Transcript NEUROLOGY IN ICU

NEUROLOGY IN ICU
Dr.Ravi Srinivasan
NEUROLOGY
MANY IMPORTANT ISSUSES
Essential clinical history in patients
with loss of consciousness
History
Time course-abrupt
gradual
fluctuating
Preceding focal signs
Previous episodes
h/o recent illness
h/o recent fall
Altered behaviour
Drugs
Medical psychological history
Alcohol drug abuse
Possible causes
SAH, seizure, bleeding
Tumour, venous thrombosis
Metabolic,subdural hematoma.
Focal lesion
TIA, seizure
Infection, metabolic
Subdural, epidural bleed
Toxic, metabolic, infection
Toxic-metabolic.
Metabolic, psychiatric
Toxic-metabolic
Vital signs interpretation in comatose
patients
Vital signs
Fever
Potential illnesses
Hypothermia
Cold exposure, hypothyroidism,
hypoglycemia, shock,
Drugs(alcohol,barbiturates,opioids,
sedatives)
Hypertension
Infection, heatstroke, thyrotoxicosis,
Drug ingestion
(cocaine,amphetamines,Tca,
anticholinergic)
Pheochromocytoma,
drugs (cocaine,amphetamine,
phencyclidine)
Vital signs interpretation in comatose
patients
Hypotension
Addisons, sepsis, MI,
Blood loss, hypothyroidism
Tachycardia
Bradycardia
HTN-Bradycardia
Alcohol, amphetamines,
ethylene glycol
Uremic coma, myxedema
coma.
Kocher-cushing reflex.
Respiratory patterns in coma
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Cheyne stroke
-Bihemispheric damage, metabolic
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Kussmaul breathing
-Metabolic acidosis, post
mesencephalic lesions
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Agonal gasps
-Bilateral lower brainstem lesions
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-Bihemispheric,midbrain,pons
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Central neurogenic
hyprventilation
Apneusis
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Cluster
-Bihemispheric or pons
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ataxic
-Dorsomedial medulla RAS
-Lateral tegmentum of lower pons
Cutaneous and mucosal exam in
comatose
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Petechiae &ecchymosis
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Hypermelanosis
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Cherry red skin
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Gray blue cyanosis
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Telangiectasia
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Ecthyma gangrenosum
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Splinter hemorrages
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pigmentedmacules
TTP,ITP,DIC,meningococcemia,
vasculitis,endocarditis
Addisons,chemotherapy,porphyria,m
elanoma
.CO poisoning
.Methemoglobinemia
Chronic alcoholism,vascular
malformations
Pseudomonas sepsis
Anemia,sepsis,leucemia,endocarditis
Tuberous sclerosis,
neurofibromatosis
Evaluation of comatose
• Spontaneous activity, motor response, eye position
and movements, pupillary reflexes, brainstem
reflexes and asymmetry between right and left
responses.
• Decorticate (flexor) posturing-lesion above level of
red nucleus.
• Decerebrate posturing (extensor)-damage to lower
midbrain or upperpons, severe damage and less
chance of recovery.
• Ciliospinal reflex
Main ophthalmologic findings in
comatose
• Vitreous sub hyaloid
hemorrhages
• Papilledema,retinal
exudates&bleed
• Papilledema
• Cholesterol embolus
• Subconjunctival
hemorrhage
• Periorbital eccymoses,
Battle sign
-SAH
-hypertensive
encephalopathy
-ICT increase
-carotid atheroma
-endocarditis
-head trauma
Eye movements in coma
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Conjugate horizontal roving
Conjugate horizontal ocular
deviation
Wrong way eyes
-Excludes midbrain, pons lesion
-Contralateral pon/ipsilateral
frontal
-Paradoxically to,contralateral
deep hemispheric leson.
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Downward ,inward eyes
-Thalamic,upper midbrain lesion
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Ocular bobbing
-Bilateral pontine damage
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Ocular dipping
-Diffuse cortical anoxia
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Dysconjugate eye
movements
-Brainstem damage
Abnormal pupillary responses in coma
Bilateral small ,reactive
b/l dilated and unreactive
b/l dilation&reactive
Unilateral miosis
Metabolic encephalopathy, B/l
thalamic, pontine lesions,
hydrocephalus,narcotics,OP,barbitura
tes
Midbrain damage or compression
Seizure
Thalamus, sympathetic efferents from
posterior hypothalamus, tegmentum,
descending to the cervical cord
Pupillary responses and coma
Unilateral, unreactive & enlarged
-unilateral ptosis
-bilateral ptosis
Unilateral,small,reactive, ipsilateral
ptosis
-with face anhydrosis
-anhydrosis entire side of body
-without anhydrosis
Compression of ipsilateral III nerve
-Fascicular lesion
-Nuclear lesion
-Extracranial defect T1-T2 to carotid
bifurcation
-Between hypothalamus and spinal
cord
-ICA vs cavernous sinus vs SOF vs
orbit
Glasgow coma scale
FOUR score scale
Eye response
Brainstem reflexes
4-eyelid open or opened, tracking or blinking to command
3-eyelids open, not tracking
2-eyelids closed, open to loud voice, not tracking
1-eyelids closed, open to pain, not tracking.
0-eyelids remain closed with pain
4-pupil & corneal reflex present
3-open pupil wide & fixed
2-pupil/corneal reflexes absent
1-pupil & corneal reflex absent
0-absent pupil, corneal & cough reflexes
Motor response
4-thumbs up, fist, or peace sign to command
3-localizing to pain
2-flexion response to pain
1-extensor posturing
0-no response to pain or generalized myoclonus/status
Respiration
4-not intubated, regular breathing pattern
3-not intubated, cheyne-stokes breathing pattern
2-not intubated, irregular breathing pattern
1-breathes above ventilator rate
0-breathes at ventilator rate
Neuro muscular blockers in ICU
succinylcholine
5-10min
-t1/2
renal
rapacurium
12-17
60-120
-
mivacurium
12-18
2
renal
atracuronium
30-40
20
renal
vecuronium
20-60
60-130
renal
rocuronium
30-67
80-100
renal
pancuronium
120-180
110-140
renal
tubocurarine
80-120
240
renal
doxacurium
90-120
100+
renal
pipecuronium
80-100
137+
renal
hepatic
hepatic
hepatic
Sedatives in ICU
diazepam
50-120
Icp, cbf,
lorazepam
3-7
midazolam
7-10
morphine
4-11
fentanyl
10
thiopental
2-4
phenobarbitone
48-144
haloperidol
10-19
Cbf, cpp, icp
propofol
40-50
Cbf,icp,cpp
ketamine
2-14
Cbf,icp
Cbf,icp
Cbf,icp,cpp
Cerebral herniation :clinical syndromes
Uncal herniation
Hemispheric/lateral
middle fossa
Ipsilateral III
compression
Central herniation
Supra tentorial diffuse
brain edema,
haemorrage,
midline tumors
Initial obstruction
hydrocephalus,
thalamus,
hypothalamus
displacement
Dilated ipsilateral pupil
with preserved or
sluggish reaction to
light.
CnIII,ophthalmoplegia,
ipsilateral hemipareis
Decrease
consciousness, small
& reactive pupils,
normal eye
movements.
Fixed pupils, cheyne
stroke respiration,
opthalmoplegia,
decorticate posturing
Cerebral herniation clincal syndromes
Midbrain compression
Advanced stage of
central herniation,
upward infra tentorial
lesions
Midbrain and upper
pons
Decerebrate
posturing, midposition
pupils, sometimes
irregular and loss of
pupillary,
oculocephalic and
oculo vestibular
reflexes
Foramen magnum
herniation
Infra tentorial lesions
Medulla-lower pons,
All brainstem reflexes
are lost, flaccid
paralysis, ataxic
respiration, then
ceasing
cerebellar tonsils
Types of herniations
Medical ICU
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Metabolic encephalopathy-28.6%
Seizures-28.1%
Hypoxic ischemic encephalopathy-23.5%
Stroke-22.1%
• Sepsis is major cause of neurological complication38.8%
Primary CNS processes
• Acute stroke-1-4% in non neuro icu.
Angiographic studies
De clotting of Av shunts
Vascular line insertions
Air embolism
Cardioversion
Anticoagulation
Thrombolytic therapy
Primary CNS processes
• Meningitis & encephalitis-change in mental
state with fever, csf analysis and
antibiotics.
• Posterior reversible leuco encephalopathyacute hypertensive crisis involving brain,
vaso genic edema, control with labetolol,
nicardipine etc.
Conditions associated with acute hypertensive crisis &
hypertensive encephalopathy
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Toxemia of pregnancy
Drugs-cyclosporine
tacrolimus
interferon
fludarabine
cisplatin
gemcitabine
erythropoetin
Uncontrolled essential hypertension
Secondary hypertensionSLE,AGN,CRF
Primary CNS processes
• New onset seizure-0.8-4%,focal most common.
• Myoclonic seizures-metabolic, drugs,hypoxia.
• Non convulsive status-10%(50%of TBI),
52% mortality in critically ill
• Myoclonic status epilepticus-12hrs of cardiac
resuscitation, persists up to 48 hrs, poor prognostic
sign, unresponsive to medication.
Common precipitants of seizures in
ICU
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Metabolic: renal,
hepatic,
electrolyte,
Endocrine
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Hypoxia/ischemia
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Sepsis
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Stroke
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Primary CNS inflammations
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Withdrawal
delirium tremens
BZD
narcotics
Drugs:
Anti arrythmics- lidocaine, flecainide
Antibiotics-imipenam, ciprofloxacin,
norfloxacin, penicillin derivatives
Antidepressants-amit,
nortript,doxepin
Bronchodilators-theophylline
Immunosupressive drugscyclosporine,OTR3,FK506
Secondary CNS processes
• Encephalopathy is the most common
neurological complication in medical ICU.
• Prolonged sedation
• Drug intoxication
Not weanable patients
• Critical illness neuro myopathy
-Axonal/demylinating
• Electrolyte imbalance
Sodium disturbances
• Hypo natremia-incidence of1%,prevalence of 2.5%.
Postoperative patients
Lethargy, confusion, coma ,seizures.
Central pontine myelinolysis
• HypernatremiaLethargy, obtundation, coma
Progressive shrinkage of brain leading to cerebral
vascular damage and sub dural hamatoma
Calcium disturbance
• Hyper calcemia- ionised calcium levels
and rate of rise.
Delirium, depression, coma.
• Hypo calcemia-commonly associated with
sepsis.
Irritability, tremors and seizures
Magnesium disturbances
• Hypo magnesemia-commonly associated
with hypo calcemia.
Tremor, tetany, myoclonus and seizures.
• Hyper magnesemia- cns depression with
lethargy, confusion and weakness.
Serum levels>6meq/l causes coma
Acid base disturbances
• Severe acidemia-<7.2,metabolic,respiratory,mixed
Increase of icp, decrease seizure threshold,
stimulate chemoreceptor trigger zone.
• Severe acute alkalemia-ph>7.60
Cerebral vasoconstriction, decreased oxygen
extraction
Respiratory depression, tetany,coma,siezures
renal
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Uremic encephalopathy-BUN doubles, drowsiness,
asterexis, myoclonus
Post dialysis disequilibrium-rapid dialysis, first dialysis,
extreme baseline pre dialysis BUN
Younger patients, previous neurological deficits
Cerebral edema along osmotic gradient
Combative behavior, headache, myoclonic jerks, cramps,
cortical blindness, coma, seizures
Avoided by continuous veno venous hemodialysis
liver
• Acute hepatic failure-hyper ammonemia,
hepatic encephalopathy.
Gr IV -80% mortality
• Hypoglycemia/hyperglycemia-confusion,
coma, seizures, focal neurological deficits.
Sepsis encephalopathy
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Most common (70%) in medical icu.
Highest mortality
Multi organ failure
Decreased cerebral O2 extraction ratios,
disordered amino acid transport, micro
abscesses, inflammatory mediators, dys
regulation of neurotransmitters, direct
cytotoxicity, disruption of blood brain
barrier
Surgical ICU
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Cholesterol embolisation-vascular catheterisation
diffuse encephalopathy, retinal hemorrhage, transient
hemiparesis, livedo reticularis, purple toes, renal failure,
muscle weakness
Muscle/renal biopsy-stacked needle shaped crystals
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Fat embolism-trauma and long bone fracture/surgery
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Multifocal ischemic stroke-Cardiothoracic surgery.
watershed infarcts, LV thrombus, aortic atherosclerosis
,aortic cross clamping, infective endocarditis, arrythmias.
MRI limited by pacemakers
Hypoxic ischemic encephalopathy
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Hypotension, hypoxemia, asphyxia,
laryngeal edema
Severity and duration of hypoxia
Transient confusion, antegrade amnesia, focal, multi focal
or global cns damage or brain death.
Fixed pupils, myoclonic status, sustained upward gaze
poor prognosis
• Delayed post anoxic encephalopathy
Lucid interval of 1-4 weeks
Diffuse hemispheric demyelination, cognitive cerebellar,
pyramidal and coma.
Anoxic coma
• Pupils, corneal reflex, motor response to pain
,myoclonic status, SSEP, serum neuron specific
enolase.
• No response or extension to pain, EEG with
malignant characteristics, absent bilateral sseppoor prognosis
• Elevated NSE at 24 and 48 hrs >33ng/ml -poor
prognosis
• EEG with alternating high voltage slow waves with
low voltage irregular fast activity-good prognosis
Offering prognosis
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Etiology, severity, secondary CNS damage, age.
5-pont Glasgow outcome scale,6-point pediatric cerebral
performance category scale, GCS, FOUR score-motor
score, sphincter control, self care, communication,
pupillary reactivity
Children and young adults, toxic or metabolic
abnormalities-better
Absence of brainstem reflexes, low GCS, hypoxia
,hypotension-worst
MRI,MRS, DTI.
Brain death and organ donation
• Irreversible loss of brain function including
brainstem
• Traumatic brain injury and SAH
• Prerequisites to diagnosis
• Identify patients who are likely to progress to brain
death
• Consent, ethical
• Optimize and treat any physiological disturbance
associated with brain death to protect organs for
transplantation
hypothermia
• To minimize secondary brain damage
• Avoid hyperthermia-excito toxicity, free radical
generation, inflammation, apoptosis.
• Therapeutic hypothermia-core body temp <33 c
• Massive ischemic stroke, TBI, anoxia
• External cooling devices, iv cold saline infusions, iv
cooling catheters.
• Electrolyte abnormalities, cardiac
arrhythmia,infection.
Management of status epilepticus
What is Delirium?
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An acute confusional state with
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Fluctuating mental status
Disordered attention
Disorganised thinking OR altered
consciousness
DSM IV definition: “a disturbance of consciousness with
inattention accompanied by a change in cognition or
perceptual disturbance that develops over a short
period (hours to days) and fluctuates with time”
Synonyms: ICU psychosis, septic encephalopathy, ICU
syndrome, acute brain failure, acute confusional state
How is Delirium Categorised?
Hyperactive
Mixed
Hypoactive
1.6% of cases, “ICU psychosis”, agitation,
restlessness, “picking”, emotional lability
54.1% % of cases
43.5% of cases, “encephalopathy”, often
unrecognised, withdrawal, flat affect, apathy,
lethargy, decreased responsiveness, may be
misdiagnosed as depression
Why does delirium happen?
Opioids & benzo’s
2o brain infection
Decreased cerebral
metabolism
Hypoxia
Serotonin
Acetylcholine
Dopamine
Toxins
Metabolic
derangement
Systemic disease
1o intracranial
disease
Withdrawal
syndromes
DELIRIUM(S) - causes
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D
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M
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Drugs, dementia
Eyes & ears (poor vision and hearing)
Low O2 states (CHF, COPD, ARDS, MI, PE)
Infection
Retention (urine and stool)
Ictal states
Underhydration/undernutrition
Metabolic upset
Subdural, sleep deprivation
Treating delirium
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Non-pharmacological (most studied outside ICU)
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Up to 40% risk reduction achieved
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Repeated reorientation of patients
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Early mobilisation
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Visual and hearing aids (and wax removal!)
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Early catheter, line etc. removal
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Minimise restraints and sedatives
Treating delirium - haloperidol
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Typical antipsychotic
2-5 mg iv/po q6H (reduce in elderly)
Adverse effects – extrapyramidal, prolonged QTc, torsades (3.8%),
neuroleptic malignant syndrome
More effective than lorazepam
? mortality reduction in ventilated ICU patients
Dopamine blockade + disinhibition of ACh
Anti-inflammatory effects
Girard & Ely, Handbook of Clinical Neurology 2008; 90: chapter 3
Treating delirium – atypical antipsychotics
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Olanzepine, quetiapine, risperidone
Alter multiple neurotransmitters including DA, NA, serotonin, ACh,
histamine
Suggestion of decreased extrapyramidal side-effects compared to
haloperidol
As effective as haloperidol
Girard & Ely, Handbook of Clinical Neurology 2008; 90: chapter 3
Skrobik YK, Bergeron N, Dumont M et al. (2004). Olanzapine vs haloperidol: treating delirium in a critical care set- ting. Intensive Care Med 30:
444–449.107: 341–351.
Han CS, Kim YK (2004). A double-blind trial of risperidone and haloperidol for the treatment of delirium. Psychosomatics 45: 297–301 Breitbart W,
Marotta R, Platt M et al. (1996). A double- blind trial of haloperidol, chlorpromazine, and lorazepam in the treatment of delirium in hospitalized
AIDS patients. Am J Psychiatry 153: 231–237.
Awake EEG
BURST SUPPRESSION
BRAIN DEATH
DIFFUSE SLOWING
Thank you