Adult Neuro Flashcards
Increased ICP
Monro-Kelli Hypothesis
Normal Range
Monro-Kellie Hypothesis
- States that three components – brain tissue, blood, and cerebrospinal fluid (CSF) – occupy a rigid box, the skull.
- When one of these three components increases, the other components must decrease to maintain equilibrium, preventing further injury to the brain through compression of the tissue within the fixed box.
- The ability of the body to compensate is called intracranial compliance.
Normal ICP ranges from 0mmHg to 15mmg
Causes of Increased ICP
Factors that influence ICP
Causes
- Injury
- Bleeding
- Hematoma
- Hydrocephalus
- Tumor: lesion occupying inside of the brain
- Encephalitis or Meningitis
Factors that influence ICP
*Body temperature:
- Increasing cerebral metabolism may exacerbate existing brain injury by increasing the demand for oxygen and nutrients where there is existing poor blood flow (ischemia).
*Oxygenation status, especially CO2 & O2 levels
- A PaO2 below 50 mm HG can precipitate increased ICP. Vasoconstriction (decreased PaCO2) or vasodilation (increased PaCO2) of cerebral blood vessels. Cerebral vasoconstriction reduces ICP, and vasodilation increases ICP.
*Body position
- Elevating HOB and ensuring that the head is in midline facilitates drainage of blood from the jugular venous system, decreasing ICP. Avoiding sharp hip flexion ensures that large veins in the abdomen are not compressed, decreasing venous return.
*Arterial and venous pressure
- Increased pressure = increased ICP
*Anything that increases intra-abdominal/thoracic pressure (vomiting, bearing down, PEEP)
What is cerebral perfusion pressure?
What happens when it is low?
Range?
How to calculate
The pressure that pushes the blood to the brain…hence influences the cerebral blood flow.
**When CPP falls too low the brain is not perfused and brain tissue DIES
Normal CPP is 60-100 mmHg
CPP = MAP - ICP
MAP = SBP + 2(DBP) / 3
Clinical Manifestations of Increased ICP
- Increased ICP is defined as an ICP >20mmHg for over 5 minutes
- Earliest!: Mental status changes (restless, confused, not responding to questions)
- Late!: Irregular breathing (Cheyne-Stokes-hyperventilation then apnea)
- Cranial nerve changes to the optic and oculomotor nerves
*Double vision, strabismus
*Swelling of the optic nerve (Papilledema)
*Constricted, dilated or unequal pupils
*Abnormal Doll’s eye (oculocephalic reflex) - move the head, eyes stay fixed = positive sign, LATE - Decerebrate (pronated arms, flexed wrists, LATE sign, herniation taken place) and Decorticate (less severe, flexed arms and wrists, immediately after event then resolves) posturing
- Cushing’s Triad (Late!)
*Elevated systolic BP, lowering diastolic BP
(widening pulse pressure)
*Bradycardia
*Lowering or abnormal respiratory rate - Seizures
- Headache
- Vomiting (without nausea)
- Positive Babinski reflex: dorsiflexion (upward movement) of the big toe and fanning of the other toes.
Monitoring ICP
Examples
Patients with traumatic brain injury and a GCS score of 8 or less have an ICP monitor placed. (GCS 8 -> intubate)
Using a catheter or sensor.
Placed in lateral ventricle of brain, parenchyma, or subarachnoid space.
Examples:
*Intraparenchymal sensor/probe
- No drainage
*Subarachnoid bolt
- Temporary, no drainage
*Intraventricular catheter
- Ability to monitor pressure and drain CSF
- Increased risk of infection
Increased ICP
Diagnostic Tests: Labs, Radiology
Blood &Urine
- ABGs: evaluation of the PaCO2, which causes vasoconstriction (decreased PaCO2) or vasodilation (increased PaCO2) of cerebral blood vessels. Cerebral vasoconstriction can reduce ICP, and vasodilation of the cerebral blood vessels can increase ICP in brain injury.
- CBC
- Coagulation Profile
- Electrolytes: A target above the normal sodium range is chosen on the basis of the severity of cerebral edema and the specific disease process. The purpose of monitoring serum sodium is to determine whether a patient is meeting the target to maintain a continuous concentration gradient favoring the pull of water out of the brain tissue.
- Serum Osmolality: monitor effects of mannitol
- Urinalysis and osmolality
Radiology
- Computed Tomography (CT) of the head
- Magnetic Resonance Imaging (MRI)
- Cerebral blood flow with transcranial
doppler
- EEG
Medical Management of Increased ICP
Adequate Oxygenation
- Mechanical Ventilation
- ABGs
- Goal: Maintain PaO2 above 80mm Hg!
PaCO2 Management
- Goal: Maintain PaCO2 35 – 45mm Hg!
- Hyperventilation decreases PaCO2 resulting in
decreased cerebral blood flow (CBF)
- Hyperventilation no longer recommended to
manage increased ICP
Diuretics
- Reduces brain tissue volume
- Osmotic diuretics (Mannitol & Hypertonic Saline)
- Mannitol pulls water from the interstitial spaces into the vascular space, and then diuresis occurs at the level of the kidney
CHECK KIDNEY AND HEART FUNCTION
- High-concentration sodium chloride solutions pull water from the interstitial spaces into the vascular space without the dramatic fluid shifts caused when osmotic diuretics are utilized.
- Loop diuretics (Lasix)
Fluid administration
- In order to compensate for the systemic dehydration and hypovolemia that occur with the administration of mannitol, IV fluid should be administered to replace losses.
- Optimize MAP & maintain intravascular volume
- Isotonic solution (Normal Saline)
- Strict I&O
- Keep serum osmolarity < 320 mOsm/L
Blood Pressure
- Goal: MAP 70 – 90 mm Hg
- CPP: at least 70 mm Hg
- Avoid hypertension! Increases cerebral blood volume
- Antihypertensives (Nicardipine & Labetolol)
Seizure Prophylaxis
- Fosphenytoin (Cerebyx) & Levetiracetam (Keppra)
Increased ICP
Nursing Interventions
Positioning
- HOB 30-35 degrees: facilitates drainage of blood from the jugular venous system, decreasing ICP.
- Neutral head position
- No flexion of the neck or hips: ensures that large veins in the abdomen are not compressed, decreasing venous return.
Suctioning
- Only when necessary
- Limit suctioning to 10-15 seconds
- Hyperventilate before and after
Assessment
- Neuro exam (per hospital protocol)
- Vital signs: Prompt identification of hypotension and decreased oxygenation (SpO2) is important in preventing further brain injury resulting from decreased perfusion and oxygenation.
- ICP and CPP (per hospital protocol)
- Temperature control: Increasing cerebral metabolism may exacerbate existing brain injury by increasing the demand for oxygen and nutrients where there is existing poor blood flow
- Sedatives: treat pain, anxiety, restlessness
Traumatic Brain Injury
Causes
Risk Factors
Leading causes are falls, MVCs, and being struck by
an object
Certain individuals are at higher risk
* Alcohol use, drug use, team sports, not wearing seatbelts
* Men > Women
* Very young (<10 years) and elderly (>74 years)
Classifications of TBI
Determined by worst non-confounded (free of alcohol or drugs)
Mild brain injury
* GCS: 13- 15
Moderate brain injury
* GCS: 9 – 12
Severe brain injury
* GCS: 3-8
* GCS of 8, intubate
GCS
- Eye Opening: Spontaneously, to speech, to pain, no response
- Verbal Response: Oriented to person/time/place, confused, inappropriate words, incomprehensible sounds, no sounds
- Motor Response: Obeys command, moves to localized pain, flex to withdraw pain, abnormal flexion, abnormal extension, no response
Primary (Coup)
- Initial mechanical insult
Secondary (Contrecoup)
- Secondary injury
Types of TBI
Skull fractures
- Linear: skull fractures at the base of the skull are termed basilar fractures.
- Depressed: occurs when the outer table of the skull is depressed below the inner table of the surrounding intact skull. If the scalp is lacerated and the dura is torn, there is direct communication between the brain and the environment, and meningitis can occur.
- Comminuted: occurs when there are multiple linear fractures with a depressed area at the side of impact.
Penetrating injuries
- Result of low or high-velocity forces such as gunshots, knives, or sharp objects.
- Deep laceration of brain tissue and possible damage to the ventricular system.
Contusion
- Superficial bleeding that occurs on the surface of the brain, often at the point of initial impact or “coup” location
Concussion
- Occurs when a mechanical force of short duration is applied to the skull.
Diffuse Axonal Injuries (DAI)
- With this injury, widespread white matter axonal damage occurs secondary to rotational and shearing forces.
Hematomas
-
Basilar Skull Fracture
S/S
Tx
- Occurs at the base of the skull
- CSF can leak from ears and nose due to fracture
- There is potential for hemorrhage from this injury
- Battle’s Sign (bruising behind and Raccoon Eyes (late signs)
Treatment - Bedrest with HOB elevated (High-Fowler’s)
- Neuro checks
- No blowing of the nose or nasal suctioning
- No NG tube: may cause further disruption of a fracture and places the patient at risk for the tube to invade the cranium.
- Management of CSF leak: If clear fluid is draining from the ear or nose, it should not be stopped; it should be collected using loosely applied gauze.
Epidural Hematoma
Patho
Symptoms
- In an epidural hematoma, blood collects
between the skull and the dura mater - The dura is the tough covering of the brain that
covers the brain and spinal cord and is
connected to the inside surface of skull in the
suture lines, forming potential compartments or
spaces - When an epidural hematoma occurs, blood fills
a particular epidural compartment and begins to
compress brain tissue inward - The patient typically experiences a brief loss of consciousness followed by a lucid period before neurological deterioration. The lucid period may last for a few hours to 48 hours.
Subdural Hematoma
Patho
Symptoms
- A subdural hematoma refers to a collection of
blood beneath the dura and above the arachnoid
layer; which is most often caused by venous
bleeding - When the head is impacted by a blunt force, the
brain moves within the skull and dural covering.
When the brain moves within the dural covering,
tension is placed on bridging veins, causing
stretching and tearing and releasing a steady flow
of blood around the brain in the subdural space
Symptoms of a subacute subdural hematoma occur anywhere from 48 hours to two weeks after an injury.
A higher incidence of chronic subdural hematomas is seen in the elderly, chronic alcohol abusers, and those taking anticoagulants such as warfarin, antiplatelet aggregation, or aspirin.
Subarachnoid Hemorrhage
Cause/Patho
S/S
- Traumatic subarachnoid hemorrhage is the most
common type but may be due to a cerebral
aneurysm - Poor prognosis
- Occurs as a result of disruption in the veins and
arteries traversing the arachnoid layer
Clinical Manifestations - Neck pain
- Horner’s sign
*Miosis – pupillary constriction
*Ptosis – eyelid droop
*Anhidrosis – decreased sweating
Thunderclap HA
Drape over eyes
Complications of TBI
- Diabetes insipidus: occurs in the absence of ADH; urinary output increases rapidly, causing a loss of free water and severe dehydration manifesting as hypernatremia and low urine specific gravity.
- Syndrome of inappropriate anti diuretic hormone (SIADH): occurs when an excessive amount of ADH is secreted from the posterior pituitary; results in the retention of free water, causing hyponatremia and normal to low urinary output.
Medical Management of TBI (assessment/actions)
- Neurological assessments (GCS)
- Airway management
- Hemodynamic monitoring
- ICP monitoring
- Evaluation of laboratory testing
- Enteral nutrition: Patients with severe TBI demonstrate a hypercatabolic state where the body utilizes substrates at a rapid pace, causing utilization and depletion of fat and protein stores.
- Seizure precautions: at risk for seizures
- Temperature: antipyretics and cooling devices as ordered
Surgical Treatment for TBI
- Debridement & cleaning open wounds
- Craniotomy
- Surgical evacuation of epidural & subdural hematoma
Parkinson’s Disease
Patho
- Motor system disorder
- Involves the loss of dopamine producing brain cells in the substantia nigra of the basal ganglia
- Deterioration of the substantia nigra decreases the amount of dopamine in the brain. The excitatory ACh neurons continue to proliferate, remaining active while there is a continued loss of dopamine and its inhibitory mechanisms, culminating in the loss of initiation and control of voluntary movement.
Parkinson’s
Clinical Manifestations
Two or more symptoms with asymmetrical presentation:
- Resting tremors (pill-rolling tremor)
- Muscle rigidity
- Bradykinesia (slowness of movement)
- Akinesia (loss of movement)
- Postural instability (impaired balance and frequent falls)
- Mood, cognitive, and behavioral alterations
- Slow, shuffling gait
- Widening of gait
- Postural instability
- Drooling
- “Pill-rolling” tremor
- Cogwheel rigidity
- Masklike face
- Bowel or bladder function: risk for incontinence and constipation
Parkinson’s
Anticholinergic Medications
Examples, Considerations
Examples: Trihexyphenidyl (Artane) & Benztropine (Cogentin)
- These medications block the cholinergic receptors in the CNS, thereby suppressing acetylcholine activity
- Reduces tremors and drooling
- Generally avoided in older adults because of side effects including confusion, memory impairment, blurred vision, dry mouth, constipation, and urinary retention.
- Not to be used in patients with Glaucoma
Parkinson’s
Dopamine-receptor agonists
Examples, MOA, Contraindications, Side Effects
Examples: Ropinirole (Requip) & Pramipexole (Mirapex)
- Stimulates the dopamine receptors and increase the amount of dopamine available in the CNS
- Enhances neurotransmission of dopamine
- Contraindicated in patients with cardiac, renal, or psychiatric disorders
- Side effects include N&V, drowsiness, orthostatic hypotension
Parkinson’s
Sinemet (Carbidopa/Levodopa)
Examples, MOA, Consideration
Adds more dopamine to the brain
Carbidopa prevents Levodopa from breaking down in the blood
Levodopa enters the brain and turns into dopamine
Common side effects are nausea and involuntary movement
Takes about 3 weeks to be effective
Long-term use may result in “wearing off” of symptoms
Parkinson’s
Entacapone (Comtan)
MOA, Considerations
COMT inhibitor (Catechol-o-methyltransferase)
Used with Sinemet
Blocks COMT enzyme that breaks down Levodopa in the blood making it last longer
Avoid MAO inhibitors – hypertensive crisis
Avoid foods or supplements high in vitamin B6
Do not take with a meal high in protein
