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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...
Pulmonary Embolism I: Introduction01:19

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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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Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
Pleural Effusion I: Introduction01:25

Pleural Effusion I: Introduction

Pleural effusion is an abnormal fluid accumulation in the pleural cavity, a narrow space between the lungs and the chest wall. It is not a disease per se but rather a symptom or indication of an underlying disease. In normal circumstances, this space contains a small amount of fluid (5 to 15 mL), a lubricant facilitating the non-frictional movement of the pleural surfaces.
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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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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
07:36

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[Amniotic fluid embolism].

Carlos António1, Nelson Marçal, Carlos Lopes

  • 1Serviço de Pneumologia, Hospital Sousa Martins, ULS, Guarda, Portugal.

Acta Medica Portuguesa
|June 21, 2012
PubMed
Summary
This summary is machine-generated.

Amniotic fluid embolism (AFE) is a rare but fatal obstetric complication. This case report details a fatal AFE case, highlighting the importance of early diagnosis and intensive care for maternal mortality.

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Area of Science:

  • Obstetrics and Gynecology
  • Critical Care Medicine
  • Pathology

Background:

  • Amniotic fluid embolism (AFE) is a rare, often fatal obstetric emergency.
  • It is a significant contributor to maternal and fetal morbidity and mortality.
  • AFE can occur during labor, delivery, or the immediate postpartum period.

Observation:

  • This report details a young woman experiencing acute respiratory failure during labor.
  • The patient required invasive mechanical ventilation and an emergency cesarean delivery.
  • Despite intensive medical therapy, hypoxemia persisted, leading to multi-organ failure.

Findings:

  • The case demonstrates a refractory hypoxemia and progressive multi-organ failure.
  • Diagnosis was confirmed by identifying fetal material in maternal pulmonary microcirculation.
  • This highlights the pathological mechanism of amniotic fluid embolism.

Implications:

  • This case underscores the critical need for prompt recognition and management of AFE.
  • It emphasizes the challenges in treating refractory hypoxemia and multi-organ failure in AFE.
  • Understanding the pathophysiology is crucial for improving outcomes in this rare obstetric complication.