seminar on neurological complcations in medical ICU

1. Coma in non neurological intensive
care units
Santiago ortega et al
University college of Wisconsin.
The Neurologist,Nov,2009.

2. Back ground
 Increased survival among medical and
surgical ICU.
 Increasing spectrum of illness secondary to
critical illness
 1/3 of icu patients,55% mortality rate
 Increase length of stay and disability
 Systematic approach to identify potentially
reversible etiologies and prognostic factors

3. Clinical history
 Physical examination
Degree of sedation
Neurologic examination
Herniation syndromes
Coma scales

4. 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

5. Vital signs interpretation in
comatose patients
Vital signs
Fever
Hypothermia
Hypertension
Potential illnesses
Infection, heatstroke, thyrotoxicosis,
Drugingestion(cocaine,amphetamin
es,Tca,anticholinergic)
Cold exposure, hypothyroidism,
hypoglycemia, shock,
Drugs(alcohol,barbiturates,opioids,s
edatives)
Pheochromocytoma, drugs
(cocaine,amphetamine,phencycli
dine)

6. Vital signs interpretation in
comatose patients
Hypotension
Tachycardia
Bradycardia
HTN-Bradycardia
Addisons, sepsis, MI,
Blood loss, hypothyroidism
Alcohol, amphetamines,
ethylene glycol
Uremic coma, myxedema
coma.
Kocher-cushing reflex.

7. Respiratory patterns in coma
 Cheyne stroke
 Kussmaul breathing
 Agonal gasps
 Central neurogenic
hyprventilation
 Apneusis
 Cluster
 ataxic
-Bihemispheric damage, metabolic
-Metabolic acidosis, post
mesencephalic lesions
-Bilateral lower brainstem lesions
-Bihemispheric,midbrain,pons
-Lateral tegmentum of lower pons
-Bihemispheric or pons
-Dorsomedial medulla RAS

8. Cutaneous and mucosal exam in
comatose
 Petechiae &ecchymosis
 Hypermelanosis
 Cherry red skin
 Gray blue cyanosis
 Telangiectasia
 Ecthyma gangrenosum
 Splinter hemorrages
 pigmentedmacules
TTP,ITP,DIC,RMSF,meningococce
mia,vasculitis,endocarditis
Addisons,chemotherapy,porphyria,
melanoma
.CO poisoning
.Methemoglobinemia
Chronic alcoholism,vascular
malformations
Pseudomonas sepsis
Anemia,sepsis,leucemia,endocarditi
s
Tuberous
sclerosis,neurofibromatosis

9. Neuro muscular blockers in ICU
succinylcholin
e 5-10min -t1/2 renal
rapacurium
12-17 60-120 - hepatic
mivacurium
12-18 2 renal
atracuronium
30-40 20 renal
vecuronium
20-60 60-130 renal hepatic
rocuronium
30-67 80-100 renal
pancuronium
120-180 110-140 renal hepatic
tubocurarine
80-120 240 renal
doxacurium
90-120 100+ renal
pipecuronium
80-100 137+ renal

10. Sedatives in ICU
diazepam 50-120 Icp, cbf,
lorazepam 3-7
midazolam 7-10
morphine 4-11 Cbf,icp
fentanyl 10
thiopental 2-4 Cbf,icp,cpp
phenobarbiton
e
48-144
haloperidol 10-19 Cbf, cpp, icp
propofol 40-50 Cbf,icp,cpp
ketamine 2-14 Cbf,icp

11. 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

12. Main opthalmologic findings in
comatose
 Vitreous sub hyaloid
haemorrages
 Papilledema,retinal
exudates&haemorrages
 Papilledema
 Cholesterol embolus
 Subconjunctival
hemorrage
 Periorbital eccymoses,
Battle sign
-SAH
-hypertensive
encepalopathy
-ICT increase
-carotid atheroma
-endocarditis
-head trauma

13. Eye movements in coma
 Conjugate horizontal roving
 Conjugate horizontal ocular
deviation
 Wrong way eyes
 Downward ,inward eyes
 Ocular bobbing
 Ocular dipping
 Dysconjugate eye movemnts
-Excludes midbrain, pons lesion
-Contralateral pon/ipsilateral
frontal
-Paradoxically to,contralateral
deep hemispheric leson.
-Thalamic,upper midbrain lesion
-Bilateral pontine damage
-Diffuse cortical anoxia
-Brainstem damage

14. 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,barbitur
ates
Midbrain damage or compression
Seizure
Thalamus, sympathetic efferents
from posterior hypothalamus,
tegmentum, descending to the
cervical cord

15. 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

16. Glasgow coma scale

17. FOUR score scale
Eye response
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
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
Brainstem reflexes
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
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

18. Cerebral herniation :clinical
syndromes
Uncal herniation Hemispheric/later
al middle fossa
Ipsilateral III
compression
Dilated ipsilateral
pupil with
preserved or
sluggish reaction
to light.
CnIII,ophthalmopl
egia,ipsilateral
hemipareis
Central herniation Supra tentorial
diffuse brain
edema,
haemorrage,
midline tumors
Initial obstruction
hydrocephalus,
thalamus,
hypothalamus
displacement
Decrease
consciousness,
small & reactive
pupils, normal
eye movements.
Fixed pupils,
cheyne stroke
respiration,
opthalmoplegia,
decorticate
posturing

19. 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, cerebellar
tonsils
All brainstem
reflexes are lost,
flaccid paralysis,
ataxic respiration,
then ceasing

20. Differential diagnosis in non
neurological ICU
Metabolic coma
Structural coma

21. major causes of organic coma-
supra tentorial
 Unilateral
Hemorrhagic contusion
Subdural hematoma
Epidural hematoma
MCA occlusion & edema
IC bleed
Abscess
tumor
 Bilateral
Traumatic injury
Multiple infarcts (vasculitis
coagulopaty, cardiac emboli)
Bilateral thalamic infarct
Primary lymphoma
ADEM
Anoxia
Metastases
Leucoencephalopathy(chemothe
rapy,radiotherapy)

22. Major causes of organic coma-
infratentorial
 Brainstem
pontine bleed
basilar artery
occlusion
central pontine
myelinolysis
brainstem contusion
 Cerebellum
cerebellar infarct
cerebellar bleed
cerebellar abscess
cerebellar tumour

23. Medical ICU
 Metabolic encephalopathy-28.6%
 Seizures-28.1%
 Hypoxic ischemic encephalopathy-23.5%
 Stroke-22.1%
 Sepsis is major cause of neurological
complication-38.8%
Bleck et al-2 yr period

24. 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

25. Primary CNS processes
Meningitis & encephalitis-change in
mental state with fever, csf analysis and
antibiotics.
Posterior reversible leuco
encephalopathy-acute hypertensive
crisis involving brain, vaso genic
edema, control with labetolol, nicardipine
etc.

26. Conditions associated with acute hypertensive crisis &
hypertensive encephalopathy
 Toxemia of pregnancy
 Drugs-cyclosporine
tacrolimus
interferon
fludarabine
cisplatin
gemcitabine
erythropoetin
Uncontrolled essential hypertension
Secondary hypertension-
SLE,AGN,CRF

27. 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.

28. Common precipitants of seizures in
ICU
 Metabolic: renal,
hepatic,
electrolyte,
Endocrine
 Hypoxia/ischemia
 Sepsis
 Stroke
 Primary CNS inflammations
 Withdrawal
delirium tremens
BZD
narcotics
Drugs:
Anti arrythmics- lidocaine, flecainide
Antibiotics-imipenam, ciprofloxacin,
norfloxacin, penicillin derivatives
Antidepressants-amit,
nortript,doxepin
Bronchodilators-theophylline
Immunosupressive drugs-
cyclosporine,OTR3,FK506

29. Secondary CNS processes
Encephalopathy is the most common
neurological complication in medical
ICU.
Prolonged sedation
Drug intoxication

30. Sodium disturbances
 Hypo natremia-incidence of1%,prevalence of
2.5%.
Postoperative patients
Lethargy, confusion, coma ,seizures.
Central pontine myelinolysis
 Hypernatremia-increase use for ICT.
Lethargy, obtundation, coma
Progressive shrinkage of brain leading to
cerebral vascular damage and sub dural
hamatoma

31. Calcium disturbance
Hyper calcemia- ionised calcium levels
and rate of rise.
Delirium, depression, coma.
Hypo calcemia-commonly associated
with sepsis.
Irritabilty, tremors and seizures

32. 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

33. Acid base disturbances
 Severe acidemia-
<7.2,metabolic,respiratory,mixed
Increase of icp, decrease seizure thresold,
stimulate chemoreceptor trigger zone.
 Severe acute alkalemia-ph>7.60
Cerebral vasoconstriction, decreased oxygen
extraction
Respiratory depression, tetany,coma,siezures

34. renal
 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

35. liver
Acute hepatic failure-hyper ammonemia,
hepatic encephalopathy.
Gr IV -80% mortality
pH dependent partial pressure of
gaseous ammonia from blood
Hypoglycemia/hyperglycemia-confusion,
coma, seizures, focal neurological
deficits.

36. Hypoxic ischemic encephalopathy
 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.

37. Sepsis encephalopathy
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

38. Surgical ICU
 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
 Fat embolism-trauma and long bone fracture/surgery
 Multifocal ischemic stroke-Cardiothoracic surgery.
watershed infarcts, LV thrombus, aortic
atherosclerosis ,aortic cross clamping, infective
endocarditis, arrythmias.
MRI limited by pacemakers

39. Transplant ICU
Transplant organ/procedure related
Immunosuppressive therapy

40. Renal/liver transplantation
Cutaneous neuropathies ad spinal cord
infarction
Re vascularisation procedure
BP changes
Hyper coagulabilty-secondary to rapid
correction of uremia
Increase in ICT during postoperative
anicteric phase

41. Cardiac/BMT
Single/multiple cerebral infarctions-
emboli, global hypo perfusion,
arrhythmias, bypass pump, supra
therapeutic heparin
Infections, Hippocampal damage
Bmt-37% met encephalopathy,
CNS infection with minimal signs

42. cyclosporine
Tremor and restlessness
Syndome1-confusion,cortical blindness,
visual hallucinations
Syndrome2-ataxia,cerebellar tremor,
and focal weakness
Within 2 weeks, IV,normal levels
Psychosis, mutism, central pontine
myelinolyis,actionmyoclonus.

43. Tacrolimus/muromonab
 Fine tremor, paresthesias, apraxia, aphasia,
akinetic mutism.
Cortical blindness, CIDP
 Aseptic meningitis and toxic encephalopathy
Csf pleocytosis with neutrophil predominance,
mild protein elevation, normal glucose and
sterile cultures
Seizures, psychosis, visual loss

44. Offering prognosis
 Etiology, severity, secondary CNS damage, age.
 5-pont Glasgow outcome scale,6-point pediatric
cerebral performance category scale, GCS, FOUR
score-motor score, sphincter conrol, 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.

45. 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
ssep-poor 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

46. 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

47. 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.

48. Thank you