Acute Intracranial Problems/Test 3 Flashcards
Intracranial Pressure….the brain in enclosed in
a box.
- dynamic measurement of pressures within the cranial vault.
- Common to many neurological conditions
- normal 0-20 mmHg
Regulation and maintenance of intracranial pressure: Normal Influence
- Arterial pressure
- Venous pressure
- Intraabdominal/intrathoracic pressure
- posture
- temperature
- blood gasses (particularly 02)
Composition of cranium
- The cranium is a rigid container of 3 elements:
- brain
- blood
- and CFS
- Pressure of brain and contents in skull
- Total volume of the 3 elements is constant at all times
- *Any of these increased by itself or combination will increase ICP
ICP: White matter has
..slower blood flow. Gray matter has a faster bloodflow
ICP: Increase CO2-
relaxes smooth muscle, dilates cerebral vessels, decreases cerebrovascular resistance, and increases cerebral blood flow. A decrease reverses the process.
Cerebral edema will typically peak in…
3 days
Causes of Increase ICP:
- Cerebral edema
- Tumor
- Blood
- CSF
Order of incidence after cranial insult…
- Tissue edema
- increased ICP
- Compression of blood vessels
- Decreased cerebral blood flow
- Decreased O2 w/death of brain cells
- Edema around necrotic tissue
- Accumulation of CO2
- Vasodilation
- Increased ICP resulting from increased blood volume
- Death
Complications of ICP
- Inadequate cerebral perfusion
* Cerebral herniation
Diagnostic Studies for ICP/Measurements of ICP:
*“Gold standard” is ventriculostomy (catheter inserted into the lateral ventricle and coupled to an external transducer to directly measure the pressure within the ventricles, facilitates removal of CSF for sampling and allows intraventricular drug administration.
Monroe Kellie Hypothesis
- Condition that increases one or more of the intracranial contents
- Must cause reciprocal changes in the remaining contents or an increase in ICP will occur
ICP: If volume increases
Compensatory mechanism will take place
Cerebral perfusion pressure measures:
The adequacy of blood flow.
When volume within the skull overwhelms the compensatory mechanisms…
intracranial pressure begins to rise.
- difference between mean arterial and intracranial pressure
- close relationship between cerebral blood flow and CPP
- necessary to maintain adequate delivery of O2 and nutrients to the brain
Cerebral blood flow is:
*amount of blood in mL passing through 100 g of brain tissue in 1 minute-normal= 50mL/min per 100 g of brain tissue (20% of body’s oxygen and 25% of its glucose
What is the parameter to monitor adequacy of blood flow to the brain?
Cerebral perfusion pressure
When the increase of ICP, the systemic blood pressure needs to
be high enough to over come ICP, to deliver oxygen and glucose to the brain tissue
To maintain adequate cerebral blood flow
the brain has the ability to regulate its own blood flow in response to metabolic needs.
Auto regulation:
automatic alteration in diameter of cerebral blood vessels to maintain a constant diameter of the cerebral blood vessels to maintain a constant blood flow to the brain during changes in systemic arterial pressure.
To ensure a consistent cerebral blood flow (CBF) to provide for the metabolic needs of the brain tissue and maintain cerebral perfusion pressure within normal limits:
Lower limit:
50 mm/Hg MAP
Upper limit:
150 mm Hg MAP
CPP=
Cerebral perfusion pressure: determinant of cerebral blood flow
CPP affects
oxygen and glucose suppy to bran
MAP=
Mean arterial pressure
Stage 1 on the pressure volume curve shows
*there is high compliance. The brain is in total compensation, with accommodation and autoregulation intact. An increase in volume (in brain tissue, blood, or CSF) does not increase the ICP.
Stage 2 on the pressure volume curve shows
the compliance is beginning to lessen, and an increase in volume places the patient at risk of increased ICP.
Stage 3 on the pressure volume curve shows
there is a significant reduction in compliance. Any small addition of volume causes a great increase in ICP. Compensatory mechanisms fail, there is a loss of autoregulation, and the patient will exhibit manifestations of increased ICP (e.g., headache, changes in level of consciousness or pupil responsiveness.
If volume increases:_____ will take place
Compensatory mechanism
- CSF will be displaced into spinal subarachnoid space (lumbar cistern)
- Ottorhea
- Rhinorrhea
- Skull fractures with laceration of the dura an basilar fractures, have the potential to cause leakage of CSF from ears or nose.
- Check fluid for the presence of glucose or send specimen to lab
Increased intracranail pressure causes
- Cerebral edema/space occupying lesion
- the brain will shift/herniation
Types of herniations:
- cingular herniation
- transtentorial herniation
- uncal
- central herniation
- cerebellar tonsil herniation
Increased Intracranial pressure complications:
- Inadequate cerebral perfusion
* Cerebral herniation
Diagnostics for Increased Intracranial pressures
*Measurement of ICP: “gold standard” is ventriculostomy (catheter inserted into the lateral ventricle and coupled to an external transducer to directly measure the pressure within the ventricles, facilitates removal of CSF for sampling and allows intraventricular drug administration
Herniation Syndromes: Brainstem compression and herniation of the brain from one compartment to another (higher pressure area to lower)
a) cingulate herniation
b) uncal herniation
c) central, transtentorial (downward) herniation
d) external herniation
e) tonsillar herniation
Brain herniation is a
major consequence of cerebral edema
Cingulate herniation (subfalcine herniation):
Occurs when the brain is forced under the dura mater that seperates the hemispheres. A unilateral mass can cause a shift of the hemisphere and midline structures to the contralateral side, often with herniation of the cingulate gyrus under the falx cerebri
Transtentorial herniation:
As the uncus and central structures descend, they may compress the third cranial nerve. The parasympathetic fibers are on the outside of the third nerve, and so the first sign of uncal herniation may be pupillary dilation. Further compression will lead to paralysis of extraocular muscles.
Uncal
occurs when the uncal portion of the temporal lobe shifts over the edge of tentorium cerebelli. The medial temporal lobe (uncus) herniates through the gap between the cerebral peduncles and the tentorium. This commonly occurs due to an ipsilateral mass lesion in one cerebral hemisphere. s/s ipsilateral eye response
Central herniation (downward herniation)
This usually occurs when there is bilateral swelling of the cerebral hemispheres. The diencephalon and the bilateral medial temporal lobes are pushed through the tentorial opening. Downward herniation stretches the penetrating branches of the basilar artery, which may then rupture, causing secondary linear hemorrhage in the brainstem (mesencephalon and pons) This is generally fatat.
Cerebellar tonsil herniation
Through the foramen magnum. This may either be secondary to downward herniation, or due to primary swelling of the cerebellum itself, as by hemorrhage or tumor. In both cases, there is compression of the medulla (with effects on medullary cardiorespiratory centers).
Early signs of increased intracranial pressure:
*Change in level of consciousness
*HA occurs at bedtime or when awakening in the morning. Often continuous but worse in the morning. Worse with straining or movement.
*Vomiting: usually not preceded by nausea or associated with food intake. Projectile vomiting may be seen.
*Pupillary changes:
-amnesia
-restlessness, drowsiness, changes in speech, loss of judgment.
-motor weakness, drift, posturing
-cushing’s response
increased b/p, widening pulse pressure, bradycardia
As pressure on the brain stem is increased:
the vasomotor center can no longer function. -drop in b/p and increase in HR
Assessment of cranial nerve 3
Ocular signs- dilation of pupil on ipsilateral to mass/lesion (sluggish, no response to light, inability to move the eye upward and ptosis of the eyelid). A fixed unilaterally dilated pupil is a neurological emergency, herniation also produces respiratory changes. Pt. will have trouble maintaining an airway. May have slow shallow resp. this leads to hypoxia and hypercapnia. As a result: Ischemia to vasomotor center in the medulla. Cushing triad will occur: hypertension with widening pulse pressure, bradycardia and resp. pattern changes. Decrease in motor/sensory function: Contra lateral hemi paresis or hemiplegia may be seen; when compression is so severe> posturing (decorticate-flexion) (decerebrate-extenison)
Decerebrate may indicate
more serious damage and results from disruption of fibers in the midbrain and brainstem.
Failure of thermoregulatroy center is a
late sign
Clinical manifestations…precursor to herniation:
*altered respirations> decreased effort
*b/p
-systolic increases
-diastolic decreases
-pulse decrease
(widening pulse pressure, bradycardia)
Pupil reactions in cerebral compression (passage of time)
right and left eye normal progress to normal right, constricted slightly reactive on left, progress to constricted slightly reactive on righ, normal size unreactive on left, progress to normal size unreactive on right, fixed dilation on left, progress to fixed dilated on right, fixed dialed on left.
Clinical manifestations: cranial nerve 3
-Ocular signs: dilation of pupil on ipsilateral to mass/lesion (sluggish, no response to light, inability to move the eye upward and ptosis of the eyelid). A fixed unilaterally dilated pupil is a neurological emergency.
Clinical manifestations ICP: late signs
- pupillary changes: dilated/nonreactive
- unresponsive
- cushing’s response
- failure of themoregulatory center is late sign
- herniation also produces respiratory changes.
As pressure on the brain stem increases the
vasomotor center no longer functions. As intracranial pressure continues to increase, the patient’s heart rate will decrease, breathing will become shallow, periods of apnea will occur, and systolic hypertension with widening pulse pressure. Patient will have trouble maintaining an airway. May have shallow resp. this leads to hypoxia and hypercapnia
Nursing management increased ICP/Assessment
- Glascow Coma Scale neurological: VS
- Diagnostic tests
- CT
- MRI
- PET
- Cerebral angiography
- Digital subtraction angiography
Nursing management: increased ICP/Diagnoses:
- decreased intracranial adaptive capacity r/t decreased cerebral perfusion or sustained increased in ICP
- Ineffective airway clearance r/t decreased level of consciousness.
- Ineffective tissue perfusion (cerebral) related to cerebral edema
- Impaired skin integrity r/t nutritional deficit, self-care deficit, and immobility
- Self care deficit r/t altered LOC as manifested by inability to follow commands or move purposefully, inability to perform ADLs
Nursing Interventions: Treat the cause-
-ongoing assessment: LOC, pupils, VS, GCS, ICP, Motor and sensory function, urine output (esp if osmotic diuretic has been administered)
Nursing Intervention/Outcomes
- Keep ICP <20
- HOB elevation 15-30 degrees
- Neutral alignment: support the neck
- promote venous drainage through the jugular vein.
- space nursing activities
- avoid compression of the neck veins
- avoid valsalva maneuver
- stool softner
More nursing interventions for ICP:
Improve CPP
- maintain normal b/p
- hypotension will decrease CPP
- Monitor and maintain fluid balance
- osmotic diuretics (Mannitol)- goal serum osmol 290-300
- fluid balance (isotonic/hypertonic)
- blood transfusions: hematocrit (30-33%)
- electrolyte balance
More nursing interventions for ICP:
- maintain normothermia
- Maintain a patent airway
- prevent hypoxia and hypercarbia
- prevents cerebral vasodilation
- suction gently and only prn
- Want to prevent seizures
- seizures increase the brain metabolism and oxygen demand.
Medications in tx of increased ICP:
- Osmotic diuretics: Mannitol, urea
- promote fluid removal from edematous brain tissue.
- monitor: hydration, serum electrolytes and serum osmolarity
- Glucocorticoid: decadron, solucortef
- reduced edema associated with tumors or abscess (inflammation)
- monitor: glucose and WBC and temperature
Medications/decreased cerebral metabolic rate
- Anticonvulsants: Phenytoin
- Narcotics: CNS depressants, fentanyl, sufentanyl, codiene
- Sedatives, propofol, benzodiazepines
- Neuromuscular blockers, vecuronium, doxacurium
- Barbiturate coma, pentobarbital, phenobarb, theiopental, **only if hemodynamically stable and unresponsive to other tx
Surgical interventions for increased ICP:
- purpose to correct underlying cause of increased ICP
- Shunts if due to hydrocephalus
- Nursing care the same as pre and post crani
- Specifics on neurological status monitoring
