ΔMS Ken Uchino, M.D.Assistant Professor of Neurology UPMC Stroke Institute
DEFINITION COMA: the complete absence of awareness of self and the environment even when the subject is externally stimulated
ΔMS Confusion Drowsy—Inability to sustain wakefulness without external stimuli Obtundation—aroused by vigorous stimuli, interacts briefly Stupor—arounsed only by vigorous and repated stimuli, but not interactive Coma
ΔMS IT’S A SPECTRUM: ALERT ”DROWSY” ”OBTUNDED” ”STUPOROUS” COMATOSE ….much better to just describe what you see!
ANATOMY RETICULAR ACTIVATING SYSTEM: – a primitive, evolutionarily conserved diffuse (reticular) network of neurons throughout the brain – some more concentrated areas “nuclei” or “centers” – originates in brainstem – ascends through diencephalon via which it connects to rest of brain
ANATOMY Two major anatomic patterns of coma: 1. Diffuse cerebral injury (2/3) or 2. Focal injury to the brainstem (1/3)
DIFFUSE CEREBRAL INJURY Metabolic: – Electrolyte abnormalities: pH disturbance Hyper or hyponatremia Hyper or hypoglycemia Hyper or hypocalcemia – Organ failure liver, kidney – Thiamine or vitamin B12 deficiency – Drug intoxication or withdrawal
FOCAL BRAINSTEM INJURY Direct hit to the brainstem – Brainstem stroke or tumor Secondary pressure onto the brainstem – Trauma Subdural or epidural hematoma – Vascular Subarachnoid hemorrhage Intracerebral hemorrhage – Neoplasm – The mass raises intracranial pressure and herniation onto the brainstem.
Case 1 50 yo man sent confused from homeless shelter. History not obtainable. ? EtOH abuse PE: Afebrile, tachycardic. Mildy hypertensive. Really groggy. When aroused, very confused, dysarthric.
Case 1 CT normal Labs: WBC 15, otherwise CBC, Chem 7, LFTs normal. EtOH level undetcable, Urine tox: negative for drugs of abuse. Presumed dx: toxic encephalopathy, EtOH withdrawal
Case1 Febrile in the evening. The resident attempts to perform LP. After attempt at decubitous position… Attempted sitting up (with help of nurse and attending physician)… Green fluid comes out.
ΔMS H&P 1. Recent events: – When was the patient last seen? – How was the patient discovered? – Were there any preceding neurologic complaints? – Was there any recent trauma or toxic exposure? 2. Medical istory 3. Psychiatric history 4. Medications 5. Use of drugs or alcohol
General Physical Exam Vitals – Is there a fever? – Severe hypertension? Skin – Trauma, jaundice, needle marks Head – Fractures, lacerations Neck (do not manipulate if suspect Fx!) – Stiffness? Neurologic exam…
Coma exam Describe: Observe then stimulate: – Level of consciousness Brain stem Exam – Fundi, Pupils, Corneals, EOM, Gag and cough Extremities
Coma Exam: Level of Consciousness Awake “Opens eyes to voice,” “grimaces to pain,”… Localizes pain—pain where ?(central vs. peripheral) Any abnormal response? Patterned response? – Flexor posturing (Decorticate) – Extensor posturing (Decerebrate) – Myoclonus? Respiratory pattern? – “Riding the vent” vs. overbreathing
Respiration Cheyne- Stokes pattern – diencephalic/ diffuse – CHF hyperventilation – midbrain apneustic pattern – pons ataxic respiration – medulla …interesting, but not really useful in the field!
Testing LOC First, a verbal command: – Specific command (hard): “Show me two fingers!” not “squeeze my hand” – Midline command (easier): “Open your eyes” eye lid apraxia? Try it again with a noxious stimulus
Testing LOC: Noxious – Head: stimulus ear pinch, cotton swab to nares, supraorbirtal ridge pressure, pin to nares – Body Sternal rub, shoulder pinch Areolapossibly the most sensitive spot you can find…It also helps you identify the malingering patients. – Extremities Pinch arm or calf, Nailbed pressure, plantar stimulation Response Localization Withdawal Flexor (decorticate) posturing Extensor (decerebrate) posturing
Posturing Extensor posturing (Decerebrate) – Hips and shoulders extend, adduct, and internally rotate – Knees and elbows extend – Forearms hyperpronate, Wrists and fingers flex – Feet plantar flex and invert – Trunk extends, Head retracts Flexor posturing (Decorticate) – Shoulders adduct, internally rotate, and flex slightly; elbows flex; forearms pronate; and wrists and fingers flex – Lower extremities extend, adduct, and internally rotate – Hip, knee, and ankle may flex in a spinal reflex known as triple flexion
A picture speaks…• It means that the patient is not conscious.• The cortex isn’t communicating.• It’s not well localizing.
Brains stem reflexes: pupils critical in distinguishing metabolic from structural etiologies of coma
Brainstem reflexes EYE Pupils: – II in – III out EOM: – VIII in – III, (IV), VI out Corneals: – V in – VII out Gag: – IX in – X out
Extremities Reflexes – Deep tendon reflexes – Response to noxious stimuli: Is it a reflex or withdrawal? Plantar response—triple flexion
Glasgow Coma ScaleEye OpeningNone 1To Pain 2To Speech 3 Best Verbal ResponseSpontaneous 4 None 1Best Motor Response Incomprehensible sounds 2None 1 Inappropriate words 3Extension (at elbow) 2 Confused 4Abnormal Flexion 3 Oriented 5Withdrawal 4Localizes pain (attempts to 5remove stimulus) Total Score = 3-15Obeys commands (simple 6commands)
Case 2 (JJ) 78 yo woman stopped talking and had right sided weakness. On the way to the hospital, she vomited. Became unresponsive. PMH: macular degeneration, anxiety. Pt was intubated in the ER. Received lasix for HTN of 218/98.
BP 180/90 P 84 afebrile General PE: unremarkable, except intubated. Neurologic: No spontaneous movements or eye opening. Not following commands. Noxious stimuli: – She localizes pain in the left UE. She has purposeful movement in the left upper extremity (squeezing hand sponaten.). – On the right side, extensor posturing to pain on the right UE and triple flexion in the right lower extremity. Brain stem: – Her pupils are 2 mm and reactive. She has left gaze preference, but has spontaneous eye movements. Visual field is difficult to assess. She has gag reflex intact.
MANAGEMENT In the case of a diffuse cerebral injury with no known cause…give the coma “cocktail”: – THIAMINE 100 mg IV – 50% DEXTROSE 50ml IV – NALOXONE (Narcan) 0.4-0.8 mg IV – (FLUMAZENIL (Romazicon) 0.2-1.0 mg IV)
MANAGEMENT In the case of focal hemispheric or brainstem signs, obtain neuroimaging.. – CT – MRI And look for signs of increased intracranial pressure
Case 3 (CM) 75 yo F found down by husband. She has left hemiparesis, dysarthric. C/o HA. PMH: GERD, no HTN SH: Husband: she drinks and smokes as much as she can. PE: BP 106/90 A+O x3. Follows commands. Speech fluent, but dysarthric. She has left neglect. Pupils 63 mm. Left VF cut. Corneal and gag reflexes present. Facial sensation is diminished on the left. Right eyelid droop (old). Flaccid hemiplegia. Sensation: neglect. Deep tendon reflexes 1 throughout. Toes going up bilaterally.
Case 3 Day 2 BP 169/94 No eye opening to stimuli. Not following commands. Eyes downward and to the left. Pupils 3mm reactive. Corneal reflexes present. Left hemiplegic. RUE purposeful movement. RLE withdrawal. Bilateral upgoing toes.
↑ICH & hydrocephalus• CT: Nov 6 at 4:50 am• Subsequently Intubated• Ventriculostomy
Case 3 Day 3 ICP shot up early morning. Got head CT: Exam off propofol x 5min: LUE extension and RUE flexion to pain centrally as well as peripherally. Triple flexion in LE bilaterally. Pupils 2mm reactive. Left gaze deviation but some spontaneous roving movements. Corneal reflex intact.
Case 3 Day 4 Off propofol for 24 hours BP 148/68 P 120 RR 14/13 Unresponsive to sound or pain Pupils fixed at 4mm, corneal reflexes present. Absent gag reflex. Triple flexion in LE. Pt expired later that day.
Herniation Syndromes Central Transtentorial – paratonic rigidity of lower extremities – pinpoint pupils (sometimes) – hyperreflexia/ spontaneous triple flexion responses – waning level of consciousness – sudden cardiac or respiratory arrest/ death
Case 4 35 yo man unresponsive. Pt was just booked for some incident. At police station, found with empty pill bottle. Pt unresponsive. No known medical history.
Case 4 CT head normal Labs: – Urine tox for drugs of abuse normal (opiates, amphetamines, cocaine, tricyclics), salicylate and acetaminophen levels undetectable. PE: – Vitals normal – General exam: shackled to stretcher Blood in back – Unresponsive to voice, pain. Brainstem reflexes intact. Extremity reflexes in tact.
Techniques Let arm drop on face Tickle nares Surprise the patient
Case 4 Wouldn’t let eyes be opened ER residents had attempted LP without lidocaine. (The blood in back). He only flinches with needle in his back. I further macerate his back and succeed in getting CSF—normal Angry man next morning.
Case 5 40 yo woman from rural Washington state Presents to local ER c/o “throat swelling.” She also c/o blurred vision. The exam is reported to be fairly unremarkable initially. But in the ER she worsens and develops respiratory arrest. No signficant past medical history. No asthma or allergies.
Case 5 She is intubated, given steroids for presumed allergic reaction or angioedema. She is transferred to Seattle. In medical ICU she is on vent. She is treated for aspiration pneumonia, reactive airways. She remains unresponsive. Comatose. Never wakes up. Several days later neurology is consulted for post- anoxic encephalopathy. Is she going to wake up?
Case 5 Exam: Vitals normal. Riding the vent. – Unresponsive to pain, sound. – Pupils unreactive, absent corneals, cold calorics absent, no gag. Areflexic in extremities CT of head: normal. Is she brain dead?
Brain Death: the complete and irreversible cessation of all brain function absent pupillary responses (fixed, midposition) absent oculocephalic responses absent corneals, gag absent calorics response absent motor response absent respiration (pCO2>60)
Brain Death: Necessary Tests APNEA TEST – preoxygenate with 100% O2 – maintain O2 through ETT with cannula etc. – two minute duration – pCO2 of 60mmHg or higher adequate COLD WATER CALORICS – never do in a noncomatose person – ice water 30cc to each ear – wait 2 minutes for response before other side
Brain Death: Pitfalls no drugs or hypothermia to explain a precondition of diagnosis absent pupillary responses – anticholinergic drugs, especially atropine in cardiac arrest – NM blockade – preexisting eye disease absent oculocephalics – ototoxic/ vestibular toxins
Brain Death: Pitfalls apnea – NM blockade – post- hyperventilation – phrenic nerve palsies/ diaphragm paralysis no motor activity – NM blockade – locked in syndrome – sedatives
Brain Death: Confirmatory Tests Confirmatory tests are NOT necessary for the diagnosis. Tests necessary if the checklist incomplete. – Trauma, hemodynamic instability Tests: – EEG with special array, sensitivity settings ICU artifact can create problems – cerebral blood flow (Nuc Med) – Transcranial Doppler ultrasound – Evoked potential studies notlegally required to render futile care to a dead person
Summary Get good History from surrogate Examine Is it focal or diffuse?