Increased ICP Flashcards
Normal ICP
Pressure exerted from total volume of 3 components within the skull - brain tissue, blood and CSF
Relationship between 3 components within the skull
If volume of any of 3 components increases without corresponding decrease in another component the result is increased ICP (Monroe-Kelly Hypothesis)
Measure of ICP and normal and abnormal values
In ventricles, subarachniod space, subdural space, epidural space, or brain tissue using a pressure transducer
normal ICP: 5-15 mmHg
sustained ICP > 20 mmHg = abnormal
Compensatory Mechanisms to resist increased ICO by: (3)
- Changes in CSF volume
- Altering intracranial blood volume
- Brain tissue volume
However, compensatory adaptation are finite. only going to last so long and then they will cause brain damage
Compensatory Mechanism: changes in CSF volume
By displacement of CSF (into spinal subarachnoid space) or altering production and absorption rates of CSF
Compensatory Mechanisms: Altering intracranial blood volume
By compression of veins, or vasoconstriction/vasodilation, or changes in venous outflow
Compensatory Mechanism: Brain Tissue
Distension of dura, or compression of brain tissue
Cerebral Blood Flow (CBF) definition
Amount of blood (ml) passing through 100 gms of brain tissue/min -> approx 750ml/min
Brain and glucose
brain is unable to store oxygen and glucose means you always have to have blood flow and supply of glucose and oxygen
CBF: Autoregulation
Brain has ability to autoregulate its own blood flow in response to metabolic needs.
- automatic alteration in diameter of cerebral flow to maintain constant blood flow
autoregulation does not work in extreme hypo/hypertension
MAP and Autoregulation of CBF
If MAP< 50, CBF is decreased and cerebral ischemia occurs
If MAP>150, cerebral vessels are maximally constricted and further response is lost
Other Factors Affecting CBP
- PaCO2
- PaO2
Increased Carbon Dioxide in the blood (increased PaCO2) causes cerebral vasodilation, decreased vascular resistance, and increased cerebral blood flow. If carbon dioxide is decreased in the blood this is reversed and CBF is decreased
PaO2 < 50 - vascular dilation, increasing CBF. In acidotic environment, further vasodilation in attempt to increased blood flow
CBF can be indirectly reflected by calculating cerebral perfusion pressure (CPP)
What is CPP (cerebral perfusion pressure)
CPP is the pressure needed to ensure adequate perfusion to brain tissue
CPP does not reflect perfusion pressure in ALL parts of the brain
Calculation of CPP
CPP = MAP - ICP
Calculation of MAP
MAP = SBP + 2(DBP)/3
Imperative to maintain MAP when ICP is increased
Normal CPP
70-100 mmHg
Min CPP required for adequate cerebral perfusion
50-60 mmHg
CPP meaning cerebral ischemia
CPP < 50 mmHg
CPP incompatible with life
CPP < 30 mmHg
What causes increased ICP (4)
- Cerebral edema
- Contusion (bruise - can cause bleeding and swelling)
- Cerebral abscess (pocket of pus and infected fluid in the brain)
- Cerebral neoplasm
Causes of cerebral abscess
surgery, ear infection, sinus infection, brain injury, meningitis, hx of IV drug use, HIV/AIDS, immunocompromised
Crucial factor of increased ICP
preservation of brain tissue by maintaining cerebral blood flow
Cerebral Edema - different types
Increased accumulation of fluid in extravascular spaces of brain tissue
Different types:
- vasogenic cerebral edema
- cytotoxic cerebral edema
- interstitial cerebral edema
Vasogenic Cerebral Edema
- most common type
- from changes in endothelial lining of cerebral capillaries
- increase in permeability of blood-brain and increase extracellular fluid volume
- occurs mainly in white matter
Cytotoxic edema
From disruption of integrity of cell membrane
Results from destructive lesions or trauma to brain tissue, leading to cerebral hypoxia/anoxia, Na+ depletion, syndrome of inappropriate antidiuretic hormone
Fluid and protein shift from extracellular space into cells
Most often in grey matter
Interstitial cerebral edema
Result of diffusion of ventricular CSF in an uncontrolled hydrocephalus
Clinical Manifestations of increased
- headache
- confusion
- decreased LOC
Three categories of clinical manifestations
Change in LOC
Change in Vital Signs
Ocular signs
Change in LOC
flattened affect, confusion, voice changes, talking different than they were before
Changes in Vital Signs: Cushings Triad
- irregular or decreased respirations
- decreased HR
- widening pulse pressure (difference between systolic and diastolic)
Ocular Signs
Dilation of the pupils epsilateral (on the same side of the lesion), sluggish or unresponsive to light. inability to move the eyes upward, or drooping of the eyelid. Fixed unilaterally dilated pupil is an emergency and a indication of herniation of the brain
Clinical Manifestations: decreased motor function
- Decorticate (flexor)
- Decerebrate (extensor) - more serious damage
- Headache from compression of intracranial structures (arteries, veins, nerves)
- Pain is continuous
Clinical Manifestations: vomiting
Not proceeded by nausea
From direct pressure on vomiting center in 4th ventricle in medulla
Vomiting associated with increased ICP is projectile
Early Signs of Increased ICP (6)
Altered LOC
- unilateral pupil changes in size, equality, and/or reactivity
- altered respiratory pattern, bradypnea or irregular
- unilateral hemiparesis (weakness to one side of the body)
- focal findings (speech difficulty)
- papiledema (swelling of the optic nerve)
- vomiting, headache, seizures
Late Signs of increased ICP
decreased LOC (stupor)
- unilateral or bilateral pupillary changes i.e. size, equality, and/or reactivity
- cheyne-stokes respiration
- decorticate or decerebrate posturing
Terminal Signs(4)
- coma
- bilaterally fixed and dilated pupils
- resp. arrest
- absence of motor response
Pathophysiology of increased ICP
Insult to brain -> tissue edema -> increased ICP -> compression of ventricles -> compression of blood vessels -> decreased cerebral blood flow -> decreased oxygen with death of brain cells -> edema around necrotic tissues -> increased ICP with compression of brain stem and respiratory center -> accumulation of CO2 -> vasodilation -> increased ICP resulting from the increase in blood volume -> death
Causes of cerebral edema (6)
Mass lesions
Head injuries
Cerebral infections
Brain Surgery
Vascular insult
Toxic or metabolic encephalopathic conditions
Mass lesions
Brain abscess, brain tumor
Hematoma
hemorrhage
Head injuries
Contusion
Diffuse axonal injury
Hemorrhage
Post-traumatic brain swelling
Cerebral infections
Meningitis
Encephalitis
Vascular insult
Anoxic & ischemic episodes
Cerebral infarction (thrombotic or embolic)
Venous sinus thrombosis – blood clot forms in the sinus and causes blood to fill in the ventricles and it can’t drain from the blood
Toxic or metabolic encephalopathic conditions
Hepatic encephalopathy (toxin build up from liver failure)
Lead or arsenic intoxication
Uremia
Complications of increased ICP
Inadequate cerebral perfusion
Cerebral herniation
Cerebral herniation types (6)
- cingulate herniation
- tentorial herniation
- cerebellar tonsillar herniation (move downwards)
- falx cerebri (brain tissue is pushed across to the other side from the damage. a midline shift)
- tentorium cerebelli
- tentorial incisura
Brain herniation occurs as the brain is shifted from the compartment of higher pressure to the compartment of lower pressure.
Diagnostic Studies
- MRI
- CT scan
- MRA (magnetic resonance angiography)
- CTA (computed tomographic angiography)
- Above tests are used to differentiate many conditions that can cause increased ICP and to evaluate therapeutic options
Goal of care for a patient with increased ICPC
identify and treat the underlying cause of increased ICP and to support brain function
Drug Therapy
mannitol (diuretic osmotic - fluid moves into the blood vessels and is excreted)
hypertonic saline (3% draws fluid out and into the vein)
Corticosteroids to reduce swelling
Nutritional Therapy
pts with increased ICP are in hypermetabolic & hypercatabolic state -> increased need for glucose or fuel among other considerations
Significant part of interprofessional care
Pain Control
Supportive Therapy
Metabolic demands such as fever, agitation, shivering, pain and seizures can increased ICP.
- address these with induced coma. dont want brain to be active. want the brain resting and sleeping so it can heal. decreases the oxygen and metabolic demands of the brain.
Inducing hypothermia to suppress cerebral metabolism. This is often done for several days but extended hypothermia makes the patient susceptible to systemic infections and hypotension
Glasgow Coma Scale
Three areas tested: eye opening, motor response, verbal response)
not able to use it when pt is in a coma or sedated from pain management
Change: is key in determining what is happening neurologically
low glasgow coma number
Score less than or equal to 8 at 6 hours post injury - 50% die
Neurological Assessment
pupils compared for size, movement, and response (use penlight)
evaluate cranial nerves
for unconscious patients, observe their spontaneous movement
If no spontaneous movement, painful stimuli are applied
VS
Nursing Implementation (7)
Respiratory Function
Fluid & Electrolyte balance
Monitoring ICP
Body position - elevated at least 30 degrees
Protect from injury - confusion, agitation, seizures. give seizure precautions.
turn slowly, keep head midline, avoid unnecessary stimulation
Coughing, straining and the valsalva maneuver should be avoided
Psychological consideration
