Stupor And Coma (Sachen) Flashcards
Define consciouness
Total awareness of self and environment
Requires:
-arousal: level of alertness, ability to interact with environment
-awareness (content): sum of cognitive mental functions, “know what’s going on”
Describe consciousness and brain structures
Depends on arousal of cerebral cortex by brainstem ascending reticular activating system (ARAS)
- input from many sensory systems
- projects to hypothalamus, thalamus, cortex
What does impaired consciousness mean?
Diffuse or bilateral impairment of both cerebral hemispheres
Failure of brainstem ARAS
Both
Define confusion
Attention deficit, orientation disturbed, stimuli misinterpreted
Define delirium
Disorientation, stimuli misinterpreted, hallucinations (visual)
Define obtundation
Mental blunting, increased sleep, arouses to mild stimuli (voice)
Define stupor
Arouses only to noxious stimuli and not environmental, only rudimentary awareness (purposeful motor responses)
Define coma
Unarousable, unresponsive, unaware
Describe persistent vegatative
+arousal
+awareness
no reproducible response to stimuli, eyes may be open, roving eye movements, BP/pulse stable
Describe akinetic mutism
Appears +arousal
(-) awareness
No spontaneous motor activity
Describe locked in state (Monte Cristo Syndrome)
+arousal
+awareness
Normal sensation/cognition but complete paralysis except for vertical eye movements
Describe psychogenic state
+/altered arousal
+/altered changing/inconsistent physical examination
What does assessment of comatose patient include?
History General medical exam Neurological exam Laboratory evaluation Diagnosis and treatment
Describe history of comatose pt
From family, EMTs, witnesses How and when pt was found Sudden or gradual onset Prior illnesses (esp vascular) and medications Any recent symptoms (fever, confusion) History of substance abuse
Describe general exam of comatose pt
Vital signs (resp rate and pattern) Skin Breath odor Signs of trauma: raccoon eyes, battle sign, CSF leak (otorrhea, rhinorrhea) Neck stiffness: meningitis, SAH
Describe considerations for hyper/hypotension and hyper/hypothermia in comatose pt
Hypertension: pheochromocytoma, drugs (amphetamine, cocaine, phenyclidine), increased ICP, PRES
Hypotension: Addison’s, sepsis, drugs (Beta-blocker, Ca chanel blocker, TCA’s, Li, sedatives, organophosphates, opioids, methanol), progression to brain death
Hyperthermia: infection, heat stroke, drugs (amphetamines, TCA’s cocaine, salicylates, neuroleptics), serotonin syndrome, central (pontine hemorrhages)
Hypothermia: hypothyroid, hypoglycemia, exposure, drugs (opioids, sedatives, barbiturates, phenothiazine, Et-OH)
Describe skin considerations in comatose pt
Diaphoresis: thyroid storm, decrease BS, drugs (sympathomimetics, cholinergics)
Dry: hypothyroid, drugs (anticholinergics, TCAs)
Acne: long term antiepileptic use
Butterfly rash: systemic lupus
Dark pigmentation: Addison’s disease
Cold, puffy, yellowish: Myxedema coma
Edema: acute hepatic or renal failure
Purpura: meningococcal meningitis, TTP, DIC, vasculitis, aspirin OD
Rash: meningitis, viral encephalitis, rickettsia
Needle marks: Drug OD
Describe breath odor considerations in comatose pt
Dirty restroom: uremia
Fruity: ketoacidosis
Musty: hepatic failure
Onion: paraldehyde (rarely used anymore to treat seizures)
Garlic: organophosphates (insecticides, herbicides, sarin)
What is the purpose of neurological examination of comatose pt?
- Determine location and nature of process that is causing impaired consciousness with emphasis on anatomic level of brain involvement (supratentorial, subtentorial, or diffuse)
- Narrow differential possibilities
What broad category of lesions produce coma?
- Large, pressure producing supratentorial mass lesions
- cause dysfunction in upper ARAS
- cause downward herniation of brain to compress ARAS - Infratnetorial mass lesions that involve brainstem
- Diffuse or multifocal brain disease
Describe unilateral hemisphere (mass effect) supratentorial causes of coma
Intracerebral hemorrhage Large MCA infarct Subdural hematoma Epidural hematoma Brain abscess Neoplasm
Describe bilateral hemisphere supratentorial causes of coma
Subarachnoid hemorrhage Multiple infarcts Venous thrombosis Cerebral edema Acute hydrocephalus Multiple metastases
What are subtentorial causes of coma?
Pontine hemorrhage Basilar artery occlusion Central pontine myelinolysis Cerebellar hemorrhage/infarct Cerebellar/brainstem neoplasm Cerebellar abscess
What are diffuse causes of coma?
Vasculitis Hypoxia Hypercapnia Meningitis/encephalitis Hypoglycemia Hyperglycemia (nonketotic) Hyponatremia Acute hypothyroidism Hypercalcemia Heptaic failure Uremia Malignant hypertension Hypo/hyperthermia Toxins Drug intoxication Drug withdrawal Malignant neuroleptic syndrome Seizures (esp status epilepticus)
What are the essential and nearly-essential elements of the neuro exam of comatose pt?
Essential: Pupillary responses Corneal reflex Extraocular movements Cough/gag reflex Motor responses Respiratory pattern
Nearly-essential:
Neck stiffness
Carotid auscultation
Funduscopic examination
All of these should be performed in stepwise manner
Describe pupillary responses
- Sympathetic/parasympathetic balance determines size
- sympathetic path: hypothalamus->lower cervical cord->sympathetic chain->superior cervical ganlgion->up carotid a. To CN V(I), long ciliary nerve (dilator), Mueller’s muscle
- parasympathetic path: upper midbrain (Edinger Westfall nucleus)->CNIII->ciliary ganglion->short ciliary nerve (constrictor) - Nuclei/tracts controlling pupils are anatomically adjacent to ARAS. Therefore, absent or unequal responses imply brainstem lesion
With anisocoria: which is the abnormal pupil?
Rule of thumb:
If it’s the large pupil, it should fail to constrict to light.
If it’s the small pupil, it should fail to dilate in dark
Describe the rules of thumb for pupillary responses
Enlarged on one side: parasympathetic dysfunction (usually CNIII)
Enlarged bilaterally: bilateral CNIII lesion, post ictal, barbiturate intox
Constricted: sympathetic dysfunction (hypothalamus, carotid)
Pinpoint: pontine lesion, opiates pilocarpine
-Three P’s of pinpoint pupils: Pontine lesion, oPiates, Pilocarpine
Midposition and unreactive: sympathetic and parasympathetic (midbrain)
Interpretation of pupillary signs may be confused by what?
Atropine/scopolamine: dilated, fixed Opiates: pinpoint, +/- reactive Pilocarpine: pinpoint Glutethimide: dilated, fixed, unequal Hypothermia, anoxia, ischemia: possible dilated, fixed, unequal
Describe extraocular movements in neuro exam of comatose pt
Conjugate gaze depends on intact CN III, IV, and VI, their nuclei, and interconnections
Frontal gaze centers deviates eyes to opposite side
Pontine gaze centers deviate eyes to same side
Describe spontaneous roving extraocular movements
Conjugate: implies brainstem intact
Dysconjugate: implies brainstem lesion
Describe spontaneous conjugate deviation at rest of extraocular movements
Hemispheric lesion:
Destructive: toward lesion
Irritative: away from lesion
Brainstem lesion
Destructive: away from lesion
Describe the types of nystagmus and indicated lesions
Ping-pong (right-left deviation every few seconds): bihemispheric, midbrain
Convergence (slow abduction with rapid jerk back): mesencephalon
Retractory (retraction orbit): mesencephalon
Bobbing (rapid down, slow up): pons
Dipping (slow down, rapid up): bihemispheric
Describe oculocephalic maneuver (Doll’s eyes)
Reflexive
Tests mid-pons
Used to assess CN III, IV, and VI
Passive horizontal head rotation: eyes move horizontally opposite
Passive vertical head rotation: eyes move vertically opposite
Be sure neck is stable
Overridden in alert patient
Describe Caloric (oculovestibular) reflex
Reflexive
Lower pons
Otoscopic exam: be sure canal clear and TM intact
Irrigate TM with cold (usually) or warm water
Cold water irrigation with intact brainstem causes:
Eyes to deviate to irrigated side if unilateral irrigation
Eyes to deviate downward if bilateral irrigation
Describe motor responses in neuro exam of comatose pt
Purposeful: follows commands, localizes pain
Reflexive:
- decorticate: arms flexed, and legs extended (hemispheric)
- decerebrate: all extremities extended (brainstem)
- flaccid: pontomedullary or metabolic
Describe respiratory patterns in comatose pt
Cheynes-Strokes: hyperpnia regularly alternating with apnea (bilateral hemispheres or diencephalon). Seen in many disorders ranging from metabolic to structural
Central neurogenic hyperventilation: midbrain
Apneustic breathing: long inspiration followed by apnea (mid/low pons). Seen in structural lesions and anoxia, hypoglycemia, meningitis
Ataxic: completely irregular (medullary respiratory centers)
Describe supratentorial mass lesions
Initial signs usually focal
Neurological signs at any given time point to one anatomic location
Progression of signs is rostral to caudal
Motor signs are often asymmetric
Describe herniation syndromes
Caused by expanding supratentorial mass lesions
Effect is to displace brain tissue into adjacent intracranial compartments (so called rostral to caudal progression of herniation)
Describe uncal transtentorial herniation
Herniation of uncus under edge of tentorium, compressing CN III (ipsilateral dilated pupil, poor EOM, ptosis), then contralateral brainstem (ipsilateral hemiparesis), then respiratory abnormalities, posturing, fixed pupils, and death
Describe central transtentorial herniation
Herniation into foramen magnum leads to early coma, small pupils, normal EOMs, posturing and later bilateral fixed pupils, respiratory arrest, and death
Describe cingulate gyrus herniation
Herniates under falx
Describe subtentorial mass lesions
History: preceding brainstem dysfunction usual (disequilibrium, dysarthria, dysphagia, diplopia, vertigo) but may be sudden onset of coma
Localizing brainstem signs precede or accompany onset of coma and almost always include a form of oculovestibular abnormality
Cranial nerve palsies usually present
Bizarre respiratory patterns common
Characterize diffuse/metabolic coma
Confusion and stupor commonly precede motor signs
Motor signs are usually symmetrical
Pupillary reactions are usually preserved
Asterixis, myoclonus, tremor, seizures common
Acid-base imbalance with hyper or hypoventilation frequently seen
Level of consciousness may fluctuate
Describe global cerebral ischemia
Occurs whenever blood flow is inadequate to meet metabolic requirements (oxygen and glucose) of brain, as in cardiac or pulmonary arrest
Result is spectrum of disorders, ranging from reversible encephalopathies to brain death
Describe brief (
Commonly reversible encephalopathies, generally after 12 hours or less of stupor or coma
Anteograde and/or retrograde amnesia can occur
Recovery often occurs within 7-10 days but may be delayed by 1 month or longer
Describe prolonged ischemic episodes
Focal cerebral dysfunction
Patients are usually comatose for at least 12 hours and may have lasting focal or multifocal motor, sensory, and cognitive deficits
Describe persistent vegetative state
Awake but functionally decorticate and unaware of surroundings
Eye opening, eye movements, sleep-wake cycles, and brainstem and spinal reflexes may remain intact
What does the definition of brain death imply?
Irreversibility
Complete cessation of brain function (including respirations but not heartbeat)
Persistence
Describe irreversibility of brain death
Cause of coma should be known. Must be adequate to explain clinical picture and must be irreversible
Sedative intoxication, hypothermia (≤ 90F), neuromuscular blockade, and shock must be ruled out, since these conditions can produce a clinical picture that resembles brain death but are potentially reversible.
Describe cessation of brain function
Unresponsiveness: pt must be unresponsive to all sensory input, including pain and speech
Absent brainstem reflexes: including pupillary, corneal, oculocephalic, and oculovestibular reflexes. Respiratory response are absent at 8 to 10 minutes after pt’s pCO2 is allowed to rise to 60 mm Hg, while oxygenation is maintained with 100% O2 (apnea test)
Describe persistence of brain death
Criteria for brain death must persist for an appropriate length of time
Six hours with a confirmatory isoelectric (flat) EEG, performed according to technical standards of AEES
Twelve hours without confirmatory isoelectric EEG
Twenty-four hours for anoxic brain injury without a confirmatory isoelectric EEG
Describe precautionary notes about brain death
State law may impose additional requirements such as
- qualification of examiner
- confirmation by second examiner
Ancillary tests (EEG, angiography, nuc med scan) are not required unless there is uncertainty about diagnosis or apnea test cannot be performed. However, some countries do require them.
Describe the initial steps for management of comatose patient
A: Insure pt airways (spontaneous, mouth piece, ETT)
B: insure breathing and adequate oxygenations (pulse oxy, O2, ABG)
C: Insure adequate ciruclation and control any active bleeding (BP, P)-IV line, arterial line, ECG
Stabilize neck, get C-spine films if trauma suspected
Quick history (seizure, meds, drug use, trauma)
Quick exam
EKG to monitor for arrhythmias
Give glucose (1 amp=25gms), thiamine (100 mg IM)
Give specific antidote (Narcan)
Adjust body temperature
Control agitation
Stop seizures if present
Describe laboratory evaluation of comatose pt
Venous blood: glucose, electrolytes (including calcium, phosphorus, magnesium), BUN/creatinine, osmolality, drug screen, liver functions, ammonia, coagulation studies, thyroid function, blood cultures
Arterial blood: pH, pO2, pCO2, HCO3, HbCO
Urine: UA, culture, drug screen
If febrile: blood cultures
If stiff neck: LP (after CT) with CSF for cell count, glucose, protein, gram stain, cultures (bacterial, viral, and fungal)
Describe diagnostic testing
Noncontrast head CT
- acute blood
- space occupying lesion
LP
- xanothochromia (SAH)
- infection
+/- MRI
- posterior fossa
- early infarct
+/- EEG
What are specific interventions for comatose pt?
Reduce elevated intracranial pressure
- elevate head of bed
- Intubate and hyperventilate to PCO2 of 20 mm
- use mannitol for ischemic lesions
- use decadron for tumor, abscess, and perhaps cerebral hemorrhage
- Lasix 20-40 mg IV possibly
Treat seizures
- lorazepam 2 mg IV q10-15 min up to 10 mg total
- phenytoin 18 mg/kg load (about 1000 mgs) then 300 mg/day
Describe Glasgow Coma Scale 3-15
Eye opening: Never: 1 To pain: 2 To verbal: 3 Spontaneous: 4
Best verbal response: None: 1 Sounds: 2 Inapp words: 3 Disoriented; 4 Oriented: 5
Best motor response None: 1 Extensor: 2 Flexor: 3 Withdrawal: 4 Localizes: 5 Obeys: 6
Sum and individual elements are important: eg GCS = 9, E2, V3, M5
