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At least 487 records · Page 27Linked to original sources
PubMed1992

[A new method for diagnosis of amniotic fluid embolism by means of monoclonal antibody TKH-2 that recognizes mucin-type glycoprotein, a component in meconium].

Five monoclonal antibodies (moABs TKH-2, MA54, MA61, B72.3, and CC49), directed toward the O-linked mucin-type glycoprotein, showed signs of specific reactivity with human meconium. The reactivity of these moABs with meconium extract was examined by solid-phase ELISA with different native and sialidase-treated glycoproteins. All moABs react with meconium extract, whereas the reactivities of TKH-2, MA54, and MA61 are sialidase sensitive and the reactivity of TKH-2 with meconium extract was only inhibited by ovine submaxillary mucin (OSM), indicating that TKH-2 is the most sensitive and specific antibody clearly directed to the sialyl Tn antigen in meconium. The possible application of TKH-2 to diagnose amniotic fluid embolism (AFE) has been prelimiarily investigated. We demonstrated that the concentration of sialyl Tn antigen in the serum of patients with AFE was significantly increased, indicating that meconium was released into the maternal circulation. Our method for detecting sialyl Tn antigen in the serum of AFE patients is a direct way to demonstrate the release of meconium into the maternal circulation, and is a simple, rapid, non-invasive and sensitive method for the diagnosis of AFE.

Amniotic Fluid↗
PubMed1984

Cryoprecipitate therapy in amniotic fluid embolization.

Cryoprecipitate was administered to a patient with severe adult respiratory distress syndrome secondary to an amniotic fluid embolus, diagnosed cytologically. Following the administration of cryoprecipitate, cardiopulmonary and hematologic status markedly improved, and the patient recovered without apparent sequela. She is the sixth surviving patient reported to have an amniotic fluid embolus confirmed cytologically. On the basis of accumulating data on the relationship between fibronectin levels and the integrity of the reticuloendothelial system, it is quite possible that fibronectin (cold-insoluble globulin), and not fibrinogen, played the key role in her dramatic improvement and may well have been responsible for the clinical improvement in earlier patients treated with blood products containing fibronectin.

Adult↗
PubMed1987

[Amniotic fluid embolism caused by uterine rupture with severe coagulopathy].

There is reported on a 35 years old woman, who was delivered of her third child. Six days after the expected day of delivery labour was introduced. On the end of the second stage an amniotic fluid infusion happened. The patient was transferred to the ward for intensive therapy following initial treatment. Within four hours she received 22 units of blood and 27 units of coagulo-active substance because of severe coagulation defect. After restoration of coagulability of blood hysterectomy had to follow owing to uterine rupture which in the first instance was overlooked. Woman and child survived.

Adult↗
PubMed1999

Amniotic fluid embolism and isolated disseminated intravascular coagulation.

PURPOSE: Disseminated intravascular coagulation (DIC) is a well-known complication of an amniotic fluid embolus. However, clinical experience has shown that, in some patients, clinical hemorrhage may be the initial presentation. Mortality in this subset of patients is high. This report describes a patient with a suspected amniotic fluid embolus who survived and in whom the initial presentation was post partum hemorrhage. CLINICAL FEATURES: During the post delivery repair of a fourth degree perineal tear a 29 yr old prima gravida was noted to have excessive vaginal bleeding despite a well contracted uterus. Laboratory investigations revealed a decrease in hemoglobin from 126 g x l(-1) to 86 g x l(-1) and a severe disseminated intravascular coagulopathy (PT 27.5 sec, APPT 149 sec, direct fibrinogen < 0.6 g x l(-1), FDP > 640 g x l(-1)). Treatment included massive blood component therapy and, eventually, total abdominal hysterectomy. The patient subsequently recovered without sequelae. In the absence of any other explanation, the coagulopathy was considered to be secondary to amniotic fluid embolus. CONCLUSION: Amniotic fluid embolus remains an important cause of maternal mortality. Clinical reports, reviews of the literature, and the development of the national registry have all contributed to our understanding of this syndrome. Contrary to earlier beliefs, not all patients present with sudden cardiorespiratory collapse. As the present case illustrates, a less common presentation is the development of an isolated DIC in the peripartum period without antecedent hemodynamic or respiratory instability. Therefore, anesthesiologists must maintain a high index of suspicion for the disorder in order to facilitate early recognition and treatment.

Adult↗
PubMed1984

Massive amniotic fluid embolism.

A patient at 42 weeks of pregnancy called the emergency department complaining of painful uterine contractions for six hours. She was advised to come to the hospital immediately. An episode of vomiting caused a 60-minute delay in her arrival. Dyspnea, fatigue, and leg cramps developed. In the emergency department she was anxious, alert, and cyanotic. Fetal distress was diagnosed. Within 15 minutes the patient had bradycardic cardiopulmonary arrest. Resuscitation attempts and agonal caesarean section failed. Autopsy revealed massive pulmonary amniotic fluid emboli. Amniotic fluid embolus must be considered in the differential diagnosis of pregnant patients with complaints of shortness of breath and signs of shock with bradycardia.

Adult↗
PubMed1982

Tissue damage caused by activated complement and granulocytes in shock lung, post perfusion lung, and after amniotic fluid embolism: ramifications for therapy.

The complement system evolved as a beneficial antimicrobial system. However when activated during extracorporeal perfusion, as with hemodialysis or cardiopulmonary bypass, modest pulmonary dysfunction associated with granulocyte aggregation and embolization can occur. When complement activation is more massive and prolonged as with severe sepsis, trauma and acute pancreatitis or during infusions of amniotic fluid or other lipid-rich suspensions, severe pulmonary damage which we often recognize as shock lung may occur. Therapeutic ramifications of these conclusions are evident. Thus, high doses of corticosteroids (or of non-steroidal anti-inflammatory agents, such as ibuprofen--herein not discussed) have the ability to prevent aggregation and embolization of stimulated granulocytes to patent vessels downstream and also inhibit their production of toxic oxygen radicals. These beneficial properties suggest the use of these agents may be appropriate in shock states, particularly shock lung or during suspected amniotic fluid infusion. Appropriate clinical trials to substantiate this suggestion are awaited with interest.

Adrenal Cortex Hormones↗
PubMed2001

[Non-thrombotic pulmonary embolisms].

In the absence of intracardiac or intrapulmonary shunts, the pulmonary microvasculature traps all embolized particles greater than 10 microns. In the vast majority of cases these emboli are venous thrombi which lodge in larger pulmonary arteries, resulting in obstructive phenomena rather than primarily being injurious to lung parenchyma. This review deals exclusively with nonthrombotic pulmonary embolism which involves substances that lodge predominantly in the pulmonary microvessels and cause a true endothelial and parenchymal injury, as well as obstructive phenomena. The article focuses on fat embolism, amniotic fluid embolism, gas embolism, septic emboli, and tumour pulmonary embolism.

Embolism, Air↗