INCREASED INTRACRANIAL PRESSURE BOX THEORY Think of the skull as a large closed box that cannot expand. In this box is brain tissue (85%), blood (7%), and cerebrospinal fluid (CSF) (8%). Intracranial pressure (ICP) is the force exerted by the three components within the skull and is measured by the pressure of the CSF. The normal range for ICP is approximately: 80-180 mmH2O or 0-15mmHg. The contents within the rigid skull “box”, must remain relatively constant or the pressure will increase. To compensate for any sustained increase in pressure the brain can cause certain components to decrease, but this compensatory function is limited (Monro-Kellie Hypothesis). •
Ordinarily the body keeps ICP within safe limits although normal fluctuations do occur in response to physiologic factors such as: o 1-Respiratory Rate Changes o 2-Body positioning – posture o 3-Increased intra abdominal pressure o 4-Intrathoracic pressure – Coughing, sneezing, straining
To maintain a constant cerebral blood flow despite these normal fluctuations in ICP the body employs 2 mechanisms:
PRESSURE AUTOREGULATION o Brain with constant blood flow – CPP – How much pressure it takes to perfuse the brain o Cerebral Perfusion Pressure = Mean Arterial Pressure – Intracranial Pressure o (CPP=MAP-ICP) Normal Range 60-150mmHg CPP – This is how much pressure it takes to .
keep the brain perfused
o MAP= Systolic – Diastolic + Diastolic 3 • • •
• • •
Mean arterial pressure must be at least 50-60mmHg higher than ICP to maintain adequate CPP. CPP <50mmHg – irreversible neurological function and decreased cerebral perfusion. Pressure atuoregulation maintains CPP regardless of fluctuations in systemic blood pressure. If B/P increases the cerebral vasculature vasoconstricts to protect the brain from blood engorgement If B/P decreased the cerebral vasculature vasodilators to increase the blood supply to the brain. Pressure autoregulation system fails when ICP rises > 33mmHg and cerebral blood blow varies passively with systemic blood flow.
METABOLIC AUTOREGULATION • •
Cerebral blood vessels also dilate and constrict in response to CO2 and O2 levels in blood Cushings Response – Seen with decreased cerebral blood flow. The brain, in attempt to restore blood flow, Increases arterial pressure to overcome increased ICP o Cushings Triad = Bradycardia, HTN, Bradypnea CO2 is a potent vasodilator
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Hypercapnia (PCO2 >50) Hypoxemia (PO2<50)
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Trigger vasodilatation to increase Oxygen supply to the brain
These auroregulatory mechanisms maintain constant cerebral blood flow but do nothing to reduce ICP. Both of these systems fail in the presence of ICP.
COMPENSATION / DECOMPENSATION Once the 2-autoregulatory systems have failed the body goes into compensation/decompensation cycle.
1-Small volume increase is better compensated than large volume increase
2-ICP increase over long periods of time are compensated better than rapidly increased ICP
o 50cc of blood in brain is a massive bleed. •
Compensation – Cerebral Spinal Fluid Regulation CSF cushions the brain and spinal cord o Decreased Production -CSF is produced in the Chorion plexus and is o Increased Reabsorption reabsorbed in the Arachnoid villi. o Displacement -You have about 100-150cc of CSF circulating at any
Dura of Spinal Cord Foramen of Luschka Foramen of Megendie
given time. You produce about 20ml per hour. -It replenishes it self
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If the pressure continues to increase and the CSF can no longer compensate, decompensation begins with compromise of the cerebral blood flow.
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Decompensation – Venous compression with arterial flow continuing to perfuse the brain resulting in an increase in ICP resulting in a decrease in CPP resulting in: Cerebral Blood Flow Increased ICP
Cerebral Hypoxia (O2) DECOMPENSATION CYCLE “killing itself off” CO2; PO2; PH Acidosis
Cerebral Edema
Vasodilatation Venous system collapses and the arterial continues to pump to brain increasing blood supply, which increases ICP and Decreases CCP. • •
If the cycle of decompensation continues, the brain will do one of two things. o Herniate downward o The brain will no longer be perfused usually resulting in death. Examples of Herniation: Tentoriam – Keeps the cerebrum
SUPRATENTORIAL • •
Herniation above the Tentoriam and is moving down Putting pressure on the brain stem
INFRATENTORIAL •
Herniation Below the tentoriam
from sitting on the cerebellum Foramen Magnum – The opening at the base of the skull
• •
Will not move up. May begin as a Supratentorial herniation and move downward. Eventually the brain stem is crushed against the bony opening of the base of skull
CAUSES OF INCREASED INTRACRANIAL PRESSURE INCREASE IN BRAIN SIZE Handwritten notes begin • Edema here and are also in packet • Tumor • Infection • Bleeding • Foreign body (bullet) • Abscess • Metabolic (diabetic ketoacidosis) – 1st change is in LOC – because the brain controls it
ICREASE IN INTRACRANIAL BLOOD VOLUME • Aneurysm • Subarachnoid hemorrhage • Venous flow blockage – Trach ties, turning head, too many pillows • CO2 – triggers vasodilatation of O2 supply to brain • Hyperthermia
INCREASE IN CEREBROSPINAL FLUID VOLUME • Meningitis • Subarachnoid hemorrhage • Tumors Ventricles
SIGNS AND SYMPTOMS OF INCREASED ICP DETERIORATION IN LOC •
• •
The First thing you see RAS System Decreased O2 Levels
MOTOR AND SENSORY LOSS • • • •
Response to Painful Stimuli Purposeful response – if you are doing pressure to nailbeds and they pull away.
Motor Cortex – Medulla Sensation: numbness, tingling Nonpurposeful response – if you put pressure on the nail bed Motor: Paralysis and they go into a Decerebrate posturate. Posturing – Only seen in comatose clients o Decorticate: cerebral cortex has been affected Extension of the lower extremities and flexion of the lower extremities • Core of the body (Core – Cortex – Decorticate) o Decerebrate: Brain stem has been affected – Worst because of brain stem injury Extension of the lower and upper extremities Stem – Decerebrate - Extension o Flaccidity – Rag doll – Very Bad
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(Nail beds, sternal rub)
HEADACHE • • •
Compression on arteries, veins, cranial nerves Brain Tumor: Worse in the morning Increased ICP Progressively worse
PUPILLARY CHANGES • Cranial nerve III(Brain Stem) - Dilated, sluggish = herniation at tentorial notch
Do not use a flashlight
PAPILLEDEMA • •
Swelling optic disc o S/S: deplopia and decreased visual acuity Choked Disc trunk – or the edges are not real clear
VOMITING • • •
Pressure on vagus nerve, brain stem, medulla Increased ICP sudden onset with no nausea Projectile
ALTERATIONS IN VITAL SIGNS •
The last thing seen
Waley/Wong P. 984
INFANTS -Tense bulging fontanels -Separating cranial sutures -Macewen’s Sign – Crackpot the cranial sutures separate -Setting sun – The eyelids look as they are setting over the eyes them selves -High pitched cry -Infant that cant be soothed -Look for changes in behavior
o Blood Pressure Increased Systolic with diastolic volume remains around same with widening pulse pressure o Pulse Bradycardia – Pump slower more effective perfusion overcome high pressure o Respirations Depends if the medulla is affected Typical Decrease with apnea due to pressure on medulla o Temperature Increase 105-106oF Cooling blankets, Tylenol
MEASURING AND MONITORING INCREASED ICP OBSERVATION • Neuro checks – should be repeated as much as needed • Altered LOC LUMPAR PUNCTURE • CSF Pressure, Measure ICP • Cause Herniation with ICP o Can cause herniation by producing a lower pressure area • Increased r/f infection CONTINOUS INTRACRANIAL MONITORING • Ventricular Catheter
P. 1637
• • •
Subarachnoid Screw Epidural Sensor Fibra
MEDICAL MANAGEMENT OF INCREASED INTRACRANIAL PRESSURE VENTILATION • • • •
Effective short term Open airway Hyperventilation – short term Position max airway, suctioning (with hyperventilation before)
CEREBRAL PERFUSION PRESSURE CONTROL • • • •
Increase HOB 30o, neck neutral midline position Blood Pressure should be Normotensive Temperature control Neck neutral, midline position
MECHANICAL DECOMPRESSION • Ventricalostomy - drainage device to drain CSF – aseptic technique • R/F Infection • Must maintain 1” above ear DRUGS • Osmotic diuretics: Mannitol, D50W o o
o o
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Diuretics Lasix o o
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o o o
If you have a patient with some kind of cerebral thing going on and they are not on Decadron or some type of steroids or osmotic diuretic then as a nurse you would question the order If on Decadron they should also be on some type of gastric med: Axid, Pepcid, Tagamet Will mask S/S of infection Would not DC abruptly
Barbiturate (drug induced coma) o
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Usually given in conjunction with Mannitol to help clear out the intravascular volume THERAPEUTIC EFFECT: Decrease Peripheral Edema
Corticosteriods – Decadron o
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Makes the intravascular (hypertonic) draw fluid from the interstitial into the intervascular spaces. You are duiresing tissue Given for rapidly rising ICP Possible complications: Pulmonary edema (Listen Breath sounds), CHF THERAPEUTIC EFFECT: Improve LOC – Given because they have an altered LOC caused by a neuro problem. They will have Increased Urine output but that is not the therapeutic effect.
If you have a person in a drug induced coma the patient is totally dependent on you as a nurse for everything.
Anticonvulsants: Dilantin, Phenobarbital, Cerebryx o o
If a person has cerebral trauma – the blood irritates the brain leading to seizure At high risk for injury
o
DO NOT prevent seizures only help control seizures
INTRACRANIAL SURGERY • Tumor o Get out the tumor • Craniotomy – Injury, infection • High risk – unstable patients
NURSING MANAGEMENT ESTABLISH AND MAINTAIN A CONTINUED / ACCURATE DATA BASE PROMOTE REDUCTION OF THE CEREBRAL EDEMA AND INCREASED ICP •
Administration of osmotic diuretics o D50W & Mannitol Dehydrate brain, reduce cerebral edema Hypertonic thus draws fluid out of brain tissue Assess breath sounds
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Administration of corticosteroids o Dexamenthasone Reduce edema surrounding brain tumors when tumor cause increased ICP
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Promote venous drainage o Increase HOB, Head neutral and midline
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Prevention of activities that increase intracranial pressure o Lifting, straining, coughing, bending
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Fluid restriction o Increase BV = Increase ICP
PREVENT HYPOXIA AND HYPERCAPNIA •
Observe for clinical manifestation of ventilatory impairment o Respirations
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Monitor blood gases o Hypercapnia trigger vasodilation O2 to brain
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Administer Oxygen
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Maintain patent airway and improve ventilation
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No narcotics or sedatives o respirations and LOC
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Prevent and/or treat elevated temperature
VENTRICULAR DRAINAGE CONTINOUS INTRACRANIAL MONITORING PROMOTE SEIZURE CONTROL PROMOTE OVERALL GOOD BASIC NURSING CARE AND PREVENTION FROM INJURY PROVIDE EMOTIONAL SUPPORT From another set of handwritten notes
NURSING INTERVENTIONS •
• •
Maintain patent airway o Suction with care B/C I ICP (hyperoxygenate) o Auscultate lung fields o HOB Attaining Normal Resp Pattern Preserving / Improving Cerebral Tissue Perfusion o Head neutral, midline position o Use cervical collar o HOB o Avoid Hip flexion o Maintain calm environment
ASSESSMENT OF ICP • • • • • • • • • • • • • •
Obtain hx events leading to present illness / subjective data Mental status LOC – Sensitive indicator of neurologic function Cranial nerve function Cerebellar function – Balance and coordination Reflexes Motor / sensory function Pupil checks VS Glasgow Coma scale – Eye opening, verbal response, motor responses Periorbital edema (may interfere with eyes) Orientation to person, place time Motor Responses: Spontaneous, Purposeful movement, Movement only response to noxious stimuli, abnormal posturing o Cannot respond to command: apply painful stimulus (firm, gentle pressure) Flaccidity – Most severe neurologic impairment
PLANNING / GOALS • • •
Maintain airway Normalization resp. Adequate cerebral tissue perfusion ICP
• • •
Restoration of fluid balance Absence of infection Absence of complications
WHY? INCREASED INTRACRANIAL PRESSURE Frequent neuro checks. Why? • Condition quickly changes and establish a baseline. Looking for improvements Drug Induced Comas. Why? • Decreases metabolic demand on brain • Shut down Avoidance of Valsava Maneuver. Why? • Increased ICP Administer Lasix. Why? • Decreases ICP (unload intravascular spaces) Hyperventilation. Why? • Respiratory alkalosis Cerebral vasoconstriction Decreased cerebral blood volume, decreased ICP
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O2 and CO2 levels
Seizure Precautions. Why? • Cerebral changes cause seizures Elevate HOB. Why? • 20-30o will increase venous return/drainage. Careful regulation of IV fluids. Why? • Prevent Increased ICP. DO NOT want to overload with fluids Neck in Neutral, Midline Position. Why? • Promote venous drainage Administer Oxygen. Why? • Increase cerebral perfusion Administer osmotic diuretics. Why? • Dehydrate brain, Decreases cerebral edema Passive Range of Motion. Why? • Prevent Contractures Turn and deep breathe. Why? • Prevent pneumonia Administer corticosteriods. Why?
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Decreases cerebral edema
Treat elevated temperatures. Why? • Increases cerebral metabolism rate and cerebral edema Restrict fluids. Why? • Dehydration Check stools for occult blood. Why? • Corticosteroids can cause bleeding Administer Anticonvulsants. Why? • Prevent convulsions Monitor intake and output. Why? • Dehydration, diabetes insipidus No trendelengerg. Why? • Decreased venous return and increases cerebral edema Monitor electrolytes. Why? • Evaluate seizures Keep blood pressure normotensive. Why? • Increase BP Increased ICP Monitor BUN/Creat Levels. Why? • Renal Function Monitor Blood Gas Values. Why? • Respiratory Status (CO2) Continuous intracranial pressure monitoring. Why? • Condition of client Administer stool softeners. Why? • Prevent straining Ventriculostomy. Why? • Drain, and administration of drugs Intracranial surgery. Why? • Remove tumor, correct bleed Nothing snug around neck. Why? • Decreases venous drainage Avoid Extreme hip flexion and prone position. Why? • Increased intraabdominal/ intrathoracic pressure increases ICP Assist client to move in bed. Why? • Movement increases ICP No Restraints. Why? • Resistance Increases ICP Decrease anxiety level and avoid emotional upsets. Why?
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Decreases ICP
Suction as needed to maintain clear airway. Why? • Coughing Increases ICP No Narcotics or sedatives. Why? • Effects LOC