The Critically Ill Patient with a Cerebrospinal Fluid Shunt

 

The Critically Ill Patient with a Cerebrospinal Fluid (CSF) Shunt: A Critical Care Perspective

Dr Neeraj Manikath , claude.ai

Abstract

Cerebrospinal fluid shunts represent life-sustaining interventions for patients with hydrocephalus, yet their presence introduces unique diagnostic and therapeutic challenges in the intensive care unit. This review synthesizes current evidence and clinical experience to guide intensivists in managing shunt-related emergencies, with emphasis on differentiating malfunction from infection, optimizing diagnostic approaches, and coordinating neurosurgical intervention. We present practical algorithms and evidence-based strategies for the critically ill patient with indwelling CSF shunt hardware.

Introduction

Approximately 125,000 CSF shunt procedures are performed annually in the United States, with ventriculoperitoneal (VP) shunts comprising 85-90% of placements.[1] The lifetime revision rate approaches 80%, with infection rates of 5-15% and malfunction rates of 40% within the first year.[2,3] When these patients present to the ICU—often comatose or unable to provide history—the intensivist must rapidly differentiate between shunt malfunction, infection, or unrelated pathology while understanding that delayed recognition carries catastrophic consequences including herniation, permanent neurological deficit, or death.

The complexity escalates when considering that symptoms of shunt failure mimic numerous critical illnesses, imaging may be falsely reassuring, and interventions themselves carry substantial risk. This review provides a structured approach to these high-stakes clinical scenarios.

Recognizing Shunt Malfunction and Shunt Infection in the Comatose Patient

Clinical Presentation: The Diagnostic Conundrum

The comatose patient with a shunt presents a uniquely challenging diagnostic puzzle. Unlike the communicative patient who reports headache progression, the unconscious patient offers only physiological clues that overlap substantially with other critical illnesses.

Shunt Malfunction typically results from obstruction (proximal catheter in 60%, distal in 25%, valve in 15%) or disconnection.[4] The classical triad of headache, nausea, and vomiting cannot be elicited in the obtunded patient. Instead, intensivists must recognize:

• Acute deterioration in conscious level (the most reliable sign)
• Cushing's triad (hypertension, bradycardia, irregular respirations)—a late and ominous finding
• Pupillary changes (unilateral or bilateral dilation, sluggish response)
• Decerebrate or decorticate posturing
• Abducens nerve palsy (sixth nerve palsy causing esotropia—often the first cranial nerve affected by raised ICP)

Pearl: In patients with programmable shunts, inadvertent reprogramming by MRI magnets or even strong magnetic fields can cause valve setting changes mimicking malfunction. Always verify shunt settings with plain radiographs after MRI exposure.[5]

Shunt Infection presents with even greater diagnostic ambiguity. The classical presentation of fever, meningismus, and altered consciousness occurs in less than 40% of cases.[6] Most infections develop within 6 months of the most recent surgery, though late infections occur.

Key clinical features include:

• Fever with or without systemic inflammatory response (SIRS criteria)
• Unexplained abdominal pain or peritonitis (distal catheter infection in VP shunts)
• Erythema or tenderness along the shunt tract (present in only 15-20%)
• New-onset seizures (particularly concerning in previously seizure-free patients)
• Subtle deterioration over days to weeks rather than acute decompensation

Oyster: Coagulase-negative staphylococci (40-60% of infections) produce biofilms causing indolent infections with minimal systemic response.[7] Blood cultures are positive in only 10-30% of shunt infections, and normal inflammatory markers do NOT exclude infection.[8]

Distinguishing Malfunction from Infection: A Systematic Approach

This differentiation is critical because management pathways diverge dramatically:

Feature	Malfunction	Infection
Onset	Hours to days	Days to weeks (occasionally acute)
Fever	Absent	Present (60-80%) but may be absent
Timeline from surgery	Any time	Usually <6 months, 50% within 2 weeks
Ventricular size	Increased	Variable (may be normal or increased)
Shunt tap findings	Normal cell count, chemistry	Elevated WBC, low glucose, positive Gram stain/culture

Hack: The "shunt series" radiograph (AP and lateral skull, neck, chest, abdomen) should be obtained in EVERY suspected malfunction. Disconnection or migration is visible in 15-20% of malfunctions and immediately changes management.[9]

Critical Point: These conditions can COEXIST. Infection can cause catheter obstruction through inflammatory debris, and malfunction can create static CSF predisposing to infection. Always consider both diagnoses simultaneously.

The Role of Shunt Tapping and Imaging in the ICU Workup

Neuroimaging: First-Line but Imperfect

CT Head Non-Contrast remains the initial imaging modality:

• Advantages: Rapid, widely available, assesses ventricular size, identifies hemorrhage or mass lesions
• Limitations: 20-30% of shunt malfunctions occur WITHOUT ventriculomegaly on CT[10]

Pearl: Always compare with PREVIOUS imaging. Absolute ventricular size is less important than CHANGE from baseline. Patients with long-standing shunts may have permanently dilated ventricles that don't enlarge further despite elevated ICP (slit-ventricle syndrome).[11]

MRI offers superior soft tissue resolution and can identify:

• Loculated CSF collections
• Small periventricular edema (transependymal flow)
• Shunt catheter tip position
• Concurrent pathology (tumor, abscess)

However, MRI requires patient stability, time, and caution with programmable valves.

CT Ventriculography through shunt reservoir access can confirm patency when other studies are equivocal, though this requires neurosurgical consultation.

Ultrasound in patients with patent fontanelles provides bedside assessment of ventricular size trends.

Shunt Tapping: Indications, Technique, and Interpretation

Shunt tapping—percutaneous aspiration from the shunt reservoir—provides both diagnostic information and temporary therapeutic relief.

Indications:

1. Suspected shunt infection (obtain CSF for analysis)
2. Equivocal imaging with high clinical suspicion
3. Assessing shunt patency (though this requires experience)
4. Temporizing measure before definitive neurosurgical intervention

Technique Essentials:

Hack: The reservoir is typically palpable in the parietal region, 2-3cm from the burr hole. Use strict sterile technique—you're accessing the CNS. Prepare as for a central line: chlorhexidine prep, full barrier precautions, sterile gloves and drape.

1. Identify and palpate the reservoir
2. Strict aseptic technique (this procedure itself can cause infection)
3. Use a 23-25 gauge butterfly needle
4. Advance perpendicular to scalp until reservoir is punctured
5. Allow CSF to flow passively (DO NOT aspirate more than 10-20mL as this can collapse ventricles)
6. Observe flow characteristics

Interpretation:

Flow dynamics:

• Normal: Steady drip with each pulse (10-15 drops/minute)
• Proximal obstruction: No flow or very slow flow that doesn't improve with compression of distal tubing
• Distal obstruction: Brisk flow that doesn't slow when reservoir is allowed to refill

CSF Analysis:

Send for:

• Cell count with differential (bacterial infection: WBC >100 cells/μL with neutrophil predominance; normal shunt CSF: <10 WBC/μL)
• Glucose (infection: <50% of serum glucose or <40 mg/dL)
• Protein (elevated >45 mg/dL suggests infection, though often elevated in malfunction too)
• Gram stain and culture (INCLUDING fungal and anaerobic cultures)
• Consider lactate (>4 mmol/L suggests bacterial meningitis)[12]

Oyster: "Normal" CSF parameters vary by shunt type and chronicity. Long-standing shunts may have baseline protein elevation and mild pleocytosis. Interpret results in clinical context, not isolation.

Contraindications/Cautions:

• Overlying scalp infection
• Coagulopathy (relative; correct INR <1.5, platelets >50,000)
• Suspected loculated or trapped ventricles (risk of brain injury)

Advanced Diagnostic Considerations

Radionuclide Shunt Patency Study: Injection of technetium-99m into the reservoir with scintigraphic imaging can definitively assess flow through the entire shunt system. Useful when diagnosis remains uncertain after standard workup.[13]

ICP Monitoring via Reservoir: Some centers perform direct ICP measurement through the reservoir using transduced systems. This provides real-time pressure data but requires specialized equipment and expertise.

Managing Externalized Ventricular Drains (EVDs) and High ICP in the Shunted Patient

EVD Management: Unique Considerations in Shunt Patients

When shunt infection or malfunction necessitates externalization, management principles differ from de novo EVD placement:

Placement Strategy:

• Infected shunts: Complete hardware removal with NEW EVD at different site (opposite hemisphere preferred)[14]
• Malfunctioning shunts: May externalize existing ventricular catheter if proximal portion patent and position adequate

Drainage Management:

Critical Hack: Set EVD height based on DESIRED ICP, not arbitrary landmarks. For shunt-dependent patients, sudden exposure to "normal" ICP (10-15 mmHg) may cause overdrainage symptoms. Start conservative (15-20 cmH₂O above tragus) and titrate based on clinical response and ventricular size.

Overdrainage Prevention: Shunt-dependent brains are adapted to lower-than-normal ICP. Rapid drainage can cause:

• Subdural hematomas (particularly in elderly with atrophic brains)
• Slit-ventricle syndrome recurrence
• Severe postural headaches

Management protocol:

1. Continuous ICP monitoring when possible
2. Drain only when ICP exceeds threshold (e.g., >20 mmHg)
3. Clamp EVD periodically to assess tolerance (shunt trial)
4. Daily ventricular size monitoring with CT or ultrasound
5. Strict sterile technique with sampling (infection rate increases 1-2% per day)[15]

High ICP Management: Medical Therapy in the Shunted Patient

When shunt malfunction causes elevated ICP, medical management serves as a BRIDGE to definitive neurosurgical intervention, not a substitute.

Tier 1 Interventions (First-Line):

1. Head of bed elevation (30-45 degrees) improves venous drainage
2. Optimize sedation/analgesia (reduce metabolic demand; propofol preferred for wakeup assessments)
3. Maintain normocapnia (PaCO₂ 35-40 mmHg; avoid hyperventilation except as acute temporizing measure)
4. Maintain CPP >60 mmHg (may require vasopressors)
5. Normothermia (every 1°C temperature elevation increases ICP)
6. Seizure control (continuous EEG if concerns for non-convulsive status)

Tier 2 Interventions (Escalation):

7. Hyperosmolar therapy:

   • Mannitol 0.25-1 g/kg IV bolus (onset 15-30 minutes, duration 4-6 hours; monitor osmolality <320 mOsm/L)
   • Hypertonic saline 3-23.4% (bolus or infusion; target Na 145-155 mEq/L; safer for repeated dosing)[16]

   Pearl: Hypertonic saline is preferred over mannitol in neurosurgical patients due to better hemodynamic profile and no risk of osmotic diuresis complicating volume status.

8. Controlled hyperventilation (target PaCO₂ 30-35 mmHg; maximum 25 mmHg; duration <24 hours due to CSF buffering)

9. Metabolic suppression:

   • Barbiturate coma (pentobarbital loading dose 10 mg/kg over 30 minutes, then 5 mg/kg/hr × 3, maintenance 1-2 mg/kg/hr; requires continuous EEG to burst suppression)
   • Requires hemodynamic monitoring, vasopressor support, continuous EEG

Tier 3 (Last Resort):

10. Decompressive craniectomy (consider if medical management fails and patient not operative candidate for shunt revision)

Oyster: Do NOT delay neurosurgical consultation while optimizing "medical management." In shunt-dependent patients, definitive treatment IS surgical. Medical measures buy time, not cure disease.

Slit Ventricle Syndrome: The Special Challenge

Approximately 5% of chronically shunted patients develop slit ventricle syndrome—a state where ventricles cannot dilate in response to elevated ICP due to chronic decompression.[17]

Recognition:

• Severe headaches despite non-dilated ventricles on imaging
• Symptoms of raised ICP without ventriculomegaly
• May present with coma despite "normal" CT

Management:

• Requires high index of suspicion
• ICP monitoring via shunt reservoir or invasive monitor
• Anti-siphon devices or programmable valve adjustments
• May require cranial expansion procedures in severe cases

Antibiotic Penetration into the CNS and Shunt Hardware

Pharmacokinetic Principles in Shunt Infections

Shunt infections present unique therapeutic challenges:

1. Biofilm formation on hardware creates bacterial sanctuaries impermeable to antibiotics[18]
2. Blood-brain barrier limits antibiotic penetration
3. CSF flow dynamics altered by shunt change drug distribution
4. Device-related infections rarely eradicate without hardware removal

Antibiotic Selection: Evidence-Based Recommendations

Empiric Therapy (pending culture results):

Vancomycin 15-20 mg/kg IV q8-12h (target trough 15-20 μg/mL) PLUS Anti-pseudomonal coverage:

• Ceftazidime 2g IV q8h OR
• Cefepime 2g IV q8h OR
• Meropenem 2g IV q8h

Rationale: Covers coagulase-negative staphylococci (40-60%), S. aureus (20%), gram-negative rods (15-20%), and polymicrobial infections.[19]

Organism-Directed Therapy:

Organism	First-Line	Alternative	Duration
Coagulase-negative Staph (MSSA)	Nafcillin 2g q4h	Cefazolin 2g q8h	10-14 days after hardware removal
MRSA/Coag-neg Staph (resistant)	Vancomycin	Linezolid 600mg q12h	10-14 days after removal
Gram-negative rods	Ceftazidime or meropenem	Ciprofloxacin (if susceptible)	10-21 days after removal
Propionibacterium acnes	Penicillin G 4 million units q4h	Vancomycin	14-21 days after removal
Candida	Liposomal amphotericin B + flucytosine	Fluconazole (if susceptible)	14-28 days after removal

CNS Penetration: Critical Pharmacology

Good CSF Penetration (>50% serum levels):

• Linezolid
• Fluoroquinolones (ciprofloxacin, levofloxacin)
• Metronidazole
• Trimethoprim-sulfamethoxazole
• Chloramphenicol

Moderate Penetration (inflammation-dependent):

• β-lactams (ceftriaxone, ceftazidime, meropenem)
• Vancomycin (10-20% penetration; adequate for most CNS infections at high doses)

Poor Penetration:

• Aminoglycosides (<10%)
• First-generation cephalosporins
• Macrolides

Hack: For refractory infections or confirmed multidrug-resistant organisms, consider intrathecal or intraventricular antibiotics via EVD or Ommaya reservoir:

• Vancomycin 5-20 mg daily
• Gentamicin 5-10 mg daily
• Colistin 10 mg daily (for resistant gram-negatives)

This requires neurosurgical collaboration and pharmacy expertise. Monitor for chemical meningitis, seizures, and local toxicity.[20]

Hardware Management: The Fundamental Principle

Critical Point: Antibiotics alone fail in 85-90% of shunt infections without hardware removal.[21] The infected shunt creates a biofilm-coated foreign body that antibiotics cannot sterilize.

Standard approach:

1. Remove ALL infected hardware
2. Place EVD (different site, new trajectory)
3. Systemic antibiotics for 10-14 days with negative CSF cultures
4. Reimplant new shunt after documented CSF sterilization

Antimicrobial-impregnated shunts (rifampin/clindamycin or silver) reduce infection rates by 50-70% and should be considered for reimplantation.[22]

Neurosurgical vs. Medical Management of Shunt Complications

Decision-Making Framework: When to Operate

URGENT/EMERGENT Neurosurgical Consultation (Within 1 Hour):

• Glasgow Coma Scale ≤8 with suspected malfunction
• Signs of herniation (blown pupil, posturing, Cushing's triad)
• Rapid deterioration despite medical management
• Radiographic evidence of mass effect or midline shift
• Intraventricular hemorrhage with acute hydrocephalus

PROMPT Consultation (Within 2-6 Hours):

• Confirmed shunt malfunction with symptoms
• Suspected shunt infection
• Persistent elevated ICP despite tier 1-2 medical management
• CSF leak from shunt site
• Abdominal complications (bowel perforation, pseudocyst)

NON-URGENT Consultation (Within 24 Hours):

• Questionable malfunction with stable examination
• Chronic symptoms in shunt-dependent patient
• Shunt revision planning in patient with EVD

Surgical Options: The Neurosurgical Arsenal

For Malfunction:

1. Shunt revision (replace malfunctioning component)

   • Mortality: <1%
   • Infection risk: 5-8%
   • Re-malfunction within 1 year: 15-25%

2. Complete shunt replacement (when multiple component failures or infection)

3. Endoscopic third ventriculostomy (ETV) (creating physiologic CSF pathway)

   • Success rate: 70-90% in obstructive hydrocephalus with favorable anatomy
   • Shunt-independent outcome in 60-70%[23]
   • Preferred in older children/adults with acquired aqueductal stenosis

4. EVD temporization followed by reimplantation

For Infection:

Standard protocol:

• Hardware removal
• External drainage
• Antibiotics (10-14 days with negative cultures)
• New shunt placement (different site preferred)

Alternative approaches (selected cases):

• Antibiotic-impregnated catheter exchange (externalization without complete removal)—reserved for low-virulence organisms in stable patients
• Shunt retention with antibiotics—rarely successful (<15%), considered only in patients with extreme operative risk and low-virulence organisms

Complications of Surgical Intervention

Intensivists must recognize postoperative complications:

Immediate (0-48 hours):

• Hemorrhage (intraventricular, subdural, or tract)—occurs in 1-3%
• Incorrect catheter placement—into brain parenchyma rather than ventricle
• Overdrainage—acute subdural hematoma formation
• Pneumocephalus—usually benign, resolves spontaneously

Early (2-7 days):

• Infection (surgical site or new CSF infection)
• Malposition of distal catheter (bowel perforation with VP shunts)
• Seizures (5-10% incidence)[24]

Late (>7 days):

• Recurrent malfunction
• Abdominal complications (pseudocyst formation, peritonitis)
• Thrombotic complications (ventriculoatrial shunts)

The Medical Management Ceiling: Knowing Limitations

Medical intensivists provide critical support but must recognize limitations:

What medical management CAN do:

• Stabilize for safe transport to neurosurgical center
• Temporize raised ICP for hours to days
• Treat systemic manifestations (sepsis, seizures)
• Provide postoperative critical care support
• Manage comorbidities complicating surgical planning

What medical management CANNOT do:

• Definitively treat mechanical shunt failure
• Sterilize infected hardware
• Replace neurosurgical intervention
• Provide long-term ICP control in shunt-dependent patients

Pearl: In centers without immediate neurosurgical availability, intensivists should have a low threshold for arranging urgent transfer. A 2-hour transport delay is preferable to 6-hour delay in definitive management.

Clinical Pearls for ICU Practice

1. Always get old records. Prior imaging and operative reports are invaluable for determining baseline ventricular size and shunt configuration.

2. The "shunt series" radiograph is mandatory, not optional. Fifteen percent of malfunctions are immediately apparent on plain films.

3. Do not trust a single normal CT. Repeat imaging in 6-12 hours if clinical suspicion remains high.

4. CSF eosinophilia suggests hardware reaction or parasitic infection, not bacterial infection. Consider Propionibacterium in delayed postoperative presentations.

5. Abdominal pain in a VP shunt patient is a neurosurgical emergency until proven otherwise. Think bowel perforation, pseudocyst, or distal infection.

6. Programmable shunts need post-MRI confirmation of settings. Deprogramming to wide-open can cause overdrainage; to closed can cause acute malfunction.

7. When in doubt, tap the shunt. The information gained outweighs the small risk when performed with proper technique.

8. Empiric antibiotics should cover skin flora (including coagulase-negative staph) plus hospital-acquired pathogens in recent postoperative patients.

9. Document neurosurgical consultation clearly. In medicolegal reviews, delayed neurosurgical involvement is a common liability issue.

10. Communicate shunt presence to ALL consulting teams. Critical decisions about anticoagulation, lumbar puncture, and sedation vacations require this knowledge.

Conclusion

The critically ill patient with a CSF shunt demands synthesis of neurosurgical principles, critical care physiology, and infectious disease therapeutics. Success requires:

• Aggressive early diagnosis (low threshold for imaging and shunt tapping)
• Understanding that "normal" imaging does not exclude shunt failure
• Recognition that medical management temporizes but rarely cures
• Early neurosurgical partnership
• Awareness that hardware retention almost always fails in infection
• Attention to antibiotic pharmacokinetics in the CNS compartment

As shunt technology advances and patient populations age, intensivists will increasingly encounter these complex scenarios. Mastery of the principles outlined herein can be life-saving. The greatest errors occur not from lack of sophistication but from delayed recognition and intervention. When confronted with a comatose patient and uncertain shunt function, the intensivist's mantra should be: Image early, tap judiciously, consult promptly, and intervene definitively.

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Author Declaration: This review represents synthesis of current evidence-based practice for educational purposes. Local protocols and neurosurgical consultation should guide individual patient management decisions.