GC111 Raised Intracranial Pressure And Hydrocephalus
Raised intracranial pressure is an elevation of pressure within the cranial cavity above normal (>20 mmHg), often caused by mass lesions, cerebral edema, or hydrocephalus—a pathological accumulation of cerebrospinal fluid within the ventricular system due to impaired production, flow, or absorption.
Raised Intracranial Pressure & Hydrocephalus
Big Idea: The brain lives in a rigid, non-expandable box (the skull). Any increase in the volume of its contents — brain, blood, or CSF — will eventually cause a rise in intracranial pressure (ICP). Raised ICP reduces cerebral perfusion, causes brain herniation, and kills patients rapidly. Understanding the Monro-Kellie doctrine, the ICP–volume relationship, cerebral perfusion pressure, and the principles of ICP management is foundational to neurosurgery, neurology, critical care, and emergency medicine. Hydrocephalus is a specific cause of raised ICP with its own classification, clinical features, and surgical management.
Learning Objectives (from the lecture): [1]
- Common causes, pathophysiology, and clinical presentation of raised ICP
- Principles of management of raised ICP
- Pathophysiology of hydrocephalus
- Principles of management of hydrocephalus
How this fits into exams: This is one of the most consistently tested neurosurgery topics. Past papers have directly examined GCS calculation, CPP/CBF equations, communicating vs non-communicating hydrocephalus, LP contraindications, brain herniation types, NPH triad, shunt complications, and steroid use in TBI vs tumours. Expect MCQs (physiological thresholds, management principles) and SAQs (clinical scenarios with GCS calculation, herniation explanation, NPH workup).
Core Concepts and Mechanisms
ICP is measured at the level of the external auditory meatus (approximately the foramen of Monro). It can be measured by ventricular or lumbar puncture. Normal adult ICP = 10–15 mmHg; normal infant ICP = 1–6 mmHg. [1]
Why these numbers matter: The brain has no pain receptors for pressure itself — symptoms arise because raised ICP compresses structures, reduces perfusion, and causes herniation. Knowing the normal range lets you interpret monitoring data and recognise pathology.
The adult skull is a rigid box containing Brain + Blood + CSF. A mass lesion initially displaces venous blood and CSF. [1]
First principles explanation:
- Brain parenchyma ≈ 80%, Blood ≈ 10%, CSF ≈ 10% of intracranial volume [2]
- The skull cannot expand (unlike infant skulls with open fontanelles/sutures)
- Therefore, if any one compartment increases in volume, the other compartments must decrease to compensate
- Compensation mechanisms (in order):
- Venous blood outflow — fastest; venous blood is squeezed out of the cranium through jugular veins
- CSF displacement — CSF shifts from the ventricles/cisterns into the spinal thecal sac
- Once these buffers are exhausted → decompensation → exponential rise in ICP for even small additional volume increases
This is the classic "ICP vs SOL Volume" curve (the pressure-volume curve):
"Talk... and die." Initial compensation allows the patient to remain conscious, but once decompensation occurs, ICP rises exponentially and rapidly. [1]
Clinical pearl: This is why a patient can go from GCS 14 to GCS 5 in one hour — you go to lunch, they start dying. The slide literally shows: "1:00 p.m. Alert & Talking GCS=14 → 2:00 p.m. Comatose GCS=5. You went to lunch." [1]
CPP = MAP − ICP. Normal CPP = 60–80 mmHg. CBF = CPP / CVR. Normal CBF = 45–65 ml/min/100 g tissue. [1]
Why this matters:
- If ICP rises and MAP stays the same → CPP falls → CBF falls → cerebral ischaemia
- If MAP falls (e.g., from haemorrhagic shock) and ICP is normal → CPP still falls
- The brain's oxygen consumption is high and constant; it cannot tolerate ischaemia
Brain cells don't like ischaemia: obligate aerobic respiration; can only use glucose (& ketones in emergency); injured neurons can't recycle lactate → lactic acidosis; vicious cycles of glutamate release (excitotoxicity), calcium influx, energy failure & DNA damage → rapid cell death. [1]
The vicious cycle: Ischaemia → cell death → brain swelling (oedema) → further ICP rise → further ischaemia → more swelling. This is the slide titled "Vicious Cycle of Ischaemia & Brain Swelling." [1]
| Type | Mechanism | BBB Status | Location | Classic Cause | Steroid Response |
|---|---|---|---|---|---|
| Vasogenic | Fluid leaks from capillaries through damaged BBB into extracellular space (white matter) | Disrupted | Extracellular | Tumour (peri-tumoural oedema), abscess | Yes ✓ |
| Cytotoxic | Defective Na⁺/K⁺ ATPase → intracellular swelling | Intact | Intracellular | Ischaemia/infarction, hypoxia | No ✗ |
| Interstitial | CSF forced into periventricular extracellular space | N/A | Periventricular | Obstructive hydrocephalus | No |
High Yield – Steroids
Glucocorticoids are effective for vasogenic oedema (e.g., peri-tumoural oedema). They are ABSOLUTELY CONTRAINDICATED in TBI (increases mortality — CRASH trial). They are questionable and not used in stroke. [1] This is a favourite MCQ discriminator.
Space-occupying mass lesion (haematoma, tumour, abscess); Hydrocephalus (communicating/non-communicating); Brain swelling (focal/diffuse); Hyperaemia; Venous congestion. [1]
| Category | Examples |
|---|---|
| Mass lesion | Intracerebral haemorrhage, brain tumour, brain abscess, epidural/subdural haematoma |
| Hydrocephalus | Communicating (post-SAH, post-meningitis), non-communicating (tumour obstructing aqueduct/ventricle) |
| Brain swelling | Massive infarction, diffuse cerebral oedema (post-TBI, hypoxic-ischaemic encephalopathy) |
| Hyperaemia | Loss of cerebral autoregulation (post-TBI) |
| Venous congestion | Venous sinus thrombosis, jugular vein compression, midline tumour compressing sagittal sinus |
| Others | Idiopathic intracranial hypertension (IIH), seizure |
Clinical Features of Raised ICP
Headache (supine > erect; worse early a.m.); Vomiting (might transiently relieve headache); Blurring of vision & diplopia (CN VI); Deterioration in consciousness; Papilloedema (late). [1]
- Headache worse supine and early morning: Lying down increases venous return to the head → increased intracranial blood volume → increased ICP. During sleep, hypoventilation → ↑ PaCO₂ → cerebral vasodilation → ↑ ICP [3]
- Vomiting: Direct pressure on area postrema (vomiting centre) in the medulla. Vomiting transiently relieves headache because the Valsalva effect during emesis initially raises ICP, but subsequent changes in posture and CSF dynamics can temporarily relieve pressure
- CN VI palsy (diplopia): CN VI (abducens) has the longest intracranial course → most vulnerable to stretching by diffusely raised ICP. This is a false localising sign — it doesn't tell you where the lesion is
- Papilloedema: Raised ICP is transmitted along the subarachnoid space surrounding the optic nerve sheath → impedes axoplasmic flow → axonal swelling at the optic disc. It is a late sign [1][4]
- Deterioration in consciousness: Compression of the reticular activating system (brainstem) and global cerebral ischaemia
Brain "herniates" across intracranial compartments. Basal cistern obliterated. Brainstem compressed. [1]
The lecture uses the analogy: basal cistern patent = brainstem "smiling"; basal cistern obliterated = "not smiling" [1].
Types of herniation (supplemented from past papers [5]):
| Type | Structures Involved | Key Clinical Features |
|---|---|---|
| Uncal (transtentorial) | Medial temporal lobe through tentorial notch | Ipsilateral fixed dilated pupil (CN III compression), contralateral hemiplegia, ↓consciousness |
| Subfalcine (cingulate) | Cingulate gyrus under falx cerebri | Contralateral leg weakness (ACA compression), can compress ACA → infarction |
| Tonsillar | Cerebellar tonsils through foramen magnum | Brainstem compression → Cushing's triad, respiratory arrest, death |
| Upward (transtentorial) | Cerebellum herniates upward through tentorial notch | Posterior fossa mass pushing upward |
| External | Brain through skull defect | Through traumatic/surgical skull defect |
Combination of sympathetic & parasympathetic activation: Hypertension, Bradycardia, Irregular respiration (rapid & shallow). Also: Cushing ulcer, fixed dilated pupil (CN III). [1]
Why the Cushing reflex occurs:
- Brainstem ischaemia (from ICP approaching MAP)
- The vasomotor centre in the medulla responds by firing maximally → systemic hypertension (sympathetic surge to try to maintain CPP)
- Baroreceptors detect hypertension → reflex bradycardia (vagal)
- Respiratory centres in the medulla are compressed → irregular/agonal breathing
Critical Distinction
The Cushing reflex is a terminal, pre-mortem event. If you see the triad, the patient is about to die. Don't wait for it to diagnose raised ICP.
Glasgow Coma Scale (GCS)
Objective & reproducible way to assess consciousness. Admission GCS is prognostic. Trend reflects deterioration/improvement. Quantitative (3–15) but not a linear scale. Three components: Eye opening (E1-4), Motor response (M1-6), Verbal response (V1-5). [1]
| Component | Score | Response |
|---|---|---|
| Eye Opening (E) | 4 | Spontaneous |
| 3 | To voice* | |
| 2 | To pain | |
| 1 | None | |
| Verbal Response (V) | 5 | Oriented** |
| 4 | Confused | |
| 3 | Inappropriate words | |
| 2 | Incomprehensible sounds (moaning) | |
| 1 | None | |
| Motor Response (M) | 6 | Obeys commands |
| 5 | Localises pain | |
| 4 | Withdrawal (flexion) | |
| 3 | Abnormal flexion (decorticate) | |
| 2 | Extension (decerebrate) | |
| 1 | None |
*Try to wake up by calling the patient by name [1] **Oriented in person, space & time [1]
Motor score is indicative of extent of injury & prognostic. Painful stimuli applied over CNV territory. Best response of limbs. M5 – UL raised above clavicle. M4 – UL withdraw but not above clavicle. M3 (Decorticate Posture) – Injury to corticospinal tract above midbrain. M2 (Decerebrate Posture) – Injury to midbrain or upper pons. [1]
Why M is most prognostic: The motor pathways span the entire neuroaxis — their integrity reflects the global state of the brain better than eye or verbal responses.
Decorticate vs Decerebrate:
- M3 Decorticate (abnormal flexion): Arms flexed, legs extended. Lesion is ABOVE the red nucleus (in the midbrain) — the rubrospinal tract is intact and drives flexion
- M2 Decerebrate (extension): All limbs extended. Lesion is AT the midbrain/upper pons — the vestibulospinal tract dominates, driving extension
E1M5V2 (eyes closed, localises pain, moaning) vs E1M4V2 (eyes closed, flexion withdrawal, moaning) vs E1M3V1 (eyes closed, abnormal flexion, no sound) vs E1M2V1 (eyes closed, extension, no sound). [1]
E – swollen/no eye post-trauma; M – spinal cord injury, limb injury, muscle relaxant; V – language barrier, intubation/tracheostomy (VT); Total score can mean many things; Effect of shock – use post-resuscitation GCS; Effect of sedative drugs (e.g., for mechanical ventilation). [1]
Key exam point: Always use the best response. If the right arm localises but the left arm only flexes, record M5. Document components separately (e.g., E2M5V3 = GCS 10), not just the total.
ICP Monitoring
Indications: No reliable GCS (e.g., sedation, muscle paralysis); GCS ≤ 8 (requires intubation); Evolving disease conditions. Relative contraindications: Awake patients; Bleeding tendency. [1]
Why GCS ≤ 8: At this level the patient cannot protect their airway → requires intubation → you lose the ability to serially assess their neurological status → need invasive ICP monitoring.
Manometric principle for monitoring intracranial CSF pressure. Therapeutic by draining CSF for decompression. Risk of infection, iatrogenic trauma. LP contraindicated if raised ICP (with exception…). [1]
The exception: LP is safe in communicating hydrocephalus (all ventricles communicate with the lumbar space). In non-communicating hydrocephalus, LP creates a pressure gradient from above to below → transtentorial/tonsillar herniation → death. [1]
Initial GCS = E1M4V2. Intubated, ventilated & observed. ICP progressively increased from 16 to 28 cmH₂O. Definitely abnormal > 20 cmH₂O. Suggests worsening conditions → Repeat imaging studies → Escalate treatment. [1]
Management of Raised ICP
Protect uninjured brain. Salvage injured brain. Treat underlying cause. ALWAYS resuscitate first. Clinical/ICP monitoring. Control ICP & maintain cerebral perfusion. Neuroprotective therapies. [1]
ABC before ICP!! Airway, Breathing (protect C-spine), Circulation (not CT scan!), Disability, Exposure/Environment. [1]
ABC before ICP
Never skip resuscitation to get a CT scan. A dead patient doesn't need imaging. Stabilise the patient first, then investigate. [1]
| Any Doctor Can Do | Neurosurgeon/ICU |
|---|---|
| Head elevation 30° | ICP monitoring + CSF drainage (EVD) |
| Optimise ventilation | Controlled hyperventilation |
| Maintain MAP | Barbiturate coma |
| Osmotherapy (mannitol, hypertonic saline) | Surgical removal of SOL |
| Sedation | Decompressive craniectomy |
| Optimise electrolyte/glucose level | |
| Prevent/control seizures | |
| Prevent pyrexia |
Avoid neck rotation. Remove neck collar if not indicated. Head elevation ~30°. Maintain vascular volume & BP. [1]
Why 30° head elevation: Promotes venous drainage via the internal jugular veins → reduces intracranial venous blood volume → reduces ICP. Neck rotation or tight collars compress the jugular veins and impede outflow.
Normally vasoreactivity maintains stable CBF. Brain injury might impair vasoreactivity: Pressure active: ↑MAP → ↓ICP; Pressure passive: ↑MAP → ↑ICP. Aim: CPP ~60–70 mmHg. [1]
Explanation:
- In a pressure-active (intact autoregulation) brain: raising MAP causes reflex vasoconstriction → decreased cerebral blood volume → ICP actually decreases. This is desirable.
- In a pressure-passive (lost autoregulation) brain: raising MAP directly increases cerebral blood volume → ICP increases. This is dangerous.
- You don't always know which state the patient is in, so aim for a CPP sweet spot of 60–70 mmHg.
↓CO₂ → ↑Vasoconstriction → ↓ICP. But: CBF = CPP/CVR. ↑Vasoconstriction → ↑CVR → ↓CBF. Aim: PaCO₂ ~3.0–3.5 kPa. To buy time (e.g., on way to OT). [1]
PREVENT these: [1]
- ❌ Prophylactic hyperventilation
- ❌ Prolonged hyperventilation
- ❌ Without raised ICP
- ❌ Without monitoring
- ❌ Stopping suddenly (rebound vasodilation → ICP spike)
Hypoglycaemia → seizure & brain injury. Hyperglycaemia → lactic acidosis. Seizure → ↑metabolic demand, ↑brain swelling → Phenytoin (loading + infusion). Electrolyte imbalance. Fever → All contribute to acidosis. [1]
Mannitol (e.g., 100 ml 20% i.v.): Osmotic effect (needs intact BBB); ↓Blood viscosity, ↑CBF, ↓CBV; but also ↓Vascular volume, haemoconcentration, renal failure. CI: shock, ↑Na. Foley's catheter required (osmotic diuresis). Loop diuretics (e.g., frusemide). Hypertonic saline (better in multiply injured patients?). [1]
No Mannitol if Shocked
Mannitol causes osmotic diuresis → further volume depletion. If the patient is in haemorrhagic shock, mannitol will worsen hypotension → worsen cerebral perfusion. Use hypertonic saline instead. [1]
Aim at "burst suppression" on EEG. ↓Neuronal activities → ↓CBF & ↓ICP. Side effects: hypotension, myocardial depression. [1]
Why it works: Decreasing neuronal metabolic activity reduces oxygen demand → reflex cerebral vasoconstriction (metabolic autoregulation) → decreased cerebral blood volume → decreased ICP. But the trade-off is systemic cardiovascular depression.
Early cooling to 32–34°C. Neuroprotection by: ↓brain metabolic rate, ↓ATP consumption & ↓O₂ demand, ↓cell death cascades. Established therapy for post-cardiac-arrest brain injury. Controversial in stroke & trauma. S/E: pneumonia, coagulopathy. [1]
| Procedure | Description | Indication |
|---|---|---|
| EVD | Release CSF ± ICP monitoring | Hydrocephalus, raised ICP monitoring |
| Craniostomy (burr hole) | Drainage of superficial fluid collection | Chronic subdural haematoma |
| Craniotomy | Skull flap raised & replaced; removal of haematoma/tumour | Acute epidural/subdural haematoma, tumour |
| Decompressive craniectomy | Skull flap removed (not replaced) | Massive infarction, post-TBI brain swelling with refractory raised ICP |
Decompressive craniectomy: Bone flap not replaced. Effective in lowering ICP & mortality. Massive infarction or post-TBI brain swelling. Primary pathology (deficit) unchanged. Quality of survival variable. Ethical & philosophical issues. [1]
Hydrocephalus
Production: Choroid plexus in ventricles, ~450 ml/day in adults. Absorption: Arachnoid granulations at venous sinuses. Hydrocephalus if: ↑Production, Flow obstruction, ↓Absorption. [1]
CSF pathway: Lateral ventricles → Foramen of Monro → 3rd ventricle → Aqueduct of Sylvius → 4th ventricle → Foramina of Luschka (lateral) & Magendie (medial) → subarachnoid space → arachnoid granulations → superior sagittal sinus [6]
Key numbers:
| Feature | Communicating | Non-communicating (Obstructive) |
|---|---|---|
| Site of problem | Arachnoid granulations (impaired absorption) | Within ventricular system (flow obstruction) |
| Ventricle appearance | ALL ventricles dilated (including 4th) | Ventricles proximal to block dilated; 4th ventricle may be normal |
| LP safe? | YES — diagnostic & therapeutic | ABSOLUTELY CONTRAINDICATED (& lethal) |
This is a critical distinction. [1]
Acquired: ↑CSF production (choroid plexus papilloma); Flow obstruction (tumour, haematoma); ↓Absorption (meningitis, SAH). Congenital: Aqueductal stenosis, Arnold-Chiari malformation, Dandy-Walker syndrome, Neural tube defect, Congenital infection, Congenital mass lesions. [1]
| Classification | Causes |
|---|---|
| Communicating – Acquired | Post-SAH, post-meningitis (arachnoid granulation adhesions), leptomeningeal carcinomatosis, IVH, NPH |
| Non-communicating – Acquired | CPA tumours, posterior fossa tumours (cerebellar tumour obstructing 4th ventricle), colloid cyst in 3rd ventricle, aqueductal stenosis (post-infective), brain abscess |
| Congenital | Aqueductal stenosis, Arnold-Chiari malformation (Type II), Dandy-Walker syndrome, congenital infection |
| Overproduction (rare) | Choroid plexus papilloma |
Depends on age, cause, chronicity, brain compliance. Infants: large head, dilated scalp veins, tense fontanelle, sunset eyes, irritability, developmental delay. Adults: ICP symptoms, motor deficit, cognitive dysfunction, urinary incontinence, drowsiness, coma. Insidious onset, or can be rapidly fatal. [1]
Why infants are different: Sutures are open → skull can expand → ICP may remain relatively compensated for longer, but head circumference increases. In adults, the rigid skull means raised ICP symptoms develop earlier.
A surgically treatable cause of cognitive decline. Complex pathophysiology of abnormal brain compliance. ICP not high despite large ventricles. Classic clinical triad: Gait disturbance, Cognitive decline, Urinary incontinence. Responds well to CSF diversion (e.g., VP-shunting). Need to distinguish from other causes of dementia such as AD, which does not respond to shunting. [1]
Why is ICP "normal" in NPH? The pressure reaches a new equilibrium — the ventricles dilate until an equilibrium is reached where production ≈ absorption at a normal pressure, but the expanded ventricles exert local pressure effects on periventricular structures (especially the corona radiata carrying leg fibres → gait disturbance appears first).
Key differential: Alzheimer's disease. Both present with cognitive decline in elderly patients. But only NPH responds to shunting. CT/MRI shows ventriculomegaly out of proportion to sulcal enlargement in NPH (vs proportional ventricular and sulcal enlargement in cerebral atrophy/AD). [7]
Clinical suspicion. Imaging studies — ventricular dilatation, change in morphology & periventricular oedema. MRI CSF studies. Lumbar puncture — measures CSF pressure, trial drainage BUT BE CAREFUL!! EVD — rarely. [1]
For NPH specifically:
- CT/MRI: ventriculomegaly out of proportion to sulcal widening
- LP (high-volume tap 30–50 mL): observe for clinical improvement (especially gait) — this is a therapeutic trial [7]
ABC first. Temporising measures: LP if communicating; EVD if doubt or unstable/evolving condition. Definitive measures: CSF shunting (VP, VA); Endoscopic third ventriculostomy (ETV); Treat underlying cause (haematoma/tumour removal). [1]
Complications: Infection (10% or 20%); Blockage → hydrocephalus; Dislodgement/Fracture → hydrocephalus; Over-shunting → CSDH; Abdominal pseudocyst; Slit ventricle syndrome; Nephritis (VA); Bowel perforation (VP). Avoid shunting if possible! [1]
| Complication | Mechanism/Explanation |
|---|---|
| Infection | Most common organism: S. epidermidis, S. aureus. Presents with fever, meningism, raised ICP signs |
| Blockage | 80% proximal (choroid plexus/brain debris), 10% valve, 10% distal. Most common mechanical failure |
| Over-shunting | Too much CSF drained → low ICP → bridging veins stretch → chronic subdural haematoma (CSDH) |
| Slit ventricle syndrome | Chronic over-shunting → ventricles collapse → catheter tip obstructed → intermittent raised ICP |
| Abdominal pseudocyst | CSF-filled cyst forms around distal VP catheter in peritoneum |
| Bowel perforation | VP catheter erodes into bowel → peritonitis |
| Nephritis | VA shunt → immune-complex (shunt) nephritis |
| Scenario | Think About |
|---|---|
| Recurrent hydrocephalic symptoms | Blocked shunt → test shunt if competent |
| Raised ICP + focal deficit | CSDH? (especially elderly on aspirin — from over-shunting) |
| Postural headache (worse erect) | Intracranial hypotension from over-shunting (without CSDH) |
| Fever + abdominal pain | Shunt infection → peritonitis? OR peritonitis → shunt infection? → Externalise shunt + antibiotics |
Allows post-op transcutaneous adjustment of shunt valve setting. Tailored to individual patients' needs. Affected by external magnetic field. Check before and after MRI. [1]
Fenestrate III ventricle floor. Bypass obstruction & restore CSF flow. Avoid permanent shunting. Enable tumour biopsy. [1]
When to use ETV: For non-communicating (obstructive) hydrocephalus only. The 3rd ventricle floor is fenestrated endoscopically → CSF can flow directly from the 3rd ventricle into the basal cisterns, bypassing the blocked aqueduct. This is NOT effective in communicating hydrocephalus because the problem is at the arachnoid granulations, not flow obstruction.
Raised ICP can have insidious onset or be rapidly fatal. CPP = MAP − ICP (~60–80 mmHg). CBF = CPP/CVR (45–65 ml/min/100g). GCS = E+M+V (3–15). ICP monitoring when GCS unreliable or evolving condition. ABC before ICP. Steroids for tumour but not TBI or stroke. No prophylactic/prolonged/uncontrolled hyperventilation. No mannitol if shocked. No LP if raised ICP unless absolutely sure communicating hydrocephalus. [1]
Integration with Related Material
- Meningitis → meningeal adhesions → communicating hydrocephalus and raised ICP
- Post-meningitic hydrocephalus is communicating → LP is safe
- ICP monitoring in raised ICP from stroke
- Surgical decompression of supratentorial infarct: quality of life not improved, best in young patients with non-dominant infarct
- Cerebellar infarct → direct brainstem compression → drainage of hydrocephalus, posterior fossa decompression
- Obstructive hydrocephalus: lateral ventricles dilated out of proportion to sulcal spaces
- SAH → IVH → obstructive hydrocephalus
- Differentiate from "hydrocephalus ex vacuo" (cerebral atrophy — proportional ventricular and sulcal enlargement)
- Papilloedema = optic disc swelling from raised ICP only
- Transient visual obscurations (TVOs): fleeting monocular visual disturbance
- Evaluation: immediate CT/MRI to r/o SOL → LP only if neuroimaging normal
- CRASH trial showed dexamethasone increases mortality in TBI
- Never give steroids for traumatic brain injury
While not the focus of this lecture, it is mentioned as a cause of raised ICP and is frequently tested:
- Typical patient: Obese young woman with headache and visual disturbance [7]
- CT brain: Normal (to rule out SOL)
- LP: Elevated opening pressure (> 25 cmH₂O) with normal CSF composition
- Management: Weight reduction, acetazolamide (1st line), frusemide (2nd line), optic nerve sheath fenestration or LP shunt if refractory [7]
Likely Exam Questions
Q1 (2020/2023 style): Maintaining normal ICP and adequate cerebral perfusion is crucial. Which is CORRECT?
- A. CBF is directly proportional to systolic BP → Wrong (CBF = CPP/CVR, not directly proportional to SBP)
- B. CPP should be maintained at ~70 mmHg → Correct (lecture says 60–80, some guidelines say ~70) [1][11]
- C. ICP is increased by hyperventilation → Wrong (hyperventilation DECREASES ICP)
- D. ICP is normally 15–20 mmHg in neonates → Wrong (1–6 mmHg in infants) [1]
Q2 (2018 SAQ style): 68-year-old woman with left basal ganglion haemorrhage. Opens eyes and flexes limbs to pain, utters inappropriate words.
Q3: What are the three cardinal symptoms of NPH? → Gait disturbance, cognitive decline, urinary incontinence [1][5]
Q4: Key differential diagnosis presenting with similar features? → Alzheimer's disease [1]
Q5: Two investigation modalities to support NPH diagnosis? → CT/MRI brain (ventriculomegaly out of proportion to sulcal enlargement); LP with high-volume CSF tap (assess clinical improvement) [1][5]
Q6: One effective treatment? → VP shunting [1]
Q7: Three complications of VP shunt? → Infection, blockage, over-shunting (→CSDH) [1][5]
| Trap | Correct Answer |
|---|---|
| "Give steroids for raised ICP in head trauma" | NEVER — steroids increase mortality in TBI |
| "Give mannitol to all patients with raised ICP" | NOT if shocked — will worsen hypotension |
| "Do LP in all hydrocephalus" | ONLY communicating — LP in non-communicating = herniation/death |
| "Hyperventilate prophylactically" | NEVER prophylactic or prolonged — only to buy time |
| "ICP 15 mmHg is always abnormal" | Normal adult ICP = 10–15 mmHg; definitely abnormal > 20 cmH₂O |
| "Papilloedema is an early sign of raised ICP" | It is a LATE sign |
| "GCS 8 means the same thing regardless of components" | E2M4V2 ≠ E1M5V2 — always report components separately |
| "NPH = high ICP" | ICP is normal — the pathology is abnormal compliance with local pressure effects |
| "ETV works for all hydrocephalus" | Only for non-communicating (obstructive) hydrocephalus |
| "CPP = SBP − ICP" | CPP = MAP − ICP (not systolic BP!) |
High Yield Summary
Raised ICP: Normal adult ICP = 10–15 mmHg. Abnormal > 20 cmH₂O. Causes: SOL, hydrocephalus, brain swelling, hyperaemia, venous congestion.
Monro-Kellie Doctrine: Brain + Blood + CSF in rigid skull. Compensation (venous outflow, CSF displacement) then decompensation (exponential ICP rise). "Talk and die."
CPP = MAP − ICP (aim 60–80 mmHg). CBF = CPP/CVR (normal 45–65 ml/min/100g).
Clinical features: Morning headache, vomiting, CN VI palsy, papilloedema (LATE), deteriorating consciousness. Terminal: Cushing triad (HTN, bradycardia, irregular breathing), fixed dilated pupil.
GCS: E(1-4) + M(1-6) + V(1-5) = 3–15. Motor score most prognostic. M3 = decorticate (above midbrain). M2 = decerebrate (midbrain/pons).
Management: ABC FIRST → Head 30° → Maintain CPP 60–70 → Osmotherapy (mannitol CI: shock) → Controlled hyperventilation (PaCO₂ 3.0–3.5 kPa, never prophylactic) → Seizure/fever/glucose control → Steroids ONLY for tumour (CI in TBI/stroke) → Surgical: EVD, craniotomy, decompressive craniectomy.
Hydrocephalus: Communicating (↓absorption, LP safe) vs Non-communicating (obstruction, LP KILLS). CSF production ~450 ml/day. Causes: SAH, meningitis, tumour, congenital.
NPH: Wet (incontinence), Wacky (dementia), Wobbly (gait). Responds to VP shunt. DDx: Alzheimer's.
Shunt complications: Infection, blockage (80% proximal), over-shunting → CSDH, abdominal pseudocyst, slit ventricle, bowel perforation, nephritis (VA).
ETV: For obstructive hydrocephalus only. Fenestrates 3rd ventricle floor → bypasses obstruction.
No LP if raised ICP unless sure communicating hydrocephalus.
Active Recall - Raised ICP and Hydrocephalus
[1] Lecture slides: GC 111. Raised intracranial pressure and hydrocephalus.pdf [2] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Increased ICP section) [3] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (Brain tumour headache section) [4] Senior notes: Ryan Ho Opthalmology.pdf (Papilloedema section) [5] Past papers: 2018 Fourth Summative SAQ.pdf (Q8); 2022 Fourth Summative SAQ.pdf (Q9) [6] Senior notes: Maksim Surgery Notes.pdf (Hydrocephalus section) [7] Senior notes: Maksim Medicine Notes.pdf (NPH and IIH sections) [8] Lecture slides: GC 051. Fever and confusion_meningitis and encephalitis; suppurative brain infection.pdf [9] Lecture slides: GC 087. Sudden hemiplegia dysphagia.pdf [10] Lecture slides: Neuroradiology Cases studies_Updated by Chu C Y_June 2023.pptx.pdf [11] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q63); 2023 Fourth Summative MCQ.pdf (Q58)