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DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
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The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
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Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
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Acute pancreatitis presents a complex medical emergency characterized by rapid onset inflammation of the pancreas, demanding timely diagnosis and management to prevent complications. The condition primarily manifests through severe upper abdominal pain that often radiates to the back. This pain intensifies following the consumption of fatty foods. Accompanying symptoms such as nausea, vomiting, abdominal distention, fever, dyspnea, cyanosis, and jaundice can vary in intensity but significantly...
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Updated: Jun 5, 2026

Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas
05:31

Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas

Published on: January 26, 2024

[Postpartum eclampsia and fulminant HELLP syndrome].

M Schott1, A Henkelmann, Y Meinköhn

  • 1Klinik für Anaesthesiologie, Intensivmedizin und Schmerztherapie, Klinikum Nordstadt, Klinikum Region Hannover, Haltenhoffstrasse 41, Hannover, Germany. martin.schott@germanynet.de

Der Anaesthesist
|December 25, 2010
PubMed
Summary
This summary is machine-generated.

Postpartum eclampsia and HELLP syndrome are rare but dangerous. Early detection of placental separation and hypertension is key to managing these severe postpartum complications and ensuring maternal and fetal survival.

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Last Updated: Jun 5, 2026

Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas
05:31

Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas

Published on: January 26, 2024

Area of Science:

  • Obstetrics and Gynecology
  • Critical Care Medicine
  • Hematology

Background:

  • Postpartum eclampsia and HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome represent rare but life-threatening obstetric emergencies.
  • These conditions pose significant risks to both maternal and fetal well-being, necessitating prompt recognition and management.

Observation:

  • A case report details a 38-year-old parturient who developed severe postpartum complications, including eclampsia and HELLP syndrome, following emergency cesarean delivery for fetal bradycardia.
  • The patient presented with new-onset hypertension, seizures, anemia, renal failure, and severe coagulopathy, complicated by diffuse abdominal bleeding and hyperfibrinolysis.

Findings:

  • The patient's anemia was attributed to severe hemolysis and coagulopathic bleeding, distinct from typical postpartum hemorrhage.
  • Management involved intensive care, blood product transfusions, antifibrinolytic therapy, and renal replacement therapy.
  • Successful recovery was achieved without sequelae after 26 days of hospitalization.

Implications:

  • Placental separation and peripartum hypertension can herald severe gestosis and associated complications like disseminated intravascular coagulation (DIC) and acute renal failure.
  • Differentiating hemolysis from hemorrhage in postpartum HELLP syndrome is critical.
  • Early detection of warning signs and a multidisciplinary approach are vital for managing postpartum gestosis and its complications effectively.