Embolic Manifestations Research Articles

Amniotic fluid contains tissue factor, a potent initiator of coagulation

A primary clinical manifestation of amniotic fluid embolism is coagulopathy. Prior studies have identified a poorly characterized yet potent procoagulant property in amniotic fluid that increases with gestational age. One possible source of procoagulant activity is tissue factor, a primary biologic initiator of coagulation. We used sensitive immunoassays and functional assays to identify substantial quantities of tissue factor antigen and tissue factor-specific procoagulant activity in amniotic fluid, which increased with gestational age. Moreover, tissue factor accounted for virtually all of the coagulant potential of amniotic fluid. Amniotic tissue factor appeared intact and membrane bound and, when reconstituted into synthetic microvesicles of optimal phospholipid content, displayed nearly full activity. Calcium chelation and sonication experiments suggested that the presence of inhibitors and the physical configuration of membrane-bound tissue factor in amniotic fluid might explain the modest reduction in tissue factor procoagulant activity relative to total antigen levels observed in vivo. We postulate that the substantial quantities of functionally active tissue factor in amniotic fluid account for the coagulation changes accompanying amniotic fluid embolism and could indirectly contribute to the characteristic hemodynamic derangements of amniotic fluid embolism.

Amniotic fluid contains tissue factor, a potent initiator of coagulation

A primary clinical manifestation of amniotic fluid embolism is coagulopathy. Prior studies have identified a poorly characterized yet potent procoagulant property in amniotic fluid that increases with gestational age. One possible source of procoagulant activity is tissue factor, a primary biologic initiator of coagulation. We used sensitive immunoassays and functional assays to identify substantial quantities of tissue factor antigen and tissue factor-specific procoagulant activity in amniotic fluid, which increased with gestational age. Moreover, tissue factor accounted for virtually ail of the coagulant potential of amniotic fluid. Amniotic, tissue factor appeared intact and membrane bound and, when reconstituted into synthetic microvesicles of optimal phospholipid content, displayed nearly full activity. Calcium chelation and sonication experiments suggested that the presence of inhibitors and the physical configuration of membrane-bound tissue factor in amniotic fluid might explain the modest reduction in tissue factor procoagulant activity relative to total antigen levels observed in vivo. We postulate that the substantial quantities of functionally active tissue factor in amniotic fluid account for the coagulation changes accompanying amniotic fluid embolism and could indirectly contribute to the characteristic hemodynamic derangements of amniotic fluid embolism. A primary clinical manifestation of amniotic fluid embolism is coagulopathy. Prior studies have identified a poorly characterized yet potent procoagulant property in amniotic fluid that increases with gestational age. One possible source of procoagulant activity is tissue factor, a primary biologic initiator of coagulation. We used sensitive immunoassays and functional assays to identify substantial quantities of tissue factor antigen and tissue factor-specific procoagulant activity in amniotic fluid, which increased with gestational age. Moreover, tissue factor accounted for virtually ail of the coagulant potential of amniotic fluid. Amniotic, tissue factor appeared intact and membrane bound and, when reconstituted into synthetic microvesicles of optimal phospholipid content, displayed nearly full activity. Calcium chelation and sonication experiments suggested that the presence of inhibitors and the physical configuration of membrane-bound tissue factor in amniotic fluid might explain the modest reduction in tissue factor procoagulant activity relative to total antigen levels observed in vivo. We postulate that the substantial quantities of functionally active tissue factor in amniotic fluid account for the coagulation changes accompanying amniotic fluid embolism and could indirectly contribute to the characteristic hemodynamic derangements of amniotic fluid embolism.

Native valve Staphylococcus epidermidis endocarditis: Report of seven cases and review of the literature

This report describes seven patients from three university hospitals whose native valve infective endocarditis was caused by Staphylococcus epidermidis. The literature on endocarditis caused by S. epidermidis is also reviewed and the clinical features of patients with native valve endocarditis due to this organism are compared with those of patients from a general series of infective endocarditis cases. Compared with infective endocarditis caused by other organisms, S. epidermidis endocarditis tends to occur more frequently in male patients. Patients with S. epidermidis endocarditis exhibit fewer embolic complications and skin manifestations. The frequency of congestive heart failure is lower in this group. The relative indolent course and apparent rarity of native valve S. epidermidis endocarditis necessitate a high index of suspicion for early diagnosis.

Embolic mononeuropathy in subacute bacterial endocarditis

A 49-year-old man presented with temperature up to 39.5 degrees C, a sudden peroneal nerve lesion, and a cardiac murmur. The peroneal nerve lesion was likely caused by an embolic occlusion of an artery supplying the nerve. Until now, six cases of embolic mononeuropathy in endocarditis have been reported in the literature. Embolic mononeuropathy is a very rare manifestation of subacute bacterial endocarditis and quite often complicates, as do other more common embolic manifestations, the correct diagnosis.

Systemic Gas Embolism Complicating Mechanical Ventilation in the Adult Respiratory Distress Syndrome

Most forms of barotrauma related to mechanical ventilation are known to occur in both adult and pediatric patients. The pressure-driven transfer of gas from the alveolar compartment to the systemic circulation, a devastating complication of ventilatory support in infants, is not generally recognized as a consequence of ventilatory support in adults. Two young adult patients who received ventilatory support with high levels of positive pressure for pneumonia and the adult respiratory distress syndrome developed massive sub-pleural air cysts, interstitial emphysema, and tension pneumothoraces. Despite receiving appropriate treatment for these problems, the patients had recurrent episodes of cerebral infarction, myocardial injury, and a characteristic pattern of livedo reticularis. This distinctive triad of findings, otherwise unexplained and occurring in the setting of cystic barotrauma, is highly suggestive of systemic gas embolism. Although our patients presented with dramatic clinical features, we believe that patients with ventilator-related gas embolism may present more commonly with subtler signs, such as puzzling disturbances in heart rhythm or mental status, seizure activity, hypotension, localized pain, or other embolic manifestations readily ascribed to other causes in critically ill patients.

Cutaneous manifestation of atrial myxoma

A left atrial myxoma may present in a manner that diverts attention from its cardiac origin. This case report documents a cutaneous clinical presentation that initially was thought to represent a peripheral vasculitis or connective tissue disease. Biopsy specimens revealed a peripheral arterial myxomatous embolus in the skin, and echocardiogram results were diagnostic for atrial myxoma. Embolic manifestations may occur in up to 40% of cases. We hope that description of this patient will alert others to suspect this tumor in unexplained or peculiar forms of vasculitis and to consider an echocardiogram as part of the diagnostic workup.

Atheroembolic renal disease: clinico-pathologic correlations.

It has been known for long time that the course of atherosclerotic disease may be complicated by systemic manifestations of cholesterol embolism (1). The kidney is frequently involved in this phenomenon (2) which may give rise to diverse clinical pictures. The clinical diagnosis of atheroembolic renal disease may be easy in the presence of other embolic manifestations (livedo reticularis, digital ischemic necrosis, retinal emboli) and a clinical history of angiography, angioplasty and recent abdominal aortic surgery. In these cases, the cutaneous and muscular biopsies may provide valid and not invasive diagnostic support (3). When atheroembolism appears spontaneously, in the absence of causal events, and the clinical history is of acute or chronic renal failure of unknown origin, only renal biopsy with pathognomonic findings of needle-shaped cholesterol crystals within the vessel lumen permits diagnosis, distinguishing atheroembolic lesions from those of nephroangiosclerosis or other pathologies.

High fever (greater than 39 degrees C) as a clinical manifestation of pulmonary embolism.

This is a review of seven patients with pulmonary emboli manifested as high fever (temperature greater than 39 degrees C) seen over a 3 year period by an infectious disease consultant for unexplained fever. The patients' ages ranged from 16 to 81 years. Bed confinement was the underlying condition of all but one patient. Fever resolved with intravenous heparin therapy in three patients and one patient recovered without heparin therapy. Three patients died. Regardless of the degree of fever, pulmonary emboli should be among the list of differential diagnoses in patients with unexplained fever, especially in those who are confined to bed.

Antibiotic treatment of Staphylococcus aureus endocarditis. A review of 119 cases.

Clinical and bacteriological information of Staphylococcus aureus endocarditis was reviewed in 119 cases from all over Denmark. Overall mortality was 71%. Survival correlated with antistaphylococcal treatment, short duration from onset of infection to start of treatment, and long duration of treatment. In spite of relevant treatment, mortality was significantly lower in cases infected with penicillin-susceptible strains than when penicillin-resistant strains were isolated. There were no differences in the effect of various anti-staphylococcal treatment regimens; in particular, there were no differences in mortality with regard to beta-lactam antibiotics alone as compared to beta-lactam antibiotics in combination with aminoglycosides. However, embolic manifestations occurred more often after start of treatment with combination therapy than with beta-lactam antibiotics alone.

The cutaneous manifestations of cholesterol crystal embolization

The cutaneous manifestations of cholesterol crystal embolization

The Cutaneous Manifestations of Cholesterol Crystal Embolization

In an effort to provide a greater understanding of the cutaneous features of cholesterol crystal embolization (CCE), we reviewed the clinical features of all histologically proved cases reported in the English-language literature, exclusive of cases in which there was only central nervous system or cardiac involvement. We found that the skin is involved in 35% of patients with CCE. Livedo reticularis is the most common skin manifestation (49%), followed by gangrene (35%), cyanosis (28%), ulceration (17%), nodules (10%), and purpura (9%). Cholesterol crystal embolization was most common in older men and was frequently associated with anticoagulant therapy (36%) or vascular procedures (31%). Because of its protean systemic manifestations, CCE was often mistaken for vasculitis (16%) and periarteritis nodosa (12%). Mortality was very high (72%). Histologic confirmation of cutaneous CCE was possible in 92% of cases where a skin biopsy specimen was obtained. We conclude that the diagnosis of cutaneous CCE should be suggested and easily confirmed histologically in the appropriate clinical setting.

Psychological Manifestations of Embolization

Back to table of contents Previous article Next article ArticleNo AccessPsychological Manifestations of EmbolizationLAURENS D. YOUNGLAURENS D. YOUNGSearch for more papers by this authorPublished Online:1 Apr 2006https://doi.org/10.1176/ajp.138.7.996AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail "Psychological Manifestations of Embolization." American Journal of Psychiatry, 138(7), p. 996 Access content To read the fulltext, please use one of the options below to sign in or purchase access. Personal login Institutional Login Sign in via OpenAthens Purchase Save for later Item saved, go to cart PPV Articles - American Journal of Psychiatry $35.00 Add to cart PPV Articles - American Journal of Psychiatry Checkout Please login/register if you wish to pair your device and check access availability. Not a subscriber? Subscribe Now / Learn More PsychiatryOnline subscription options offer access to the DSM-5 library, books, journals, CME, and patient resources. This all-in-one virtual library provides psychiatrists and mental health professionals with key resources for diagnosis, treatment, research, and professional development. Need more help? PsychiatryOnline Customer Service may be reached by emailing [email protected] or by calling 800-368-5777 (in the U.S.) or 703-907-7322 (outside the U.S.). FiguresReferencesCited byDetailsCited byNone Volume 138Issue 7 July 1981Pages 996-996 Metrics PDF download History Published online 1 April 2006 Published in print 1 July 1981

Surgical management of massive pulmonary embolism

Between 1972 and 1976, 24 patients have been treated by open pulmonary embolectomy with the aid of cardiopulmonary bypass (CPB). In 17 (71 percent) acute pulmonary embolism occurred 3 to 60 days after a surgical procedure. The remaining seven (29 percent) patients had chronic medical diseases. The interval between clinical manifestation of acute pulmonary embolism and the performance of open embolectomy ranged from 8 to 36 hours. The definitive diagnosis in all patients was made by pulmonary arteriography. Candidates for pulmonary embolectomy were selected by assessment of hemodynamic stuides: shock, arterial Po2 less than 65 mm. Hg, acidosis, pulmonary artery pressure higher than 20 to 30 mm. Hg, and central venous pressure elevated (patients in Class III or IV according to the Greenfield classification). The definitive indication for embolectomy was occlusion of the main pulmonary artery of more than 50 percent as well as occlusion of the right or left pulmonary artery. Of the seven patients operated upon between 1973 and 1974, three (43 percent) died in the early postoperative period. Between 1975 and 1976 the operative mortality rate in 17 patients was 23 percent (four patients). Our results show that prompt diagnosis of acute massive pulmonary embolism and better selection of patients may improve significantly the survival rate after open pulmonary embolectomy with CPB.

Acute bacterial endocarditis

Acute endocarditides, defined by the intensity of the infectious syndrome, increase rapidly in incidence, both in absolute number and in relation with classical subacute endocarditides. 60 cases were studied out of a lot of 130 cases of bacterial endocarditides. They are characterized by the nature of the portals of entry, particularly in hospital, the nature of the causal germs (staphylococci and gram-negative germs essentially), their habitually primary character, the importance of embolic manifestations. Cardiac failure through valvular mutilation is common, but surgical valve replacement is not always possible in view of the visceral or infectious context. Their overall prognosis is a very bad one: lethality 67 percent as against 15 percent for subacute endocarditides. An important part of prevention lies in a better hospital hygiene.

Mural Endocarditis Associated with Recurrent False Aneurysm of the Left Ventricle

Acute bacterial endocarditis developed in a 65-year-old man two years after surgical resection of a false aneurysm of the left ventricle. The patient had cerebral embolic manifestations, and coagulase-positive Staphylococcus aureus was cultured from each of six blood samples. A pericardial friction rub and a changing pansystolic murmur appeared during the third week of hospitalization. The presence of a false aneurysm was once again demonstrated on ventriculographic studies. This was successfully repaired, employing cardiopulmonary bypass. The sequence of events in this patient suggests that bacterial endocarditis at the site of a previous cardiomyotomy might have led to the development of the second pseudo-aneurysm.

Massive Left Atrial Thrombus Complicating Mitral Stenosis with Atrial Fibrillation: Results of Surgical Treatment

Thirty-five patients with massive atrial thrombus complicating mitral stenosis and atrial fibrillation were treated surgically. The mean age in this series is lower than that reported in the West. Furthermore, the incidence of preoperative embolic manifestations has been less frequent in our experience. We believe it is desirable to document the presence of a thrombus by selective left atrial cineangiography. Surgical treatment was accomplished with an acceptable mortality. The vital role played by the use of low-molecular-weight dextran and early anticoagulation in decreasing the incidence of postoperative cerebral embolism is emphasized. Follow-up data in the survivors has shown excellent functional status with no late embolic phenomena in any subject.

Leftward Shift of Frontal Plane QRS Axis as a Frequent Manifestation of Acute Pulmonary Embolism

Analysis of the frontal plane QRS axis was made in 115 patients with acute pulmonary embolism studied at this medical center. A leftward shift of axis was twice as frequent as a rightward shift, and left axis deviation was twice as common as right axis deviation at the time of the acute embolism. It is concluded that a leftward shift of the frontal plane electrical axis in acute pulmonary embolism may be considered one of the electrocardiographic manifestations of the disorder.

Left axis deviation as an electrocardiographic manifestation of acute pulmonary embolism

Summary A previously unreported shift of the frontal plane QRS electrical axis to the left is described in a patient with documented acute pulmonary embolism. Recognition that such an electrocardiographic abnormality may occur in pulmonary embolism may be of value in reaching a tentative clinical diagnosis prior to definitive studies.

Unusual electrocardiographic manifestation of pulmonary embolism

A case of acute pulmonary embolism is presented because of its unusual electrocardiographic manifestation. The scalar ECG showed the transient development of abnormal Q waves with T-wave inversion in the precordial leads V 2 through V 5. A simultaneous vectorcardiogram showed the initial forces to be directed to the right with a loss of the anterior forces. A thorough postmortem examination failed to reveal an acute myocardial infarction.

Pulmonary Embolism

Few diseases are as common, as potentially lethal, and yet as frequently unrecognized as pulmonary embolism. When pulmonary emboli have been carefully sought at postmortem examination, the incidence has been found to be in excess of 25%.^1-3At the Peter Bent Brigham Hospital, pulmonary embolism is one of the three most common causes of death.¹Yet, the correct premortem diagnosis is made in only about 50% of the cases. The number of deaths due to pulmonary embolism may be decreased by early recognition and prompt treatment, thus minimizing the risk of additional episodes of potentially lethal embolism. <h3>Recognition of Pulmonary Embolism</h3> The well-known difficulty in recognizing pulmonary embolism is, in part, due to the fact that it can present as four different clinical syndromes: <h3>1. Pulmonary Infarction.—</h3> Although pulmonary infarction is the most familiar manifestation of pulmonary embolism, it is one of the least frequent complications of embolism.