Death from cardiac failure in a child with ruptured cerebral arteriovenous malformation

Kevin S Haug1, Barry G Baylen, Richard B Mink

  • 1Department of Pediatrics, Division of Pediatric Critical Care, David Geffen School of Medicine at UCLA, Torrance, CA, USA. kevin.haug@ucdmc.ucdavis.edu

Insights

A ruptured cerebral arteriovenous malformation in a child caused severe cardiac failure and death. This case highlights the critical, potentially lethal cardiovascular risks in pediatric patients following a cerebral insult.

Area of Science:

  • Neurology
  • Cardiology
  • Pediatrics

Background:

  • Cardiac dysfunction following neurological injury, known as neurogenic stunned myocardium, is well-documented in adults with subarachnoid hemorrhage.
  • Cardiovascular complications in children after brain injury are less common and typically associated with traumatic brain injury, with no reported fatalities.

Observation:

  • A 13-year-old boy experienced rapid cardiac failure and death following a ruptured cerebral arteriovenous malformation (AVM) with subarachnoid hemorrhage.
  • Diagnostic data, including electrocardiograms, cardiac enzymes, echocardiograms, and pulmonary artery catheterization, confirmed severe ventricular dysfunction due to myocardial ischemia and infarction.

Findings:

  • This case demonstrates a fatal outcome in a pediatric patient due to severe cardiac dysfunction after a ruptured cerebral AVM.
  • The event suggests that ruptured cerebral AVMs can precipitate life-threatening cardiac complications in children, mirroring but exceeding the severity seen in other pediatric brain injuries.

Implications:

  • Early recognition and management of cardiac dysfunction are crucial in pediatric patients with ruptured cerebral AVMs and subarachnoid hemorrhage.
  • Aggressive supportive care is necessary to maintain adequate perfusion and limit secondary brain injury in these high-risk pediatric cases.

Related Concept Videos

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...
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...
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...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
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...