Neurologic Intensive Care

Question 1

Monro-Kellie doctrine

Answer 1

ICP is a function of the volume and compliance of each component of the intracranial compartment

** Under physiologic conditions, the intracranial contents include (by volume):

●Brain parenchyma – 80 percent

●Cerebrospinal fluid – 10 percent

●Blood – 10 percent

Question 2

intracranial hypertension definition

Answer 2

pressures ≥20 mmH2O

Question 3

CSF production rate

Answer 3

SF is produced by the choroid plexus and elsewhere in the CNS at a rate of approximately 20 mL/hour (500 mL/day)

Question 4

Causes of intracranial hypertension

Answer 4

Question 5

intracranial hypertension clinical findings

Answer 5

Global symptoms of elevated ICP include
1) headache, which is probably mediated via the pain fibers of cranial nerve V in the dura and blood vessels
2) depressed consciousness due to either the local effect of mass lesions or pressure on the midbrain reticular formation
3) vomiting

Signs include
1) CN VI palsies
2) papilledema
3) spontaneous periorbital bruising
4) a triad of bradycardia, respiratory depression, and hypertension (Cushing triad)

Focal symptoms of elevated ICP may be caused by local effects in patients with mass lesions or by herniation syndromes.
Herniation results when pressure gradients develop between two regions of the cranial vault.

Question 6

Most common anatomic locations affected by herniation syndromes

Answer 6

• subfalcine (υποδρεπανικός)
  η έλικα του προσαγωγίου πιέζεται κάτω από το δρέπανο, με αποτέλεσμα συμπίεση της πρόσθιας εγκεφαλικής αρτηρίας και επακόλουθη ετερόπλευρη πάρεση κάτω άκρου, καθώς και διαταραχές συμπεριφοράς
• central transtentorial
  δυσλειτουργία στελέχους
  εκδηλώνεται με κώμα, άποιο διαβήτη και σύνδρομο Parinaud (αδυναμία κατεύθυνσης βλέμματος προς τα πάνω, κόρες μέσου εύρους, σύσπαση βλεφάρου, «σημείο δύοντος ηλίου»)
• uncal transtentorial (αγκιστρωτής έλικας)
  συμπιέζεται το σύστοιχο κοινό κινητικό νεύρο, προκαλώντας μυδρίαση με κατάργηση του φωτοκινητικού αντανακλαστικού, καθώς και η σύστοιχη οπίσθια εγκεφαλική αρτηρία, προκαλώντας έμφρακτο στην κατανομή της
  Επιπλέον, εμφανίζεται ετερόπλευρη ημιπάρεση και, μερικές φορές, ομόπλευρη ημιπάρεση λόγω παγίδευσης του ετερόπλευρου εγκεφαλικού σκέλους πάνω στο σκηνίδιο (φαινόμενο εντομής του Kernohan)
• upward cerebellar (ανάστροφος διασκηνιδιακός της παρεγκεφαλίδας)
  συμπίεση του μεσεγκεφάλου
  Κλινικά εκδηλώνεται με κώμα, μύση (αντιδραστική), απουσία ή ασυμμετρία οφθαλμοκεφαλικού αντανακλαστικού και κινήσεις απεγκεφαλισμού
• cerebellar tonsillar/foramen magnum
  οι παρεγκεφαλιδικές αμυγδαλές παρεκτοπίζονται στο ινιακό τρήμα, με αποτέλεσμα καρδιοαναπνευστική δυσλειτουργία (άπνοια, υπέρταση) και ανακοπή
• transcalvarial (εγκεφαλοκήλη)
  ο εγκέφαλος προβάλλει έξω από την κρανιακή κοιλότητα μέσω κρανιακού ελλείμματος (είτε χειρουργικού – κρανιεκτομή, είτε λόγω κατάγματος του κρανίου)

Question 7

Herniation syndromes

Answer 7

Supratentorial lesions are associated with uncal and central herniation depending on the location of the lesion.
Infratentorial structural lesions may also cause herniation, either transtentorially upward, producing midbrain compression, or downward through the foramen magnum with distortion of the medulla by the cerebellar tonsils.

Uncal άγκιστρο
Subfalcine υποδρεπανικός

Question 8

Types of ICP monitors

Answer 8

Intraventricular
Intraparenchymal
Subarachnoid
Epidural

Question 9

standard resuscitation techniques in increased ICP

Answer 9

● Head elevation

● Hyperventilation to a PCO2 of 26 to 30 mmHg (contraindicated in the setting of traumatic brain injury and acute stroke)

● Intravenous mannitol (1 to 1.5 g/kg)

Question 10

Increased intracranial pressure management protocol

Answer 10

Question 11

Fluids, blood pressure and fever management in increased ICP

Answer 11

only isotonic fluids (such as 0.9 percent saline).
Serum osmolality should be kept >280 mOsm/L, and often is kept in the 295 to 305 mOsm/L range

BP should be sufficient to maintain CPP >60 mmHg.
Hypertension should generally only be treated when CPP >120 mmHg and ICP >20 mmHg

aggressive treatment of fever, including acetaminophen and mechanical cooling, is recommended in patients with increased ICP.

Question 12

Mannitol dosing

Answer 12

IV (using 20% solution): 0.5 to 2 g/kg once; may repeat 0.25 to 1 g/kg per dose every 4 to 6 hours based on response and clinical status

Question 13

Mannitol contraindications and warnings

Answer 13

1) anuria; severe hypovolemia; active intracranial bleeding except during craniotomy; preexisting severe pulmonary vascular congestion or pulmonary edema

2)
Fluid/electrolyte imbalance: May cause hypervolemia and electrolyte disturbances; monitor for new onset or worsening cardiac or pulmonary congestion. Also may cause profound diuresis with fluid and electrolyte loss; close medical supervision and dose evaluation are required. Correct electrolyte disturbances; adjust dose to avoid dehydration.

Nephrotoxicity: May cause kidney dysfunction, especially with high doses; use caution in patients taking other nephrotoxic agents, with sepsis, or preexisting kidney disease. To minimize adverse kidney effects, monitor serum osmolality or osmolar gap

Question 14

When should corticosteroids be administered in increased ICP

Answer 14

Glucocorticoids were associated with a worse outcome in severe head injury.
They should not be used in this setting.

In addition, glucocorticoids are not considered to be useful in the management of cerebral infarction or intracranial hemorrhage

By contrast, glucocorticoids may have a role in the setting of intracranial hypertension caused by brain tumors and central nervous system infections.

Question 15

Dexamethasone dosing in brain tumor edema

Answer 15

Initial: IV: 10 mg once followed by maintenance dosing

Maintenance: IV, Oral: 4 mg every 6 hours

Note: Consider taper after 7 days of therapy; taper slowly over several weeks

Question 16

Hyperventilation in increased ICP indications

Answer 16

Therapeutic hyperventilation should be considered as an urgent intervention when elevated ICP complicates cerebral edema, intracranial hemorrhage, and tumor.

Hyperventilation should be minimized in patients with traumatic brain injury or acute stroke. In these settings, vasoconstriction may cause a critical decrease in local cerebral perfusion and worsen neurologic injury, particularly in the first 24 to 48 hours

Question 17

Which conditions increase cerebral blood flow

Answer 17

CBF increases with hypercapnia and hypoxia

That’s why is hyperventilation (hypocapnia) used
It decreases cerebral blood flow, which reduces cerebral blood volume and, ultimately, decreases the patient’s intracranial pressure

Monro Kellie doctrine

Question 18

Does hyperventilation (hypocapnia) cause vasodilation or vasoconstriction?

Answer 18

Hyperventilation causes vasoconstriction

Question 19

Does hypotension improve increased ICP?

Answer 19

Although it might seem that lower BP would result in lower ICP, this is not the case.

Hypotension, especially in conjunction with hypoxemia, can induce reactive vasodilation and elevations in ICP.

Question 20

Cerebral perfusion pressure (CPP) definition

Answer 20

CPP is defined as mean arterial pressure (MAP) minus ICP.

CPP = MAP - ICP

Question 21

Acute management in cardiac arrest after return of spontaneous circulation

Answer 21

Cooling to 32–36°C should be achieved within the first 4–6 hours and should be maintained for a period of 24 hours.
Hypothermia is maintained for approximately 24 hours, and rewarming is accomplished slowly and passively to avoid rebound ICP response and potassium disarrangements that could trigger fatal arrhythmias.

Question 22

Poor prognostic features after cardiac arrest

Answer 22

Question 23

Algorithm for prognosis determination in pre-therapeutic hypothermia era

Answer 23

Question 24

Algorithm for suggesting neurological prognosis in Hypoxic-ischemic brain injury

Answer 24

Question 25

malignant and benign types of EEG in Hypoxic-ischemic brain injury

Answer 25

Malignant
* complete or near-complete suppression
* burst suppression
* generalized periodic complexes
* low-voltage output pattern (≤10 microvolts)
* intermittent or continuous seizures
* lack of reaction to stimuli
* alpha-theta pattern

Benign
Continuous backround with preserved backround reactivity

Question 26

Alpha coma definition

Answer 26

In some patients with coma, 8 to 12 Hz activity is seen;
this resembles normal alpha rhythm, but extends beyond the posterior cerebral regions and does not react to stimuli.

This so-called “alpha coma” is associated with pontine lesions, and has also been described with hypoxic-ischemic encephalopathy following cardiac arrest, traumatic brain injury, and drug overdose.

This should not be confused with a normal EEG pattern, which suggests a psychogenic origin for the patient’s unresponsiveness.

Question 27

Neuroimaging in Hypoxic-ischemic brain injury

Answer 27

CT images are usually normal immediately after a cardiac arrest, but by day 3, they often show brain swelling and inversion of the gray-white densities (with the use of quantitative measures) in patients with a poor outcome

MRI parameters associated with poor outcome include:
* widespread and persistent cortical DWI abnormalities
* the combination of cortical and deep gray matter DWI/FLAIR abnormalities and severe global ADC reduction

Still, 20%–50% of patients with good outcomes have DWI abnormalities on MRI and some patients have poor outcomes despite a normal MRI

Question 28

Coma localization and evolution

Answer 28

It is caused by either:
* dysfunction of the reticular activating system above the level of the mid-pons
* dysfunction of both cerebral hemispheres

Coma is a transient state.
Patients recover, die, or evolve into a more permanent state of impaired consciousness:

A) Persistent vegetative state –
Φυτική κατάσταση
describes patients who are completely unconscious but have spontaneous eye opening during cyclical periods of arousal. Such patients often have reflexive vocalizations (sounds but not words), facial expressions, and movements that can be misinterpreted by hopeful observers as reflecting awareness of their internal or external environment
Required features of PVS are:

• No evidence of awareness of self or environment and no ability to interact with others.
• No evidence of sustained, reproducible, purposeful, or voluntary behavioral responses to visual, auditory, tactile, or noxious stimuli.
• No evidence of language comprehension or expression.
• Sleep-wake cycles manifested by the presence of intermittent periods of spontaneous eye opening.
• Sufficiently preserved hypothalamic and brainstem autonomic function to permit survival with medical and nursing care.
• Bowel and bladder incontinence
• Some degree of preserved cranial nerve reflexes and spinal reflexes.

B) Minimally conscious state –
Κατάσταση ελάχιστης συνείδησης
describes patients with severe alteration in consciousness who nonetheless can be shown to have some degree of preserved awareness of the external world.
They can at least occasionally demonstrate purposeful movements or responses.
These can include following simple commands, making gestural or verbal responses to questions, making intelligible verbalizations, smiling or crying in response to evocative sounds or images, reaching accurately toward the location of an object, or fixating on and pursuing visual stimuli.

C) Brain death is defined as the irreversible cessation of cerebral and brainstem function.
There is no respiratory drive, and thus there are no spontaneous breaths regardless of hypercarbia or hypoxemia.
There are no responses arising from the brain (including cranial nerve reflexes and motor responses) to stimuli, although spinal reflexes may persist.

Question 29

Which condition may cause a delayed postanoxic encephalopathy?

Answer 29

Carbon monoxide poisoning

Question 30

Cause of petechial rash in a patient with bone fracture and loss of consciousness

Answer 30

Fat embolism

Question 31

What is true about BP management early in subarrachnoid hemorrhage?

Answer 31

In SAH, hypertensive therapy should be avoided until the culprit aneurysm is secured (clipped or coiled).

Question 32

respiratory patterns in comatose patients

Answer 32

Apneusis: a respiratory pause at full inspiration and occurs from bilateral pontine lesions.
often with pinpoint pupils and likely decerebrate posture.

Cheyne–Stokes respiration: a pattern of periodic breathing in which hyperpnea alternates with apnea and the depth of breathing increases and decreases gradually.
It is seen in patients with forebrain impairment in the setting of intact brainstem respiratory reflexes, but it is also present in patients with severe cardiopulmonary disease.

Hyperventilation may be seen in metabolic encephalopathies such as in uremia and hepatic encephalopathy, but has also been reported in patients with midbrain lesions.

Ataxic breathing is an irregular respiratory pattern (gasping respiration) seen with lesions damaging the respiratory rhythm generator in the upper medulla.

Question 33

Coma clinical findings localization

Answer 33

Decorticate rigidity (αποφλοίωση):
* flexion of the upper extremities at the elbows and extension of the lower extremities
* associated with hemispheric dysfunction or a lesion above the red nuclei resulting in disinhibition of the red nuclei, with facilitation of the rubrospinal tracts (which are thought to enhance flexor tone in the upper extremities).
* seen in lesions involving the forebrain down to the level of the rostral midbrain, and above the red nuclei.

Decerebrate posture (απεγκεφαλισμός):
* extension and hyperpronation of the upper extremities with extension of the lower extremities
* caused by a lesion in the brainstem at or below the superior colliculi and the red nuclei, but above the vestibular nuclei.
* the vestibular nuclei are intact

(Lesions below the vestibular nucleus will abolish a posture
response, and are generally associated with flaccid limbs)

Pinpoint pupils are seen in pontine lesions, below the red nucleus