ICU Fellowship – How to Approach a Neuro Hot Case?

Dr Swapnil Pawar September 5, 2021 63 5

ICU Fellowship – How to Approach a Neuro Hot Case?
Dr Swapnil Pawar

Blog Written by Dr Swapnil Pawar

Outside the room – some of the common stems –

…yr M/F admitted with …. trauma/ loc/ confusion/ seizures and its day < week to > few weeks type of scenarios

So in those 2 minutes, start thinking about how you are going to assess the neurology of this patient.

Inside the room –

observation phase – key clues to notice –

Monitor – AF, ICP monitor – what is ICP and what is CCP – what’s the trend, look at the waveform ( p1,P2, P3 )

Infusions – some of the common patterns –

No infusions at all
Heavy sedation and paralysis
Noradrenaline along with sedation
nimodipine infusion
antiepileptic infusions
3% or 20% saline infusions

other devices attached –

Codman/ EVD – make an attempt to check the height of the column – that will tell you whether the plan is to wean and take the drain out

Notice whether it is intermittently draining or is on continuous drainage.

Look at the CSF – colour and ask for micro reports.

Ventilator – notice the mode, FiO2 and compliance. Sometimes patients can have neurogenic pulmonary edema or aspiration pneumonia.

Examination Phase –

Start systematically. Ask whether stopping sedation is appropriate. This will depend on the context.

Check responsiveness & higher functions –> Assess GCS – individual components. graded escalation technique.

Often candidates get confused at this stage – whether to give painful stimuli or not. If so, how to do it. It really boils down to what’s your objective. If the patient is conscious and obeying commands and you apply the painful stimuli, that’s failing. if the patient is on industrial doses of sedation and or paralysis – giving painful stimuli is fail. So use the painful stimuli if you are worried about focal neurology or the patient is unconscious despite sedation. By applying painful stimulus you are confirming 2 things – you are assessing the motor score and you are checking for symmetry. Supra-orbital painful stimulus is the preferred one.

Check cranial nerve functions – This is another area where candidates go wrong.

Intubated patients are the easiest ones. Only cranial nerves that you can examine

Light reflex (CN II [Optic] and III [Oculomotor]):

Light impulse is carried to CN III via CN II.
Light shone into either eye causes simultaneous CN III stimulation (which makes the pupil

constrict). Both pupils constrict to light that is shone into either eye (direct and consensual

response).
If the pupil reacts to light shone into either eye, it is probably not a CN III cause.

Corneal reflex (V1 branch of CN V [Trigeminal] and CN VII [Facial]):

Touching the cornea causes both eyes to blink. The sensation is detected by the first branch of CN V (V1 branch), which stimulates CN VII to protect the eyes; nasal tickle tests the same pair.
Be careful to “sneak in from the side” when touching the cornea (with a whisp of gauze piece). If the patient blinks because they see you, you have tested CN II and VII. If they blink because they hear you, you have tested CN VIII (Acoustic) and VII.
Blinking of only one eye suggests weakness on the side of the face with the absent blink

Doll’s Eyes or Oculocephalic reflex (CN III [Oculomotor], VI [Abducens] and VIII [Acoustic] and pons)

Normally, when the head is turned, the vestibular apparatus (CN VIII) is activated, causing the

eyes to move in the opposite direction. CN VIII communicates to both CN III and VI in the

pons to produce horizontal eye movement.
CONTRAINDICATED IF C-SPINE UNCLEARED
Vertical eye movement is located at top of the brainstem (CN III); involves frontal lobe eye fields.
Stoke can be associated with the abnormal gaze.

Alternatively, you can check occulovestibular reflex by performing cold caloric test.

Gag Reflex (CN IX [Glossopharyngeal] and X [Vagus]):

Test one side at a time. Checking this in intubated patient can be challenging.

Coughing and Breathing (CN X and Medulla):

Assess for cough reflex during suctioning.

Check motor function – it includes testing for tone, Power and reflexes.

Motor Assessment:

Muscle tone
Observe patients for symmetry of movements. Observe spontaneous/localizing movements, as well as response to painful stimuli.
If the patient is able to obey commands, describe motor response using the 0-5/5 Motor Scoring Scale.
You should be able to classify the weakness of the patient – 1. Proximal vs Distal

Check Reflexes –

Biceps Brachii Tendon C5, C6 ; Triceps Tendon C7, C6 ; Brachioradialis Tendon C6, C5 ; Quadriceps Tendon (knee jerk) L4, L3, L2 ; Achilles Tendon (ankle jerk) S1

UMN Vs LMN –

Motor weakness associated with increased tone and deep tendon reflexes (3 or 4+), with/without clonus suggests an upper motor neuron cause for the weakness.

Motor weakness associated with flaccid paralysis and decreased deep tendon reflexes (< 2+) suggests a lower motor neuron cause for the weakness.

Sensory function –

Mostly not needed for ICU intubated patients. might need it for spinal cord patients. It’s important to identify correct dermatomes. You are not expected to check every single dermatome but doing it in certain dermatomes is a good idea including the abdomen.

Cerebellar function –

if you notice nystagmus on your eye examination and the patient is able to obey commands you can quickly assess for dysdidachokinesia by clapping or by performing heel to knee test.

Interpretation – Some of the relevant patterns for CICM exam –

Consciousness –

Structures Required for Consciousness Two neural structures are required for consciousness: the brain stem reticular activating system; and one cerebral hemisphere. Thus, a patient is unconsciousness if injury has occurred to both cerebral hemispheres or to the brain stem reticular activating system.

Speech –

Expressive aphasia (front, motor, non-fluent, Broca) is usually seen following a lesion involving Broca’s area (lateral pre-motor cortex). Expressive aphasia is marked by significant difficulty producing language, but with preserved understanding. Patients with this form of aphasia typically have a right hemiparesis, due to involvement of the adjacent motor cortex.

Receptive aphasia (back, sensory, fluent, Wernicke) is seen with a lesion involving the supramarginal and angular gyri in the temporal lobe (Wernicke’s area). This aphasia is characterized by fluent, nonsensical speech with numerous paraphasic errors, and markedly impaired understanding. Patients with receptive aphasia frequently have contralateral homonymous hemianopia due to involvement of the adjacent optic radiations

Hemiplegia can result from a unilateral lesion of the brain stem, internal capsule, or cerebral cortex.

Brain stem lesions result in crossed hemiplegia.

For example, a left pontine lesion will result in left facial weakness of lower motor neuron type and right-sided hemiplegia.

Similarly, a lesion in the left midbrain will result in left-sided oculomotor weakness with right hemiparesis and right facial weakness of upper motor neuron type. This constellation of signs is called Weber syndrome.

Lesions above the level of the brainstem result in uncrossed hemiplegia.

For example, a lesion in the left internal capsule would result in right hemiplegia and right facial weakness of the upper motor

neuron type.

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