Surgery chapters
Raised intracranial pressure, CSF circulation and cerebral blood flow
How pressure inside the skull is kept normal, how CSF is made and absorbed, how cerebral blood flow is regulated, and how raised intracranial pressure presents and is treated.
- The skull is a rigid box: when a mass grows, CSF and venous blood are pushed out first, then ICP rises steeply (Monro-Kellie doctrine).
- Brain perfusion depends on CPP = MAP − ICP; keep CPP at least 60 mmHg, avoid hypotension, hypoxia and both high and very low PaCO2.
- Late signs of herniation are a fixed dilated pupil on the side of the lesion and Cushing's triad (hypertension, bradycardia, irregular breathing).
On this page
Overview
The brain sits in a closed bony box with three things inside it: brain tissue, blood and cerebrospinal fluid (CSF). Any extra volume (blood clot, tumour, swelling, blocked CSF) must be balanced by a loss of something else, or pressure rises.
Raised intracranial pressure (ICP) is a neurosurgical emergency. It cuts brain perfusion, causes herniation and kills. Almost every topic in neurosurgery (head injury, haemorrhage, tumours, hydrocephalus, infection) comes back to ICP, so this chapter is the foundation for the rest of the section.
Normal values to remember
| Parameter | Normal value | Note |
|---|---|---|
| ICP (adult, at rest) | 5–15 mmHg (about 10) | Sustained > 20–22 mmHg linked to poor outcome |
| Mean arterial pressure (MAP) | 90–110 mmHg | Head injury target MAP 80–90 mmHg (neuro-ICU) |
| Cerebral perfusion pressure (CPP) | 75–105 mmHg | Keep ≥ 60 mmHg after brain injury |
| Cerebral blood flow (CBF) | About 55 mL per 100 g per minute | Ischaemia below about 20; lower still → infarction |
| CSF volume | About 150 mL | Production about 20 mL/hour (roughly 500 mL/day) |
The Monro-Kellie doctrine
- The skull is a rigid container and the brain is almost incompressible.
- The total volume of brain + blood + CSF must stay constant.
- When a mass expands, the system first compensates by squeezing CSF (into the spinal theca) and venous blood (into the jugular veins) out of the head. ICP stays near normal.
- Once this reserve is used up, a small further increase in volume causes a steep (exponential) rise in ICP. This is the "point of decompensation" on the pressure-volume curve.
Early on, a growing clot can enlarge with a normal ICP. Deterioration is then sudden. This explains the lucid interval of an extradural haematoma.
Monro-Kellie = "a full suitcase". You can push out the soft things (CSF, venous blood) once; after that the lid bursts.
Cerebral blood flow and its control
Cerebral perfusion pressure
CPP = MAP − ICP. Flow to the brain depends on this pressure difference.
Patient A: MAP 90 mmHg, ICP 10 mmHg
CPP = 90 − 10 = 80 mmHg → adequate
Patient B after head injury: MAP 70 mmHg, ICP 30 mmHg
CPP = 70 − 30 = 40 mmHg → well below 60, brain at risk of ischaemia
Fix both sides: raise MAP (fluids, vasopressors) and lower ICP
Pressure autoregulation
- In the healthy brain, arterioles constrict or dilate to keep CBF steady across a MAP of about 50–150 mmHg (the range shifts upwards in chronic hypertension).
- Severe brain injury disrupts autoregulation. Flow then follows blood pressure passively: low MAP causes ischaemia; very high MAP causes swelling and higher ICP.
Chemical regulation
| Change | Effect on cerebral vessels | Effect on ICP |
|---|---|---|
| High PaCO2 (hypoventilation) | Vasodilation | Rises |
| Low PaCO2 (hyperventilation) | Vasoconstriction | Falls, but at the cost of reduced flow |
| Low PaO2 (hypoxia) | Vasodilation | Rises; and the brain is starved |
Hyperventilation lowers ICP quickly but can cause cerebral ischaemia. Aim for normocapnia (PaCO2 about 35 mmHg, 4.5–5.0 kPa). Use brief, moderate hyperventilation (PaCO2 25–30 mmHg) only for acute deterioration or signs of herniation while definitive treatment is arranged. Prophylactic hyperventilation below 25 mmHg is not recommended.
CSF: production, flow and absorption
- Produced mainly by the choroid plexus, most of it in the lateral ventricles (smaller amounts from the third and fourth ventricles and the ventricular walls). Rate about 20 mL/hour.
- Pathway: lateral ventricles → foramen of Monro (interventricular foramen) → third ventricle → cerebral aqueduct (of Sylvius) → fourth ventricle → exits through the midline foramen of Magendie and the two lateral foramina of Luschka → subarachnoid space and basal cisterns.
- Absorbed through the arachnoid villi (granulations) into the superior sagittal sinus (venous blood).
- Volume about 150 mL, so it is replaced several times a day.
The aqueduct is the narrowest point of the system. Block it and the lateral and third ventricles dilate while the fourth stays small (obstructive hydrocephalus). Block absorption at the villi (after meningitis or subarachnoid haemorrhage) and all ventricles dilate (communicating hydrocephalus).
"Monro to three, Sylvius to four, Magendie in the middle, Luschka on the sides."
Causes of raised ICP
| Group | Examples |
|---|---|
| Mass lesions | Haematoma (extradural, subdural, intracerebral), tumour, abscess, tuberculoma |
| Cerebral oedema | Vasogenic (tumour, abscess: leaky vessels; responds to steroids), cytotoxic (ischaemia, hypoxia, trauma: cell swelling), interstitial (hydrocephalus) |
| Excess CSF (hydrocephalus) | Obstructive or communicating |
| Raised venous pressure | Venous sinus thrombosis, neck compression (tight collar), raised intrathoracic or intra-abdominal pressure |
| Increased blood volume | Hypercapnia, hypoxia, seizures, fever |
| Unknown mechanism | Idiopathic intracranial hypertension |
Clinical features
Symptoms and signs in adults
- Headache: worse in the morning, on coughing, straining or bending forward.
- Nausea and vomiting.
- Blurred vision, transient visual obscurations and double vision (compression of cranial nerves; the long-coursing sixth nerve is a classic "false localising" palsy).
- Papilloedema on fundoscopy. It takes time to develop, so its absence does not exclude acutely raised ICP.
- Falling conscious level: drowsiness, then coma.
Infants (open sutures)
- Tense, bulging anterior fontanelle, increasing head circumference, separated sutures, prominent scalp veins.
- "Sunsetting" eyes (loss of upgaze) from dorsal midbrain compression (Parinaud's syndrome).
Late signs: herniation
| Herniation | What moves | Key signs |
|---|---|---|
| Subfalcine | Cingulate gyrus under the falx | Often silent; may compress anterior cerebral artery (leg weakness) |
| Uncal (lateral transtentorial) | Medial temporal lobe (uncus) over the tentorial edge | Ipsilateral fixed dilated pupil (third nerve), contralateral hemiparesis, falling GCS |
| Central (transtentorial) | Diencephalon and midbrain downwards | Small then mid-position pupils, decorticate then decerebrate posturing |
| Tonsillar ("coning") | Cerebellar tonsils through the foramen magnum | Compresses medulla: Cushing's triad, apnoea, death |
The parasympathetic fibres that constrict the pupil run on the outer surface of the third nerve, so they are compressed first. Unopposed sympathetic tone gives a dilated, sluggish then fixed pupil on the side of the mass.
Rarely the mass pushes the opposite cerebral peduncle against the tentorium, giving hemiparesis on the same side as the lesion (a false localising sign). The pupil is the more reliable side marker.
Cushing's triad = hypertension (widening pulse pressure), bradycardia, irregular respiration. It is a late, pre-terminal sign of brainstem compression, not an early warning.
Investigations
- CT head (non-contrast) is the first-line test: shows haematoma, tumour, oedema, hydrocephalus, midline shift and whether the basal cisterns are open or effaced.
- MRI shows tumours, posterior fossa lesions and anatomy for endoscopic surgery better, but takes longer.
- Lumbar puncture: do not perform if a mass lesion or obstructive hydrocephalus is suspected, until CT is done. The pressure difference can drag the tonsils down (coning). LP is useful only when CT excludes a mass and the hydrocephalus is communicating, or in idiopathic intracranial hypertension.
- ICP monitoring: an intraparenchymal transducer ("bolt") or an external ventricular drain (EVD). An EVD can both measure pressure and drain CSF to lower it.
The ICP waveform
| Wave | Meaning |
|---|---|
| P1 (percussion) | Arterial pulsation |
| P2 (tidal) | Brain compliance; P2 higher than P1 = poor compliance (stiff, swollen brain) |
| P3 (dicrotic) | Venous pulsation |
Management of raised ICP
General and first steps
- ABC: secure the airway, give oxygen, avoid hypoxia and hypotension (each one alone worsens outcome).
- Head of the bed raised (about 30°), head in the midline, loosen tight collars and ties to help venous drainage.
- Sedation and analgesia; muscle relaxants if ventilated.
- Normocapnia on the ventilator; avoid high and very low PaCO2.
- Treat fever, seizures and hyperglycaemia; avoid hypotonic fluids (use normal saline); keep sodium normal to high-normal.
Osmotherapy
| Agent | Use | Cautions |
|---|---|---|
| Mannitol 20% (20 g per 100 mL) | 0.25–1 g/kg; 1 g/kg rapid bolus for acute deterioration (new dilated pupil, hemiparesis) on the way to CT or theatre | Osmotic diuretic: do not give if hypotensive or hypovolaemic; keep serum osmolality below about 320 mOsm/kg |
| Hypertonic saline (3% to 23.4%) | Lowers ICP as well as mannitol | Preferred when the patient is hypotensive (not a diuretic) |
70 kg patient with a newly dilated pupil, blood pressure normal
Dose 1 g/kg = 70 g
20% mannitol contains 20 g per 100 mL
Volume = 70 ÷ 20 × 100 = 350 mL given rapidly
Removing the cause
- Evacuate the mass: haematoma, abscess, tumour (craniotomy, burr holes).
- CSF diversion: EVD for acute hydrocephalus; shunt or endoscopic third ventriculostomy for long-term control.
- Steroids (dexamethasone) reduce vasogenic oedema around tumours and abscesses (once abscess is excluded or covered). They are not used for head injury.
Refractory ICP
- Barbiturate (thiopentone) coma: only with a stable blood pressure.
- Decompressive craniectomy: removing a bone flap lets the swollen brain expand. It controls ICP and can save life (malignant middle cerebral artery infarct, cerebellar infarct, some head injuries) but does not reverse established deficits.
- Therapeutic hypothermia: lowers ICP but long-term benefit is unproven.
Steroids help oedema around a tumour but increase mortality when given routinely in traumatic brain injury.
Low-pressure headache
The opposite problem. After LP or overdrainage from a shunt, the headache is worse on standing and better lying flat. Raised-pressure headache is worse lying down and on straining.
Expect: the Monro-Kellie doctrine and what compensates first (CSF and venous blood), the CPP formula and its target (at least 60 mmHg), normal ICP and CBF values, the range of autoregulation, the effect of CO2 on cerebral vessels and why hyperventilation must be limited, the CSF pathway from choroid plexus to arachnoid villi and the superior sagittal sinus, signs of uncal herniation (ipsilateral blown pupil, contralateral weakness), Cushing's triad as a late sign, LP being dangerous before CT, mannitol dose and its contraindication in hypotension, and steroids being useful for tumour oedema but not head injury.
Quick revision
- ICP 5–15 mmHg; CPP = MAP − ICP; keep CPP ≥ 60 mmHg.
- CBF about 55 mL/100 g/min; ischaemia below 20.
- Autoregulation: MAP 50–150 mmHg; lost after severe injury.
- High CO2 dilates vessels and raises ICP; hyperventilate only briefly.
- CSF: choroid plexus → Monro → third ventricle → aqueduct → fourth → Magendie/Luschka → arachnoid villi → sagittal sinus.
- Uncal herniation: ipsilateral fixed dilated pupil + contralateral hemiparesis.
- Cushing's triad: hypertension, bradycardia, irregular breathing = coning.
- CT before LP; LP can cause coning.
- Mannitol 20% 1 g/kg bolus in emergencies; not if hypotensive; hypertonic saline is the alternative.
Written by The House Job from standard surgical references (Bailey & Love; ATLS Student Course Manual).
FAQ
What is the Monro-Kellie doctrine?
The skull holds a fixed total volume of brain, blood and CSF, so a new mass is first balanced by pushing out CSF and venous blood; once that reserve is used, ICP rises steeply.
What is a safe cerebral perfusion pressure after head injury?
At least 60 mmHg, calculated as mean arterial pressure minus intracranial pressure.
Why is lumbar puncture dangerous in raised intracranial pressure?
Draining CSF from below creates a pressure gradient that can pull the cerebellar tonsils through the foramen magnum and compress the medulla.
Why does the pupil dilate in temporal lobe herniation?
The uncus presses on the third nerve, and its outer parasympathetic fibres that constrict the pupil are damaged first, leaving sympathetic dilation unopposed.
When is hypertonic saline better than mannitol?
In a hypotensive or hypovolaemic patient, because mannitol is a diuretic and can drop the blood pressure further.