Contents of brain
- Brain 88%
- CSF 9%,
- Blood 2-3%
CPP = MAP-ICP
- Raised ICP impairs CPP/CBF → ischemia + oedema → further increases of ICP → brain herniating from dural opening and increase retraction oedema
Recognition
- Pre-op
- Significant mass effect,
- Dilated ventricles,
- Hypertension (>140mmHg) or hypotension (<90mmHg)
- Intra op
- Tense brain
- Herniation of brain through durotomy
- Difficult retraction
Aetiology
- Extracranial Causes
- Airway obstruction,
- Hypoxia/hypercarbia (hypo-ventilation)
- Hypertension exceeding cerebral autoregulatory capacity,
- Hypotension causing cerebral hypoperfusion and reflex vasodilation
- Venous hypertension from outflow obstruction caused by head rotation or increased thoracoabdominal pressure
- Certain medications such as volatile anaesthetics, nitro-glycerine, or sodium nitroprusside
Non-invasive management
- CBV can be reduced by increasing venous return or reducing arterial inflow
- Check jugular veins are not kinked
- Raise HOB (10-30deg can reduce ICP with little effect on CPP)
- Reduce intra-thoracic/abdominal pressure
- Optimize pre-op
- Deepen anesthesia, add neuromuscular blockade, NGT/ OGT
- Laparotomy for critical cases with raised intra-abdominal pressure
- PEEP
- Should reduce intrathoracic pressure
- But keeps alveoli open.
- 5-10cmH20 PEEP usually required with Fi02 0.6.
- PEEP 10-15 if lung/thoracic injury
- Hyperventilation
- Reduces PaC02, reduces H+ of CSF
- Vasoconstriction but drops CPP
- Reduces arterial Inflow
- Transient effect as choroid plexus create ammonium ions to neutralise and so effect lasts mins to hrs
- BP control
- Usually autoregulatory control maintains CPP.
- Hypotension causes vasodilatation and raised ICP
- If not intact CBF and BP are directly proportional with raised BP causing cerebral oedema.
- Reducing BP will drop CBF. In such cases CPP 60-80 mmHg should maintain adequate CBF.
- Anaesthetic agents
- Variable effect on ICP by their effect on
- Cerebral metabolism (CMR02)
- CBF
- Volatile anaesthetics depress CMR02 but are cerebral vasodilator
- Halothane>desflurane/isoflurane>sevoflurane
- They also drop BP
- Propofol decreases CMR02, with a concomitant reduction in CBF, resulting in decreased CBV and ICP
- Barbiturates, benzodiazepines, and etomidate can all decrease ICP by decreasing CBV, CBF, and CMR02 without leading to anaerobic metabolism
- Barbiturates can also drop BP
- Ketamine historically avoided as thought to increase ICP but this is not so in the I&V patient.
- Useful in patients with opioid tolerance
- Opiates increase ICP, esp morphine
- Systemic histamine release causes vasodilatation and drops BP
- Remifentanil reportedly has no adverse effects on cerebral hemodynamics, CPP, or ICP
- NO is a vasodilator
- But in sedated hyperventilated patients it does not raise CBF as (like volatile agents) it does not blunt vasoconstrictive response to hypocarbia
- BZDs prolong emergence from anesthesia and so are generally avoided if waking the patient
- Midazolam decreases CBF and CMR02, with similar effects on ICP, CPP, and jugular bulb oxygen saturation in patients with trauma
- Therapeutic hypothermia does reduce CMR02 and CBF, decreasing ICP
- The most feasible and rapid way to induce hypothermia in the operating room is with isotonic refrigerated IV fluids
- Hyperosmolar therapy (Mannitol/HTS)
- Reduce ICP in mins and can drop ICP by up to 10mmHg over an hour
- Vasoconstriction & decreased blood rheology
- Increase IV volume causing CO & increased CPP
- Mannitol
- Has a rebound effect due to:
- Diuresis causing reduced IV vol and CPP — causing autoregulatory vasodilatation to maintain CBF
- Diuresis (if not replaced) causes raised Hct & viscosity
- Unlike HTS it slowly crosses into the BBB
- In response brain cells metabolism idiogenic osmoles (taurine, glycine, glutamine, sorbitol and inositol) leading to increased intracellular osmolality and so increased brain tissue volume
- Rapid mannitol infusion (5mins) causes greater penetration into BBB and renal clearance (should be given over 20mins)
- Mannitol causes renal impairment
- Should aim serum Osm <320mOs/l
- Mannitol may adversely affect coagulation more than HTS
- HTS
- Should be titrated to serum Na+ of 160mEq/l max
- Leads to a longer duration and greater magnitude of ICP reduction when comparing isovolemic or equimolar dosages without rebound effect
- A recent meta-analysis of randomized controlled trials comparing HTS and mannitol in patients with TBI showed no ICP difference at 30 minutes, but significantly greater decrease with HTS at 60 and 120 minutes
- HTS may be preferred in patients with hypovolemia or hyponatremia, whereas mannitol may be better in cases of cerebral hypoperfusion, because it is safer and more effective in increasing CBF, and both are similar in terms of CPP increase
- Given the increase in BP seen with HTS, and the opposite with mannitol, HTS may be preferred in aneurysmal SAH, because euvolemia and hypertension are generally recommended in this setting.
Invasive management
- CSF drainage
- Lumbar drain
- EVD
- Opening of cisterns
- Intracranial measures
- Resect known mass — e.g. tumour/haematoma
- Rapid rise may be due to hemorrhage, USS can be useful here
- Resect non-eloquent brain tissue
- Risks or frontal lobectomy inc hydrocephalus, SMA syndrome, injury to basal ganglia/insula
- Therefore try to avoid entering frontal horn on ventricle and SMA region
- For temporal lobectomy aim 4.5cm from pole on dominant side and 5/5cm non-dominant
- Cerebellum: avoid deep nuclei and medial parenchyma (risk mutism)
- If compressing venous sinus to halt bleeding, venous congestion and swelling can occur.
- Need to reduce pressure/deal with bleed.
- Extracranial measures
- Duraplasty
- Sectioning falx
- Hinge craniotomy
- Extending craniotomy
- Decompressive craniectomy
- If the cause for acutely increased brain bulk is unknown, a reasonable option is to place an ICP monitor or external ventricular drain, close the scalp with bone flap off, and obtain an immediate computed tomography scan
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