Related Experiment Video

Updated: May 4, 2026

Clinical Application of Microscope-Assisted Minimally Invasive Anterior Lumbar Interbody Fusion
04:42

Clinical Application of Microscope-Assisted Minimally Invasive Anterior Lumbar Interbody Fusion

Published on: June 16, 2023

1.4K

Cerebral vascular accidents after lumbar spine fusion

Alejandro Marquez-Lara1, Sreeharsha V Nandyala, Steven J Fineberg

  • 1From the Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, IL.

Spine
|January 4, 2014
PubMed

Insights

Cerebral vascular accidents (CVAs) after lumbar fusion are rare but serious, increasing mortality and costs. Identifying risk factors like advanced age and comorbidities can help surgeons mitigate these events.

Area of Science:

  • Neurosurgery
  • Spinal Fusion Surgery
  • Cerebrovascular Neurology

Background:

  • Lumbar fusion (LF) effectively treats degenerative spinal pathology.
  • Cerebral vascular accidents (CVAs) are rare but potentially catastrophic complications following LF.
  • Understanding CVA impact is crucial for patient safety and surgical outcomes.

Purpose of the Study:

  • To determine the incidence of CVA after lumbar fusion.
  • To identify risk factors associated with postoperative CVAs.
  • To analyze hospital resource utilization and early outcomes in patients experiencing CVAs post-LF.

Main Methods:

  • Retrospective cohort study utilizing the Nationwide Inpatient Sample database (2002-2011).
  • Analysis of patients undergoing elective anterior, posterior, or combined lumbar fusion.
  • Identification of patients with postoperative CVAs and assessment of demographics, comorbidities (Charlson Comorbidity Index), length of stay, costs, and mortality.

Main Results:

  • Out of 264,891 LFs, 340 (1.3 per 1000) developed a postoperative CVA.
  • CVA patients were older, had higher comorbidity burden, longer hospital stays, and increased costs ($41,454 vs. $25,885).
  • Mortality rates were significantly higher in patients with CVA (73.7 vs. 0.8 per 1000).
  • Risk factors included age >65, neurological disorders, paralysis, congestive heart failure, and electrolyte imbalance.

Conclusions:

  • Postoperative CVAs significantly increase complications, mortality, and hospital costs after lumbar fusion.
  • Identifying high-risk patients (e.g., older, with specific comorbidities) pre-operatively is essential.
  • Further research is needed to characterize risk factors and develop mitigation strategies for postoperative CVAs.
Abstract

More Related Videos

Novel Mini-open Transforaminal Lumbar Interbody Fusion05:52

Novel Mini-open Transforaminal Lumbar Interbody Fusion

Published on: June 6, 2025

1.0K
Surgical Approach and Complications of Stand-alone Lateral Trans-Psoas Interbody Fusion05:30

Surgical Approach and Complications of Stand-alone Lateral Trans-Psoas Interbody Fusion

Published on: February 14, 2025

1.8K

Related Concept Videos

Herniated Intervertebral Disc l: Introduction01:29

Herniated Intervertebral Disc l: Introduction

Intervertebral disc herniation refers to the displacement of the nucleus pulposus (the gel-like inner core of the disc) through a tear or weakened area in the annulus fibrosus (the outer fibrous ring). The displaced disc material extends beyond the normal boundaries of the disc space and may compress or irritate nearby spinal nerve roots or, less commonly, the spinal cord.Etiology and Risk FactorsHerniation commonly results from degeneration, in which aging reduces disc hydration and...
40
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...
19
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...
30
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
52
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...
20