1. This document provides guidance on the evaluation and management of patients presenting with coma, transient ischemic attack (TIA), and ischemic stroke.
2. For patients presenting with coma, the assessment involves a detailed history, physical and neurological examination to localize the lesion. Coma etiologies are categorized based on presence of focal signs or meningism.
3. For TIA patients, risk stratification using the ABCD2 score helps determine short term risk of stroke. Acute ischemic stroke is managed with thrombolytic therapy if within 4.5 hours of onset, following strict inclusion/exclusion criteria.
4. Secondary stroke prevention focuses on antiplatelet/anticoagulant drugs based
7. Categorized Coma
Coma without focal signs or meningism
Anoxic-ischemic, metabolic, toxic,
drug-induced, infection, post-ictal state
Coma with meningism
SAH, meningitis, meningoencephalitis
Coma with focal signs
Intracranial hemorrhage, infarction, tumour,
abscess
11. History
Difficult and sometime impossible.
Patient past health and illness.
seizure, diabetes, hypertension
substance abuse
depression, suicide attempts
etc..
Current medication.
27. Supratentorial mass lesion with
secondary brain stem compression
ipsilateral third nerve palsy
contralateral hemiplegia
Brain stem lesion
Abnormal OCR, calorics
Asymmetrical motor responses
28. Toxic/metabolic
Normal pupils: single most important criterion
(except opiate poisoning)
Ocular motility: rove randomly in mild coma and
come to rest in primary position with deepening
coma
Absent OCR and calorics
Decorticate and decerebrate rigidity or flaccidity,
multifocal myoclonus
30. Maintain airway, breathing, and circulation
(ABC’s)
Urgently correct any hypothermia, if
profound.
If trauma has occurred or is strongly
suspected
Stability of the cervical spine before
moving the head.
Initial Management of
Coma
31. Initial Management of
Coma
Rule out hypoglycemia esp DM.
Check basic blood work (blood
count, E’lyte, BS, BUN, Cr, LFT, PT,
PTT, ABG, possibly CO level if
suspected) and urine drug screen.
32. Coma Cocktail
50 ml of 50%glucose IV
100 mg of thiamine IV
Naloxone or Flumazenil for opiate or
BZP overdose.
33. Comatose patient with
suspected SAH
Rule out SAH : brain CT scan without contrast.
Lumbar puncture if SAH is still strongly suspected
but not seen on brain CT scan.
If SAH : neurosurgical consultation and urgent
cerebral angiography.
34. Generally delay CSF examination in CT-negative patients with sudden headache
by 12 h from the onset to ‘allow’ the yellow colour to develop.
35. Comatose patient with
fever or septic syndrome
Examine for any likely systemic focus (abscess,
peritonitis) of infection.
Panculture blood and urine, CXR.
Perform LP to exclude meningitis and begin initial
broad-spectrum antibiotic coverage.
If LP is contraindicated : brain CT scan with and
without contrast.
Brain MRI if suspect Herpes simplex encephalitis
36. CT brain of Increased ICP
Lateral midline shift
Loss of suprachiasmatic or basal cisterns
Fourth ventricle effacement
Obliteration of supracerebellar or quadrigeminal
plate cisterns with patent ambient cisterns
42. Transient
Ischemic Attack
(TIA)
“A transient episode of neurological dysfunction
caused by focal brain, spinal cord, or retinal
ischemia, without acute infarction”
Stroke. 2009;40:2276-2293.
43. Risk Stratification
• ABCD2 score
• Age >60 years (1)
• BP>140/ 90 mmHg (1)
• Clinical symptoms :
• focal weakness with the spell
(2)
• speech impairment without
weakness (1)
• Duration
• <60 minutes (2)
• 10 to 59 minutes (1)
• Diabetes (1)
The 2-day risk of
strokeScore Risk
0-1 0%
2-1 1.3%
4-5 4.1%
6-7 8.1%
Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals. Stroke.
2009 Jun;40(6):2276–93.
44. Risk Stratification
Johnston SC, Rothwell PM, Nguyen-Huynh MN, Giles MF, Elkins JS, Bernstein AL, et al.Validation and refinement of scores to predict
very early stroke risk after transient ischaemic attack. Lancet. 2007 Jan 27;369(9558):283–92.
45. Stroke
“Sudden loss of blood circulation to an area
of the brain, resulting in a corresponding
loss of neurologic function”
47. Baseline laboratory
FBS, CBC, Lipid, BUN, Cr, Electrolytes,
Coagulogram ,Urine exam
Cardiac work up : CXR, EKG
Non-contrast CT brain
Work up for Etiology of Stroke
49. Stroke in the young <45 yr
No evidence of Cardio-embolism or
atherosclerosis risk factor
ESR, ANA, anti-HIV, VDRL, LFT.
Protein C, Protein S, Antithrombin III, factor V
laiden, prothrombin gene, Homocysteine.
Antiphospholipid syndrome : anticardiolipin,
Lupus anticoagulant
50. Suspected of intra or extra-cranial
artery stenosis
Carotid bruit, Amouroxis fugax
Lacunar infarction with mRS>2
Vascular Work up
54. Onset of stroke
Sudden onset of focal neurological deficit
Basic life support and capillary blood
glucose to exclude hypoglycaemia
Onset <4.5 hr
Stroke Fast Track
Emergency Lab
CBC, BS, BUN, Cr
Cogulogram, E’lyte, EKG
Emergency
Non-Contrast CT
Acute Ischemic Stroke
Start Thrombolytic Treatment
within 4.5 hr of Stroke onset
Normal or Hypodensity
Onset 4.5-72 hr
Emergency Lab and
Non-Contrast CT
Acute Ischemic Stroke
Treatment
55. N Engl J Med 1995;333:1581-7
Treatment with iv t-PA within 3 hours of the onset of
ischemic stroke improved clinical outcome at 3 months.
National Institute of Neurological Disorders and Stroke (NINDS) study group
56. Significantly improved clinical outcomes in
patients with acute ischemic stroke
N Engl J Med 2008;359:1317-29.
ECASS III
mRS
65. Anticoagulant in AIS
Early administration of UFH or LMWH
does not lower the risk of early recurrent
stroke including among people with
cardioembolic sources.
Not recommended for treatment of patients with
acute ischemic stroke (Class III; Level of Evidence A).
79. ≥ 5 minutes of continuous
seizures
≥2 discrete seizures between
which there is incomplete recovery
of consciousness
Definition
Neurocrit Care (2012) 17:3–23
80. Convulsive Status Epilepticus
Focal motor SE and EPC not included in these definition
Non-Convulsive Status Epilepticus (NCSE)
Electrographic seizure without clinical GCSE
Two distinct phenotype : “Wandering confused”,
“Subtle status”
Classified by Semiology
Neurocrit Care (2012) 17:3–23
81. Cause of SE : Acute Process
Neurocrit Care (2012) 17:3–23
Metabolic disturbances: E’lyte, hypoglycemia, renal failure
Sepsis
CNS infection: meningitis, encephalitis, abscess
Stroke: ischemic stroke, ICH,SAH, CVST
Head trauma with or without epidural or subdural hematoma
Drug : toxicity, withdrawal (opioid, BZP, barbiturate, alcohol),
Non-compliance with AEDs
Hypoxia, cardiac arrest
Hypertensive encephalopathy, PRES
Autoimmune encephalitis : anti-NMDA, anti-VGKC,
paraneoplastic syndrome
82. Cause of SE : Chronic Process
Neurocrit Care (2012) 17:3–23
Preexisting epilepsy: breakthrough
seizures or discontinuation of AEDs
Chronic ethanol abuse in setting of
ethanol intoxication or withdrawal
CNS tumors
Remote CNS pathology (stroke,
abscess, TBI, cortical dysplasia)
83. Diagnostic Work up
Neurocrit Care (2012) 17:3–23
Monitor vital signs.
CT scan of brain.
DTx, BS, CBC, basic metabolic panel, Ca,
Mg, AED levels.
Continuous EEG monitoring
Consider : Brain MRI, CSF study,
toxicology (INH, TCA, CsA, theophylline, cocaine,
sympathomimetics, alcohol, organophosphates)
85. Stage of Status
Epilepticus
Current Opinion in Neurology 2011, 24:165–170
Rapid action, Parenteral, Lipid soluble
Early 0 - 30 min Lorazepam, Diazepam
Establish 30 - 60 min Phenytoin, Phenobarbital,
Valproate, Levetiracetam
Refractory > 60 min Propofol, Thiopental, Midazolam
86. Drugs use in Stage of
Early Status Epilepticus
Route of administration Adult dose
Diazepam i.v. bolus ( <2-5 mg/min) 10-20 mg
Lorazepam i.v. bolus 4 mg
Midazolam Buccal or intranasal, i.m. 5-10 mg
Clonazepam i.v. bolus (<2 mg/min) 1-2 mg at 2 mg/min
Current Opinion in Neurology 2011, 24:165–170
87. Drugs use in Stage of
Established Status Epilepticus
Route of
administration
Loading Dose Continuous dose
Phenytoin
i.v. bolus
(<50 mg/min)
15-20 mg/kg
after 8 hr 300-500
mg/d q8h
Fosphenytoin
i.v. bolus
(<100 mg PE/min)
15-20 mg PE/kg
after 8 hr 300-500
mg/d q8 h
Phenobarbital
i.v. bolus
(<100 mg/min)
10-20 mg/kg
after 8 hr 180-240
mg/d q12h
Valproate
i.v. bolus
(<50mg/min)
15-30 mg/kg 1-2 mg/kg/hr
Levetiracetam
i.v. bolus
in 15 min
Optimal dose not known,
often use 2000-4000 mg
10-30 mg/kg q12h
Topiramate * naso / orogastric 500 mg q 12h x 2days
150-750 q 12h
usual effective
300-1600
Current Opinion in Neurology 2011, 24:165–170
แนวทางรักษาโรคลมชัก
* small report
88. Drugs use in Stage of
Established Refractory Epilepticus
Route of administration
Midazolam
Bolus : 0.1–0.3mg/kg at 4mg/min
Infusion : 0.05–0.4mg/kg/h
Thiopentone
Bolus : 100–250 mg bolus over 20s then
further 50mg boluses every 2–3min until controlled
Infusion : 3–5mg/kg/h to maintain burst suppression
Pentobarbital
Bolus : 10–20mg/kg bolus at 25mg/min
Infusion : 0.5–1mg/kg/h increasing to 1–3mg/kg/h to
maintain burst suppression
Propofol
Bolus : 2mg/kg
Infusion : 5–10mg/kg/h to maintain burst suppression
Current Opinion in Neurology 2011, 24:165–170