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.