Care of Acute Neuro Patients Flashcards
Cerebrum
- Frontal-concentration, abstract thought, information storage/memory, motor function
- Broca area-motor control of speech
- Parietal-analyzes sensory data
- Essential to awareness of body position in space, size and shape discrimination, right and left orientation
- Temporal-auditory receptive areas; memory of sound, understanding language and music
- Occipital-visual interpretation and memory
Midbrain
center for auditory and visual reflexes (CN III, IV originate)
Pons
helps regulate respiration (CN V-VIII originate)
Medulla
Reflexes: respiration, BP, HR, cough, vomiting, swallowing, sneezing
(CN IX-XII originate)
Cerebellum
provides smooth controlled movement; controls fine movement, balance, and proprioception (positional sense, awareness of position of extremities without looking at them)
Normal CSF charecteristics
- Clear color
- Low specific gravity (Thin liquid), 1.007
- Protein
- Glucose, is present a glucose test can be used to confirm
- WBC minimal (If WBC are present this can indicate an infection)
- No RBC (its clear)
Art blood supply of the brain
Probably dont need to know
Common Carotid Artery Internal Carotid Arteries Anterior(ACA) and Middle (MCA) Cerebral Arteries Anterior and Posterior Communicating Arteries form Circle of Willis
Circle of Willis
Frequent site of brain aneurysms, if left untreated it can lead to death easily
Cranial nerve I
Olfactory
* Sensory
* Smell
Cranial nerve II
- Optic
- Sensory
- Vision: Tested by visual acuity and vision fields
Cranial nerve III
- Oculomotor
- Motor
- Pupil reflex, eyelid elevation and eye muscle movement (EOMs); test pupils with light, squeeze eyes shut then open, test eye movement upper outer, upper inward and medial
PERRLA: Pupils, Equal, Round, Relective to light, Accommodation
Cranial nerve IV
- Trochlear
- Motor
- Down and inward movement of the eye
Cranial nerve V
- Trigeminal
- Both
- M: Jaw movement, chewing and clench cheeks
- S: Face and neck sensation, light touch and temp
Cranial nerve VI
- Abducens
- Motor
- Lateral eye movement
Cranial nerve VII
- Facial
- Both
- M: Raise eyebrows, smile, show teeth, puff out cheeks
- S: Taste on anterior 2/3 of tongue
Cranial nerve VIII
- Acoustic
- Sensory
- Hearing
Cranial nerve IX
- Glossopharyngeal
- Both
- M: Pharyngeal movement and swallowing, gag reflex, ability to swallow, uvula elevating with a
- S: Taste on posterior 1/3 of tongue
Cranial nerve X
- Vagus
- Both
- M/S: Swallowing and speaking
Cranial nerve XI
- Accessory
- Motor
- Shoulder muscle movement, shrugging
Cranial nerve XII
- Hypoglossal
- Motor
- Tongue movement and strength
Tongue should be midline
Altered level of consciousness:
Reduced state of wakefulness, awareness or alertness to stimuli
Minimally conscious state
Patient has inconsistent but reproducible signs of awareness
Coma
Clinical state of unarousable unresponsiveness with no purposeful movements or responses to internal or external stim
Patho for altered LOC
- Caused by dysfunction of cerebral hemispheres, cells in nervous system or neurotransmitters in the RAS
- Can be caused by stroke, toxicity, infection, or metabolic causes
Reticular Activating system (RAS)
- Responsible for wakefulness/sleep wake cycle, attention, ability to focus, arousal, muscle tone
- Located in hypothalamus and brainstem
- Vascular supply from circle of willis
- Receives input from spinal cord, sensory pathways, thalamus and cortex
Causes of altered LOC: Trauma
- Stroke
- Head Injury
- Cerebral bleed
- Tumor
Causes of altered LOC: Toxic
- Drug overdose
- Alc intox
- Carbon monoxide
Causes of altered LOC: Infection
- Meningitis
- Encephalitis
- Brain abscess
Causes of altered LOC: Metabolic
- DKA
- Hepatic or renal injury or failure
- Hyponatremia
- Hypoxia
- Seizures
- Heat stroke
- Hypothermia
Ways to assess changes in LOC
- Glascow coma scale (3-15)
- Cranial nerves
- Cerebellar function: Balance and coordination
- Reflexes: Gag,pupils, DTR, Babinski
- Motor function: Muscle strength
- Sensory function: Ability to feel temp (warm and cold, sharp/light touch or vibration)
Babinski reflex
- Normal for adults: Stroke from heel to toes, the toes should crunch down
- Abnormal: Stroke from heel to toes, the toes spread and go up
GCS: Eye opening response
4.) Eyes open spontaneously
3.) Eyes open to commands
2.) Eyes open to pain
1.) No eye opening
GCS: Motor response:
- None
- Decerebrate posturing
- Decorticate posturing
- Withdrawal from pain
- Purposeful movement to pain (Bats at your hand)
- Obeys commands
GCS: Verbal
- None
- Incomprehensible: Grunts or non words
- Inappropriate: words are discernible
- Confused: but able to answer questions
- Orientated
What’s worse decor or decerb
Decerb
Blood Work for altered LOC
- CMP: Electrolytes, glucose, calcium, liver function, kidney function, serum osmolality
- CBC with diff: Noting abnormally high or low counts (Infection)
- Coagulation studies (PT/INR/ PTT), (Can be hypoxia from anemia)
- Ammonia level (hepatic encephalopathy)
- Ketones (DKA)
- Tox screen (Drugs)
- ABG
Serum osmolality
Really good at telling us the fluid status
Imaging for altered LOC
- CT/MRI
- No lumbar puncture in suspected increase in ICP, can cause brain herniation
- Perfusion CT: See vasculature
- MR Spectroscopy: Can identify location of tumor stroke, epilepsy
- EEG: detects abnormal brain waves
- PET: Shows metabolic changes
- SPECT: Shows a detailed 2d map of the brain
- Cerebral angiogram: assess brain vasculature
Medical mgmt of altered LOC: Airway
- Pt intubated vs tracheostomy needed
- Can the pt protect their own airway
- Mechanical ventilation until determined
Done first
Medical mgmt of altered LOC: Circulation
- BP, HR: Is it adequate to perfuse body and brain
- Peripheral IV, ART line, Central line, Pulmonary art cath
- IV fluids and meds
Done Second
Medical mgmt of altered LOC: Determine the underlying cause
- Determine neuro pathology
- Treat the underlying cause
- Prevent complications
Done third
Causes of increased ICP and thus brain herniation
- Space occupying lesion (Tumor, abscess, hematoma, contusion, subarachnoid hemorrhage
- Generalized brain swelling (Liver failure (Hepatic encephalopathy) hypertensive encephalopathy)
- Increased venous pressure (HF, obstruction of the superior mediastinal veins or jugular veins, venous thrombosis,)
- Obstruction of CSF flow (Hydrocephalus, meningeal disease)
- Increased production of CSF
Monro-kellie doctrine
Cerebral Edema
Swelling of the brain resulting in an increase in volume of brain tissue
Autoregulation
- Brain’s ability to change the diameter of its blood vessels to maintain consistent CBF during alterations in systemic BP
- Normally its in a state of equilibrium (CSF, Blood brain tissue)
- Mechanism: Shift or displacement of CSF, increased absorption or decreased production of CSF, decreased cerebral blood volume
- Occurs constantly based on changes in intrathoracic pressure (Coughing sneezing straining), posture, BP O2 and CO2 levels
- CAN BECOME IMPAIRED WITH PATHOLOGIC AND SUSTAINED INCREASED ICP
Monro-Kellie Hypothesis/Doctrine
- Essentially the skull vault is composed of 3 things, brain, blood and CSF, if one of those increase and the others don’t decrease you’re gonna have a hemorrhage
- If one of these increase it causes a change in the volume of one or both components.
- Loss of autoregulation;normal mechanisms exhausted; increased ICP and decreased cerebral blood flood -> Brain injury, ischemia and cell death
Normal ICP
0-15 mmHg
Normal Cerebral Perfusion Pressure (CPP)
70-100 is ideal
Above 60 is ok
Below 50 is bad
At what CPP does irreversible brain damage occur
Below 50 mmHg
How to calculate CPP
MAP-ICP
Indicates the pressure which blood has to flow against in the skull which limits perfusion to the brain
Cushing’s Triad
- Increase in SBP (widening Pulse pressure)
- Decrease in HR
- Decrease in RR
Cushing’s Response
- Nervous system response to acute elevation in ICP
- Autoregulation becomes ineffective
- Changes in mental status occur
- Vital signs change as well (Cushing’s triad)
Decreased CPP leads to
Cerebral ischemia, infarction, brain death
Pulse pressure
- Difference between the systolic and diastolic bp
- Not the same thing as MAP
MAP
- Mean arterial pressure
- Average art pressure in one cardiac cycle, varying due to CO and SVR
- (2DBP+SBP)/3
Herniation
- Life threatening event which an area of the brain exits the skull vault through one of the rigid intracranial barriers
- Classified based on structure it exits through
- Path of least resistance, with a build up of pressure in the skull the brain has to go somewhere
- CT of the brain showing a midline shift indicates URGENT intervention
monro kellie
S+S of increased ICP+ impending herniation: Pre-herniation
- HA, Vomiting
- Changes in LOC (restless agitation, confusion, increased sleepiness), high highs low lows
- Cushing triad
S+S of increased ICP+ impending herniation: Herniation
- Dilated, fixed unilateral pupils (Blown pupil) or fixed bilateral unequal pupils
- Decorticate or decereberate posturing
- Oculomotor paresis (EOM)
- Homonymous hemianopia- visual field cut
- Hemiparesis
- Loss of reflexes: Oculocephalic, oculovestibular, corneal
Treatment, increased ICP/herniation: Goals
- Identify increased ICP early, prevent dmg
- Relieve increased ICP
- Decrease Cerebral edema
- Lower volume of CSF
- Decrease Cerebral blood flow
- Maintain cerebral perfusion
Treatment: Increased ICP/herniation
- Oral intubation, avoid nasotracheal intubation
- Correct blood pressure, maintain CPP to 60-70
- Place ICP Monitoring device and ART line
Why do you avoid nasotracheal intubation for increased ICP
- Increases coughing, gagging, which increases intrathoracic pressure which in turn increases ICP
Methods to monitor ICP: Intraventricular cath
- Gold standard
- Connected to drainage bag for excessive CSF drainage
- Complications: Infection, hemorrhage during placement, difficult to place with small ventricles, ventricular collapse, occluded cath
Methods to monitor ICP: Intraparenchymal
- Thin cable with electronic or fiber optic transducer at tip placed directly on the brain parenchyma through a burr hole on the skull
- Lower risk of infection, hemorrhage and easier to place
- Cons: Cannot drain csf, can lose accuracy over time and mechanical failure due to complex design
Methods to monitor ICP: Subarachnoid
- Bolt with fluid coupled system, hollow screw placed through skull, dura punctured and CSF communicates with the fluid column and transducer
- Lower risk of infection and hemorrhage
- Cons: Can clog with debris, unreliable, and less accurate
Methods to monitor ICP: Epidural
Optical transducer that rest against the dura, often inaccurate, limited use
When are ICP monitoring devices typically used
When no reliable neuro exam can be performed due to sedation, anesthesia, low GCS (<9)
Mild GCS score
12-15
Moderate GCS score
9-12
Severe GCS score
3-8
Comatose
ICP monitoring equipment: Calibrating a transducer
- Zeroed to atmospheric pressure at the level of the tragus (Level of the foramen of monro) and leveled with a 0 mark on the drainage bag
- Drain set at a specific height above tragus for drainage (15cm H20); So when ICP exceeds that amount it will drain off
- Always level transducer for position changes (T+P)
- Ensure all connections are secure and no leakage of fluids (Infection risk as its connected directly to the brain)
Treatment for increased ICP: Methods to control ICP
- Maintain an ICP goal of <20 mmHg
- Remove CSF via a ventriculostomy
- Elevate HOB 30 degrees to enhance cerebral venous drainage and keep head and neck midline, avoid neck rotation and flexion
- Sedation (Control agitation pain and excessive muscular activity, which all increase ICP)
- Hypervent (Decreases PaCO2, goal is 26-30 only really used in emergency
- Hydration: Maintain Euvolemic state (Isotonic fluids only .9%)
- restrict oral free water
- No .45% NS or DSW because they contain more water
- Keep osmolality 295-305 (High and dry)
- Mannitol to decrease cerebral edema and ICP (Osmotic diuretic)
- Keep CPP greater than 60 (Use vasopressors not fluids)
- Antihypertensives only in cases of severe HTN (180/95) and only if they are able to maintain their CPP
- Corticosteroids: Used for edema for Tumor or infection only
- Minimize suctioning (Increases ICP)
- Avoid valsalva maneuver (Stool softeners)
- Treat the fever (increases metabolism, which increases ICP) maintain normothermia
- Anticonvulsants
Mgmt of increased ICP: Normal measures fail
- Hypothermia (Controversial, don’t want them to shiver)
- Pentobarbital coma: Decreases metabolic command
- Decompressive craniectomy: Cut a chunk of skull off so the brain can expand
Mgmt of increased ICP: mgmt of underlying cause
- Remove blood clot
- Resect tumor
- Divert CSF if hydrocephalus
- Treat metabolic disorder
Mgmt of increased ICP: Supportive measures
- Vent support
- Seizure prevention
- F/E maintenence
- Nutrition
- Skin care
- Pain and anxiety
- Oral cvare
- Monitor for infection
ICP waveforms
- Should have 3 peaks
- P1-P3
ICP waveforms: P1
- Percussion wave due to art pulsation
- It represents SBP
- Should be the tallest wave
ICP waveforms: P2
- Represents brain compliance, tidal wave
- If P2 is greater than P1 there is increased intracranial volume and pressure, decreased brain compliance Impending herniation
ICP waveforms: P3
- Dicrotic wave
- Aortic valve closure
Lundberg waves on ICP tracing: Lundberg A waves
- Plateau waves
- Transient, recurring elevations in ICP
- Lasting 5-10 min
- Ranges 40-100 mmHg
- Indicates changes in volume, early cerebral perfusion compromise
- Decreased brain compliance, impending herniation
Very bad
Lundberg waves on ICP tracing: Lundberg B waves
- Last 30 sec-2 min
- Unclear value in clinical practice
- Normal
Lundberg waves on ICP tracing: Lundberg C waves
- Small rhythmic oscillations
- 4-8 per min
- Appear related to rhythmic variations in art BP and resp
Other Neuromonitoring: SjvO2
- Oxy sat in jugular venous bulb or vial cath in brain
- Can identify changes in cerebral oxygenation
- Desaturations can reflex early cerebral ischemia before increase in ICP occurs
- Can improve outcomes
- Reflects overall brain perfusion no specific injured area
Other Neuromonitoring: Fiberoptic cath in parenchyma
Monitors oxy and temp
TBI: Four primary mechanisms
- Direct impact
- Sudden or rapid acceleration and decelerations
- Penetrating injury
- blast injury
TBI: Primary injury
- Consequence of direct contact to the head or brain during initial injury
- External: Contusion, lacerations, external hematomas, skull fractures
- Intracranial: Subdural hematoma, concussion, diffuse axonal injury
TBI secondary injury
- Evolves over hours and days after initial injury due to lack of glucose and oxygen deliver to the cells
- Intracranial: Hemorrhage, cerebral edema, intracranial hypertension, hyperemia, seizures, vasospasm
- Systemic: hypotension, hyperthermia, hypoxia, hypercarbia, infection, electrolyte imbalances, anemia
TBI: What can occur after the injury
- Cerebral edema: cerebral hypoxia and ischemia, cerebral metabolic impairment, cerebral vasospasm, increased intracerebral pressure
- Cell death
- Increased glutamate
- Mitochondrial dysfunction, impairment of glucose metabolism
- Blood brain barrier dmg
- Excitotoxicity
- Complement activation and inflammation and ROS generation
TBI: Skull fracture, skull base
- Causes persistent localized pain
- Can produce hemorrhage from nose, pharynx or ears
- Battle sign, racoon eyes
- Basal skull fracture: suspected when csf escapes from the ears and nose
- Risk for meningitis due to open dura
- Csf is clear, very watery
- Test for beta 2 transferrin, collect in a small tube
Mgmt of skull fracture: Non-depressed
Close observation
Mgmt of skull fracture: Depressed
Surgery to elevate the skull and debridement
Closed TBI
- Head accelerates then rapidly decelerates or collides with another object
- Causes brain tissue dmg but no open dura
Open TBI
Object penetrates the skull, entering the brain through the dura and dmgs the brain tissue
TBI types: Concussion
- Temp loss of neuro function without apparent structural dmg to the brain
- Mgmt: Observation and prevent secondary injury
- Monitor for changes in LOC worsening HA dizziness, seizure, abnormal pupil response, vomiting irritability, slurred speech, numbness or weakness in arms or legs
- Repeat concussions lead to chronic traumatic encephalopathy
Diffuse axonal injury
Terrible, involves the shearing of nerve fibers as the brain rotates in the skull
TBI Types: Intracranial hemorrhage
- Hematoma in the brain
- Epidural: above the dura
- Subdural: Below the dura
- Intracerebral: Within brain
- S+S depend on how slow or quick the hematoma expands and compresses tissue
TBI Types: Intracranial hemorrhage, Fast bleed
Can be fatal, due to the brain having no time to compensate
Typically do worse
TBI Types: Intracranial hemorrhage: Slow bleed
Generally do better than a fast bleed due to there being time for the brain being able to compensate
TBI Types: Epidural hematoma (EDH)
- Between the skull and the dura
- Aften due to laceration of meningeal artery from skull fracture
- Hemorrhage causes rapid pressure on the brain
- Medical emergency: Surgery to make a burr hole or craniotomy to decrease ICP, remove clot, control bleeding, placement of a drain to prevent accumulation of blood
Epidural hematoma S+S
- Brief loss of consciousness, but then awake
- Lucid, conversant but then increased restlessness, agitation, confusion, signs of herniation
TBI Types: Subdural Hematoma (SDH)
- Collection of blood between the dura and brain
- Often venous in origin
- Acute or chronic depending on size of vessel and amount of bleeding
Subdural Hematoma: Acute SDH
- Usually due to a fall
- S+S: Change in LOC, Pupil changes, hemiparesis
- Increased BP, Decreased HR/RR, comatose indicates a rapidly expanding hematoma
- Treatment needs emergent craniotomy to remove the clot
Subdural hematoma: Chronic SDH
- Brain has time to compensate
- Hematoma develops slowly, weeks to months
- Brain atrophied so there is more room to expand
- Blood changes characteristics in 2-4 days, becoming thicker and darker
- Brain adapts to this and you can see fluctuating neuro, personality changes, mental deterioration, focal seizures
- Mgmt: Surgical evacuation of the clot (Burr holes or craniotomy)
TBI Types: Intracerebral Hemorrhage/Hematoma
- Bleeding into the parenchyma of the brain
- Usually due to force exerted over small area of head (Missiles, bullets, stabbing)
- S+S: INsidious, headache, neuro changes
- Treatment: Supportive care, ICP control, careful fluid mgmt, lyte monitoring , antihypertensives
- Surgery: Craniotomy, craniectomy to remove clot and control hemorrhage
- Site may not be accessible or lack of clearly defined margin prevents removal of clot
TBI Types: Diffuse axonal injury
- Due to severe head injury
- From widespread shearing and rotational forces that produces dmg through the brain
- Damage is diffuse across the entire brain
- Poor prognosis: recovery depends on severity of injury
- No awake, lucid period; patient is coma immediately with posturing (Decor/decerb) and global cerebral edema
- Can have prolonged coma
Mgmt of TBI: Assessment
- MRI/CT
- Assume cervical spine injury until ruled out
- Transported on a board with head and neck aligned in neutral position
- Cervical collar
- C-spine Xrays
Mgmt of TBI: Goals
- Preserve brain homeostasis and prevent secondary injury
- Cerebral edema after TBI peaks 48-72 hours after injury
Mgmt of TBI: Causes of secondary injury
- Cerebral edema
- Hypotension
- Respiratory depression
- Hypoexmia
- F/lyte imbalance
Mgmt of TBI:Treatment
- Stabilize ABC
- Maintain CPP
- ICP mgmt
- Control hemorrhage
- Maintain optimal ABG
- Fluid and electrolyte balance
- Maintain proper positioning to promote venous drainage
- Seizure prophylaxis
- Manage pain and anxiety and agitation
- NG tube: prevent regurg/aspiration
Neuro mgmt of TBI and Coma: Initial injury
- When did injury occur, what caused it, direction and force of the blow
- Loss of consciousness at time of injury and for how long, was the pt arousable
Neuro mgmt of TBI and Coma: Neuro checks
- Done at least every hour
- GCS to determine LOC
- Assess motor function compare all extremities and L/R on command, speech and noxious stim
- Pupils- Bilateral, sluggish, brisk to light, equal size or unequal
- Behavior-Emotional lability, aggressive, uninhibited
- Document thoroughly
- Notify provider of changes immediately
Anisocoria
Pupils unequal
Monitor VS for changes related to increased ICP, Early signs
- Cushing triad: Bradycardia, systolic hypertension, widening pulse pressure, resp depression
Monitor VS for changes related to increased ICP: Later signs
Bradycardia, Hypotension, tachypnea
Monitor VS for changes related to increased ICP: Hyperthermia
- Maintain a temp under 100.4/38c (Increased temp increased metabolic demand on the brain
- Fever may indicate brain stem dmg
- Don’t want them to shiver either as that can increase ICP
Neuro mgmt of TBI and Coma: S+S of increased ICP and CPP
- Know elevated ICP mgmt
- Proper position of head and body
Neuro mgmt of TBI and Coma: Anticonvulsants
- Drug level monitoring, need to maintain a therapeutic range
- Side effects
mgmt of TBI and Coma: Respiratory
- Airway: Maintain the airway, is the patient able to protect their own airway, if no they getting tubed
- Oxygen sat and pulse ox
- ABG: hypoxemia, hypercarbia, brain sensitive to hypoxia and deficits can worsen if hypoxic
- Lungs sounds: Present? clear or adventitious?
- Resp pattern: Regular irregular (Unless vented) cheyne stokes
- RR: Low normal or high?
- Cough reflex intact or absent: guard against aspiration, check cuff on ett or trach
- CBC: Anemia HH plt function, WBC
- Chest X-ray: Atelectasis, contusion, pneumothorax, neurogenic pulmonary edema
- Sputum cultures
- Minimize suctioning if increased ICP as it can increase ICP: If needed make it should
- Monitor for ARDS, pneumonia , fluid overload
- Good oral hygiene to help prevent against vent associated pneumonia
- PEEP, use cautiously can increase intrathoracic pressure increasing ICP
mgmt of TBI and Coma: Cardiovascular
- Assess vitals: HR+BP
- Monitor for and treat arrhythmias: Determine the underlying cause
- BP mgmt
- IV fluids vs vasopressors, vasopressors are better
- Manipulate CO to maintain adequate CPP
- Maintain good MAP
- Maintain CPP (60-70)
- Monitor for venous thromboembolism (DVT and PE)
- 12 lead ECG: Ischemia/ infarction
mgmt of TBI and Coma: Lyte and fluids
- Want to maintain normal levels
- Strict I+O
- Daily weight
- Serum and urine electrolytes
- Glucose level
- Serum osmolality
- Urine specific gravity and ketone
- Monitor skin turgor and mucous membranes
mgmt of TBI and Coma: Lytes and fluid monitoring for
- Hyponatremia
- Effects of osmotic diuretic
- Diabetes insipidus (DI)
- SIADH
- Hyperglycemic hyperosmolar syndrome
mgmt of TBI and Coma: Lytes and Fluids interventions
- Correct hyponatremia: Fluid restriction 3% hypertonic saline Do not correct rapidly increase by 4-6 mEq/L over 24 hours
- Correct Hypokalemia
- Insulin for hyperglycemia
- If giving mannitol, monitor for pulmonary edema and HF (Fluid staying in vasculature rather than excreted), want to see increased urine output
mgmt of TBI and Coma: GI
- Monitor and prevent ileus
- Bowel sounds and abd distension
- Nutrition early: improves outcomes and prevents ileus
- Enteral feeds: NG, NJ PEG
- Needs an active bowel to be used (Bowel sounds and no ileus)
- HOB up to prevent aspiration
- High cal high protein
- TPN: not usually prefered
- Constipation mgmt: From bed rest, NPO, fluid restrictions, pain meds
- Bowel incontinence
- Altered LOC
- SKin care
- GI bleeding prophylaxis (Basically everyone needs this)
- PPI
- Monitor for bleeding (Change in stool color, decreased H+H, gastric aspirate)
mgmt of TBI and Coma: GU
- Diuretics
- Strict I+O
- Mannitol
- Monitor fluids and lytes
- Incontinence
- Skin care
- Foley cath, condom cath
- Monitor for infection
mgmt of TBI and Coma: Musculoskeletal
- Assess ROM, development of deformities or spasticity
- Passive ROM
- PT/OT
- Splints: Hands feet and ankles
- Proper positioning of patient with increased ICP
- HOB 30 degrees
- Minimal elevation of legs
- Head and neck aligned neutrally
mgmt of TBI and Coma: Integumentary
- Assess skin integrity and oral mucosa q8 hrs or more frequently
- Assess under trach collar or ties or et tube
- Turn and position Q2 hrs
- OOB to chair 3x daily if able
- Early ambulation if able
- Skin care per institution policy
- Allevyn
- Speciality bed
- Frequent oral care
- Minimizes infection risk
- Monitor for breakdown of lips from ET tube
- Lubricant for lips
mgmt of TBI and Coma: Agitation and restlessness, causes
- initial brain injury
- Emerging from coma
- Increasing ICP
- Fever
- Hypoxia
- Pain/discomfort
- Full bladder
- Restraints
mgmt of TBI and Coma: Preventing injury/ problem solving in agitated/ restless pt
- Ensure oxygenation is adequate, bladder not distended, dressings, cast, splints not constricting flow
- Padded side rails
- Wrap hands so they cannot pull out tubes and to prevent self injury, avoid restraints
- Speciality bed, bed is at floor level
- Reduce stimuli
- Adequate lighting
- re-Orientate pt
- Avoid opiates to control restlessness/agitation
- minimize disruption in sleep wake cycle, cluster nursing care , lights on, shade open, dark in evening
- Limit waking pt if able
- Keep sheets dry if incontinent
mgmt of TBI and Coma: Fever causes
Due to hypothalamic dmg
cerebral irritation
hemorrhage
infection
mgmt of TBI and Coma: Interventions
- Check temp every 2-4 hours (Continuous thermometer)
- Identify cause of fever
- Treat with acetaminophen and cooling devices
- Maintain normothermia
- Do not cause shivering: Increases ICP and metabolic demand
- Culture blood urine and sputum
- Antibiotics as prescribed
mgmt of TBI and Coma: Post TBI seizures
- Can occur immediately (within 24 hours) early (1-7 days ) or late (7+ days)
- Causes increased ICP and decreased oxygenation
- Admin anticonvulsant prophylaxis
- Can be weaned off once past acute phase unless had a seizure
Complications of increased ICP: Brain stem herniation
Increased pressure creates downward pressure of the brain stem, resulting in cessation of blood flow to the brain, causing irreversible anoxia and brain death
Complications of increased ICP: DI
- Due to decreased secretion of ADH, from pituitary
- Makes you pee a ton, decreasing urine osmolality and serum hyperosmolarity
- Urine is clear
- Mgmt: IV fluids, electrolytes, Vasopressin DDAVP
Dehydration is major concern
Complications of increased ICP: SIADH
- Excessive ADH secreted
- Stops you from peeing, volume excess
- Serum Na is dilute as a result of the volume excess
- Treated with fluid restriction with no free water and in severe cases 3% saline
Hallmark of brain death
- The person is dead when the brain is dead
- Zero possibility of recovery
- Needs to be verified by 1-2 physicians
- Pt needs to be
- Removed from sedation, neuromuscular blocking agents CNS depressants
- Normal body temp (36 degrees)
- SBP over 100 (Can use vasopressors)
- No sevre lyte, acid base or endocrine disturbances
3 cardinal signs of brain death
- Coma
- Absence of brain stem reflexes
- Apnea
3 cardinal signs of brain death: Coma
Complete loss of consciousness
3 cardinal signs of brain death: Absence of brain stem reflexes
- Pupillary reflex: Pupils are fixed, mid size or dilated not reactive to light
- Corneal reflex: Drop of saline in the eye, person should blink if not its absent
- Oculovestibular reflex: Irrigate each ear canal with ice water, absent if the eyes do not move to irrigated ear within 1 min
- Gag Reflex
- Cough reflex: Person coughs when suctioning
- Occulocphalix reflex: Hold eyes open, turning head side to side, normally the eyes turn in opposite side the head is turning
3 cardinal signs of brain death: Apnea
- Removal from vent with no spontaneous breaths
- Preoxy 100% for 10 min, vent 10 bpm Peep is 5 cmH20 if SPO2 >95 do abg, disconnect from vent continue with O2 100% 6l through ETT
- Monitor for rep movements for 8-10 min , if none do an ABG at 8 min
- If no respirations and PCO2 is >60 mmHg apnea test is positive
Ancillary test brain death:
- Cerebral angiography-gold standard; confirms absence of blood flow to brain
- CT angio or MR angio-shows cessation of cerebral blood flow
- EEG—will show no brain activity
- Somatosensory evoked potentials (SSEPs): no somatosensory evoked potentials in response to bilateral median nerve stimulation and no brain stem evoked potentials in response to auditory stimuli, can confirm EEG findings
- Transcranial doppler ultrasound—can assess pulsations of middle cerebral arteries, vertebral and basilar arteries
What happens after brain death is determined
- Need to maintain adequate tissue perfusion for potential organ donation
- If family declines organ donation, cardiopulmonary support is withdrawn
- Anticipatory grieving of the family help the family understand
- Organ donation, needs brain death confirmation in order to proceed
- Need to collab with a lot of other professions in this
Nursing mgmt if care is not withdrawn
- Provide proper suctioning of the endotracheal/tracheostomy tube to remove secretionsfrom the airway. This also helpsto prevent blockage of endotracheal or tracheostomy tubes.
- Clean all the body parts, especially the face, back, and perineal area.
- Provide dressing to open wounds (if any) and cover them with gauze pieces.
- Every patient goes through a different situation despite having the same diagnosis. Nurses should manage the patients accordingly.
- Visualization of patient treatment and prognosis, as well as counseling daily, may slowly help family members cope with the patient’s degrading health status.
- Change the patient’s position every 2 hours to prevent bedsores.
- Check the intravenous cannula sites for redness and swelling.
- Make sure that the “Do not attempt resuscitation order” (DNR) is in place
- Provide emotional and psychological support to the family and relatives of the patient, as they may deny seeing their loved ones in the end stage.
- Find out and inform the organ donation center as soon as a patient is declared brain dead.
- Respect the patient’s cultural and religious backgrounds.
- Record and report all the procedures that are done for the patient throughout the hospital stay.
