CNS Injury Flashcards
Results when the head suddenly and violently hits an object or when an object pierces the skull and enters brain tissue
TBI
- Neurologic deficit can occur instantaneously as a consequence of the primary injury or from secondary injuries that follow within minutes, hours, or days
- Consists of direct neuronal damage ± edema ± secondary ischemia-related neuronal death
What is the difference between primary and secondary TBI pathophysiology?
- primary is a direct result of external transfer of KE to various structure of the brain: due to contact (concussive), or acceleration/deceleration (MVA)
- secondary is due to cerebral edema or vasoconstriction/ platelet aggregation; goal = want to stop progression from primary injury to secondary!
In a primary TBI, what creates a focal injury? diffuse injury?
Focal – hematoma, contusions
Diffuse - shearing, stretching forces
A pt who has the following symptoms has a [mild/ moderate/ severe] TBI:
remain conscious or may experience a loss of consciousness for a few seconds or minutes, headache, confusion, lightheadedness, dizziness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, a change in sleep patterns, behavioral or mood changes, and trouble with memory, concentration, attention, or thinking
mild
How will a pt present with a moderate or severe TBI?
same sx of mild, WITH:
a headache that gets worse or does not go away, repeated vomiting or nausea, convulsions or seizures, an inability to awaken from sleep, dilation of one or both pupils of the eyes, slurred speech, weakness or numbness in the extremities, loss of coordination, and increased confusion, restlessness, or agitation
What are the overall goals of TBI tx? Short term goals?
Overall: - Reduce Morbidity and Mortality - Optimize long term functional outcomes Short term: - Establish ABC’s - Maintain oxygen balance - Prevent secondary neuronal injury - Prevention/Treatment of associated medical complications
What are the initial resuscitation goals of TBI?
- SBP >90 mmHg
2. PaCO2 < 35 mmHg
What are the postresuscitation goals of TBI?
- Improved outcomes with cerebral perfusion pressure CPP >60 mm Hg and ICP <20 mm Hg (CPP =MAP–ICP)
- Maintain oxygen saturation >90 mmHg
- Seizure Prevention
- Maintain fluid/electrolyte homeostasis
- Stress ulcer prophylaxis
- Prevent thromboembolitic event
- Maintain normothermia
- Monitor vital signs and neurologic status
What are the strategies used to decrease ICP?
- Osmotic Agents/Diuretics - remove fluid from brain to vascular system (Mannitol, Loop diuretics, Hypertonic Sodium Chloride - increase sugar in blood concentration)
- Sedation - decreases brain activity (Pentobarbital, Propofol, Fentanyl, Morphine) - pt may not be fully conscious or aware for PT
- Neuromuscular Blockers- decreases brain activity
(Vecuronium, Pancuronium, Cisatracurium) - may cause pt to be weaker
What are the acute tx options for TBIs?
- Strategies to decrease Intracranial Pressure
- Strategies to increase MAP
- Seizure Medications for TBI
What are the strategies used to increase mean arterial pressure?
- Maximize fluid status with Normal Saline and Lactated Ringers- fluid stays in vascular system, not brain
- Vasopressors/inotropes may be used in shock and after fluid status is optimized (Dopamine, Dobutamine, Norepinephrine, Epinephrine, Phenylephrine)
- both aimed to maintain BP
What drugs are used to prevent seizures?
- Phenytoin
- Carbamazepine
- both decrease neurological activity
- can continue beyond 7 days if pt has seizure
MOA: Enhancement of sodium channel activation; Reducing current through T-type calcium channel; Enhancement of GABA activity; Antiglutamate Activity
ADRs:
- Initiation: N/V, Dizziness, Drowsiness
- Chronic therapy: peripheral neuropathy, osteomalacia, acne, mentally cloudy/dull feeling, gingival hyperplasia
- Severe/Life threatening: Hepatic Failure, Stevens-Johnson Syndrome (rash), Teratogenic (can cause birth defects)
Phenytoin
What drugs does phenytoin have drug interactions
“dirty” drug, many interactions particularly with anti-seizure, antidepressants, anticoagulants:
- Depakote (anticonvulsant)
- Carbamazepine (anticonvulsant)
- Fluoxetine (antidepressant) - increases PHT levels
- Warfarin (anticoagulant) - PHT increase or decrease INR
MOA: Enhancement of sodium channel activation; Reducing current through T-type calcium channel; Enhancement of GABA activity; Antiglutamate Activity
ADRs:
- Initiation: Nausea, Vomiting, Drowsiness, Dizziness, and Neutropenia
- Chronic Therapy: Hyponatremia, water retention, Osteomalacia, Anemia,
- Severe/Life Threatening: Liver toxicity, decrease in WBC and Neutrophils, Teratogenic
Carbamazepine
