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APPROACH TO ALTERED MENTAL
STATUS
Sean Wilde
Margriet Greidanus
March 29 2012
Outline:
Practical ED based Approach Some important keys and pearls Discuss thinking about altered MS in
presentation categories Practice it with cases Discussion of selected diagnoses
Important not to missNot covered in other topics
Disorders of Consciousness
Hypervigilent
Obtunded
Drowsy/Lethargic
StuporComa
Confused
Look ‘em up Dementia
Chronic, slowly progressive, non-emergent Delerium
Acute, fluctuating, **investigate**25% hyperactive50% hypoactive25% mixed
Assessment Tools:GCSAVPUACDUSimplified Motor ScaleConfusion Assessment Method (CAM)
CAM for Delerium
Acute onset and/or Fluctuating Course
AND
Inattention
WITH EITHER
Disorganized thinking
OR
Altered Level of Consciousness91-97% sensitivity85-94% specificityJ Am Geriatr Soc. 2008 May ; 56(5): 823–830
Beware: “Grandpa’s just a little confused today”
Approach to the Clearly Altered
2 Causes of altered LOC
Arousal (R.A.S.) Behavior(Cerebral activity)
Bihemispheric dysfunctionUsually metabolicDiffuse cerebral disease
(infection, edema)
Brainstem dysfunctionReticular activating
systemBrainstem lesionsHerniation
Step 1: Unleash the A(BC)-Team
Unclear history?
C-spine
Step 2: Absent an emergent A or B…
Look for neurological
findings before you
sedate/paralyze
Step 3: Emergent Interventions
Dextrose Only if glucose < 4 1 amp (25g) D50
Oxygen Narcan
Reasonable if any clinical/historical suspicion of narcotic use 0.4-2mg IV/SC
○ Start small, increase. Full dose in code. Response? Ongoing boluses vs infusion (2/3 effective dose)
Thiamine If worried about nutritional deficiency Q- Before or after glucose? A- In the ED, who cares
No Flumazenil Risk of seizure induction
The Coma Cocktail:Do DON’T, or don’t DON’T?
GCS < 8: When Wouldn’t I Intubate?
If the airway is acutely threatened, or oxygenation/ventilation poor, then yes.
Otherwise, the indication for intubation is urgent, but not emergent.
Look first for rapidly reversible or self-limited causes of decreased LOCHypoglycemia, opioid overdosePost-ictal, EtOH intoxication
Step 4: Full vitals with ACURATE temperature
Temperature can quickly direct your differential
Rectal most accurate Can still trick you.
Rechecks
Emergent Temperature Control
Think of it like Blood PressureHealthy body can autoregulateThermal damage occurs when regulation fails
Hypo/Hyperthermia in an altered patient is a critical finding requiring
emergent correction!
Other emergent considerations
Treat shock state Antibiotics
Sepsis, meningitisOften indicated empirically
SteroidsMeningitisAdrenal crisis
BenzosSeizures, agitation
Step 5: DetailsSecondary Survey History
Evidence of trauma Evidence of infection Signs of shock Toxidromes Focal neuro symptoms Brainstem reflexes Seizure related injuries
Onset, course, symptoms
Meds/substance use Medical history Trauma
Step 6: Work-upMost of the Time When Indicated
CBC, ERChem, LFTs, INR, PTT
Calcium, TSH ABG EKG Blood cultures Urinalysis/culture/tox CT head
EtOH, ASA, apap, osm, toxic alcohols
Trauma films/CT Chest x-ray Lumbar Puncture MRI EEG
Step 7: Diagnosis and Management
Supportive Care
Correct physiologic abnormalities
Treat underlying cause
Antidote?
Think in presenting Categories…
Focal and Altered Hot and
Altered
Cold and AlteredTrauma
and Altered
Bradycardic and Altered
Shock and Altered
Sudden vs. progressive
But don’t fixate or exclude too early
So, what should I memorize?
Common Causes
Rare Dangerous
Treatable
X
Most Common CausesPediatrics Adults
CNS infections Trauma Toxic ingestions DKA Severe dehydration Congenital
malformations Metabolic disorders Prolonged seizures
Infections / sepsis Trauma Intoxication/Withdrawal Toxic ingestions Seizures Hypoglycemia Intracranial bleeding Hypoxia/CO2 narcosis Electrolyte abnormalities
Cases
The Hot and Altered Patient Infectious Toxidromes
Sympathomimetic, anti-cholinergicPsychotropic meds
EnvironmentalExertional or exposure Heat Stroke
Other Febrile illnessesThyrotoxicosis, thyroid stormNeoplasmsInflammatory conditions
Toxidrome differentiation
Look at the Skin
Diaphoretic: sympathomimetic
Dry: anti-cholinergic ○ decreased bowel sounds○ urinary retention
Serotonin SyndromeRapid onsetMyoclonusOcular clonusIncreased reflexes (hyperkinesia)Difference b/wn upper and lower extremities
Neuromuscular Malignant SyndromeOnset over daysBradykinesiaLead pipe rigidity (think Parkinson’s)Extremity exam: upper = lower.
Heat Illnesses
Spectrum from mild (cramping, rash) to severe (coma and death)
Exertional heat strokeYoung, healthy athletesAcute onset, exertion in high heat
Non-Exertional heat strokeTypically young or elderly in heat wavesSlow onset, abnormal lytes common.
Water Intoxication
Acute Hyponatremia (<125)N&V, malaise, dizziness, fatiguePeripheral edemaProgression to cerebral edema
Risk Factors:Exercise > 4hoursFemaleLow body mass indexFree water consumption
Non-Convulsive Status Epilepticus
Persistent neurological seizure activity without obvious visible seizure activity
Difficult diagnosisControversial and developing clinical and
EEG criteria Add to DDx of
“Altered/Comatose/Bizarre behavior of no obvious cause”
Non-Convulsive Status Epilepticus
Non-Convulsive Status Epilepticus
NCSE- Risk Factors
Known epilepsyEven remoteUnder-medicated
CNS infections (all types) Any recent or remote seizure risk factors
Stroke, tumor, neurosurg, CNS catastrophe/trauma
Drug intoxication/withdrawal Recent witnessed convulsive seizure
NCSE- When to suspect Altered MS with no other obvious cause Prolonged post-ictal period
>1-2 hours Subtle motor activity
Minor tremors, twitching or eye deviations Awake but altered with:
Slowing, disorientationSomatomotor symptomsAutomatismsSensory hallucinationsProlonged prodromal auraNew confusion or abnormal behavior in the elderly
J Neurol Neurosurg Psychiatry 2003;74:189–191
Most predictive Clues Ocular movement
abnormalities History of seizures Remote seizure risk
factors:StrokeNeoplasiaDementiaPrevious neurosurgery
Small studyPoor designNot much else out there
NCSE- Management approach
Urgent EEG/Neurology to confirm/categorize if at all unclear of dx.
Treatment less urgent than convulsiveNCSE still probably damages neurons, but
not nearly as much as convulsiveMostly from animal studies and case series
Benzos are first line for all types4mg IV lorazepam X 2.
Treatment diverges then if it is Absence
NCSE- If Benzo’s fail…Altered but preserved
consciousness
Impaired Consciousness
Comatose(esp post grand
mal)
VPAPhenobarb
Avoid: Phenytoin
Carbamazapine
PhenytoinPhenobarb
VPA
(std Status tx)
Full standard status Tx
Rapid progression
to GA (midaz, propofol)
Could be Absence
Case #2
Altered Elderly
Salicylate Toxicity Early signs
Hearing changes, tinnitusTachypneaCan be febrile
LateCNS toxicityAG Metabolic acidosis
Consider in:Septic appearing elderly (most common misdiagnosis)Herbal OD (wintergreen)Any sick pt with AG metabolic acidosis and resp alkalosis.
Suspected Meningitis Approach
Blood cultures during ABCs Antibiotics and dexamethasone
Ceftriaxone 2g IVVancomycin 1g IV
CT LP Antivirals
Acyclovir 10mg (0.15-0.3mg/kg)
CT before LP if: Age > 60 Immunocompromised Altered or decreasing LOC Seizure within 1 week Known CNS disease
AVN, tumor, stroke Malignancy Hx Papilledema Focal neurological finding (incl. aphasia)
97% negative predictive value for abnormal CT
N Engl J Med 2001, Hasbun et al.
Steroids in meningitis
Bacterial lysis increases CNS inflammation
Steroids attenuate if given before/concurrently
Demonstrated benefit in Strep Pneumo (adults) and H. Influenza (Peds)
Probably no harm in others Only Dexamethasone studied Caution in overtly immunocompromised
Gaham, Can J Emerg Med 2003;5(5):348-9
Viral or Bacterial?
Viral or Bacterial?
Caution in interpreting CSFSignificant overlap of findingsNormal is not always reassuringGram stain – 80% sensitive at best
Organism in blood culture: 50-91% of time
Empiric Acyclovir?No good guidelinesReasonable if high viral suspicionProbably not as urgent as antibiotics
Case #3
Cold and Altered
Adrenal Crisis
Severe hypotensionFluid/pressor refractory
Dehydration and hypoglycemia Abdominal Pain / GI symptoms CNS disturbance
Confusion, disorientation, lethargy Sepsis
With or without feverCan be hypothermic
Myxedema Coma Metabolic, multi-organ dysfunction Features:
Mental status changesHypotensionHypothermia (<35.5)
Clues90% elderly women in winterBradycardia, hypoventilationHypothyroid body habitusPleural/cardiac effusionsAbsence of shiveringDelayed reflexes (esp relaxation phase)
Some definitions Meningitis:
Infection/inflammation in subarachnoid spaceMeningeal signs and symptoms
Encephalitis:Infection and inflammation in brain parenchymaDistinct neurologic abnormalities
Encephalopathy:Global brain dysfunctionAltered LOC as primary featureMovement disorders and eye findings prominentMultiple forms/causes
Viral Encephalitis: Suspect in New psychiatric symptoms Cognitive deficits
AphasiaAmnesiaAcute confusional state
Seizures Movement Disorders Often fever and meningeal signs
Viral Encephalitis
HSV-1 Herpes Zoster Virus CMV Epstein-Barr Arboviruses
West Nile, Equine viruses, etc Rabies
Viral encephalitis
HSVProminent psychiatric featuresMemory disturbanceaphasia
Acyclovir 10mg/kg IV q8H MRI/EEG PCR studies on CSF
Case #4
Focal and Altered
Glioblastoma
Brain Abscess
Consider in well looking pt with:Triad
○ Headache (100%)○ Fever (50%)○ neuro deficits/seizures (33%)
Possible meningeal symptoms (up to 50%)Signs/symptoms of increased ICP (50%)
~60% with clear source ID consult- multidrug coverage incl
anaerobes
Thiamine Deficiency Anyone with a chronic nutritional deficiency
is at risk2-3 weeks of deficiency to develop Sx
EtOH abusePoor intakeIncreased demand (EtOH metabolism)
GI surgery (weeks to months ago)Absorbed in duodenum
Cancer/AIDS Severe systemic disease
Consider Thiamine in any of… Staple diet of polished rice Chronic EtOH abuse and malnutrition GI surgical procedures Chronic vomiting/diarrhea Cancer/chemotherapy Systemic disease state Magnesium depletion Unbalanced nutrition
Multiple Presentations Dry beriberi
Wernicke’s encephalopathy○ Progresses to Korsakoff’s syndrome
Distal polyneuropathy Wet beriberi (Asians higher risk)
High output (common)○ CHF, orthopnea, pulmonary/peripheral edema
Low Output○ Hypotension, lactic acidosis, no edema
Infantile Beriberi2-12 months, soy formula or breastfed by deficient
mother
“Classic” Wernicke’s Encephalopathy Mental Status changes (82%)
Confusion to coma spectrum Can mimic acute psychosis
Occular Abnormalities (29%) Nystagmus Various gaze palsies Optic disk edema/retinal hemorrhages
Motor Disturbances (29%) Incoordination (cerebellar and vestibular dysfunction) Gait ataxia
All the above (<10%) None of the above (19%)
Bottom Line?
Thiamine is cheap and safe
You can miss a lot of subtle presentations of deficiency
Give it liberally in the altered patient
How much?
High dose or normal dose? 100mg IV daily is standard prophylactic dose Lancet neurology 2007 review
High dose “suggested” for probable cases based on suggestion of retrospective studies
500mg over 30min TID X 2-3 days, then taperNot clearly demonstrated
Cochrane ReviewNo validated regimen in the literature
Timing?Prolonged glucose administration without thiamine can be
harmfulNo demonstrated harm from a single bolus of glucose pre-
thiamine
Common Encephalopathies Uremic Hepatic Wernicke’s Herpes (HSV) Hypertensive Hypoxic/hypercapneic Toxic Numerous other rarer causes
Hepatic Encephalopathy
Hx Liver disease Asterixis Stigmata of Liver Disease Precipitants:
GI bleed (may be occult)SBP
Serum ammonia level Treat with NG lactulose infusion
Uremic Encephalopathy
Missed Dialysis
Increased BUN/Creatinine ratio
Asterixes
Needs emergent Dialysis
Interesting Diagnosis: Case 15yo F Brought in by principle on school Ski trip Sitting on chair lift and suddenly asked
“where are we?” Unable to recall any events since waking that
morning. Continues to ask the same questions over
and over again shortly after being answered
Recalls her name, hometown, friends and family
Still able to ski down at her regular ability
Well prior, no PMhx or meds No known trauma/ingestions Other than memory, completely normal
Physical, ROS and Neurological exam.
Transient Global AmnesiaBenign, temporary loss of anterograde memory
with sparing of immediate recall, remote memories and deeply imprinted identity and
skills.
TGA: Features Isolated short-term memory loss Inability to imprint new memories Frequent perseveration
“Broken record”Orientation questions
Preserved consciousness Otherwise completely normal exam HA, nausea, emesis may be present Duration typically 2-12 hours
Always < 24hrs
I swear I don’t remember what happened…
TGA Triggers:
Physical Exertion Swimming Sex Valsalva
Drug Use Viagra Marijuana
Emotional/psychological stress
TGA: Causes
Possibly due to intracranial venous stasisIschemia of memory centresBased on studies of inducibility of stasis in
sufferers Probably not epilepsy, migraine variant Is not a TIA Higher risk in young with migraine hx.
TGA: Hodge and Warlow Criteria (1990)
TGA: DDX considerations R/O Delirium!! TIA/CVA
Suspect posterior circulation Migraine variant Complex Partial Seizures
Aura, automatismsNon-convulsive status
Transient epileptic amnesiaEEG if lasts <1hr / resolves with benzos
Fugue (psychogenic amnesia)Preserved new memoriesLoss of self-identity and auto-biographical memories
Rule out trauma
TGA: Prognosis
Excellent Small recurrence rate Not associated with long term
complications or risks TIA/CVA risk is same as general
population
TGA: Ix and Management If all criteria met:
No Ix neededReassurance and support for patient and distressed family
members is the primary management Duration < 1 hour
EEG: consider transient epileptic event Duration > 24 hours
Look for something else Any suspicion of other neuro or systemic findings
warrants full lab and imaging investigationMetabolicPosterior CVA
Approach to Altered Patient: Summary Develop a standard approach Manage and diagnose concurrently
Think first of the rapidly reversibleEarly neuro exam- is it focal?Low threshold for empiric infection tx
Think in presenting categories that work for you
Have a list of what to always think about in unclear cases.