Related Experiment Video

Updated: May 10, 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

Unusual clinical course of preeclampsia heralded by generalized edema

Takashi Kojima1, Takahiro Yamada, Takashi Yamada

  • 1Department of Obstetrics, Hokkaido University Graduate School of Medicine.

The Journal of Obstetrics and Gynaecology Research
|July 3, 2013
PubMed

Preeclampsia monitored by the amount of proteinuria usually does not show amelioration during pregnancy. A 37-year-old nulliparous woman was admitted to our hospital at gestational week (GW) 24(-1/7) due to rapid weight gain (6.2 kg/4 weeks) and oligohydramnios. Hypertension (151/91 mmHg) appeared at GW 25(-0/7) and proteinuria not detected at GW 24(-0/7) became significant (0.55 g/day) at GW 25(-2/7) . During the 2 successive weeks after administration of betamethasone at 12 mg twice and transabdominal amnioinfusion with 250 mL of Ringer's acetate solution at GW 25(-3/7) , generalized edema, proteinuria and thrombocytopenia markedly improved: bodyweight, 78.0 to 69.0 kg; proteinuria, from 7.1 to 1.3 g/day; and platelet count, from 111 to 230 × 10(9) /L. However, intrauterine infection accompanied by non-reassuring fetal status necessitated emergency cesarean section at GW 28(-3/7) . Extraordinary bodyweight gain can herald the occurrence of preeclampsia and this weight gain together with signs of preeclampsia can ameliorate even during pregnancy, although its mechanism is unclear.

Keywords:
gestational edemapreeclampsiathrombocytopeniavascular permeability

More Related Videos

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats07:36

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

Published on: November 20, 2015

Related Concept Videos

Nephrotic Syndrome I : Introduction01:24

Nephrotic Syndrome I : Introduction

Nephrotic Syndrome is a chronic kidney disorder defined by clinical findings such as severe proteinuria, hypoalbuminemia, hyperlipidemia, and edema. These symptoms result from damage to the glomeruli, the kidney’s filtering units, increasing their permeability to proteins.Definition and Meaning:Proteinuria, defined as the loss of more than 3.5 grams of protein per day in adults, is a crucial feature of nephrotic syndrome. This condition is often accompanied by edema, the accumulation of fluid...
Pulmonary Edema II: Pathophysiology01:18

Pulmonary Edema II: Pathophysiology

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...
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

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...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

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...
Nephrotic Syndrome III : Nursing Management01:24

Nephrotic Syndrome III : Nursing Management

Nursing management for nephrotic syndrome adapts as the disease progresses, with strategies evolving to address advancing symptoms and complications.Early-Stage Management In the early stages, nursing interventions for nephrotic syndrome resemble those used in managing acute glomerulonephritis, focusing on symptom monitoring, fluid balance, and managing mild to moderate edema.Vital Signs: Regularly monitor blood pressure, pulse, respiratory rate, and temperature to promptly identify...
Heart Failure III: Clinical Manifestations01:26

Heart Failure III: Clinical Manifestations

Heart failure (HF) manifests primarily as dyspnea, fatigue, and fluid retention, resulting in peripheral and pulmonary edema. Symptoms may vary depending on which ventricle is more affected, left or right.Left-Sided Heart FailureAlso known as left ventricular failure, this condition results from the left ventricle's inability to fill or eject sufficient blood into the systemic circulation. It leads to pulmonary congestion, which occurs when the left ventricle fails to eject blood effectively...