Persistent Intracranial Hypertension in a Cranial Vault Remodeling Patient With Open Skull Fractures From Horse Kick

Matthew E Braza1, John A Girotto2

  • 13591Spectrum Health/Michigan State University College of Human Medicine Integrated Plastic Surgery Residency, Grand Rapids, MI, USA.

Insights

Severe traumatic brain injury in a child with prior craniosynostosis surgery required intensive management for intracranial hypertension. Prompt multi-team care and helmet use are crucial for recovery.

Area of Science:

  • Pediatric Neurosurgery
  • Traumatic Brain Injury Management
  • Craniofacial Surgery

Background:

  • A 4-year-old female with a history of cranial vault remodeling for bilateral coronal craniosynostosis experienced a severe traumatic brain injury.
  • The injury involved open skull fractures resulting from a horse kick, presenting a unique clinical challenge.

Observation:

  • The patient developed persistently elevated intracranial pressure (ICP) post-injury.
  • Management included neurosurgical decompressions, maximal medical therapy, and various ICP monitoring devices, with limited initial success.

Findings:

  • Despite initial complications, the patient's intracranial pressure eventually improved.
  • She achieved a full neurological recovery, indicating resilience and effective, albeit delayed, treatment.

Implications:

  • Horse kick injuries can cause severe traumatic brain injuries with significant morbidity.
  • Elevated intracranial pressure in patients with prior cranial vault remodeling warrants careful consideration of potential etiologies.
  • A multidisciplinary team approach and consistent helmet utilization are vital for managing craniosynostosis patients, especially after traumatic brain injury.

Related Concept Videos

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...
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...