raised intracranial pressure

Question 1

what is the etiology of rICP?

Answer 1

Idiopathic intracranial hypertension

CNS inflammation, infection, and/or abscess

Space-occupying lesions: 
Intracranial hemorrhage or hematoma
Aneurysm 
Intracranial tumors
 brain abcess 

Infection: meningitis, encephalitis

Elevated venous pressure (e.g., as a result of heart failure)

Increased CSF (hydrocephalus)

Question 2

pathophysiology of rICP

Answer 2

Physiological ICP is ≤ 15 mm Hg in adults (in supine position);

ICP > 20 mm Hg indicates intracranial hypertension, which requires treatment.

↑ Intracranial pressure → ↓ perfusion pressure within the brain → compensatory activation of the sympathetic nervous system to maintain cerebral perfusion → ↑ systolic blood pressure → stimulation of aortic arch baroreceptors → activation of the parasympathetic nervous system (vagus) → bradycardia

Question 3

clinical features of rICP

Answer 3

Cushing triad: also called Cushing reflex or Cushing response and is thought to reflect brainstem compression. This sign indicates a need for urgent treatment

↑ Pressure on brainstem → dysfunction of respiratory center → irregular breathing
Cheyne–Stokes respiration.

widening pulse pressure

and bradycardia

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Reduced levels of consciousness- low GCS

Headache

Vomiting

Pupil changes (constriction at first, later dilation—do not mask these signs by using
agents such as tropicamide to dilate the pupil to aid fundoscopy

Visual acuity; peripheral visual field loss.

Psychiatric changes

Diplopia - Due to sixth nerve palsy

unreliable sign
Papilledema - takes several days

Question 4

what are the clinical manifestation in infants of rICP?

Answer 4

In infants: macrocephaly, bulging fontanel,
sunset sign - downward deviation of the eyes due to hydrocephalus

Headache comes off as irritability

Question 5

what are the different herniations that could occur due to rICP and its clinical manifestation?

Answer 5

Subfalcine herniation
 cingulate gyrus (medial frontal lobe) is forced under the rigid falx cerebri

compression of:

Contralateral hemisphere -obstruction of the foramen of Monro → hydrocephalus

may be silent unless the anterior cerebral artery is compressed and causes a stroke—eg contralateral leg weakness ± abulia (lack of decision-making)
Pericallosal arteries → hemiparesis (predominantly lower limbs)

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Uncal herniation: lateral supratentorial mass, which pushes the ipsi- lateral inferomedial temporal lobe (uncus) through the temporal incisura and against the midbrain

Compression of:

• Ipsilateral oculomotor nerve palsy → fixed and dilated ipsilateral pupil (mydriasis)
• Ipsilateral posterior cerebral artery → cortical blindness with contralateral homonymous hemianopia
• Contralateral cerebral peduncle → ipsilateral paralysis + Kernohan phenomenon: a paradoxical ipsilateral weakness

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Foramen magnum herniation: structures of the posterior fossa (e.g., cerebellar tonsils, medulla) herniate at the foramen magnum → plantar reflexes occur first, impaired consciousness, decerebrate posturing, irregular breathing , apnea, impaired circulation, death

Question 6

diagnosis of rICP?

Answer 6

Neuroimaging findings of intracranial hypertension:

Midline shift

Mass lesions:
1)  Traumatic brain injury - Epidural hemorrhage
Subdural hematoma
Intracerebral hemorrhage
parencymacontusions 

2) CNS infections: e.g., brain abscess
3) Brain tumors (with or without surrounding vasogenic edema)

Effacement of the basilar cisterns!!!!!!

Effacement of cerebral sulci

Evidence of brain herniation (e.g., uncal herniation or tonsillar herniation)

Changes in ventricular size (e.g., enlarged with hydrocephalus

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Invasive ICP monitoring

ICP should be evaluated in combination with CPP to guide therapeutic interventions and help prevent secondary brain injury and brain herniation.

Indications
Traumatic brain injury: ICP monitoring in severe TBI reduces in-hospital and two-week postinjury mortality.

Mass lesions: e.g., brain tumors, ICH, SAH, SDH, EDH

Diffuse brain injury due to:
Infectious causes: e.g., meningitis, encephalitis

Intraventricular catheters with an external ventricular drain (EVD) or intraparenchymal catheters (IPC) are most commonly used to monitor

Question 7

what is the acute management of icp?

Answer 7

Goals: Maintain cerebral blood flow (CBF) and prevent secondary brain injury.

ABCDE
GCS

laryngeal manipulation can raise ICP!!!!!!

Modifications to reduce risk:

Prior to intubation
Initiate ICP management measures
Perform and document rapid baseline neurological examination (e.g., GCS, pupils, presence of lateralizing signs).

pretreatment with fentanyl !!!!!!

Have the most experienced provider perform the intubation.

Select an induction agent that does not affect ICP (e.g., etomidate).

Early involvement of neurosurgery and a neurocritical care specialist is essential.

Correct hypotension, maintain MAP >90mmHg and treat seizures

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conservative

1) Correct hypotension, maintain MAP >90mmHg and treat seizures
1) Elevate the head of the bed to 30–40°

2) Sedation and analgesia
Prevents unnecessary spikes in ICP due to pain, agitation, and patient-ventilator dyssynchrony
Combinations of benzodiazepines, opioid analgesics, and dexmedetomidine are generally used

3) 7) If intubated, short term (<30min) controlled hyperventilate to PaCO2 (aim 3.5–4kPa): This causes cerebral vasoconstriction and reduces ICP almost immediately. Maintain PaO2 >12kPa
4) Temperature management: Maintain normothermia; fever should be treated with antipyretics

5) Identify and expedite lesions that are amenable to emergency neurosurgical procedures.
- tumor
- Hematoma evacuation (e.g., for EDH, SDH)

CSF drainage - external ventricular drain
indications
obstructive hydrocephalus (can be caused by TBI, ICH, and ischemic stroke)
Diffuse cerebral edema
Intracranial lesion causing mass effect

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Hyperosmolar therapy
Indications:
Elevated ICP refractory to conservative measures

6) IV hypertonic saline (HTS)
IV mannitol - 20 percent - peak efficacy in 20 mins aswell
duration4-6 hrs

Osmotic agents (eg mannitol) can be useful but
may lead to rebound ICP after prolonged use
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ADVANCED STEPS

Consider advanced therapies for persistently refractory elevated ICP (e.g., barbiturate coma).

Decompressive craniectomy

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Glucocorticoids: e.g., dexamethasone
Recommended only if elevated ICP is caused by vasogenic edema secondary to:
CNS infection or inflammation (e.g., bacterial or tuberculous meningitis)
Neoplasms

Avoid in patients with ICH.

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Restrict fluid to <1.5L/d

Question 8

complications of intracranial hypertension?

Answer 8

Cerebral edema
Definition: excess accumulation of fluid within the brain parenchyma as a result of damage to the blood-brain barrier and/or the blood-CSF barrier

exact same treatment as icp