ICL 10.9: Evaluation of the Unconscious Patient Flashcards
what is consciousness?
“the state of awareness of self and environment, and normal responsiveness to external stimulation and inner need”
what are the qualifications where you would consider someone as conscious?
consciousness is a state in which both of the following are preserved:
- ability to be aware of oneself and one’s environment
- ability to respond appropriately to environmental stimuli
what are the 5 levels of consciousness?
- awake/alert: fully attentive, aware and responsive
- sleepy: awake but appears sleepy with decreased attention and slow responses
- obtunded: asleep, wakes to verbal or light physical stimulation, falls back to sleep easily if stimulus stops
- stupor: deep sleep requires noxious and persistent stimulation to maintain arousal/participate in exam
- coma: eyes closed, unresponsive to external stimuli, with the exception of brainstem and spinal reflexes
what is the ascending reticular activating system?
ARAS is a complex poorly defined neural network that involves input &/or output with all of the following:
- brainstem reticular formation
- hypothalamus & forebrain
- thalamus
- cortical, cerebellar & spinal feedback
ARAS starts in the brainstem reticular formation and it’s located more in the upper brainstem so the upper 1/2 of the pons to the midbrain
it’s divided into 3 functional 4 neurochemical components
what are the 3 functional components of the ascending reticular activating system?
- efferents –> thalamus
- efferents –> hypothalamus and forebrain
- direct diffusion projections –> cortex
what are the 4 neurochemical divisions of the ascending reticular activating system?
there are key nuclei in the ARAS portion of the reticular formation that produce the main neurotransmitters of consciousness = Ach, serotonin, histamine and norepinephrine
what is the function of the hypothalamus in consciousness?
even though it’s considered that arousal starts in the ascending reticular formation, the arousal system includes initiation in the hypothalamus
so the lateral hypothalamus releases orexin 1 and 2 on the various nuclei in the ARAS pathway in the brainstem to stimulate the release of their respective NTs
what is the function of cortical, cerebellar and spinal feedback in relation to consciousness?
these are super important because think about how you wake up based on when you perceive light or how you don’t want to sleep when you smell smoke so there’s feedback from all the senses into the ARAS activation system
so there’s visual, auditory, smell, tactic feedback etc. to make sure we have the mechanisms to preserve our survival so we don’t sleep through important things
how do we localize impaired consciousness?
- bilateral cortex problems = ARAS pathway has diffuse output to the cortex so anything that diffusely effects the bilateral cortices can cause impaired consciousness –> usually these are toxibolic syndromes, hyper/hypoglycemia, global ischemia, etc.
- bilateral thalamus problems = most pathways go through the thalamus so each thalamus communicates its arousal pathways to the ipsilateral cortex so if you knock out both thalami you can impair consciousness
- contralateral cortex and thalamus = if you were to have a lesion that effects an entire cortex and the contralateral thalamus, you can also impair consciousness that way
so when you’re trying to see what’s causing lost consciousness, you need to try and localize it to the brainstem, thalamus or the cortex?
what are the 6 disorders of consciousness?
- locked-in state
- catatonia
- akinetic Mutism
- minimally conscious State
- unresponsive wakefulness syndrome
- coma
what causes locked-in syndrome?
classically seen in basilar strokes
but can also be seen in:
1. MS
- infection
- tumor
- hemorrhage
- trauma
what is locked-in syndrome?
aka cerebromedullospinal disconnection OR de-efferented state
it’s where the anterior pons and midbrain are effected usually due to a basilar stroke
the reticular formation and dorsal midbrain are spared though!
what are the signs of locked-in syndrome?
because the dorsal motor nuclei are spared that means the oculomotor nerve is spared, they still have vertical eye movements, and can still blink – the reticular activating tracts and sensory tracts are also still in tact!
what’s effected is basically all of their motor outputs
what are the 3 forms of locked-in syndrome?
all of these forms include full consciousness, sensation, emotional and startle responses so they’re cognitively still there
- pure = spares only vertical eye movements & blinking – so this is how a lot of them communicate
- incomplete = wide range of spared motor function depending on how extensive the stroke or infection was
- total = no spared function, not even eye movements and blinking – in this case it’s really hard to differentiate them from someone who is comatose
how do you differentiate between the locked in state and a comatose patient?
many of these patients initially present with impaired or loss of consciousness so that’s why it’s so important to test the occulocephalic reflex when examining an unconscious patient
so most physicians do the dolls eye test where they move the head side to side to make sure the eyes stay on the target but you also need to move the head up and down and make sure it stays on the target as well so you don’t miss any vertical eye movements before they’re awake and able to blink/move their eyes up and down
this might be the only thing that differentiates them from a comatose patient!!! a locked-in syndrome patient will have spared vertical eye movements
some patients actually feel that they have a reasonable quality of life in the locked in state because they have power chairs and lift systems and are able to communicate with their family and recognize them – this is what really differentiates the patients from coma because some feel that the are still in a meaningful state of life
what is catatonia?
a state in which a person appears unresponsive or unconscious
it simulates akinetic mutism, stupor or light coma
it’s often associated with psychiatric disorders, severe depression etc.
what will be seen on a PE of a catatonic patient?
- brainstem reflexes intact
- oculocephalic testing consistent with awake state = eyes move/track with the head
- resistance to eye opening
- waxy flexibility = if you position their limb in a certain way they’ll maintain it for a long time
- catalepsy = hold uncomfortable postures for a long time
- adventitious movements like repetitive motor mannerisms or choreiform jerking (consider EEG to make sure it’s not seizures)
what is akinetic mutism?
silent & inert – profound apathy
it’s a complete lack of spontaneous speech or movement due to a lack of motivation or drive. Patients are fully aware and visual tracking is preserved
patients are conscious, aware of their surroundings and depending on the localization can register and retain what happens during time in that state
what part of the brain is effected with akinetic mutism?
localization can be due to injury to the midbrain, anterior thalamus or uni-/bilateral medial frontal lobe lesions
usually associated with diminished dopamine pathways
we see a lot of this with ACA stroke patients where nurses will say they stopped following commands or they can’t get them to do anything – it’s not that the patient isn’t capable, it’s that they don’t have the motivation to do it
what is a minimally conscious state?
it’s a spectrum of states! these people can be anywhere from being comatose to a akinetic mute state
it can be transitional; like people coming out of a coma can go through this spectrum before being totally awake –> or they can get stuck along this spectrum at various severities of impaired consciousness
this is the most important loss of consciousness condition to be aware of because with every day there’s improvements in the patient so you need to look at the subtle changes to be able to identify progression along the different stages
how can you identify if someone is in a minimally conscious state?
with every day there’s improvements in the patient so you need to look at the subtle changes to be able to identify progression along the different stages
EYES
dysconjugate –> roving –> midline –> fixation –> tracking
MOTOR
flaccid –> posturing –> withdrawal –> localize –> following
what is the unresponsive wakefulness syndrome?
a return of arousal without the return of awareness following a coma –> this is basically what happens if you never make it into a minimally conscious state –> so coma patients will eventually die from medical complications or they’ll transition into an UWS
a person in a vegetative state may open their eyes, wake up and fall asleep at regular intervals and have basic reflexes, such as blinking when they’re startled by a loud noise, or withdrawing their hand when it’s squeezed hard – they’re also able to regulate their heartbeat and breathing without assistance
however, a person in a vegetative state doesn’t show any meaningful responses, such as following an object with their eyes or responding to voices. They also show no signs of experiencing emotions nor of cognitive function.
UWS causes the brain to halt the ability to create thoughts, experience sensation, and remember past events. Patients in a vegetative state are awake, but show no signs of awareness
this is what was previously known as a vegetative state and it’s considered persistent if it goes on for more than 3 months –> with traumatic brain injury it’s considered persist UWS if it persists for more than a year and this is because with traumatic brain injury there’s a lot of axonal damage that could potentially remyelinate over the year so you have to wait before giving them the diagnosis of persistent UWS
what is the clinical presentation of someone in an unresponsive wakefulness syndrome?
from a cognitive standpoint, the patient remains unresponsive and mostly unconscious and does not appear to have awareness of self, environment or needs
eyes might open to pain; may progress to spontaneous opening or a diurnal pattern – there might be intermittent blinking or brief fixation/tracking of faces and objects but it’s never consistent and it doesn’t progress into anything more
from a motor perspective they might swallow spontaneously, grind their teeth, front or moan – they can also assume some primitive postures and reflexes of the limb like cortical thumbing that babies do
what causes an unresponsive wakefulness state?
- diffuse cortical injury like from a cardiac arrest
- diffuse subcortical injury like with diffuse axonal injury from a traumatic brain injury
- thalamic injury like from influenza
what is a coma?
eyes closed, unresponsive to external stimuli, with the exception of brainstem and spinal reflexes
what are the levels of coma?
you can classify a coma via:
- quantitatively – scores: GCS & FOUR
- qualitatively – exam features
- electrophysiologically – variety of EEG patterns in comatose individuals
what is the Glasgow coma scale? (GCS)
it’s a scale that assesses the level of consciousness of a patient
for adults it’s broken down by eye opening response, verbal response and motor movement
the lowest score you can get is a 3 and that means even to noxious stimuli there’s no response
the highest you can get is a 15 which means your eyes open spontaneously, you’re oriented and conversing, and can obey motor commands
the middle is an 9; less than 8 is considered comatose –> if you open your eyes to painful stimuli, make incomprehensible sounds or have an abnormal posture that’s no longer comatose; the moment you start to withdraw from pain that’s a response to stimuli and the person would no longer be considered comatose!
what is the problem with the GCS coma scale?
in intubated patients it’s not very accurate
how are you going to get a verbal response with a trach tube??
you can modify the GCS but it gets really confusing because people use it differently so instead use the FOUR score
the FOUR score means you have the same eye and motor responses but it also takes into account EOM and brainstem reflexes and breathing patterns and this score is better at predicting outcome in intubated patients than the GCS
what is brain death?
Legal definition of death based on a clinical diagnosis
it means cessation of all brain AND brainstem function
Unified Determination of Death Act (UDDA) – 1980s
what are the components of claiming someone is braindead? Like what are the requirements to say someone is official braindead?
- evidence of an irreversible causative lesion
- rule out any potential confounders like metabolic conditions so make sure toxicology, pH, electrolytes, endocrine, temperature are in the normal range
- neurological exam consistent with brain death
- apnea test to confirm lack of respiratory effort despite significant hypercapnia (excessive CO2)
- ancillary testing if either the neurological exam or apnea test cannot be done
what are the 3 parts of a brain death exam?
- level of consciousness
- brainstem reflexes assessment
- apnea test
how do you assess the level of consciousness during a brain death exam?
- response to presence
- response to verbal
- response to pain
make sure you uncover your patients to make sure you can see any reflexes or movements that are happening
how do you assess the brainstem reflexes during a brain death exam?
- blink to threat (CN 2/3)
- pupillary light reflex (CN 2/3)
- corneal reflex (CN 5/7)
- oculocephalic vertical & horizontal (CN 3, 4, 6, 8 *C-spine)
- cold caloric (tympanic membrane)
- gag (CN 9/10)
- cough (CN 10/10)
how do you assess apnea during a brain death exam?
- get a baseline ABG
- apneic oxygenation 8-10 mins
- look for chest rise
- follow up ABG-PaCO2 > 60 or ⇡20
so provide oxygen but don’t let ventilator run and without ventilation CO2 will rise and once it gets over 60 and there’s no initiation of breath, that would confirm a positive apnea test
what are the ancillary tests you can do if the other components of a brain death exam can’t be done?
- EEG
- nuclear medicine perfusion test
- ultrasound
what results will you see in a nuclear medicine perfusion test of a braindead patient?
send radionuclei tracer through the blood stream and what you’ll see is the external carotid branches will fill so the nose will look black on the image but the skull will be white meaning that because the brain is dead it’s no longer recruiting perfusion (sagittal sinus will still fill though because the scalp drains into it)
the pituitary gland will also light up because it has collateral from the external carotid circulation so that’s doesn’t mean anything either
what results will you see in an EEG of a braindead patient?
you’re checking for electrocerebral silence which is the flatline equivalent of an EKG
what results will you see in an ultrasound of a braindead patient?
you ultrasound the middle cerebral artery and you can see a specific pattern that’s consistent with no blood being passed through it to the brain
when can’t you check tone and reflexes?
after the patient has been intubated and sedated!
what part of the brain does acute apnea localize to?
this is associated with Cushing’s triad that’s seen in tonsillar herniation due to medulla compression!
what part of the brain does Biot’s breathing localize to?
Biot’s is irregular cluster breathing
it localizes to the pons
what part of the brain does agonal breathing localize to?
medulla
it’s like someone taking one long laborious breath like once a minute; like imagine what you think of when someone is about to die and is taking those slow breaths
what part of the brain does hyperpnea localize to?
thalamic and midbrain lesion
what part of the brain does bradypnea localize to?
medulla
what part of the brain does Cheryne-Stokes breathing localize to?
forebrain or metabolic issues like CHF
it’s a medullary on/off regulation in response to CO2 levels
when there’s a delay in blood flow from the heart to the carotid bodies and the chemoreceptors ramp up until you blow off so much CO2 from the delayed feedback that you go apnic and then CO2 builds up and you ramp up again
so Cheyne Stokes is very rhythmic and sinusoidal
slide 33
what part of the brain does apneustic breathing localize to?
pons
looks like a slanted zig-zag line….this signify the force of the breath like sucking in and holding it in then quickly breathing out
what does Kussmaul breathing signify?
acidosis
zig zag line because patients breath in deep and then forcefully exhale
what does air trapping signify?
COPD
what does a lot of sighing indicate?
medulla injury
56-year-old patient who was found unresponsive in his room at the start of shift by his nurse. He was last seen well at last-night shift check.
VS: 115 (sinus) 160/95 / 26 (tachypnea) / O2Sat 100% / AF
He grimaces and groans to sternal rub and withdraws all 4 extremities symmetrically to peripheral pain. His pupil are 4 mm and briskly reactive. The remainder of his CN exam is intact. He does not follow any commands. He is hyporeflexic, mute Babinski and normal tone
He is well perfused, skin is warm and he is diaphoretic. Breath and heart sounds are normal. Pulses are thready
work through this: do localization, general exam, history, history, workup and differential
localization: there’s no CN abnormalities, you can’t really localize so it’s non-focal
general exam: hypertensive and tachycardic and are diaphoretic
history: acute
workup: do a metabolic workup but also make sure you’re not missing something wrong with the thalamus higher up past the brainstem
what you end up finding is that the patient has a glucose of 40 so they’re hypoglycemic
maybe just go look at slide 35
27-year-old woman brought to ED with history of severe HA/emesis worsening x 4 hours. On arrival is she unresponsive and was intubated for airway protection.
VS: 97 (NSR) / 170/100 / 35 (hyperpnea) / O2Sat 100% / AF
She does not follow any commands, has decorticate posturing & bilateral grimace to pain. Her pupils are 6 mm, unreactive. Vertical EOMI, loss of abduction bilaterally. Remainder of brainstem reflexes intact. She is hypereflexic, with +Babinski and rigid tone
Crackles over anterior lung fields bilaterally, otherwise unremarkable general exam
work through this: do localization, general exam, history, history, workup and differential
decorticate posturing = red nucleus in the midbrain
pupils are dilated and unreactive = CN 3, midbrain
vertical eye movements intact but abduction is impaired = CN 6
everything else is fine except some upper motor neuron signs
so mostly midbrain problems other than CN 6 which was probably stretched in this case instead of being directly compressed
probably an anterior lesion since only CN 6 was effected, CN 7 was fine because there was no facial weakness which is more dorsally located and also since 7 wasn’t effected it supports even more that CN 6 was just stretched instead of something effecting the whole pons
pulmonary edema in a young patient isn’t common….so some differentials would be cerebral venous sinus thrombosis, SAH with hydrocephalus, tumor with hemorrhage, bacterial meningitis
but then you find out she’s on oral contraceptives and smokes so high clotting risk! she has a superior sagittal sinus thrombus which you see in the CT – her brain is super swollen which pushes down on CN 6
