Download Introduction To Neurological Intensive Care

Introduction to Neurological
Intensive Care
M. S. Damian, Cambridge/Ipswich
Medical neurointensive care
issues deal primarily with:
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Altered conscious states
Coma and failure to awaken
Seizures and status epilepticus
Acute paralysis causing respiratory
distress or failure of airways protection
What are the prime issues for
neurological assessment in critical care?
• Are there focal neurological abnormalities?
– Focal findings = structural lesion
– No focal findings = metabolic disease
• How long since consciousness lost?
– Outcome in come is linked to duration
– Every condition is reversible at the beginning
– “Time is brain”
Altered Consciousness and Coma
2 main components of consciousness:
Arousal or wakefulness = “level of
consciousness“:
The ascending reticular activating
system (ARAS) extends through the
dorsal brainstem at the floor of the 4th
ventricle, then branches out through
the thalamus and diencephalon to
both hemispheres.
Awareness and responsiveness =
”contents of consciousness“ includes
attention, orientation, motivation,
sensation, perception, self-awareness,
memory and cognition.
Causes of Impaired Consciousness
500 consecutive cases - Plum & Posner
Metabolic/diffuse disorders:
63%
• Intoxications 30%
• Anoxia/Ischemia 17%
• Hepatic Coma 3.5%
• Endocrine Coma 2.5%
• Acid-base disturbance 2.5%
• Encephalitis 2.8%
• Hypothermia 1.8%
• Uremia 1.6%
• Pulmonary diseases,
malnutrition, psychiatric
disorders, others 2.5%
Hemispheric Disorders: 24%
• ICH 9%
• Subdural hematomas 5%
• SAH 2.6%
• Epidural hematomas 1%
• Cerebral infarction 1.8%
• Brain tumor, abscess, pituitary
apoplexy, thalamic infarct 3.4%
Infratentorial Disorders: 13%
• Brain stem infarction 8%
• Brain stem hemorrhage 2.2%
• Others: 2.8%
Causes of Impaired Consciousness
500 consecutive cases - Plum & Posner
Metabolic/diffuse disorders:
63%
• Intoxications 30%
• Anoxia/Ischemia 17%
• Hepatic Coma 3.5%
• Endocrine Coma 2.5%
• Acid-base disturbance 2.5%
• Encephalitis 2.8%
• Hypothermia 1.8%
• Uremia 1.6%
• Pulmonary diseases,
malnutrition, psychiatric
disorders, others 2.5%
Hemispheric Disorders: 24%
• ICH 9%
• Subdural hematomas 5%
• SAH 2.6%
• Epidural hematomas 1%
• Cerebral infarction 1.8%
• Brain tumor, abscess, pituitary
apoplexy, thalamic infarct 3.4%
Infratentorial Disorders: 13%
• Brain stem infarction 8%
• Brain stem hemorrhage 2.2%
• Others: 2.8%
29 y/o university student, 1 day confused and somnolent: Vague history →
emergency CT considered normal → skew deviation was missed →
neurologist advised “MR tomorrow” in phone consultation.
Patient is now demented and dystonic
Phone advice without seeing the patient is never a Good Call!
Phone consultations: Bad call!
Assessment of metabolic
encephalopathy
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Search for subtle focal clinical signs
Make sure laboratory tests are complete
Analyse acid-base abnormalities
Look for clinical characteristics of specific
conditions
Hepatic encephalopathy and coma
Hepatic encephalopathy is clinically
classified in 4 stages:
Stage 1 features anxiety and restlessness,
or apathy, shortened attention span, and
altered sleep patterns. Altered handwriting
is an indicator
Stage 2 features personality change,
disorientation, and psychosis. Asterixis,
ataxia, dysarthria and abnormalities of
muscle tone appear.
Stage 3 features delirium, bizarre
behaviour, drowsiness or stupor. Seizures,
myoclonus, and hyperreflexia appear.
Stage 4 is hepatic coma with flexor or
extensor responses, and commonly
increased tone, brain swelling
progressing to deep coma and brain
death.
Hepatic coma results from the combined
effects of electrolyte disturbance and
neurotoxins, including benzodiazepine
analogs, glutamate, and ammonia, most
often arterial value exceeding 120
micromols/L, and of a systemic
inflammatory response, mitochondrial
failure, BBB failure, and altered brain
perfusion. Flumazenil infusion may
improve the conscious state where brain
swelling is not the cause of coma.
Causes of Anion Gap Metabolic Acidosis
Anion gap =Na+ - (Cl- + HCO3-); normal = 12-15
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Exogenous
Salicylates
Methanol
Ethylene glycol
Iron
Paraldehyde
Cyanide
Carbon monoxide
Isoniazid
Endogenous
• Uremia
• Ketoacidosis
• Lactic acidosis
Hypertensive
encephalopathy and
posterior white matter
disease
Endocrine Derangement
Left: cortical damage in hypoglycemia;
Right: Hashimotos encephalopathy
Septic encephalopathy
Disease outside the brain must be
considered: critical illness myoneuropathy,
other neuromuscular disease, or
myelopathy?
Careful review for toxicity: cumulative
effects of sedative drugs are underestimated
(prolonged half-lives; third-spacing).
Endogenous toxins through organ failure?
Left: mutifocal bleeding (ECMO patient);
Right: septic emboli with endocarditis
Bihemispheric brain injury must be excluded
(endocarditis, multiple infarcts, abscesses;
multifocal haemorrhage; anoxic injury; brain
swelling).
Nonconvulsive status epilepticus is
underdiagnosed.
The septic process itself may cause
persistent cognitive deficits and brain
atrophy after recovery ( images bottom left
and right).
A 51 year old patient with cognitive loss following severe
sepsis. MRI on left during sepsis; MRI right performed 3
months later shows enlarging CSF spaces
Medication effects
Left: Leukoencephalopathy due to 5FU-Metimazole
(chemotherapy for bowel cancer)
Below: PRES and hemorrhage with tacrolimus
after stem cell transplantation
Anoxic-ischaemic coma after resuscitation
• 50-100 per 100 000 per year undergo CPR
• 25% are admitted to hospital
• 10% are discharged alive
• 5% are alive after 1 year
Pathophysiology of hypoxic brain injury
y
cit
i
x
o
c
Ex
t
ito
ATP deficit
NA/K pump failure
Energy failure
Depolarisation
Glutamate release
Metabotropic Ca++
channels open
Voltage-gated Ca++
channels open
ROS 
Intracellular Ca-influx
Phospholipase 
Mi
dy tocho
CPR
sfu
n
nct drTia
Mitochondrial
i
l
injury + swelling on
Reperfusion
r
Aquaporin(AQP8/9) e
channels activated
→H2O influx
a Inflammation
t Cytokine 
Cytochrome
C release
m
Caspase activation e
ROS 
n
Apoptosis
t Secondary
Ischaemia / Hypoxia
ROS 
Protease 
Cell Death
hypoperfusion
Diencephalic hypoxic injury after asthma
attack causing respiratory arrest. Prolonged
coma with prominent autonomic
dysregulation.
Neurological complications in known
medical conditions
Complications of systemic infection (septic encephalopathy;
critical illness myoneuropathy; endocarditis)
Anoxia and cardiac arrest
Endocrine disorders
Renal disease (uremic encephalopathy, disequilibrium
syndrome; hypertensive encephalopathy)
Hepatic encephalopathy and fulminant liver failure
Disorders of hemostasis and coagulation
Acute vasculitic complications
Complications of organ transplantation
Tests: Laboratory
How severe must laboratory abnormalities be to explain coma?
• Hyponatremia: <110 mmol/L coma, <120 mmol/L
may cause drowsiness if rapid onset
• Hypernatremia: >160 mmol/L
• Hypercalcemia: >3.4 mmol/L
• Hypermagnesemia: >3 mmol/L
• Hypercapnia: >70 mm Hg pCO² (9.3kPa)
• Hypoglycemia: < 2.5 mmol/L
• Hyperglycemia: > 40mmol/L
• Hypophosphatemia < 0.2mmol/L
Individual toleration varies substantially, and
severely ill patients may have multiple coexisting
abnormalities
Tests : Electrophysiology
Seizure? EEG during right facial twitch
Neurological Assessment of the
Unresponsive Patient: 4 components
• Inspection
• Brain stem reflexes
• Motor function
• Sensory testing
1. Inspection
• Tone: Normal – spastic/rigid – symmetric or
asymmetric – flaccid – varies
• Posture: Normal – decorticate – decerebrate hemiparetic
• Movements: repetitive – simple – complex –
spontaneous or to stimuli – none – face or limbs?
• Respiration: – rate and pattern (see below)
• Pupils: – size – shape – equal or anisocor
• Fundoscopy
2. Brainstem reflexes:
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Pupillary examination and pupillary reflexes
Corneal reflex
Eye movements and Oculocephalic Reflex
Gag reflex
Cough
Respiratory pattern
Pupillary Abnormalities in Coma
From: Wijdicks EFM 2001
The corneal reflex (CN 3 and 7)
Brain Control of Eye Movements: 3 separate types of
eye movement represent a large area of the brain
Saccades (frontal control)
Smooth pursuit (parietal)
http://cnx.org/contents/29ea21c4-4625-4e86-82be
[email protected]:15
1.) Nuclei of oculomotor nerve
2.) Trochlear nucleus
3.) Pons
4.) Fourth ventricle
5.) Abducent nucleus
6.) Vestibular nucleus
7.) Medial longitudinal fasciculus
Oculomotor Assessment in Coma
•Very reliable for identifying lesion location
•Supratentorial lesions cause conjugated
abnormalities of eye movements
Vergence towards or away from lesion
Abnormalities of saccadic gaze (frontal lesions)
Abnormalities of smooth pursuit (ipsilateral parietal lesions)
Preserved passive ocular motility
•Metabolic disorders cause slowed passive
movements and mild divergence
•Asymmetric/disconjugate eye positions always
signify brain stem dysfunction
•Characteristic oculomotor syndromes exist for some
specific lesions (INO, abnormal vertical
motility, ocular bobbing, skew deviation)
Rotate the head while observing the movements of both eyes.
Exclude cervical trauma first!
Respiratory Patterns in Craniocaudal
Progression of Coma
• Cheyne-Stokes respiration: slow periods of
hyperventilation that alternate gradually with periods
of hypoventilation (bihemispheric / metabolic)
• Central neurogenic hyperventilation: rapid
breathing 40-70 respirations/min (midbrain lesion)
without variation
• Apneustic breathing: slow with prolonged pauses
between inspiration and expiration (pontine lesion)
• Rapid cycle breathing (uncertain localization, but
unfavourable)
• Cluster breathing: clusters of breaths followed by
apneic periods of variable duration (caudal pontine)
• Ataxic breathing (Biot’s): irregular respiratory rate
and rhythm (medullary; soon to followed by apnoea)
The gag (pharyngeal) reflex (CN 9 and 10)
and assessment of the tongue (CN12
3. Motor Function in the Assessment
of Coma
• Brain stem reflexes
• Motor function (tone, response
to pain, tendon reflexes and
plantars, note especially
symmetry left-to-right and
arms-to-legs)
• Sensory testing
• Scores
4. Sensory Function in the Assessment
of Coma
• Brain stem reflexes
• Motor function
• Sensory testing
 Test pain
 Elicit maximum
response
 Examine for
sensory levels
• Score
Eyes
4 = open + tracking
3 = open spontaneously
2 = to speech
1 = to pain
0 = closed
Brainstem
4 = Pupil + corneals +
3 = one pupil dilated
2 = pupil or corneals absent
1 = pupil and corneals absent
0 = cough absent
Motor
4 = obeys
3 = localizes
2 = flexion
1 = extends
0 = none or myoclonus
Respiration
4 = normal pattern
3 = Cheyne Stokes
2 = irregular
1 = breathes above ventilator
0 = breathes at ventilator
Scores in the
Assessment of Coma:
The FOUR Score
[EFM Wijdicks 2005]
STANDARDISED NEUROLOGICAL
ASSESSMENT of the COMATOSE
PATIENT
Inspection: Speech
Facial (droop R/L; grimacing)
Tone
Posture
Movements
(complex/repet/stereo)
Respiration (rate and pattern)
On Admission
Date__________
Review
Date___________
Review
Date___________
Speech
Oriented
Confused
Inappropriate words
Incomprehensible
No sounds
Tone
Normal
Spastic
Rigid
Flaccid
Posture
Normal
Decorticate
Decerebrate
Hemiplegic
Symmetrical
Asymmetrical
Variable
Fundoscopy (R/L)
Autonomic findings
Notable other observations
Brain stem reflexes: Pupils (size and
reflexes)
Spontaneous eye movements
Eye movements to pain
Oculocephalic reflex
FOUR score criteria
Eye response (E)
4 = eyelids open/opened/tracking/blinking
3 = eyelids open but not tracking
2 = eyelids closed but open to loud voice
1 = eyelids closed but open to pain
0 = eyelids remain closed with pain
Corneal reflex (R/L)
Masseter reflex
Pharyngeal sensation (gag)
Tracheal sensation (cough)
Eye response
Motor response
Pupillary (Y/N)
FOUR
score
Brainstem
reflexes
Corneal (Y/N)
Cough (Y/N)
Score
Respiration
Total FOUR score
Imaging results
Motor response (M)
4 = thumbs-up, fist or peace sign
3 = localising to pain
2 = flexion response to pain
1 = extension response to pain
0 = no response to pain, or
myoclonic status epilepticus
Brainstem reflexes (B)
4 = pupil and corneal reflexes present
3 = one pupil wide and fixed
2 = pupil or corneal reflexes absent
1 = pupil and corneal reflexes absent
0 = absent pupil, corneal and cough reflexes
Respiration (R)
4 = not intubated, regular breathing pattern
3 = not intubated, Cheyne-Stokes breathing
2 = not intubated, irregular breathing
1 = breathes above ventilator rate
0 = breathes at ventilator rate, or apnoea
What are epileptic seizures?
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Clinical manifestations of abnormal hypersynchronous discharges of
cortical neurons
Symptoms depend on the location of the epileptic discharges in the
cortex and on the pattern how they propagate in the brain (Cavazos
2010)
Why is optimal seizure management
important?
• Convulsive status epilepticus is life-threatening
• Seizures elevate ICP
• Seizures may provoke cardiac failure
• Nonconvulsive status alters conscious state
• Antiepileptic drugs may affect consciousness
• Drug interactions may affect other treatment
Seizures drive up CBF and rSO2 
elevate ICP
Approach to Suspected Seizures on ICU
Unexplained impaired consciousness or recurrent episodic stereotypies
1. Document the clinical features:
– Duration of event (more than seconds?)
– Pattern of movement (stereotyped episodes?)
– Complex or elementary movements
– Externally triggered events? (normally not)
– Tremor or clonic movements? (not tremor)
2. Seek EEG confirmation
– Preferably before medication
– Only EEG changes during a clinical episode are proof
Caveat:
– Negative interictal EEG is not an exclusion
– EEG “epileptiform” changes are not absolutes
3 main groups of patients with
neuromuscular disease may require
treatment in the ICU
I.
Patients with severe new onset acquired
neuromuscular disease (eg. GBS)
II. Patients with pre-existing chronic
neuromuscular diseases who develop acute
complications (eg. Myasthenia)
III. Patients whose neuromuscular condition
arises in the ICU (eg. ICUAW / critical illness
neuromyopathy)
M. S. Damian, Addenbrookes
Hospital, Cambridge
Patient found to be weak in the ICU
(slow wean; ptosis; limb weakness)
Clinical examination: Consciousness affected? Muscle tone increased?
Plantars up? → 3x “No” suggests neuromuscular disease
↓
MRI: Exclude brain (if face affected) or spinal (limbs only) disease
↓
CSF and baseline labs: protein? Cell count? CK? Tox screen?
↓
NCV, RepStim and EMG: Nerve root vs. nerve vs. NMJ vs. Muscle?
↓
Special labs: Anti-GM1/GM2/GD1a/GQ1b; Anti-AchR/MuSK/VGKC;
DNA tests
↓
Muscle/Nerve biopsy: If NCV and RepStim inconclusive
M. S. Damian, Addenbrookes
Hospital, Cambridge
3 major subtypes of ICUAW:
1.) Acute myosin loss myopathy
– Also in steroids without neuromuscular blocking drugs
– Selective loss of the thick (myosin) filaments
– Recovery is normally good, but takes several months
Absent A-band
M. S. Damian, Addenbrookes
Hospital, Cambridge
ICUAW
2. Acute type 2 fibre atrophy
3. Acute necrotizing myopathy
M. S. Damian, Addenbrookes
Hospital, Cambridge
Beware of your limitations!
Specialised Neurointensive Care
improves outcomes
▲ Neurocritical care unit; ▲ General ICU with full-time neurological support;
Δ General ICU with limited neurological support
Questions?
M. S. Damian, Addenbrookes
Hospital, Cambridge