Trauma / ICU Flashcards
Types of Herniation (4)
High-output Heart failure + increased head circumference in neonate = what and why?
what do you do about it?
- Vein of galen malformation (venous hypertension + compression of aqueduct of sylivis)
- Cardiac sx = large left-to-right shunting through cerebral AV fistula
- Embolization of cerebral vein
Typical threshold for ICP that can lead to concern and why
at > 20 mmHg, CSF is shiften to spinal subarachnoid space
Equations:
Mean aterial pressure
Central perfusion pressure
Cerebral blood flow
MAP= diastolic BP + 1/3 (SBP-DBP)
CPP = MAP - ICP
CBF = CPP / CVR
What is P1, P2, and P3?
P1 = Percussion wave (represents arterial pulsation)
P2 = tidal wave (represents intracranial compliance)
P3 = dicrotic wave (represents aortic valve closure)
What does this signify?
P2 > P1
decreased intracranial compliance
Trauma patient is unable to move eyes up.
What is this called?
what does it signify?
Perinaud’s phenomenon
injury to superior calliculus
Patient with signs of uncal herniation also develops ipsilateral weakness
What is this called?
what causes this?
name another possible finding
Kernahan’s notch phenomenon:
False-localizing sign due to compression of contralateral cerebral peduncle to tentoral edge
can also rarely have IL CN III weakness
Herniation syndromes:
- Contralateral leg weakness
- pupillary dilation
- Rostrocaudal deterioration
- Duret’s hemorrhages
- diabetes insipidis
- bilateral occpitial infarction
- Decreased LOC + cardiac / respiratory abnormalities
- CL leg weakness = subfalcine herniation (due to compression of ACA)
- Pupillary dilation = Uncal herniation (due to compression of CN III)
- Central / diencephalic herniation
- Rostracaudal deterioration
- duret’s hemorrhages (due to stretching/shearing of basilar perforators)
- DI (due to pituitary stalk shearing)
- Bilateral occipital infarcts (due to PCA compression)
- tonsillar herniation (sx due to compression of lower brain stem and upper cervical cord)
What herniation syndrome does this make you think of?
Duret’s hemorrhages
Central (diencephalic) herniation
Factors that increase risk of herniation in stroke patients
(5)
- hypodensity in > 50% of MCA territory
- early nausea / vomiting
- NIH scale > 20 (left hemisphere)
- NIH scale > 15 (right hemisphere)
- MCA + either ACA or PCA involvement
Conservative (i.e. non medical, non surgical) management for increased ICP
(6)
- Head of bed > 30 degrees
- Head midline
- Pain / Temperature control
- Goal metrics
- ICP <20 mm Hg
- CPP > 60 mm HG
- hyperventilation (goal pCO2 30-35 mmHg)
lab value contraindicating Mannitol for increased ICP
osmolar gap >10
Osmolar gap = Measured osmolality (MO) - calculated osmolality (CO)
CO = (2xNa + (BUN/2.8) + (Glucose / 18) + (ethanol / 3.7))
Glasgow coma scale and threshold for Mild, moderate, and severe injury
Mild = 13-15
Moderate = 9-12
Severe =/<8
What type of injury does this resulf from
DAI of corpus callosum
acceleration / decelleration injury
Return to play guidelines for concussion
Grade 1: confusion <15 minutes
Grade 2: confusion > 15 minutes
Grade 3: ANY LoC
Cauda Equina syndrome versus conus medullaris syndrome
Radicular pain:
motor Weakness:
Sensory Distribution:
Reflexes:
Bladder symptoms:
Impotence:
Treatment for bradycardia in patient with acute spinal cord compression
Atropine
Eye findings in TBI and their signifiers:
Pupils mid-position and fixed (2)
Pupils fixed and dilated (3)
Pinpoint pupils (3)
Gaze preference away from paretic side
Gaze preferene toward paretic side
Skew deviation
ocular bobbing
- Mid-position and fixed
- sympathetic / parasympathetic disruption (midbrain lesion)
- Drug induced (atropine)
- Fixed and dilated
- extensive medullary lesion
- hypothermia
- barbituates
- Pinpoint
- sympathetic dysruption but preserved parasympathetic
- pons or higher lesion (disruption of dorsal long fasciculus)
- narcotics
- Gaze AWAY FROM paretic side
- pontine / thalamic lesion
- (oculocephalic maneuver WILL NOT overcome preference)
- Gaze TOWARD paretic side
- frontal cortical lesion
- Oculocephalic WILL overcome preference
- Skew deviation
- midbrain
- ocular bobbing
- pons
Brain lesions and relative respiratory / motor responses
TBI patient with this imaging finding
Cortical Ribboning (hypoxia)
TBI patient with this imaging finding
Basal ganglia injury (hypoxia)
TBI patient with this imaging finding
Border zone injury (hypoxia)
1/2
TBI patient with this imaging finding
Border zone injury (hypoxia)
2/2
Predictors of poor outcome in TBI
Day 1 (2) Day 1-3 (2) Day 3 (2)
- Day 1
- Myoclonus
- Status epilepticus
- Day 1-3
- absent N20 on SSEP
- Neuron-specific enolase (NSE) > 33 ug/L
- Day 3
- absent pupil / corneal reflexes
- Extensor or absent motor responses
before initiating brain death exam, must unsure the following (7)
- Irreversible coma with known cause
- neuroimaging explains coma
- Absence of any CNS suppression (barbituates must be <10 ug/mL)
- absence of severe acit-base, electrolyte, or endocrine abnormality
- Normothermia
- normotension (SBP >100 mmHg)
- NO spontaneous respirations
Steps of brain-death exam
- Exam (8)
- Brain death criteria met if (2)
(after determining if patient meets criteria to start exam)
- Exam
- pupils (midsize or dilated), and non-reactive to light
- (-) corneal reflex
- (-) oculocephalic reflex (if C-spine isn’t injured)
- (-) doll’s eye
- (-) facial movement to noxious stimuli
- (-) gag
- (-) cough
- (-) motor response to noxious stim in all extremities
- Spinally mediated reflexes don’t prevent diagnosis of brain death)
- Ventilator adjusted to provide normal hypercarbia (paCO2 35-45 mmHg)
- Pre-oxygenate patient with 100% fiO2 for >10 minutes (goal Pa O2 >200 mmHg)
- Disconnect ventilator but provide O2 via suction catheter at level of carina
- Brain death met if:
- No spontaneous respirations
- ABG drawn at 8-10 minutes >60 mmHg or 20 mmHg rise from normal baseline
When to abort Brain death exam (3)
- hypotension (SBP decreases below 90 mmHg)
- O2 sats <85% for >30 seconds (may retry after reoxygenation)
- Spontaneous respirations are seen
Ancillary test to determine brain death and expected results (5)
- SSEP
- Bilateral anbsence of N20-P22 response with median nerve stim
- EEG
- No electrical activity (EEG must be at least 30 minutes)
- Cerebral angiography
- No intracerebral filling at level of carotid bifurcation or CoW
- Transcranial doppler (TCD)
- small systolic peaks in early systole without diastolic flow or reverberating flow
- Nuclear studies
- no uptake of isotope in brain parenchyma (“hollow skull phenomenon”)
MRI changes during bleed and time frame for each
Hyperacute:
Acute:
Early Subacute:
Late subacute:
Chronic:
“I bleed, I die, bleed die, bleed bleed, Die Die”
Hyperacute (<24 hours)
- T1 Isointense, T2 Bright
Acute (1-3 days)
- T1 isointense, T2 Dark
Early subacute (3-7 days)
- T1 Bright, T2 Dark
Subacute (7-14 days)
- T1 Bright, T2 bright
Chronic (>14 days)
- T1 dark, T2 dark
Patient presents with hypertensive Emergency
what is the goal reduction in BP?
How does this change if the patient has had a stroke?
Goal reduction
- 10-20% reduction in first hour
- 5-15% reduction over next 23 hours
Stroke:
- Patients shouldn’t have reduciton in BP for 3 days unless
- they are receiving tPA and have BP > 185/100
- BP >220/120
patient is admitted to ICU with subarachnoid hemorrhage
What is the leading cause of death?
what are two factors that increase risk?
Vasospasm (3-4 days after hemorrhage)
Increase risk:
Severity of bleed
closeness to intracranial vessels
Patient presents with recurrent headaches following TBI which is worse when sitting upward
What is the best test to determine cause?
MRI with contrast
(looking for pachymeningial enhancement suggestive of CSF leak)
Features of LeFort Fractures
Common structure broken
Unique features of
Type I
Type II
type III
Common structure: Pterygoid process
- Type I:
- lateral margin of nasal fossa
- “floating Palate”
- Type II
- Inferior orbital rim
- “floating maxilla”
- Type III
- Zygomatic Arch
- “floating face”
Normal Cerebral Perfusion Pressure (CPP)
80 mmHg
