Neurologic Intensive Care Flashcards
References: Continuum, Neurocritical care 2024
Monro-Kellie doctrine
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
intracranial hypertension definition
pressures ≥20 mmH2O
CSF production rate
SF is produced by the choroid plexus and elsewhere in the CNS at a rate of approximately 20 mL/hour (500 mL/day)
Causes of intracranial hypertension
intracranial hypertension clinical findings
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.
Most common anatomic locations affected by herniation syndromes
-
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)
Herniation syndromes
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
Types of ICP monitors
Intraventricular
Intraparenchymal
Subarachnoid
Epidural
standard resuscitation techniques in increased ICP
● 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)
Increased intracranial pressure management protocol
Fluids, blood pressure and fever management in increased ICP
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.
Mannitol dosing
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
Mannitol contraindications and warnings
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
When should corticosteroids be administered in increased ICP
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.
Dexamethasone dosing in brain tumor edema
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
Hyperventilation in increased ICP indications
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
Which conditions increase cerebral blood flow
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
Does hyperventilation (hypocapnia) cause vasodilation or vasoconstriction?
Hyperventilation causes vasoconstriction
Does hypotension improve increased ICP?
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.
Cerebral perfusion pressure (CPP) definition
CPP is defined as mean arterial pressure (MAP) minus ICP.
CPP = MAP - ICP
Acute management in cardiac arrest after return of spontaneous circulation
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.
Poor prognostic features after cardiac arrest
Algorithm for prognosis determination in pre-therapeutic hypothermia era
Algorithm for suggesting neurological prognosis in Hypoxic-ischemic brain injury
malignant and benign types of EEG in Hypoxic-ischemic brain injury
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
Alpha coma definition
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.
Neuroimaging in Hypoxic-ischemic brain injury
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
Coma localization and evolution
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.
Which condition may cause a delayed postanoxic encephalopathy?
Carbon monoxide poisoning
Cause of petechial rash in a patient with bone fracture and loss of consciousness
Fat embolism
What is true about BP management early in subarrachnoid hemorrhage?
In SAH, hypertensive therapy should be avoided until the culprit aneurysm is secured (clipped or coiled).
respiratory patterns in comatose patients
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.
Coma clinical findings localization
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
Neurologic Emergencies and common acute threats 1
Neurologic Emergencies and common acute threats 2
