Choroid plexus coagulation in infants with extreme hydrocephalus or hydranencephaly

Sylvia Shitsama1, Nunthasiri Wittayanakorn, Humphrey Okechi

  • 1Division of Neurosurgery, Department of Surgery, Kijabe Hospital, Kijabe, Kenya.

Insights

Endoscopic choroid plexus coagulation (CPC) stabilized severe hydrocephalus in 43.3% of infants in Kenya. This procedure offers a potential alternative to ventriculoperitoneal shunts for managing congenital hydrocephalus and hydranencephaly.

Area of Science:

  • Neurosurgery
  • Pediatric Neurology
  • Medical Technology

Background:

  • Severe congenital hydrocephalus and hydranencephaly present significant challenges in Kenya.
  • Ventriculoperitoneal (VP) shunts have high complication rates, and endoscopic third ventriculostomies (ETVs) show limited efficacy in these patients.
  • Endoscopic choroid plexus coagulation (CPC) is explored to reduce cerebrospinal fluid (CSF) production.

Purpose of the Study:

  • To evaluate the effectiveness of CPC as a standalone treatment for infants with severe hydrocephalus or hydranencephaly.
  • To assess CPC's success in stabilizing head size and resolving symptoms without requiring VP shunt placement.

Main Methods:

  • Retrospective review of medical records for infants undergoing CPC at Kijabe Hospital (November 2010 - April 2013).
  • Inclusion criteria: severe congenital hydrocephalus or hydranencephaly, complete records, and preoperative imaging.
  • Success defined by symptom resolution, head size stabilization, and avoidance of VP shunt.

Main Results:

  • Thirty evaluable infants were followed for a median of 120 days.
  • CPC was successful in 43.3% of cases (13/30), including 8/20 with hydrocephalus and 5/10 with hydranencephaly.
  • Seventeen failures (56.7%) were observed, primarily due to increased head circumference (14/17) or CSF leakage (3/17), with 10 requiring subsequent VP shunt insertion. Six deaths occurred.

Conclusions:

  • CPC can stabilize macrocephaly in approximately 40% of infants with severe congenital hydrocephalus and hydranencephaly.
  • CPC presents a viable alternative treatment option to VP shunt placement in this patient population.
  • Further research may optimize CPC techniques and patient selection for improved outcomes.
Abstract

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...
27
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
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...
20
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
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...
20