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Related Concept Videos

Pulmonary Embolism I: Introduction01:29

Pulmonary Embolism I: Introduction

Pulmonary embolism (PE) occurs when a thrombus, fat or air embolus, amniotic fluid, or tumor tissue blocks one or more pulmonary arteries. These blockages originate in the venous system or the right side of the heart.EtiologyPE primarily arises from deep vein thrombosis (DVT) and other hypercoagulable states, such as inherited thrombophilias. Additional etiological factors include venous stasis, commonly seen in obesity, and endothelial injury from surgery and trauma. Less common causes include...
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A blood clot, or thrombus, is a semi-solid mass composed of fibrin, platelets, and red blood cells. When it forms within a vessel, it can obstruct blood flow, known as thrombosis. If part of the clot detaches, it becomes an embolus that can travel and block distant vessels. When this occurs in the pulmonary arteries, it causes a condition known as pulmonary embolism (PE).Origin and ImpactMost often, the embolus originates from a thrombus in the deep veins of the lower limbs, a condition called...
Cerebral Edema ll: Pathophysiology01:22

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Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
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Pulmonary Edema II: Pathophysiology01:18

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Pulmonary edema is the accumulation of fluid in the interstitial and alveolar spaces of the lungs, impairing gas exchange and oxygen delivery. It may be cardiogenic or noncardiogenic, but both reduce oxygenation and lung compliance.Cardiogenic Pulmonary EdemaCardiogenic edema results from increased hydrostatic pressure in pulmonary capillaries, usually due to left ventricular dysfunction from myocardial infarction, heart failure, or valvular disease. Ineffective cardiac pumping causes blood to...
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Related Experiment Video

Updated: Jun 17, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
07:36

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Published on: November 20, 2015

Amniotic fluid embolism.

A Rudra1, S Chatterjee, S Sengupta

  • 1Department of Anaesthesiology, K.P.C. Medical College, Kolkata, India. sumanc_24@yahoo.co.in

Indian Journal of Critical Care Medicine : Peer-Reviewed, Official Publication of Indian Society of Critical Care Medicine
|December 31, 2009
PubMed
Summary
This summary is machine-generated.

Amniotic fluid embolism (AFE) is a rare but often fatal condition where amniotic fluid enters the mother's bloodstream, causing severe systemic effects. Despite advances, AFE remains poorly understood and difficult to diagnose, with high maternal and fetal mortality rates.

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Area of Science:

  • Obstetrics and Gynecology
  • Critical Care Medicine
  • Immunology

Background:

  • Amniotic fluid embolism (AFE) is a catastrophic obstetric emergency.
  • It involves the entry of amniotic fluid into the maternal circulation, triggering a complex cascade of events.
  • The precise underlying mechanisms of AFE remain poorly understood.

Purpose of the Study:

  • To review the current understanding of Amniotic fluid embolism (AFE).
  • To highlight the pathophysiology, clinical presentation, diagnostic challenges, and management strategies for AFE.
  • To emphasize the grave maternal and fetal consequences associated with AFE.

Main Methods:

  • Literature review of Amniotic fluid embolism (AFE) cases and pathophysiology.
  • Analysis of diagnostic criteria, including clinical presentation and laboratory findings.
  • Examination of current management approaches, focusing on supportive care.

Main Results:

  • AFE can occur during various stages of labor and delivery, including cesarean sections.
  • Pathophysiology involves an immune-mediated response affecting multiple organ systems (respiratory, cardiovascular, neurological, hematological).
  • Clinical manifestations include pulmonary edema, convulsions, disseminated intravascular coagulation (DIC), arrhythmias, and cardiac arrest.

Conclusions:

  • Definitive diagnosis of AFE can be confirmed by identifying fetal elements in maternal blood, though often diagnosed clinically.
  • Management relies on a multidisciplinary approach and intensive supportive care for failing organ systems.
  • Despite improved care, AFE continues to have a high mortality rate for both mother and fetus.