Coma in non neurological intensive care units

Santiago ortega et al

University college of Wisconsin.

The Neurologist,Nov,2009.

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

Clinical history Physical examinationDegree of sedationNeurologic examinationHerniation syndromesComa scales

Essential clinical history in patients with loss of consciousness

HistoryTime course-abrupt gradual fluctuatingPreceding focal signsPrevious episodesh/o recent illnessh/o recent fallAltered behaviourDrugsMedical psychological historyAlcohol drug abuse

Possible causesSAH, seizure, bleedingTumour, venous thrombosisMetabolic,subdural hematoma.Focal lesionTIA, seizureInfection, metabolicSubdural, epidural bleedToxic, metabolic, infectionToxic-metabolic.Metabolic, psychiatricToxic-metabolic

Vital signs interpretation in comatose patients

Vital signs

Fever

Hypothermia

Hypertension

Potential illnessesInfection, heatstroke, thyrotoxicosis,

Drugingestion(cocaine,amphetamines,Tca,anticholinergic)

Cold exposure, hypothyroidism,

hypoglycemia, shock,

Drugs(alcohol,barbiturates,opioids,sedatives)

Pheochromocytoma, drugs (cocaine,amphetamine,phencyclidine)

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.

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

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,meningococcemia,vasculitis,endocarditis

Addisons,chemotherapy,porphyria,melanoma

.CO poisoning

.Methemoglobinemia

Chronic alcoholism,vascular malformations

Pseudomonas sepsis

Anemia,sepsis,leucemia,endocarditis

Tuberous sclerosis,neurofibromatosis

Neuro muscular blockers in ICUsuccinylcholine 5-10min -t1/2 renalrapacurium 12-17 60-120 - hepaticmivacurium 12-18 2 renalatracuronium 30-40 20 renalvecuronium 20-60 60-130 renal hepaticrocuronium 30-67 80-100 renalpancuronium 120-180 110-140 renal hepatictubocurarine 80-120 240 renaldoxacurium 90-120 100+ renalpipecuronium 80-100 137+ renal

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

phenobarbitone

48-144

haloperidol 10-19 Cbf, cpp, icp

propofol 40-50 Cbf,icp,cpp

ketamine 2-14 Cbf,icp

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 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

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

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,barbiturates

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 response4-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 response4-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 reflexes4-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

Respiration4-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

Cerebral herniation :clinical syndromes

Uncal herniation Hemispheric/lateral middle fossa

Ipsilateral III compression

Dilated ipsilateral pupil with preserved or sluggish reaction to light.

CnIII,ophthalmoplegia,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

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

Differential diagnosis in non neurological ICU

Metabolic coma

Structural coma

major causes of organic coma-supra tentorial

UnilateralHemorrhagic contusionSubdural hematomaEpidural hematomaMCA occlusion & edemaIC bleedAbscesstumor

Bilateral Traumatic injury Multiple infarcts (vasculitis coagulopaty, cardiac emboli) Bilateral thalamic infarct Primary lymphoma ADEM Anoxia MetastasesLeucoencephalopathy(chemothe

rapy,radiotherapy)

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

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

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 encephalopathy-acute hypertensive crisis involving brain, vaso genic edema, control with labetolol, nicardipine etc.

Conditions associated with acute hypertensive crisis & hypertensive encephalopathy

Toxemia of pregnancy Drugs-cyclosporine tacrolimus interferon fludarabine cisplatin gemcitabine erythropoetinUncontrolled essential hypertensionSecondary hypertension- SLE,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

Metabolic: renal, hepatic, electrolyte, Endocrine

Hypoxia/ischemia

Sepsis

Stroke

Primary CNS inflammations

Withdrawal delirium tremens BZD narcoticsDrugs:Anti arrythmics- lidocaine, flecainide

Antibiotics-imipenam, ciprofloxacin, norfloxacin, penicillin derivatives

Antidepressants-amit, nortript,doxepin

Bronchodilators-theophylline

Immunosupressive drugs-cyclosporine,OTR3,FK506

Secondary CNS processes

Encephalopathy is the most common neurological complication in medical ICU.

Prolonged sedationDrug intoxication

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

Calcium disturbance

Hyper calcemia- ionised calcium levels and rate of rise.

Delirium, depression, coma.Hypo calcemia-commonly associated

with sepsis.

Irritabilty, 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 thresold, stimulate chemoreceptor trigger zone.

Severe acute alkalemia-ph>7.60

Cerebral vasoconstriction, decreased oxygen extraction

Respiratory depression, tetany,coma,siezures

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

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.

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.

Sepsis encephalopathy

Most common (70%) in medical icu.Highest mortalityMulti organ failureDecreased 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

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

Transplant ICU

Transplant organ/procedure related

Immunosuppressive therapy

Renal/liver transplantation

Cutaneous neuropathies ad spinal cord infarction

Re vascularisation procedureBP changesHyper coagulabilty-secondary to rapid

correction of uremiaIncrease in ICT during postoperative

anicteric phase

Cardiac/BMT

Single/multiple cerebral infarctions-emboli, global hypo perfusion, arrhythmias, bypass pump, supra therapeutic heparin

Infections, Hippocampal damageBmt-37% met encephalopathy,

CNS infection with minimal signs

cyclosporine

Tremor and restlessnessSyndome1-confusion,cortical blindness,

visual hallucinationsSyndrome2-ataxia,cerebellar tremor, and

focal weaknessWithin 2 weeks, IV,normal levelsPsychosis, mutism, central pontine

myelinolyis,actionmyoclonus.

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

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.

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

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.

Thank you