Coma in non neurological intensive care units Santiago ortega et al University college of Wisconsin. The Neurologist,Nov,2009.
May 06, 2015
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