yearly number of patients with pulmonary embolism documented in the S. Chiara Hospital of Pisa is increased, in spite of the unchanged diagnostic procedures. Aim of this work is to verify if this trend is accompanied by earlier diagnosis with an improvement in the clinical outcome of pulmonary embolism, and if a relevant diagnostic failure is still present in our hospital. A comparison of pulmonary embolism cases collected from 1969 to 1971 and from 1980 to 1982 showed that the number of diagnoses made within one week from the onset of symptoms is increased (+24.8%), whereas the number of diagnoses made after more than one month is reduced (-18.1%). At the same time we observed that cases with a standard PaO2 less than 40 mmHg are reduced (-23.1%) while cases with a standard PaO2 greater than 50 mmHg are increased (+29.9%). An earlier diagnosis of pulmonary embolism contributed to treat a larger percentage of patients (+29.7%) and to lower the early mortality (-17.4%). This diagnostic trend can be ascribed to an increased readiness in raising the clinical suspicion of pulmonary embolism and to the prompt availability of perfusion lung scan, that is the center of our diagnostic strategy. Data of our 1,010 patients, compared with those of autoptic series and with the number of admissions, surgical operations and deaths in the wards of our hospital, suggest some persistent diagnostic failure in patients with well documented embolic risk; such as injured, burned, patients affected by neoplasm or motor lesion, patients operated for orthopedic or gynaecologic problems.

A comparison of the effects of two regimens of urokinase infusion not associated to heparin and of continuous heparin infusion was made assessing the rate of emboli and arterial hypoxemia resolution in patients with acute pulmonary embolism. Twenty-nine patients with acute pulmonary embolism, each one diagnosed by means of perfusion lung scan and selective pulmonary arteriography, were admitted to the study and randomly allocated to three treatment groups: A, 10 patients, urokinase: 800,000 CTA units/day for three days followed by oral anticoagulants; B, 9 patients, heparin: mean daily dose 30,000 units for seven days followed by oral anticoagulants; C, 10 patients, urokinase: 3,300,000 CTA units in 12 hours followed by oral anticoagulants. Pulmonary lung scan and PaO2st (PaO2 standardized to PaCO2 of 40 mmHg) were repeated at 1, 3, 7, and 30 days in all the groups of treatment. The mean daily rate of improvement, assessed from both the perfused lung segments and the PaO2st increment, in group C was highest in the first 24 hours and lowest from the first to the third day of treatment. However, from the third to the seventh day of treatment and onwards the mean daily rate of improvement was roughly the same in all the groups. After one month, lung perfusion and the PaO2st had considerably improved, but had not attained full recovery in any of the treatment groups.(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.

Pulmonary embolism was suspected in 45 neurosurgical patients who were treated between January, 1980, and December, 1981. Hypoxemia with respiratory alkalosis and sudden tachycardia gave rise to this suspicion more often than any other sign or symptom. Perfusion lung scanning confirmed the presence of pulmonary embolism in 23 of these cases. A retrospective analysis of the clinical course of these 23 patients suggested that one or more previous episodes of pulmonary embolism had occurred in 16 cases (69.6%), and had been either overlooked or misdiagnosed. Treatment was started immediately after diagnosis. Twenty-one patients were given heparin; however, two could not be treated because of contraindication to using anticoagulant drugs. Two patients died during treatment. The 21 surviving patients were assessed and 11 of them submitted again to perfusion lung scanning 1 week after diagnosis: 14 had improved, but seven did not show significant changes either clinically or on perfusion lung scanning. Nine treated patients developed hemorrhage, but it was readily controlled. In two of the nine patients, hemorrhage involved the surgical area. It is stressed that pulmonary embolism may be suspected and diagnosed in neurosurgical patients at an early stage. Heparin may be given and the survival rate appears to be better than previously reported figures.