Increased Intracranial Pressure: Causes, Symptoms, and Management | Lecture notes Nursing

Increased Intracranial Pressure

Intracranial Pressure (ICP): pressure exerted by the components of the skull: brain tissue (80%),

cerebrospinal fluid (8-10%), and cerebral blood (10-12%); normally less than 20mmHg, but more

important to look at trends.

Monro-Kellie Hypothesis: within a rigid component (the skull), if one component increases, another

must decrease to maintain a constant pressure.

Measuring ICP

Mean Arterial Pressure (MAP): mean pressure of systemic arteries; need a minimum of

60mmHg to adequately perfuse organs.

Cerebral Perfusion Pressure (CPP): MAP specific to brain, normally 50-70mmHg (per book, 70-

95mmHg…); CPP = MAP – ICP. Watch when concerned about IICP.

Regulation of ICP

Pressure Autoregulation: in which cerebral baroreceptors cause arteriole smooth muscle to

contract/dilate based on changes on MAP (inversely related to ICP)

o↑MAP  vasoconstriction  ↓ICP (less blood in cranium)

o↓MAP  vasodilation  ↑ICP (more blood in cranium)

Chemical Autoregulation: in which chemoreceptors detect chemical changes and activate

smooth muscle accordingly; carbon dioxide is the most potent cerebral vasodilator. Others

include oxygen and hydrogen ions.

o↑pCO2  vasodilation  ↑ICP (want less CO2 in brain)

o↓pCO2  vasoconstriction  ↓ICP (want more CO2 in brain)

o↓pO2  vasodilation  ↑ICP (want more O2 in brain)

o↑H+  vasodilation  ↑ICP (want less H+ in brain)

Compensation: in which the body shifts fluid (most commonly CSF ↔ lumbar column, also

blood ↔ body to a lesser extent) to compensate for changes in ICP; depends on the rate of

expansion and the location of lesions (e.g. impeded near outflows).

Cycle of Progressive Brain Swelling

1. An event causes sustained IICP.

2. IICP causes decreased cerebral blood flow (due to Monro-Kellie hypothesis).

3. Cerebral ischemia causes tissue hypoxia.

4. Tissue hypoxia leads to hypercapnia and a decrease in pH.

5. Hypercapnia causes continued cerebral vasodilation and edema, continuing the cycle.

Causes of Increased Brain Volume

Tumors (including benign, as they still take up space)

Cerebral edema (swelling of brain tissue)

Intracranial bleeds (keep reading for more)

Meningeal Irritation: i.e. in meningitis. Assess for nuchal rigidity, photophobia, ∆LOC, positive

Kernig’s or Brudzinski’s sign, fever.

oKernig’s Sign: pain/resistance occurs after flexion and extension of knee.

oBrudzinski’s Sign: knee/hip flexion occurs with head flexion while patient is supine.

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Increased Intracranial Pressure

Intracranial Pressure (ICP): pressure exerted by the components of the skull: brain tissue (80%), cerebrospinal fluid (8-10%), and cerebral blood (10-12%); normally less than 20mmHg, but more important to look at trends. Monro-Kellie Hypothesis: within a rigid component (the skull) , if one component increases, another must decrease to maintain a constant pressure. Measuring ICP  Mean Arterial Pressure (MAP): mean pressure of systemic arteries; need a minimum of 60mmHg to adequately perfuse organs.  Cerebral Perfusion Pressure (CPP): MAP specific to brain, normally 50-70mmHg (per book, 70- 95mmHg…) ; CPP = MAP – ICP. Watch when concerned about IICP. Regulation of ICP  Pressure Autoregulation: in which cerebral baroreceptors cause arteriole smooth muscle to contract/dilate based on changes on MAP (inversely related to ICP) o ↑MAP  vasoconstriction  ↓ICP (less blood in cranium) o ↓MAP  vasodilation  ↑ICP (more blood in cranium)  Chemical Autoregulation: in which chemoreceptors detect chemical changes and activate smooth muscle accordingly; carbon dioxide is the most potent cerebral vasodilator. Others include oxygen and hydrogen ions. o ↑pCO 2  vasodilation  ↑ICP (want less CO 2 in brain) o ↓pCO 2  vasoconstriction  ↓ICP (want more CO 2 in brain) o ↓pO 2  vasodilation  ↑ICP (want more O 2 in brain) o ↑H+^  vasodilation  ↑ICP (want less H+^ in brain)  Compensation: in which the body shifts fluid (most commonly CSF ↔ lumbar column, also blood ↔ body to a lesser extent) to compensate for changes in ICP; depends on the rate of expansion and the location of lesions (e.g. impeded near outflows). Cycle of Progressive Brain Swelling

An event causes sustained IICP.
IICP causes decreased cerebral blood flow (due to Monro-Kellie hypothesis).
Cerebral ischemia causes tissue hypoxia.
Tissue hypoxia leads to hypercapnia and a decrease in pH.
Hypercapnia causes continued cerebral vasodilation and edema, continuing the cycle. Causes of Increased Brain Volume  Tumors (including benign, as they still take up space)  Cerebral edema (swelling of brain tissue)  Intracranial bleeds (keep reading for more)  Meningeal Irritation: i.e. in meningitis. Assess for nuchal rigidity, photophobia, ∆LOC, positive Kernig’s or Brudzinski’s sign, fever. o Kernig’s Sign: pain/resistance occurs after flexion and extension of knee. o Brudzinski’s Sign: knee/hip flexion occurs with head flexion while patient is supine.

Traumatic Brain Injury (TBI): aka craniocerebral trauma , injury to scalp, skull, or brain; leading cause of death resulting from IICP. May cause brain hemorrhage.  Primary Brain Injury: physical injury directly to the brain; e.g. skull fractures, brain tissue disruption, and torn cerebral vessels initially caused by the injury  Secondary Brain Injury: more dangerous injury that involves multiple metabolic mechanisms that result from interruption of blood flow and oxygen to undamaged cells, leading to cerebral edema. Anaerobic metabolism and inflammation occur, precipitating neuronal death. Brain Injury Terms  Open vs Closed: disruption to the skull vs a concussion/hematoma (more common/dangerous).  Coup vs Contrecoup: bruising/concussion, point of injury vs opposite side. Classification Loss of Consciousness GCS Score Mild < 15min 13- Moderate 15min – 6hr 9- Severe > 6hr ≤ 8 Cerebral Hemorrhage: accumulation of arterial or venous blood into brain; S/Sx don’t appear until the bleed is large enough to compromise ICP (minutes–weeks).  Epidural Hematoma: a neurosurgical emergency, bleeding between the skull and dura mater, usually of the middle meningeal artery (i.e. arterial bleed). Symptoms develop quickly (momentary loss of consciousness, period of lucidity, then rapid deterioration). High risk in children as the dura is not as attached to the skull.  Subdural Hematoma (SDH): venous bleed between the dura and arachnoid/pia mater, usually bilaterally from the rupture of meningeal veins after a blow to the head. Often appear unconscious without immediately regaining consciousness. o Classification: acute, ≤ 48hrs; subacute, 48hrs–2/3wks; chronic, weeks–months. o Risk Factors: elderly (brain atrophies; anticoagulant usage); alcoholism (high risk for falls, plus coagulation abnormalities).  Intracerebral Hemorrhage (ICH): bleeding into cerebral parenchyma, usually related to contusions, hemorrhagic CVA, and ruptured aneurysms; produce most significant edema/IICP.  Intraventricular Hemorrhage (IVH): blood in ventricles of the brain, secondary to SDH or ICH Cerebral Blood Volume: 15-20% of CO goes to the brain to meet metabolic needs. Increases occur with anything that decreases MAP (e.g. anti-hypertensives) or increases CO 2. Review ICP autoregulation. CSF Increases: increased production (uncommon), decreased absorption, or obstructed circulation. Hydrocephalus: increased CSF volume due to obstruction from tumors, infections, scar tissue, or fetal development abnormalities, resulting in ventricle enlargement (IICP). Damage depends on the rate of pressure increase and the length of time to resolve.  Noncommunicating Hydrocephalus: in which CSF cannot escape circulation due to obstruction (tumor, scar tissue, or fetal development abnormality).  Communicating Hydrocephalus: impaired reabsorption of CSF (e.g. blood impeding outflow while body continues to produce new CSF).

Non-Surgical Interventions  Maintain Oxygenation: hyperventilation may be indicated (↑O 2 č ↓CO 2  vasoconstriction  ↓ICP) but decreases perfusion. Only done emergently. Monitor ABGs for normocapnia.  Prevent Transient ICP Increases: suction minimally as needed (must prevent aspiration and coughing). Prevent straining (Valsalva maneuvers), coughing/sneezing, and isometric exercises (e.g. pulling against restraints, pushing on footboard).  Fluid Management: generally on a fluid restriction to keep patient slightly dehydrated; NS and D5W (if patient needs glucose) are IVF of choice. Can also use vasoconstrictors or drain CSF via lumbar drain or ventriculostomy.  Positioning: maintain neutral alignment without constricting collars to facilitate outflow; HOB 0- 30° as tolerated. Prevent any hip flexion/raising of lower extremities (↑abdominal pressure).  Nutrition: initially IVF only (need to test gag reflex, swallow studies), moving onto continuous EF after three days (or TPN if necessary). Monitor bowel elimination (constipation ↑ICP, but diarrhea ↑metabolism).  Safety: Protect corneas and provide a calm environment (patient may be confused, agitated). Use mitt restraints to protect lines (other restraints can precipitate isometric exercises).  VTE Prophylaxis: especially if on ventilator – PCBs are best, as anticoagulants may further intracranial bleeds. Pharmacologic Therapies  Osmotic Diuretics: e.g. mannitol. Dehydrates all body tissues, pushing fluid into vasculature. Short-lived (12hr) so watch for “flash edema,” IICP. Crystallizes, so use filter needle to prepare.  Loop Diuretics: e.g. furosemide. Selectively dehydrates (damaged) brain tissue and decreases CSF production. Can use with mannitol to push fluid from tissue  blood  kidneys.  Antipyretics: due to common fever, which increases metabolism and CO 2 production; can also use cooling blankets. If fever persists (or metabolic demands increase), a barbiturate coma can be used, but only as a last resort (patient loses all reflexes). Axillary temps only.  Antiepileptics: e.g. phenytoin (Dilantin); used especially within the first week due to seizure risk. Phenytoin causes gum hyperplasia, so oral care is important.  Vasoactive Medications: to adjust MAP (↑MAP  ↓ICP). Refer to 3..  Opioids/Sedation: reduces oxygen/metabolic demand and prevents transient ICP increases from coughing while suctioning, etc. Surgical Interventions  Craniotomy: removal and subsequent replacement of portion of skull to address insult to ICP; can be performed via the supratentorial or infratentorial (posterior fossa/cerebellum/brain stem) approaches.  Craniectomy: like craniotomy, without immediate replacement of excised skull (often stored in abdomen) to permit swelling; cranioplasty replaces the excised skull.  Burr Holes: small drill holes to diagnose issues and evacuate small masses from the brain  Transsphenoidal Approach: surgery through the nares/upper lip to perform pituitary surgery (e.g. remove tumors); less invasive than craniotomies.  New Techniques: include – o Stereotaxis: positioning mechanism with CT to precisely locate deep structures o Microsurgery: causes minimal damage to surrounding healthy tissue o Laser Surgery: very precise, but cannot pierce bone. o Gamma Knife: high-dose radiation that can pierce bone.

 Ventriculostomy: surgical creation of an ostomy into the ventricles of the brain to directly measure ICP and drain CSF, etc. Drain is protected by a sterile, occlusive dressing (should be transparent to assess for CSF leak – S/Sx headache) o Contraindications: coagulopathies, small or collapsed ventricles, severe generalized cerebral edema o Complications: increased risk of infection (very invasive – watch for glucose in CSF drainage), bleeding, neuronal destruction o Other ICP Monitors: epidural probe, subarachnoid screw/bolt Preoperative Care: understand circumstances of admission and assess patient’s baseline; provide teaching about procedure and address patient’s overwhelming fear and anxiety. Postoperative Care: overall, watch for IICP, cerebral edema, and prevent secondary complications.  Incision/Dressing o Craniotomy: turban-style dressing that is removed 24hrs-3days postop. Monitor incision site for bleeding, infection, and CSF leak (halo-like appearance indicates infection). o Transsphenoidal: nasal packing that is removed in 3-4days; again watch for halo appearance of drainage. Requires frequent mouth care. Assess muscle donor site (used to build nasal flora).  Positioning o Supratentorial: HOB 30°, neutral neck alignment, hip flexion < 90°. Patients usually progress “quickly.” o Infratentorial: patient has more nausea with an unsteady gait due to cerebellar involvement. Positioning is MD preference, with neutral neck alignment. o Craniectomy: keep non-operative side up (also do this with large tumor removals). o Unconscious: position patient on non-operative side to prevent aspiration; ensure airway is patent.  Mobility: as always want patient OOB as soon as possible, but watch for cranial nerve (CN VIII) problems and cerebellar damage/edema in infratentorial patients.  Elimination: remove Foley as soon as possible (infection risk), but watch for DI/SIADH. Start bowel regimen early to prevent constipation (↑ICP).  F&E: keep patient slightly dehydrated, watching for DI/SIADH. Postoperative Complications  Arrhythmias: not specific to surgery, but rather to fluid/K+^ imbalances; monitor I/Os and BMP.  Respiratory: e.g. aspiration, airway obstruction, atelectasis, pneumonia. Good pulmonary hygiene is key. IS may be ok, but might ↑ICP.  Visual Problems: varies based on surgical approach – o Infratentorial: extraocular eye movements, ptosis, change in acuity. o Transsphenoidal: change in acuity and field cuts (can be bitemporal , affecting the lateral aspects of each eye; or homonymous , same side of each eye).  Hydrocephalus: can occur at anytime post-op; treated via ventriculostomy temporarily or with a permanent ventriculo-peritoneal (V-P) shunt (shunts fluid from lateral ventricle to peritoneal cavity) in cases of chronic hydrocephalus.  CSF Leak: notify MD immediately at first site of a leak and if leak increases in site. Often seal spontaneously but may use a lumbar drain to relieve pressure. Prophylactic ABX.  Others: cerebral hemorrhage, seizures (use phenytoin).

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