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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There were 37 maternal deaths among the 109,221 livebirths registered during the period 1977-86 in Bahrain, Arabian Gulf. The maternal mortality rate was 33.9/100,000 for the 10-year study period; however, disaggregation reveals a decline in this rate from 42.3/100,000 in 1977-81 to 26.9/100,000 in 1982-86. This decline presumably reflects streamlining of the Ministry of Health's maternity services, including a central maternity hospital with all modern facilities that serves as a referral center for all of Bahrain, 2 peripheral hospitals with provision for blood transfusion and surgical deliveries, and 3 maternity units managed by fully qualified midwives. About 80% of deliveries are covered by these maternity services; only 2.5% of deliveries occur in the home. Despite this highly developed maternity care system, 18 of the maternal deaths were due to direct obstetric cause: hemorrhage, 7; pre-eclampsia and eclampsia, 5; abortion septicemia, 2; bowel perforation during cesarean section, 1; thromboembolism, 2; and amniotic fluid embolism, 1. The causes of the 19 indirect maternal deaths were: pulmonary embolism, 5; infection, 7; cardiac failure, 2; cerebrovascular accident, 2; pulmonary hypertension, 1; and uncertain, 2. Of interest is the finding that sickle cell disease was the underlying cause of maternal death in 12 of the 37 deaths in this series. Sickle cell disease was implicated in 3 of the deaths from hemorrhage, all 5 deaths from pulmonary embolism, 2 deaths from septicemia, and the 2 cases of cardiac failure. In this series, 50% of the patients with sickle cell disease had thromboembolic crises following treatment of anemia with packed cell transfusion. Blood transfusion, especially of packed cells, should be given with caution to these patients since it may precipitate vaso-occlusive crisis by increasing blood viscosity. Since sickle cell disease represents a high risk during pregnancy in this Arab population, such patients should have frequent prenatal check-ups and deliver in a well-equipped hospital.
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PMID:Maternal mortality in Bahrain with special reference to sickle cell disease. 321 81

Pulmonary hypertension may develop whenever chronic obstruction of pulmonary arterial blood flow occurs. Although repeated pulmonary embolism is thought to be the usual underlying cause, there is little clinical evidence to support this theory. Studies of the pulmonary vascular endothelium have shown that perturbations of the normal endothelium can create a procoagulant environment, which could lead to the development of thrombosis in situ at the level of the large or smaller pulmonary vessels. Some patients develop proximal pulmonary thromboemboli, which may be the result of retrograde propagation of thrombus after an initial pulmonary embolus. Others present with unexplained pulmonary hypertension secondary to thrombotic occlusion of the pulmonary microvasculature. A perfusion lung scan will show abnormalities that should lead to correct clinical diagnosis and confirmatory evaluation. Thromboendarterectomy in selected cases provides dramatic clinical improvement in patients with proximal thromboemboli. Vasodilators may be effective in some patients with obstruction at the arteriolar level. Both groups should be treated with chronic warfarin anticoagulant therapy to protect against progression of thromboembolism.
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PMID:Pulmonary hypertension from chronic pulmonary thromboembolism. 327 15

Echocardiography provided the initial diagnosis of significant pulmonary hypertension, unrelated to left heart pathologic conditions, in 10 patients: four with acute pulmonary embolism; five with chronic pulmonary hypertension, primary in three patients and secondary to tumor emboli in the other two patients; and one with Eisenmenger's syndrome due to previously unsuspected atrial septal defects. Referral diagnoses were pericardial disease in five patients (including three with suspected tamponade), and right ventricular infarction versus pericarditis, atrial septal defect, dyspnea, inferoposterior infarction (by electrocardiography), and Ebstein's malformation in one patient each. The echocardiographic diagnoses were confirmed by lung scan (ventilation/perfusion mismatches were interpreted as high probability for pulmonary emboli in all four patients considered to have acute pulmonary emboli by echocardiographic study), pulmonary angiography (one patient), cardiac catheterization (four patients), and autopsy (three patients). No patient had evident aortic or mitral valvular, myocardial, or other left heart pathologic condition. In acute pulmonary embolism, mean right ventricular diameter was increased at 4.2 cm (range 3.2 to 6 cm) and right ventricular wall thickness was normal (mean 4.5 mm, range 3 to 5 mm). Moderate or marked right ventricular hypokinesis was noted in two patients each. Doppler examination, performed in three patients, revealed tricuspid regurgitation in all, with an increased flow velocity suggestive of mild to moderate systolic pulmonary hypertension (right ventricular minus right atrial pressures of 28 to 36 mm Hg). Patients with chronic pulmonary hypertension also had right ventricular dilatation (mean 4.4 cm diameter, range 3 to 5.4 cm) and hypokinesis (marked in four and moderate in one patient), but wall thickness was increased in all (mean of 9 mm, range 6 to 14 mm) and the flow velocities in the tricuspid regurgitant jets, detected by Doppler in all patients, suggested higher right ventricular minus right atrial pressures of 44 to 104 mm Hg (mean 64 mm Hg). The single patient with Eisenmenger's syndrome had right ventricular dilatation (3.2 cm), hypertrophy (10 mm), and hypokinesis (mild). Only the patient with Eisenmenger's syndrome had Doppler or contrast echocardiographic evidence for an intracardiac or extracardiac shunt. In the absence of left heart pathologic conditions, right ventricular dilatation and hypokinesis strongly suggest pulmonary arterial or primary right ventricular disease.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Echocardiographic recognition of pulmonary arterial disease and determination of its cause. 334 42

Chronic pulmonary embolism is a rare disease which can occur at first with pulmonary hypertension. In these cases it may be difficult to distinguish between primary pulmonary hypertension. We examined nine patients with Chronic Pulmonary Embolism (CPE) (three females and six males, mean age 45 +/- 13 years, range 21-67 years) and ten patients with Primary Pulmonary Hypertension (PPH) (seven females and three males, mean age 35 +/- 13 years, range 10-56 years) who came to our attention during the years 1973-1986 (mean follow up 3 years). All patients had an electrocardiogram, chest x-ray, echocardiogram, cardiac catheterization with pulmonary angiography; seven patients with CPE and eight with PPH had perfusion lung scans. Progressive dyspnoea was the main feature in all the patients; four out of nine with CPE and none of the ones with PPH had a previous history of thrombophlebitis. In all the patients the electrocardiogram, chest x-ray and echocardiogram showed signs of pulmonary hypertension, so that a clear distinction between the two groups was not possible. Cardiac catheterization showed pulmonary pressure values higher in patients with PPH as compared to the ones with CPE (systolic pressure 96 mmHg vs 70 mmHg, diastolic pressure 49 mmHg vs 31 mmHg, mean pressure 65 mmHg vs 45 mmHg). Pulmonary angiography in more than half of the patients with CPE showed a "cut off" of two or more lobar branches of the pulmonary arteries. In the patients with PPH pulmonary angiography showed a dilatation of the main pulmonary artery and a diffuse bilateral hypoperfusion. Perfusion lung scan in all the cases of CPE showed zonal perfusion defects, while in all cases of PPH, with the exception of one, it was largely normal. Venograms in the districts of the inferior vena cava demonstrated thrombosis in two out of six patients with CPE. Negative venograms were found in the five patients with PPH who had this investigation performed. One patient with CPE had a surgical embolectomy, the other eight had anticoagulant oral treatment. During the follow-up period three patients with CPE and five with PPH died within five years and within fifteen months respectively, of the diagnosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Differences in patients with chronic pulmonary embolism and primary pulmonary hypertension]. 338 46

Isolated right ventricular infarction has been found in cases of right ventricular hypertrophy, but there are no reports on right ventricular infarction secondary to massive pulmonary embolism. Six autopsied patients with massive pulmonary embolism and pure right ventricular infarction, suspected to be secondary to the embolism, were selected from a population of 216 autopsies. Pulmonary embolism was the suspected diagnosis in five cases due to typical clinical, electrocardiographic and haemodynamic data. Right ventricular infarction was a post-mortem finding, not previously diagnosed. In every case the thickness of the right ventricular myocardium was normal. The necrosis of the right ventricle was transmural in four cases and subendocardial in two and the entire right ventricular wall (anterolateral as well as posterior) was involved. No mural thrombi were present and in no case did the necrosis involve the left ventricle. In one case the coronary arteries were normal, in the other five significant lesions of the right or left coronary arteries were observed. These lesions may have been, in part, responsible for the necrosis of the right ventricle when the massive pulmonary embolism was added. We conclude that right ventricular infarction may be secondary to pulmonary hypertension in the setting of massive pulmonary embolism, even in the absence of right ventricular hypertrophy and with normal or stenotic coronary arteries.
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PMID:Acute right ventricular infarction secondary to massive pulmonary embolism. 340 69

When shock complicates an acute increase in RV afterload, initial therapy should be directed toward restoration of an adequate BP (RV coronary perfusion pressure) and CO. Current results indicate that norepinephrine, a drug with direct inotropic and pressor effects, may be an excellent agent for acute resuscitation and short-term maintenance of hemodynamic stability when frank circulatory instability complicates pulmonary embolism. Following hemodynamic stabilization, thrombolytic therapy should be initiated. Recent evidence suggests that the lytic agent can be given by bolus technique, but more work is required to determine the optimum dosing regimen. In the absence of shock, when a moderate decrease in CO complicates pulmonary embolism, isoproterenol or hydralazine may be used to improve flow. However, both of these agents may decrease systemic vascular resistance and BP. Accordingly, the latter parameter should be carefully monitored to ensure that excessive falls in BP and RV coronary perfusion pressure do not occur. Whereas in certain conditions volume expansion is appropriate therapy to increase CO, in acute pulmonary hypertension with excessive RV afterload, volume expansion may worsen RV function. Recent canine studies indicate that an increase in vascular closing pressure is the predominant mechanism explaining the increase in PAP and apparent increase in PVR complicating pulmonary embolism. Accordingly, in addition to decreasing vascular resistance, therapy to decrease RV afterload could be directed toward decreasing the vascular response producing excessive closing pressures.
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PMID:Pathophysiology and therapy of right ventricular dysfunction due to pulmonary embolism. 353 3

Records of 34 patients with established causes of pulmonary arterial hypertension were retrospectively reviewed. The ventilation-perfusion scans were blindly classified according to standardized criteria as normal or high, low, or intermediate probability of pulmonary embolism as the cause of pulmonary arterial hypertension. Twelve of 13 patients with primary pulmonary hypertension had normal or low-probability scans, but the perfusion pattern was not helpful in distinguishing between histologic subtypes. All eight patients with large-vessel thromboembolic hypertension had high-probability scans; however, three of 13 patients with nonembolic secondary pulmonary hypertension also had high-probability scans. While a normal or low-probability scan excluded proximal pulmonary emboli as a cause of pulmonary hypertension, a high-probability scan may be associated with a variety of other nonembolic causes of secondary pulmonary hypertension.
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PMID:Pulmonary arterial hypertension: value of perfusion scintigraphy. 361 69

Pulmonary hypertension is a known complication of chronic obstructive pulmonary disease (COPD). A worsening dyspnea in a patient with COPD is usually a sequela of the pulmonary disease. However, it may be due to pulmonary embolism, a complication which is difficult to diagnose in such patients. We present a patient with COPD in whom two-dimensional and Doppler echocardiography confirmed the diagnosis of pulmonary emboli by documenting right ventricular thrombus and pulmonary hypertension. This case report emphasizes the usefulness of these noninvasive cardiac imaging techniques in the detection and evaluation of pulmonary embolism in patients with COPD.
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PMID:Right ventricular thrombus and pulmonary emboli in a patient with emphysema: an echocardiographic and Doppler documentation. 367 3

Using the method of equilibrium radionuclide ventriculography (RNV), the right ventricular ejection fraction (RVEF) at rest and at a standard workload of 250 kpm per min was determined in 25 control subjects and in 30 patients with pulmonary hypertension (8 patients with chronic obstructive bronchopulmonary disease, 12 with recurrent pulmonary embolism and 10 with pure mitral stenosis). In the same week as RNV, pulmonary artery pressure was registered in patients with pulmonary hypertension at rest and at standard workload. RVEF was significantly higher (45 +/- 5%) in normal subjects than in patients with pulmonary hypertension (33 +/- 5%) and during exercise increased, whereas in patients with pulmonary hypertension it did not markedly change or decreased. The RVEF correlated at rest (r = -0.6293, p less than 0.001) and during exercise (r = 0.6980, p less than 0.05) with the degree of pulmonary hypertension at rest and during exercise. The results show a good correlation between the RVEF and the degree of pulmonary hypertension in patients with pulmonary hypertension at rest and during exercise.
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PMID:Equilibrium radionuclide right ventriculography at rest and during exercise in patients with pulmonary hypertension. 369 5

Haemodynamic studies were undertaken in 30 patients with chronic post-embolic pulmonary hypertension (CPEPH), and the findings were compared with those found in acute thromboembolism of the pulmonary artery. The study showed that radiocardiographic examination is a useful supplementary method for diagnosing postembolic lesions of pulmonary arteries and for dynamic examination of patients after pulmonary embolism. The appearance of a "single-hump" curve on the radiocardiogram was an unfavourable prognostic sign and attested both to an increase of pulmonary hypertension or to a latent heart failure. The importance of radiocardiographic examination for determining the prognosis of the disease and for choosing the most suitable method of its treatment is analysed.
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PMID:Haemodynamics in patients with chronic post-embolic pulmonary hypertension. 369 6


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