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Related Concept Videos

Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
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...
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...
Increased Intracranial Pressure l: Introduction01:14

Increased Intracranial Pressure l: Introduction

Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...

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Related Experiment Video

Updated: May 18, 2026

Modeling Intracerebral Hemorrhage in Mice: Injection of Autologous Blood or Bacterial Collagenase
10:44

Modeling Intracerebral Hemorrhage in Mice: Injection of Autologous Blood or Bacterial Collagenase

Published on: September 22, 2012

[Subepithelial pelvic hematoma].

J J Aguilar-García1, B Vargas-Serrano

  • 1UGC de Radiodiagnóstico, Hospital Universitario Virgen del Rocío, Sevilla, España. jjag96@hotmail.com

Actas Urologicas Espanolas
|September 25, 2012
PubMed
Summary
This summary is machine-generated.

Subepithelial pelvic hematoma, or Antopol Goldman lesion, can mimic tumors. Early diagnosis through imaging and clinical suspicion is key to avoiding unnecessary surgery.

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Massive Pontine Hemorrhage by Dual Injection of Autologous Blood
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Massive Pontine Hemorrhage by Dual Injection of Autologous Blood

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Last Updated: May 18, 2026

Modeling Intracerebral Hemorrhage in Mice: Injection of Autologous Blood or Bacterial Collagenase
10:44

Modeling Intracerebral Hemorrhage in Mice: Injection of Autologous Blood or Bacterial Collagenase

Published on: September 22, 2012

Massive Pontine Hemorrhage by Dual Injection of Autologous Blood
06:33

Massive Pontine Hemorrhage by Dual Injection of Autologous Blood

Published on: May 29, 2021

Area of Science:

  • Radiology
  • Urology
  • Pathology

Background:

  • Subepithelial pelvic hematoma (Antopol Goldman lesion) is a rare entity.
  • It can clinically and radiologically mimic renal or pelvic neoplasms.
  • Misdiagnosis has historically led to nephrectomy in many cases.

Observation:

  • A 43-year-old woman presented with acute left flank pain after physical exertion.
  • Imaging studies included ultrasonography, computed tomography, and magnetic resonance imaging.
  • A lesion in the left renal sinus was identified.

Findings:

  • Radiologic findings were suggestive of subepithelial pelvic hematoma.
  • No evidence of an underlying lesion was detected.
  • The patient was managed conservatively with lesion resolution confirmed on follow-up.

Implications:

  • High clinical suspicion and advanced imaging are crucial for diagnosing Antopol Goldman lesions.
  • Accurate diagnosis can prevent misdiagnosis and unnecessary nephrectomy.
  • Understanding the imaging characteristics of this rare condition improves patient management.