Clinical- 3 Flashcards
What is a coma?
A state of unconsciousness where the pt doesnt respond to environmental stimuli and cannot be awaken
Where in the brainstem are the disturbances to cause the coma?
reticular activating system ABOVE the midpons or of both cerebral hemispheres
What are the 5 defining characteristics of comas?
- eyes closed
- no speaking
- cant move
- cant respond to verbal stimuli
- cannot respond to pain
What is the first thing u should do when treating a coma?
establish ABCs
What is the next procedure to do for Dx in a coma?
blood labs for CBC, hepatic/renal panels, serum glucose/electroltes, PT/PTT
What 2 easy things should you rule out (which are easily correctible) in the cause of the coma?
hypoglycemia and opiate OD
How can u evaluate the metabolic cause of the coma?
blood gas and pH studies
What happens if the coma pt has szrs?
treat it
Why do u give 25g of dextrose?
tosee if its a hypoglycemic cause
Why do u give 100mg of thiamine for the comapt?
prevents dextrose precipitation and prevents exasterbation of Wenicke’s encephalopathy
Why do u gie 0.4-1.2mg naloxone for the come pt?
to see if its an opiate OD
Why do u NOT give flumenazil for the coma pt?
cuz it can precipitate status epilepticus
What causes a SUDDEN onset of coma?
vascular origin, esp brainstem stroke or subarachnoid hemorrhage
What is the cause of rapid progression from hemispheric signs to a coma?
intracerrebral hemorrhage
What are some cuases for a slower/longer progresison for the coma?
tumors, abscesses, or chronic subdural hematomas
What is the cause for a coma that follows a confusional state or agitated delirium w/o lateralizing signs or Sx?
metabolic
What are raccoon eyes?
periorbital ecchymoses
What is battle sign?
swelling or bruising over the mastoid bone behind the ear
What is hemotympanum?
blood behind the tympanic membrane
What is CSF rhinorrhea/otorrhea?
CSF coming out of nose or ear
Coon eyes, battle sign, hemotympanium, or CSF rhinorrhea/otorrhea are all signs of what?
basilar skull Fx from head trauma
What are the early diencephalic findings of the coma pt?
small pupils (<2mm), reactive, reflex intact, motor response is purposeful and asymmetric
What ar ethe late diencepalic findings of coma?
similiar to early but pain causes decorticate posturing (lol neuroanatomy)
What are the sign for midbrain coma?
pupils fixed and midsized (5mm), reflex in adducion is impaired, decerebrate (eeee)
What are the signs of pons/medulla involvement in comas?
fixed, midsized pupils, loss of abduction and adduction, flaccid
When do u get decorticate positioning?
. Decorticate posturing is indicative of lesions involving the thalamus either directly or from large hemispheric masses above it.
When do u get decerebreate posturing?
This posture occurs when midbrain function is compromised and implies a more severe brain dysfunction than decorticate posturing.
What are the Sx of an uncal herniatioN?
The medial portion of the temporal lobe (uncus) is forced across the cerebellar tentorium and on to the rostral brainstem causing ipsilateral pupillary dilation and impaired adduction of the eye (uncal syndrome) before losing consciousness.
What happen sin cheyne-stokes respirations?
there is alteration between apnea and hypernea
True or False: cheyne-stokes and central hyperventilation are not useful in localizing the cause of coma.
True. They’re also seen with metabolic disturbacnes and structural lesions
Where is the lesion to cause ataxic and gasping ventialtions?
pontomedulla
What is the classic finding for metabolic encephalopathy?
the presence of reactive pupil even with impaired brainstem function.
What are the 2 classes of drugs to treat cerebral edema?
glucocorticoids and osmotic diuretic agents.
The drugs dexamethasone, prednisone, methylprednisone, and hydrocortisone belong to which class?
Glucocorticoids
The drugs mannitol and hypertonic saline belong to which class?
Osmotic diuretic agents.
Subdural hematoma (SH)- cause
trauma
SH- pathogenesis
shearing of bridging veins
SH- clinical findings
headache and altered consciousness with comes and goes. CL hemiparesiss, IL miosis
SH- Tx
surgical evaculation
Epidural Hematoma (EH)- cause
trauma to lateral skull
EH- pathogensis
tearing of MMA
EH- clinical findings
heaedache, vomiting, obtundation, srs, and focal signs
EH- tx
prompt surgical evacuation
Intercerebral hemorrhage (IH)- cause
chronic HTN
IH- pathogenesis
transentorial heriation –> nuchal rigidity, eyes deviate toward side of hemorrhage and away from hemiparetic side.
IH clinical findings
headache, N/V, hemiparesis
IH- Tx
limited, as these are usually brief
Brain abscess (BA)- cause
metastasis of infection > direct infection > unknown source of infection > infection with recent or remote head trauma > infection assocaited with cyanotic congential heart disease
BA- clinical findings
headache, focal signs, hyperthermia, ↑ WBC count
BA- Tx
antibiotics and/or surgery (if there is a big ass mass)
Which pts typically have pontine hemorrhages?
HTN pts
What is the hallmark of pontine hemorrhages?
apoplectic onset
Which artery is screwed up in pontine hemorrhages?
basilar a.
Sx of pontine hemorrhages?
ocular bobbing (quick downward movement, slow return to normal position), pinpoint pupils, and loss of lateral eye movements
Global cerebral ischemia (GCI)- cause
Cardiac arrest
GCI- pathogenesis
encephalopathy that leads to coma
GCI- clinical Sx
rapid pupil dilation, opisthotonic posture (hyperextension and spasticity)
GCI- Tx
prompt re-establishment of cerebral perfusion
GCI- prognosis
good if u return blood quickly. bad if u cant get pupillary reactivity within 1 day or consciousness within 4 days
The intoxication of which drug is the most common cause of coma?
Sedative-hypnotic drugs
btw middle-aged women LOVE trying to commit suicide by ODing on this. Classic 2 bottles of wine + bottle of sedatives = 5150 UP IN HERE.
What the 2 classes of drugs that are sedative-hypnotic drugs?
barbituates and benzos
What is the progression for sedative-hypnotic drug comas?
drug intoxication –> nystagmus in all directions + dysarthria + ataxia –> coma –> presents with UMN lesion-like Sx
What are the Sx of sedative-hypnotic drug comas?
absence of extraocular movements with preserved pupillary reflex
What is the Tx to sedative-hyponotic drug comas?
Be supportive and maintain adequate ventilation and circulation. Dialysis may be used to reduce the drug intoxication.
What are the Sx to alcohol-induced comas?
produces a similar syndrome without nystagmus during wakefulness, impairment of lateral eye movements, or progression to coma.
What are the Sx to opiate-induced comas?
Characterized by pupillary constriction similar to miotic eye drops, pontine hemorrhage, Argyll Robertson pupils, and organophosphate poisoning
How can you Dx opiate OD’s?
Naloxone
What are the complications to hepatic encephalopathy?
Somnolence, delirium, and ultimately coma due to severe liver disease
What are the Sx to hepatic encephalopathy?
Patients will present with increased muscle tone, hyperreflexia, alternating hemiparesis, and decorticate or decereberate posturing
What causes hepatic encephalopathy?
inability to detoxify ammonia
What happens in persistent vegetitative state?
Happens when you eat too much salad. Patients who go into a coma because of cerebral hypoxia or ischemia, will sometimes “wake up.” These patients will show an ability to spontaneously open their eyes but they cannot comprehend or produce language and cannot produce purposeful movements. That are in what is called a minimally conscious state where they are “awake but not aware.”
Where is the damage to cause locked-in syndrome?
damage to the brainstem below the midpons (the reticular formation above this area is responsible for consciousness)
So if I say: not awake and not aware. What am I?
hepatic encephalopathy
So if I say: awake and aware. What am I?
locked-in syndrome
So if I say: awake and not awake. What am I?
persistent vegitative state
What are the 4 factors to determine brain death?
1) Patient must be unresponsive to sensory input such as pain and speech.
2) Brainstem reflexes are absent, attempts to elicit eye movements passively via oculocephalic (doll’s head) and vestibuloocular (cold caloric) maneuvers are unsuccessful. Respiratory responses are also absent, when PCO2 is raised to 60mmHg, the patient does not respond.
3) The brain dysfunction is irreversible. In order to determine this, the cause of coma must be known.
4) Time is also a factor: 6 hours with a confirmatory isoelectric (flat) EEG, 12 hours without a confirmatory isoelectric EEG, and 24 hours for anoxic brain injury without a confirmatory isoelectric EEG.
