brain/trauma Flashcards
what is the leading cause of death in all trauma cases?
TBI
Mechanism of Injury
Acceleration (head bounces off one surface of brain)
Acceleration-deceleration (brain bounces off one surface of brain and stops really fast) / Coup-contrecoup injuries (MVA)
Rotational forces
Penetration injuries
Pathophysiology (same as organ damage)
Primary injury
- Direct injury to the parenchyma (brain tissue)
- Hemorrhage and compression of nearby structures
Secondary injury
- Biochemical and cellular response to initial trauma (inflammatory mediators)
- Can exacerbate primary injury – flood of interstitial and serum volume can make injury worse -> increase ICP (cerebral ischemia)
- Consequences of increased intracranial pressure:
(a) Risks of cerebral hypoperfusion
(b) Cerebral edema
Traumatic Brain Injury (head injuries)
Scalp Laceration
Skull Fracture
Concussion
Contusion
Epidural Hematoma (various degrees)
Subdural Hematoma
Intracerebral Hematoma
Subarachnoid Hemorrhage
Diffuse Axonal Injury (consistent with shaken baby syndrome or ejected from high speed vehicle) – scan with MRI
Cerebrovascular Injury – hemorrhagic/ischemic stoke
ASSESSMENT TBI
1) Ensure secure airway.
- Hypoxia is an independent risk factor for mortality
- Supplemental O2 appropriate for the patient
2) All patients should be monitored w/ pulse ox and frequent checks
3) Maintain MAP >90mmHG with fluids (or vasopressor maybe). Another indicator of mortality
- AVOID DEXTROSE- damaging to injured brain
- AMS? -> can give amp to correct BG if needed
4) All head injuries are C-Spine injury until proven otherwise
- CT scan
5) Glasgow Coma Scale (quickest way to assess MS)
High = 15, low = 3
6) Degree of injury and type of injury
- Mild injury
- Moderate injury
- Severe injury
7) Check pupils (will tell a lot about TBI)
- Fixed and dilated pupils will have lesions/injury on the same size
- Vision changes -> suggestive of damage to opposite side of brain
- Dilated pupils with concussion -> unilateral
8) Consider seizure prophylaxis (Keppra)
9) Post-trauma convulsions tx w/ lorazepam/valium
10) Focused physical assessment: suggests serious brain injury
(a) Ecchymoses
- Battles sign (retro- auricular bruising) -> under ears, suggest basilar skull frature
- Raccoon eyes – suggest skull fracture
11) Scalp Lacerations (hide scalp fractures), avulsions (part of scalp is missing), fractures, hemotympanum (blood behind eardrums – suggest basilar skull fracture), babinski (brief neuro assessment)
types of motor response to pain
Localizing: reach where pain is at
Withdrawal – using nailbed pressure (subtle way to assess motor response)
Decorticate: flex towards CORE
Decerebrate: extend away from body
Flaccid: WORST -> no motor response
Fencing sign: signal a momentary loss of communication between cerebellum and brainstem
ASSESSMENT of Reversible Causes of MS changes (KNOW)
D: Dextrose 50% (hypoglycemia) – especially septic patient, can cause brain injury
O: Oxygen 100% (hypoxemia)
N: Naloxone (Narcotic- pinpoint pupils) – use for OD
T: Thiamine w/ fluids (Alcohol withdrawal) -> doesn’t reverse w/d but reduce risk of seizures and delirium tremens
Reflexes
Sensory stimulus evokes motor response.
Cutaneous reflexes graded as normal, abnormal, or absent (ie, plantar reflex)
Deep tendon reflexes: biceps, brachioradial, triceps, patellar (easiest to assess), and Achilles
4+: A very brisk response; evidence of disease, electrolyte imbalance, or both; associated with clonic contractions
3+: A brisk response; possibly indicative of disease
2+: A normal response
1+: A response in the low-normal range
0: No response; possibly evidence of disease or electrolyte imbalance
Frontal Lobe
Motor function
Cognitive functions
- Judgment (pre-frontal cortex)
- Personality
- Reasoning (pre-frontal cortex)
Broca’s speech center –
- Ability to talk
- Word salad when not developed (Non-sensical phrases that)
Long term memory
Parietal Lobe
Sensory interpretation
Temporal Lobe
Hearing
Wernickes Area
- Sensory speech – understanding what is said
Memory - hippocampus
tip:
The temporal lobe interprets what we hear. Wernicke’s speech area is the area that interprets the words we hear. The temporal lobe also houses short term memory which is necessary to learn new things.
Occipital Lobe
Visual brain (how we see things)
- The visual system is a complex pathway which begins with the eye and ends in the occipital lobe where the image is interpreted.
Cerebellum
Integration of motor function
Muscle tone
Equilibrium (balance) (where we are in space)
Brainstem (below cerebellum)
Essential for life – breathing, eating, BP, sexual attraction, reaction to certain stimuli – overrides amygdala
Ascending (sends information to brain) & descending motor (allows us to move in a certain way) & sensory tracts
Cranial nerves
Reticular formation – arousal
Cardiopulmonary regulation
tip:
Cerebral peduncles is the entrance of the motor pathways from the cerebral hemisphere to the brainstem. These fibers may be compressed in herniation causing motor deficits. Cranial nerves 3 regulates eye movements up, down, medial (toward the nose), down & out, & up & out. It also contains the parasympathetic fibers for pupil constriction & eyelid closure. The fourth cranial nerve controls medial & downward eye movement. Substantia nigra are the neurons that make dopamine. An inadequate supply of dopamine is thought to be responsible for Parkinson’s disease.
Amygdala – located within the limbic and connects the cortex and brainstem
Primarily responsible for memory and relay of info to the cortex
May be blunted by constant stimulation from the brainstem
If constantly stimulated with flight/fight, brainstem wants to take over role of whole amygdala and won’t let the cerebellum think through rationally -> illicit reaction before thinking about (ex. PTSD)
Monro-Kellie Hypothesis
Intracranial space has three components
- Brain substance 80% (majority of space)
- Cerebrospinal fluid (CSF) 8-12%
- Blood (3-10%)
An increase in volume of one intracranial component must be compensated by a decrease in one or more of the other components
This compensation is limited and is influenced by time
cerebral hematoma
first thing dropped -> CSF, then blood
how do we assess patient on vent with increased ICP?
- reduce sedation to assess LOC (move arms, legs, push toes, fingers)
- Babinski, pupillary response, DTRs
- cough/gag
- HR/RR/BP
Clinical manifestations TBI
Perfusion
- CPP=MAP-ICP
- (MAP=Mean Aterial Pressure; ICP = Intracranial Pressure; CPP=cerebral perfusion pressure)
- Reduced CPP is a concern during head injury. As bleeding increases ICP, body will compensate to raise MAP.
When beginning to decompensate, symptoms of Cushing’s triad may develop**
- Widening pulse pressure (1st sign)
- Decrease Respiratory Rate (oscilitory RR -> Cheyne stokes)
- Decreased Heart Rate
If the ICP increases to match the MAP = Bad news
- CSF pressure is 0 -> no blood flow to brain, brain herniation occurs
- Severed brain stem
tip:
Closed vault + bleeding = body wil
Intracranial pressure gets too high -> cushing’s triad
Decreased HR -> CSF/blood has left cranial vault and brain parenchyma is the only compensatory mechanism by pressing on brainstem to leave foramen magnum
MAP augments CPP
Auto regulation
MAP 50-150 mm Hg no change in CBF
- Post injury, we want the MAP a bit higher than normal
Acidosis, alkalosis and changes in metabolic rate affect CBF
Acidosis conditions cause cerebral vascular dilation
- Hypoxia, hypercapnia, ischemia
Hypoxia, hypotension, and intracranial hypertension are the leading causes of cerebral ischemia
tip:
Acidosis: Hypercapnia, hypoxemia, ischemia (all 3 drive acidosis) result in cerebral vascular dilation
Alkalosis: hypocapnia, Cerebral vascular constriction and prolonged can cause ischemia (20 mmHg)
Hyperthermia increase CBF
Hypoxemia: Pa02 level below 40 mm Hg
Cerebral Edema - 2 main types
- Vaso-genic edema (calls can’t effectively move volume in and out)
- Disruption in the blood-brain barriers and the inability of the cell walls to control movement of water in and out of the cells.
- Extracellular fluid in white matter (Brain tumors, cerebral abscess and ischemic and hemorrhagic stroke) - Cytotoxic Edema
- Swelling of the individual neurons and endothelial cells, increases fluid in the intracellular space and reduces available extracellular space, affecting the gray matter (Anoxia or hypoxic injury) - May result in Herniation (both combined)
Cerebral hematoma
skull flap removed (store in patient s abdomen for repositioning)
Don’t aggressively palpate skill
Management TBI
Consult a neurosurgeon
Prevent Hypotension and hypoxemia
Attempt to maintain a SBP >90mmHg to maintain MAP
- MAP= (2[DBP]+SBP) / 3
If hypotensive administer 1-2 L of isotonic crystalloid solution immediately. Avoid over hydration as attempts are made to restore adequate blood pressure.
- NEVER D5W
Hyperosmolar Therapy/osmotic diuresis
(a) GOAL= increase serum osmolarity to 300-320 –OR- increase serum sodium to 145-150mmol/L
(b) Mannitol
- Bolus infusion over 10-30 minutes – takes about 20-30 minutes to work
- Dose 0.25 to 2 g/kg body weight
- Acts on the loop of Henle to increase the osmotic pull of the collecting ducts
- Reduces ICP by pulling water from the cerebral parenchymal cells. (diuresis brain)
Hypertonic Agents:
- Induce hypernatremia to increase cerebral perfusion pressures and decrease ICP.
- Solutions 3%-23.4%
- Bolus of 250 ml of 3% Saline will increase serum Na 5 mEq/L
Respiratory support:
- PEEP increases the mean airway pressure and decreases the MAP and CPP
- Normocapnia (pCO2 35-45) is essential because PaCO2 effects vasoconstriction.
Hyperventilation/hyperoxia:
- Low PaCO2 increases risk cerebral ischemia by constricting cerebral vasculature
- Avoid Hyperventilation in first 24 hours
- First elevate HOB (30 degrees or higher), sedation, paralysis, Mannitol, CSF drainage should be tried first.
- Suction no more than 5-10 seconds, and no more than 2 passes due to coughing (don’t be super aggressive with suctioning)
CNS Depressants:
(a) Opioid sedatives help lower ICP by reducing metabolic demand and relieve anxiety and pain.
- Short-acting opioids are best
- IV fentanyl: 2-20 mcg/kg over 1-2 min, up to 50mcg/kg, or sufentanil 1-8mcg/kg/min
- IV Morphine Sulfate for pain
(b) Sedatives
- Cause little change in CBF, ICP and cerebral metabolic rate
- Potentiate the effects of analgesic agents
- Lorazepam, Midazolam in combination with Fentanyl
(c) Neuromuscular blocking agents (paralytic agents)
- Vecuronium or doxacurium
- Lower ICP and decrease agitation
- Patient must be sedated and intubated with adequate set rate on vent.
Steroids – Decadron
(a) Corticosteroids remains controversial
(b) Prevents fluid from entering the cells and by increasing blood vessel diameter, thereby promoting cerebral blood flow
- Decadron in low doses has been shown in rats to decrease brain water content
(c) Brain Trauma Foundation guidelines recommend not to use
(d) Risk of using out weigh benefits
(e) Not much research to support
Anticonvulsants (seizure prophylaxis)
- Frequent and routine Neurologic assessment for treatment effectiveness
- Metabolic needs of paralyzed and non-paralyzed patients increase, administer enteral or parenteral formulas that contain protein w/ dietary consultation
- Assume spinal cord injury in all head injury patients until ruled out
- Avoid any condition that increases metabolic rate and increases the demand for O2 and glucose (slow to allow for healing)
tip:
Pulls water out cerebral parenchymal (diuresis brain itself) to reduce ICP
- need to be given through filter tubing -> it can precipitate out and cause endothelial damage to the tissues
- will also see INCREASE U/O
what occurs during hyperosmolar therapy
pulls water out of the brain
strict I&O monitoring is required
the fluid around the cell has a higher (solute) = causing the water to diffuse out of the cell
Barbiturate Coma (helps to reduce ICP)
For severe refractory elevated ICP
Last resort to save brain function
Indications: GCS <7, ICP >25 at rest for 10 min, failed maximal interventions including drainage of CSF, mannitol, analgesia, and sedation
Use for <72 hours
Need secure airway with mechanical ventilation, continuous monitoring of ICP, BP, cardiac and pulmonary artery monitoring; and continuous EEG monitoring (electroencephalogram)
Discontinue if: ICP<15 for 24-72 hours, SBP<90 mmHg with Vasopressors, progressive neurological impairment, &/or Cardiac arrest.
Blood Pressure Management TBI
Hypertension Defined as SBP>185 mmHg or DBP 110 mmHg
Avoid hypotension and arrhythmias
Treat with IV Hydralizine and Labetalol if hypertensive
Nicardipine or nitroprusside infusions (IV agents to keep BP on high level but not too high)
- Need BP continuously monitored by arterial line.
- Avoid other Calcium channel blockers as they can increase cerebral edema by stimulating vasospasm
- May use oral beta blockers and ACE-Inhibitors.
monitoring TBI mgmt
ICP monitoring
CSF Drainage
CPP management
Management: Intracranial Pressure Monitoring
Brain is contained within inflexible skull, any change in volume is reflected as a change in pressure
Monitor changes minute by minute
Recommend in any patient with severe brain injury
- GCS </=9
- CT scan evidence
- Bleed or fluid accumulation
Types of Monitors: Ventriculostomy Catheter
Location Ventricle of BRAIN
Fiber-optic (can be guided into brain injury)
Specific to area of brain injury
Fluid filled (ventricle)
- Able to drain CSF fluid
- Global monitoring (similar to arterial line, zero line)
- Zero and calibrate transducer even small changes are reflected
- Foramen of Monro is optimal reference point (tragus)
- Any break or interruption in continuous fluid column will create artifact
manometer
helps to measure pressure in brain
same as ABP
ICP waveforms
correlates with EKG
Cerebral Perfusion Pressure (CPP)
Blood pressure gradient across the brain
Calculated: CPP = MAP−ICP
Goal: range 70-80
- Auto-reglatory functions may increase CPP up to 100-120 mm Hg
Must be maintained near 80 mmHg to provide adequate blood supply to the brain, but >90mmHg may cause injury
CPP <30 mm Hg results in neuronal hypoxia and cell death
Normal ICP <20mmHg
Sedation Monitoring
Ramsay Scale
- Six levels of sedation
- “Is the patient awake?” “How does the patient respond?”
- Subjective of nurse
The Sedation Agitation Scale
- Scale 1-7 dependent on level of agitation
The Richmond Agitation-Sedation Scale (most popular in southeast Michigan)
- 10 levels of response
- 0 baseline
- +4 agitated
- -5 comatose
tip:
RASS -3 (most ventilated patients)
Neuromuscular Monitoring
Used when neuromuscular blockade or chemical paralysis
“Twitch” Monitor or train-of-four monitor
Note number of movements with a given electrical impulse
Low voltage delivered to ulnar nerve and watch for finger twitch
tip:
Gives electrical impulse, look for response
0 twitches, all motors are blocked
4 twitches, no receptors are blocked
Summary: Nursing Implications
1) Q 1 hr neuro exam: Notify MD immediately for S/S of herniation (as ordered)
- Widening pulse pressure followed by low HR (common to see), low RR
2) HOB > 30 degrees, neck neutral position (promote jugular venous drainage)
Maintain ICP <20-25
- Decompressive craniectomy, Mannitol, Hypertonic saline
3) Prevent hypoxemia and hypotension
4) Pre-sedate before procedures/care (pre-analgesic)
5) Feed early and advance to goal
6) Attention to fluid & electrolyte balance (any injury to brain cause cause all 3)
- (SIADH/CSW/DI)
7) Treat fever (can increase cerebral metabolism) - Tylenol/cooling blankets
8) Bowel routine/stool softeners, GI and DVT prophylaxis
9) OT/PT/speech/Rehab consults on day 1
10) Involve/educate/support family
Categories of Injury
1) Primary Head Injury
- Scalp laceration
- Skull fracture
- Concussion
- Diffuse axonal injury
- Contusion (no central fluid consolidation like hemorrhage)
2) Hematoma
3) Infection
4) Brain swelling or edema
Categories of Injury: Primary head injury - Scalp laceration
Most common head injury
May result in profuse bleeding caused by the great vascular supply to the scalp (Eliquis, xalrelto -> may see issue)
- Monitor for hypovolemia
Apply direct pressure to control bleeding
- First assess for skull fracture
Suture/staple laceration after thorough examination and cleansing
- Lidocaine 1% with epinephrine should be used on scalp lacerations to control bleeding
- Do not use lidocaine with epinephrine for lacerations on nose or ears
Categories of Injury: Primary Head Injury - Skull fracture
1) Simple: no displacement of bonw
- Protect the cervical spine (most will come with C-collar on
- some may to be cleared with CAT scan and some may need)
- observe scalp laceration
- may indicate underlying brain injury
2) Depressed: bone fragment depressing the thickness of the skull
- Scalp laceration usually present
- Asymptomatic or may have altered level of consciousness
- Surgery is required to elevate and debride the wound
- Prophylactic broad-spectrum antibiotics
- Tetanus toxoid if indication
- Institute seizure precautions
3) Basilar: fracture in the floor of the skull
- Raccoon eyes-periorbital ecchymosis (running nose, water discharge coming out of ears -> suggestive of CSF)
- Battle sign-mastoid ecchymosis (behind ear)
- Otorrhea and/or rhinorrhea (positive dextrostix test, halo or target sign, & salty taste in mouth. Do not obstruct flow)
- Prophylactic antibiotic coverage
- Oral intubation and oral gastric tube are indicated instead of nasal intubation and nasogastric tube (potential for NG tube in brain)
Categories of Injury: Primary head injury - Concussion
Transient, reversible alteration in brain functioning. Brief loss of consciousness amnesia of events. Pathophysiology unclear, thought to be impairment of reticular activating system caused by shearing and impact.
Primary concern is an underlying hematoma
Lethargy, headache, nausea, dizziness
Do not give opioids/alcohol/drug use.
Evaluate for changes in level of consciousness
May need to admit to hospital if unconsciousness lasts longer than 2 minutes
tip:
Best guidelines: brain rest for 7 days (no tv, no phone, no reading, no stimulating activity)
- most research in football games
Categories of Injury: Focal head injury - Contusion
bruising to the surface of the brain with varying degrees of edema, coup (Direct) or countercoup (Indirect) injury. Variable LOC, nausea, vomiting, dizziness
Visual disturbances
Institute seizure precautions
Brain stem contusion; Posturing, variable temperature, variable vital signs
Categories of Injury: Primary head injury - Diffuse axonal injury
usually results in coma and death
High mortality, suspect in any patient with a correlating injury who arrives comatose
Deceleration injury coupled with MVC. Results in shearing of axons
CT will show blurring of grey and white matter junction
- Along with hemorrhage and edema
cerebral hematoma
blood collections in brain
Epidural hematoma
arterial blooding
KNOW THE HISTORY-
- Unconscious -> Injury followed by lucid period. May last several hours
Collection of arterial blood between the skull and the dura mater within the epidural space
LOC followed by lucid interval, then rapid deterioration
Stupor progresses to coma
Ipsilateral pupil dilatation
Hemiplegia
- Obtain CT scan (ASAP)
- Mannitol may be given
- Immediate surgical intervention is necessary if decreased in neurological function. Small bleeds are monitored.
Subdural hematoma
venous bleeding between the dura mater and the brain tissue
Requires forceful injury in young patients, elderly patients may develop with less severe injury
Most frequently seen type of IC bleeding (MOST COMMON TYPE)
Acute: develops over minutes to hours
- Drowsiness, agitation, confusion
- HA
- Unilateral or bilateral pupil dilatation
- Late hemi paresis
- Obtain CT scan
- Surgery is required
Chronic: develops over days or weeks
- HA
- Memory loss
- Personality changes
- Incontinence
- Ataxia
- Obtain CT scan
- Surgery is usually required, but close monitoring may be sufficient if the hematoma is small
Categories Brain Injury:Infection
Meningitis
Brain abscess
tip:
Takes a while to recover, 6 months -> IV antibiotics
Categories Brain Injury:Brain Swelling
Brain Swelling or Edema
- Secondary to any of the above
Arteriovenous Malformations
12% of AV-M’s cause symptoms
Incidence disease 1-100,000-300,000
Account for 8.6% of all hemorrhages
Advances in technology are being identified before rupture
A-V Malformations detected and treatment
Detected:
- CT scan with and without contrast reveal bleeding sites
- MRI with injection of radioactive reagents
- 4-vessel cerebral angiogram
Treatment:
- Surgical resection for small-medium size
- Endovascular Treatment- detachable coils, Onyx liquid
- Redos-urgery
Nursing Care AV-Malformation
Admission to ICU
Monitor for Neuro changes
Hemorrhage prevention
Symptom management with BP control
Treat pain
Prophylactic anti-seizure medication
Lifestyle modification
- No smoking
Cerebral Aneurysms
Caused by Atherosclerosis, hypertension, smoking and alcohol consumption
Genetic component
Symptoms
- Headache
- 3rd nerve palsies (dilated pupils)
- Extra-ocular motor deficits (Cranial nerve III,IV, VI)
- Vision changes
- Pain above and behind the eye
- Localized HA
- Nuchal rigidity
- Seizures
- Photophobia
Severity presentation depends on
- amount of bleeding
- Worst headache of life (thunderclap HA)
- Nausea
- Vomiting
- May or may not lose consciousness
- Cranial nerve deficits
- Stiff neck/neck pain
- Blurred vision
- HTN, Bradycardia
Diagnosis
- CT scan without contrast
- IF negative CT scan for blood-Lumbar puncture for RBC’s and xanthrochromia (bile) in CSF
- CT angiography
- MRI/angiography
- Angiograms
Treatment
- Surgical Clipping
- Endovascular Techniques: Guglielmi coil, Stent assisted coiling
Nursing Care:
(a) Neurological assessment
(b) Monitor signs and symptoms of complications:
- Vasospasm: Begins 3 days after bleed resolves 21 days
- Hyponatremia: Na<135, due to SIADH, or maybe due to increase loss of Na via urine. Tx with fluid restriction
- Neurogenic pulmonary edema: Support with Intubation will self corrected.
- Cardiac dysfunction: Support with inotropic therapy, pulmonary artery monitoring and vent support.
- Chronic hydrocephalus
Acute Stroke-Ischemic
Early recognition
Early treatment
Mortality 35%, with 40% of strokes occurring in people under the age of 60 years
Leading cause of disability and need for long term care.
Risk factors are HTN, smoking, obesity, cardiac disease, hypercholesterolemia, DM, cancer, use of BC pills, and PFO with atrial septal aneurysm.
Prevention is anti-coagulation for atrial fibrillation and ASA
Ischemic Stroke: treatment
Early recognition
CT Scan, MRI, Cerebral angiography
IV thrombolytic (tPA) administration
- Intra-artrial within 3 hours from symptom onset
- Can be pushed to 4.5 hours in some patients
- 24 hours for intravascular intervention for basilar artery stroke
Ischemic Stroke Management
Restoration of CBF
Prevent recurrent thrombosis
Neuroprotection
Supportive care
Ischemic Stroke: tPa
Given within 4.5 hours or less from onset of last seen functioning normally
NIHSS score (measurable defect) and results of imaging will determine if appropriate to give tPA
Dose of 0.9mg/kg with (maximum dose of 90mg IV)
- 10% bolus over 1-2 minutes
- Followed by infusion of remainder of solution over 60 minutes
- No other anti-thrombotic therapy should be given for the next 24 hrs
- Major risk is intracranial hemorrhage.
Acute Stroke-Hemorrhagic Cause
Aneurysmal
AVM
Coagulopathies
Vasculitis
Abuse of cocaine or sympathomimetic drugs
Brain death criteria
No spontaneous movement
No spontaneous respiration after 100% O2 is received for 10 minutes and the patient is tested for a period of 4-6 minutes, with PCO2 reaching 60mmHg
Absence of brain stem reflexes
- Fixed and dilated pupils
- No corneal reflexes
- Absent doll’s eyes
- Absent gag reflex
- Absent vestibular response to caloric stimulation
- Demonstration of “no flow” state to the brain through arteriography
- Flat EEG repeated over 12-24 hour period
- Rudimentary spinal reflexes, when present, should not influence determination of brain death
- Hypothermia, barbiturate poisoning, and metabolic imbalance must be ruled out as causes of CNS lesions.
Gift of Life
If patient is declared dead based on neurologic criteria, call Gift of Life before extubation to discuss with family organ donation – Never the responsibility of the RN to approach the family for organ donation
- Family sense of loved one still living through other
- Benefit of giving to others in time of sorrow
- Donor family will not have contact with those who receive organ and vise versa
- Many end-stage disease patients waiting for organ
- Even if not sure meets criteria, let Gift of Life determine and discuss with family. Maybe able to use cornea, skin, bones, as well as eyes, lungs, liver, heart and kidney
