Lecture 8: Increased Intracranial Pressure PDF

Lecture 8: Increased Intracranial Pressure ICP: ● Intracranial vault is composed of 3 components: Brain, Blood & CSF ● ↑ in size of any of the 3 compartments can → ↑ ICP ● Monro-Kellie rule: ↑ in one element must occur at expense of others Normal intracranial pressure: ● Adults: 8 to 18 mmHg (15-22...

Lecture 8: Increased Intracranial Pressure ICP: ● Intracranial vault is composed of 3 components: Brain, Blood & CSF ● ↑ in size of any of the 3 compartments can → ↑ ICP ● Monro-Kellie rule: ↑ in one element must occur at expense of others Normal intracranial pressure: ● Adults: 8 to 18 mmHg (15-22 cmH₂O) ● Children: ~ 10-20 cm H₂O & it’s even lower in babies ● ICP is not a static state Pathophysiology of ICP: ● With ↑ ICP → BF & O₂ delivery may be compromised ● CPP = cerebral perfusion pressure → CPP = MAP - ICP ● Normal CPP = 80 to 100 mmHg ● < 70 = Inadequate ● ≤ 40 = Ischemia ● ≤ 30 = Cell death Danger of ICP can disturbs brain function by: ● ↓ CPP ● Transtentorial or foramen magnum herniation Signs of ↑ ICP: ● Earliest and most reliable indicator = ↓ LOC ● Late sign = pupils dilated, fixed ● Cushing’s Triad = bradycardia, change in breathing, ↑ BP ● Ischemia or pressure on the brainstem is the reason ● Altered motor function: ○ Hemiparesis ○ Hemiplegia ○ Decorticate: flexed to core of your body ○ Decerebrate ● Loss of temperature control ● Headache ● Vomiting ● Abnormal posturing ● Abnormal CN findings: pupillary reaction (poor response to light, any size) ● Papilledema: later ● Bulging fontanelle (in infants) → awww 6raaggg Respiratory changes: ● Depend on the level of brainstem involved: ○ Diffuse Cortical involvement result in Cheyne-Stokes respiration: apnea alternating with hyperventilation ○ Midbrain: sustained regular, rapid & deep breathing, called → Central Neurogenic Hyperventilation ○ Pons: Apneustic Breathing. Breathing shows prolonged pause at end of inspiration ○ Medulla: rapid & shallow respiration with ataxic breathing in the final stages Causes of ↑ ICP: Generalized brain injury: ● ● ● ● ● Hypoxia Head injury Metabolic Infection Toxins Focal intracranial lesion: Abscess CSF obstruction: ● Vascular: subdural, epidural, ICH, AVM ● Focal traumatic lesion ● Tumor Complications of ↑ ICP: ● Herniation ● Death Classification of brain edema: check pics in lecture Vasogenic: Cytotoxic: Interstitial: ● ↑ permeability of brain capillary endothelial cells ● As in Tumor, abscess, hemorrhage, infarction, contusion & meningitis ● It follows the white matter distribution ● Failure of normal homeostatic mechanisms that maintain cell size ● Primarily represents cellular energy (ATP) failure ● Prominent in hypoxic-ischemic injury, osmolar injury, some toxins & as part of 2ndry injury sequence following head trauma ● ↑ H₂O content of periventricular white matter due to obstruction of CSF flow ● Example: normal pressure hydrocephalus Herniation syndromes: Transtentorial herniation (2): ● Medial temporal lobe is squeezed by a unilateral mass under the tent ● Herniating lobe compresses: ○ Ipsilateral 3rd CN (often first) & posterior cerebral artery ● As herniation progresses, ipsilateral cerebral peduncle can be squeezed ● In ~ 5% of pts, the contralateral 3rd CN & cerebral peduncle can be affected “Kernohan's sign” Upward transtentorial herniation: ● When an infratentorial mass (ex: tumor, cerebellar hemorrhage) compresses BS, kinking it & causing patchy BS ischemia ● Very rare ● Upward movement of the cerebellum Subfalcine herniation (1): ● Cingulate gyrus is pushed under falx cerebri by an expanding mass high in a cerebral hemisphere ● One or both anterior cerebral arteries become trapped, causing infarction of paramedian cortex ● As the infarcted area expands, pts are at risk of transtentorial herniation, central herniation or both Tonsillar herniation (3): Central herniation: ● Both temporal lobes herniate ● Bilateral, more or less symmetric damage to the midbrain: ○ Pupils fixed in midposition ○ Decerebrate posturing ○ Many of the same symptoms as transtentorial herniation ● Further compromise of the BS: ○ Loss of all BS reflexes ○ Cessation of respirations ○ Brain death ● Compression the brainstem ● Obstruction of CSF flow ● Acute hydrocephalus (with impaired consciousness, headache, vomiting) ● Later, abrupt respiratory & cardiac arrest Treatment of ↑ ICP: ● Best treatment: removal of causative lesion such as tumors, hydrocephalus & hematomas ● Hyperventilation: ○ Has been the cornerstone of ICP management ○ Hyperventilation → hypocapnia → vasoconstriction → ↓ CBF globally ○ Aggressive hyperventilation to pco2 < 25 mmHg should be avoided bcz it may ↓ CBF excessively → cerebral ischemia ● Removal of CSF ● Fluid restriction ● IV mannitol: delayed osmotic effect, with onset in 15-30 minutes & duration from 1 to 6 hours ● Steroids: ○ Helpful for patients with a brain tumor or abscess, but they are ineffective for patients with head trauma, cerebral hemorrhage, ischemic stroke, or hypoxic brain damage after cardiac arrest ● Hypertonic Saline: ○ ↑ MAP without ↑ ICP thus results in improved CPP ○ 20 – 50 % ↓ in ICP ○ Not first line Nursing Management of Patient with ↑ ICP: ● Elevate head of bed about 30 degrees ● Minimal suctioning ● Minimize coughing ● ● ● Prevent vomiting Prevent constipation CLOSE ASSESSMENT