COMA Flashcards
what are the causes for coma?
drugs
poisoning - carbon monoxide , alcohol , tricyclics
hypoglycemia
hyperglycemic, hyperosmolar nonketotic coma (HONK)
hypoxia (COPD)
septicemia
hypothermia
myxoedema
addison crisis - deficiency in cortisol
hepatic (liver cirrhosis) and uremic encephalopathy
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neurological - trauma
meningitis
encephalitis - herpes simplex
tumor
stroke
subdural , subarachnoid
hypertensive encephalopathy
epilepsy : non convulsive status
post ictal state
what is the immediate management in coma ?
A-E approach
A
spinal injury and do not move spine
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B - ABG
BiPAP - considered if hypercapnia is believed to be the cause of the altered mental status
If COPD -then BiPAP may be trialed
If hypercapnia is the result of substance intoxication or neurological disease, BiPAP is contraindicated.
hypercapnia in this context is generally intubation
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C - Hypertension is more challenging than hypotension which can be managed with vasopressors:
- Some patients have posterior reversible encephalopathy syndrome (PRES) - hypertension is the cause of the coma - usually associated with a mean arterial pressure >140 mm
- If the blood pressure is profoundly elevated (e.g., mean arterial pressure >140 mm), then gentle reduction may be reasonable
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D
asses intubation if Glasgow coma scale is 8 or below
AVPU
check blood glucose - finger prick / blood analysis - if hypoglycemia - 200ml of 10% glucose IV
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full blood count
blood cultures
arrange urget CT scan of head
serum electrolyte test:
Hyponatremia, hyperkalemia,
hypocalcemia
Hypoglycemia
Random blood cortisol level
The sample should be drawn prior to hydrocortisone administration
100 mg, then (by continuous intravenous infusion) 200 mg every 24 hours, diluted in Glucose 5%
U and e
blood toxicology
brief history
Recent complaints—headache, fever, vertigo,
Recent medical history—sinusitis, otitis, neurosurgery, ENT procedure
diabetes, asthma, BP, epilepsy,
rug or toxin exposure
Any travel? - malaria
blood ethanol
toxin screen , drug levels
Suspect opioid intoxication primarily if the respiratory rate decreased
EEG may be indicated if there are reasons to consider nonconvulsive status epilepticus
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CT angiogram : if there is suspicion for an acute ischemic stroke
CT venogram should be considered if there is suspicion of venous sinus thrombosis
lumbar puncture:
Suspicion of meningitis or encephalitis (e.g., based on fever, leukocytosis).
PCR for both HSV and VZV.
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!!!!! always check the pupils every few mins !!!!!!!
contra for hydrocortisone ?
Congestive heart failure; diabetes mellitus (including a family history of);
diverticulitis;
epilepsy;
glaucoma (including a family history of or susceptibility to)
hypertension
what are the examinations which needs to be done ?
Signs of trauma—haematoma, , bruising,
blood in nose or ears,
fracture ‘step’ deformity of skull
anterior basilar skull fracture:
panda eyes / racoon eyes ( subcutaneous hematoma)
CSF rhinorrhea
Palsies of CN I, CN V, CN VI, CN VII, and/or CN VIII
Posterior basilar skull fracture :
CSF otorrhea - CSF from the external auditory meatus
Hemotympanum
Battle sign: subcutaneous hematoma behind the ear
Palsies of CN VI, CN VII, and/or CN VIII
Skin for needle marks
meningism
opisthotonos -meningitis
Pupils - size, reactivity, gaze - pin point for heroin
any foci of infection -abscesses, bites, middle ear infection
describe the glasgow coma scale
eye opening 1- none 2 - in response to pain 3 - in response to speech 4 - spontaneous
best verbal response 1 - none 2 - incomprehensible 3 - inappropriate speech 4 - confused 5 - orientated to time , place and person
motor response 1 - no response to PAIN 2 - extensor response to pain 3 - flexor response to pain 4 - withdrawing to pain 5 - moves to localised pain 6 - obeying command
9-12 moderate
13-15 - minor injury
what is AVPU ?
a - alert
v - responds to vocal stimuli
P - responds to pain
u - unresponsive
neurological examination in coma in terms of respiratory ?
respiratory pattern
cheyenne stokes =
alternating periods of deep breathing followed by apnea
Common causes include:
-advanced heart failure with poor cardiac output
Generation of this pattern requires intact brainstem respiratory reflexes
due to bilateral forebrain dysfunction or or bilateral thalamic injury due to
-stroke
-traumatic brain injuries,
-metabolic encephalopathy
stroke, raised intracranial , congestve HF , metabolic encephalopathy, pressure, pulmonary oedema, opioid toxicity, hyponatraemia or carbon monoxide poisoning
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apneustic breathing
rare pattern that involves end-inspiratory pauses.
suggests pontine dysfunction (especially pontine infarction due to basilar artery occlusion)
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tachypnea -response to respiratory acidosis
compensating metabolic acidosis
hypoxia - copd
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ataxic -
irregular breathing patterns
brainstem damage with grave prognosis
neurological examination in coma in terms of of pupil ?
eyes - ARAS pathology (ascending reticular activation system)
pupils - with pen light
normal direct and consensual reflexes - intact midbrain
bilateral mid-position, fixed pupils
Bilateral midbrain damage with loss of sympathetic and parasympathetic output.
Profound barbiturate coma.
Hypothermia
bilateral mid-position, reactive
excludes a lesion around the level of the midbrain (where CN2 and CN3 lie)
may be toxic/metabolic coma
Lesions in the dorsolateral upper-mid pons
Neuromuscular blocking drugs
bilateral fixed & dilated=
Bilateral midbrain damage causing loss of parasympathetic output from CN3.
Anticholinergic drugs at high dose - especially atropine).
Extremely deep metabolic coma - hypothermia, barbiturates, bupropion
bilateral dilated, reactive=
Anticholinergic drugs.
Withdrawal from alcohol or benzodiazepines.
Sympathomimetics (e.g., amphetamine, cocaine
Serotonin syndrome.
Generalized seizure
Unilateral dilated and fixed =
3rd nerve compression
Midbrain lesion affecting the CN3 nucleus.
Focal seizure.
bilateral Small, reactive = drugs (cholinergic agonists) or opioids
diencephalic lesion
bilateral pin point / pontine pupil =
extensive pontine hemorrhage
unilateral small pupil
Unilateral Horner’s syndrome - loss of sympathetic outflow, often due to large hemorrhage affecting the thalamus
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A persistently small pupil (miosis)
A notable difference in pupil size between the two eyes (anisocoria)
Little or delayed opening (dilation) of the affected pupil in dim light
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Horner’s syndrome ipsilateral lateral medulla or hypothalamus lesion,
Beware patients with false eyes or who use eye drops for glaucoma
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test the vestibulo-ocular reflex (VOR)
what are the spontaneous eye movements in coma ?
horizontal conjugation deviation
- stroke - eyes deviate ipsilateral to the cortical damage and contralateral to the limb paralysis
focal seizure - eyes deviate contralateral to lesion and ipsilateral to seizing limb
=^above cases eyes can cross the horizontal line^
horizontal gaze palsy -moving the eyes past the midline to the opposite side is very difficult
( https://www.youtube.com/watch?v=NAz_g3FDPjw )
pontine lesions that affect the horizontal gaze center and the 6th cranial nerve nucleus. Strokes are a common cause, resulting in loss of horizontal gaze ipsilateral to the lesion
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horizontal conjugate roving eye movements (ping-pong gaze)
holding one corner for 2-3secs
with maybe Cheyne-Stokes breathing
reveal normal function of midbrain and pons
indicates that the coma is due to bilateral cerebral hemispheric dysfunction (e.g., a toxic/metabolic coma)
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ocular bobbing or dipping
Bobbing (rapid down, slow up) suggests a pontine lesion (such as hemorrhage
Dipping (slow down, rapid up) localizes to bihemispheric dysfunction (e.g., anoxia or a metabolic disorder)
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nystagmus (especially if bidirectional, vertical or rotatory)
Cerebellar or brainstem lesion.
Intoxication (e.g., phencyclidine)
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upward gaze
Suggests bihemispheric damage - severe anoxic injury
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downward gaze
Thalamic injury (e.g., hemorrhage). Midbrain dysfunction (e.g., Parinaud syndrome). Bilateral hemispheric dysfunction (e.g., anoxic injury)
what are the oculocephalic (doll’s eyes) / vestibulo-ocular (cold calorics) reflexes
Rapid rotation of the head to one side normally elicits eye movement in the opposite direction to stabilise the image in the centre of the visual field.
this reflex manifests in comatose state because humans suppress it
the medial longitudinal fascicules is the crucial pathway for this reflex - and the pathway can be damaged through stroke
this reflex reflects the integrity of the brainstem , frontal cortex , supra and infra tentorial regions when a person is in comatose state
Both reflexes test a similar neural circuit involving cranial nerves 3, 6, and 8
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normal :
dolls eyes test- oculocephalic reflex
when you turn your head to the left you stimulate the labyrinthine on the left - stimulating the 6th nerve and the third nerve in the contralateral side (right side) so your eyes will go to the right side (lateral rectus and medial rectus)
If the oculocephalic reflex is absent, cold caloric testing can be used to provide a stronger stimulus
caloric test - vestibule-ocular reflex
used to test VOR by stimulating the vestibular system
the eardrum is checked
Electrodes are placed around the eyes and connected to a computer used to measure eye movement
the head of the bed inclined at a 30 degree angle (to properly align the semicircular canal)
POUR hot water to one side of the ear to stimulate the labyrinth however this may damage the tympanic membrane so avoided but it will illicit the eyes to move towards the warm water, and then move slowly back
or pour cold water - causes the eyes to move away from the direction of the cold water ( fast-phase nystagmus), and then move slowly back
If this is found, it suggests:
Functional coma (pseudocoma).
Akinetic mutism.
Less severe toxic/metabolic encephalopathies
what does a failed caloric test show ?
With cold caloric stimulation, isolated failure of the contralateral eye to adduct suggests a lesion in the medial longitudinal fasciculus in the pons. This can also occur with a CN3 palsy, but CN3 palsy would also cause pupillary dilation
Isolated failure of an eye to abduct (CN6 palsy) may reflect damage to the abducens nucleus in the pons
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symmetrically abnormal vestibulo-ocular reflexes
This generally indicates brainstem pathology.
Toxic/metabolic coma can abolish vestibulo-ocular reflexes (e.g., phenytoin, tricyclic antidepressants, or sedatives)
path-physio of cough reflex in intubated patients?
cough reflex involves the vagus nerve (CN10, near the medulla). This reflex will be preserved in most coma states, it is the most durable reflexes, which is generally preserved even in severe brain injury
eliciting the cough reflex requires an intubated patient, in whom endobronchial stimulation can be applied by suctioning the endotracheal tube
Causes of an absent cough reflex include:
Damage to the medulla (e.g., tonsillar herniation, brain death).
Extremely profound toxic/metabolic coma (e.g., barbiturate or baclofen overdose).
Neuromuscular paralysis (e.g., lingering effects of rocuronium used for intubation).
always consider the possibility of a lingering neuromuscular paralytic agent
muscle tone examination in coma ?
One way to test for hemiplegia in coma is to raise both arms together and compare how they fall under gravity. If one descends fast, like a lead weight, but the other descends more gracefully, you have found a valuable focal sign of cortical dys- function.
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increased motor tone or rigidity:
Intoxication (e.g., serotonin syndrome, neuroleptic malignant syndrome, malignant hyperthermia).
Seizure.
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hyperreflexia or clonus:
Suggests serotonin syndrome,
neuroleptic malignant syndrome,
malignant hyperthermia.
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multifocal myoclonus (diffuse, random, asynchronous jerking of various muscle groups)
Generally, suggests a toxic/metabolic etiology.
This should be differentiated from diffuse, synchronous or rhythmic movements – that may suggest anoxic brain injury, nonconvulsive status epilepticus (NCSE), lithium intoxication, cephalosporin intoxication, or pesticides
motor responses to pain in coma ?
How to examine:
Apply painful stimuli to four extremities and bilateral face (either supraorbital ridge or temporomandibular joints).
Observe for motor response
Observe for motor response (e.g., purposeful avoidance of the painful stimuli, a “localizing” response to pain)
Asymmetric responses suggest a focal lesion
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when pain is applied
Decorticate posture : abnormal posturing in which a person is stiff with bent arms (flexed) and adducted , clenched fists, and legs held out straight and internally rotated with the feet plantar flexed.
bilateral damage to diencephalon - upper midbrain
======= decerebrate - worst between the two arms extended and adducted forearm is pronated fist is clenched legs are extended and plantar is flexed head and neck arched backward
bilateral damage to upper midbrain
associated with downward herniation or compression of the brainstem by posterior fossa lesions
what are the common coma syndromes ?
uncal herniation
Ipsilateral blown pupil:
Initially, the pupil is simply dilated.
With progression, oculomotor paralysis occurs (causing the eye to be fixed in a down-and-out orientation).
Contralateral hemiparesis due to compression of the cerebral pedicle
Ipsilateral weakness can occur if lateral displacement compresses the opposite cerebral peduncle (a “false localizing sign”).
Hemiparesis may be accompanied by a positive Babinski’s sign.
Impaired consciousness is almost always present by the time the pupil is fixed and dilated
If untreated, this may eventually compress the midbrain (e.g., causing bilateral fixed & dilated pupils, with decorticate or decerebrate posturing).
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downward central herniation (a.k.a. downward transtentorial herniation)
Miotic (small) pupils are initially a prominent sign.
⚠️ Initially, this may resemble an intoxication causing small pupils (e.g., cholinergic agonists, opioids, clonidine, ACE-inhibitors).
There may initially be conjugate roving eye movements, simulating a toxic/metabolic coma.
With progression of herniation:
Midbrain dysfunction emerges: pupils may become fixed & mid-position.
Vestibulo-ocular reflexes become abnormal.
Pathological breathing patterns may emerge (including Cheyne-Stokes breathing, irregular ataxic breathing, or neurogenic hyperventilation).
Decorticate and later decerebrate posturing occur, with bilateral extensor Babinski reflexes.
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brainstem displacement from a cerebellar mass:
ranial nerves:
Pupillary reflexes are often intact (since these are located in the midbrain,
Absent corneal reflexes and abnormal vestibulo-ocular reflexes are often seen.
Ocular bobbing can occur, or nystagmus
