330 Neuro CritCare, HIE, SAH Flashcards
2 Principal types of edema or swelling of brain tissue
- Vasogenic edema
2. Cytotoxic edema
Influx of fluid and solutes into the brain through an incompetent blood brain barrier
Vasogenic edema
Results from cellular swelling, membrane breakdown and ultimately cell death
Cytotoxic edema
Pathway of irreversible cell death due to inadequate delivery of substrates (oxygen, glucose) to sustain cellular function
Ischemic cascade
The Ischemic Cascade process as seen in ischemic stroke, global cerebral ischemia, traumatic brain injury
- Release of excitatory amino acids (glutamate)
- Influx of calcium and sodium ions disrupting cellular homeostasis
- Activate proteases and lipases
- Lipid peroxidation and free radical-mediated cell membrane injury
- Cytotoxic edema
- Necrotic cell death and tissue infarction
Areas of ischemic brain tissue that have not yet undergone irreversible infarction and are potentially salvageable if ischemia can be reversed
Penumbra
Factors that exacerbate ischemic brain injury causing events known as secondary brain insults
- Hypotension and hypoxia = further reduce substrate delivery to vulnerable brain tissue
- Fever, seizures, hyperglycemia = increase cellular metabolism, outstripping compensatory process
Cell death that occurs without cerebral edema and therefore often not seen on brain imaging
Apoptotic cell death
Provides the driving force for circulation across the capillary beds of the brain
Cerebral perfusion pressure (CPP)
Defined as MAP minus ICP
Cerebral perfusion pressure (CPP)
Physiologic response whereby cerebral blood flow (CBF) is regulated via alterations in cerebrovascular resistance in order to maintain perfusion over physiologic changes such as neuronal activation or changes in hemodynamic function
Autoregulation
Factors that strongly influences CBF
- pH (acidosis)
- PaCO2 (hypercapnia)
Acidosis and hypercapnia increases CBF while the opposite causes decrease.
T or F: Hyperventilation can lower ICP?
True.
Mediated thru decrease in both CBF and intracranial blood volume
CSF pathway
- Produced (principally) in choroid plexus of each lateral ventricle
- Exits the brain via foramens of Luschka and Magendie
- Flows over the cortex to be absorbed into the venous system along the superior sagittal sinus
Approximate amount of CSF
150 mL
Cerebral blood volume
150 mL
Vicious cycle seen in traumatic brain injury, massive intracerebral hemorrhage, large hemispheric infarcts with significant tissue shifts
- Obstruction of CSF outflow, edema of cerebral tissue, or increase in volume of tumor or hematoma INCREASES ICP
- DIMINISHED cerebral perfusion
- Tissue ischemia
- Vasodilation via autoregulatory mechanisms to restore cerebral perfusion
- INCREASE cerebral blood volume INCREASES ICP, LOWERS CPP, provokes further ischemia
EEG findings in metabolic encephalopathy
Generalized slowing
Screening that should be performed in patients with encephalopathy of unknown cause
Serum or urine toxicology screens
When is it preferable to perform neuroimaging study prior to lumbar puncture?
Patients with coma or profound encephalopathy
Conditions where ICP monitoring should be considered
- Primary neurologic disorders (Stroke, traumatic brain injury)
- Severe traumatic brain injury (GCS = 8)
- Large tissue shifts from supratentorial ischemic or hemorrhagic stroke
- Hydrocephalus from SAH, intraventricular hemorrhage or posterior fossa stroke
- Fulminant hepatic failure
What levels should ICP and CPP be maintained?
ICP : <20mmHg
CPP : >/= 60mmHg
See Table 330-2 for the stepwise approach to treatment of elevated ICP.
p. 1780
Condition occurs from lack of delivery of oxygen to the brain because of extreme hypotension (hypoxia-ischemia) or hypoxia due to respiratory failure
Hypoxic-Ischemic Encephalopathy (HIE)
Causes of HIE
- Myocardial infarction
- Cardiac arrest
- Shock
- Asphyxiation
- Paralysis of respiration
- Carbon monoxide or Cyanide poisoning
Another term for HIE caused by carbon monoxide/cyanide poisoning
Histotoxic hypoxia
In hypoxia-ischemia, consciousness is lost within seconds.
Time when circulation is restored affects recovery.
How long will it be for full recovery to occur?
Ideally:
WITHIN 3-5 mins = full recovery may occur
BEYOND 3-5 mins = some degree of permanent cerebral damage usually results
In extreme cases:
8-10 mins of global cerebral ischemia may still make relatively full recovery
Factor that gives better prognosis for HIE patients
Better prognosis = patients with INTACT BRAINSTEM FUNCTION
Part of the brain frequently affected in HIE that explains why selective persistent memory deficits may occur after brief cardiac arrest
Hippocampus
Hippocampal CA1 neurons are vulnerable to even brief episodes of hypoxia-ischemia
A specific form of HIE that occurs at the distal territories between the major cerebral arteries and can cause cognitive deficits, including visual agnosia, and weakness that is greater in proximal than in distal muscle groups
Watershed infarcts
Basis for diagnosis of HIE
Based on history
Usually necessary:
BP <70mmHg systolic
PaO2 <40mmHg
Cause of HIE confirmed by measuring carboxyhemoglobin and suggested by cherry red color of venous blood and skin
Carbon monoxide intoxication
Treatment goal for HIE
Restoration of normal cardiorespiratory function
Based on International Liason Committee on Resuscitation: “Unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32-24 deg C for 12-24 h when initial rhythm was Vfib.”
Advantage and disadvantage of hypothermia as part of treatment for HIE.
Advantage:
Targets neuronal cell injury cascade and has neuroprotective properties in experimental models
Disadvantage:
Coagulopathy
Increased risk of infection
Treatment for severe carbon monoxide intoxication
- Hyperbaric oxygen
2. Anticonvulsants (not given prophylactically)
Anticonvulsants for treatment of posthypoxic myoclonus
- Oral Clonazepam 1.5-10mg daily
2. Valproate 300-1200mg daily in divided doses
T or F:
Myoclonic status epilepticus within 24h after primary circulatory arrest indicates very poor prognosis even if seizures are controlled?
True
Part of the brain that may be affected in carbon monoxide and cyanide intoxication responsible for a parkinsonian syndrome of akinesia and rigidity without tremor
Basal ganglia
A confusional state characterized by disordered perception, frequent hallucinations, delusions, and sleep disturbance
Delirium
T or F:
Presence of delirium is associated with worsened outcome in critically ill patients?
True
A centrally acting alpha 2 agonist that reduce delirium and shorten duration of mechanical ventilation compared to benzodiazepines
Dexmedetomidine
Triad of Wernicke’s Disease
- Global confusion
- Impairment of eye movements (ophthalmoplegia)
- Gait ataxia
Only 1/3 of patients presents with these
Type of encephalopathy wherein systemic response to infectious agents leads to release of circulating inflammatory mediators that contribute to encephalopathy
Sepsis-Associated Encephalopathy
Cytokines: TNF, IL-1, IL-2, IL-6
Diagnosis of Sepsis-associated encephalopathy
Clinical but requires exclusion of structural, metabolic, toxic and infectious causes.
Reflexes associated with sepsis-associated encephalopathy
- Hyperreflexia
2. Frontal release signs (Grasp or snout reflex)
Prognosis after treatment of sepsis-associated encephalopathy
Treatment of underlying critical illness almost always results in substantial improvement but long term dysfunction similar to dementia can be present
Severe disability or minimally conscious states are uncommon
Disorder that presents as quadriplegia and pseudobulbar palsy
Central Pontine Myelinosis
Predisposing factors for Central Pontine Myelinosis
- Severe underlying medical illness or nutritional deficiency
- Rapid correction of hyponatremia or with hyperosmolar states
Pathology of Central Pontine Myelinosis
Demyelination without inflammation in the base of pons, with relative sparing of axons and nerve cells
Modality useful in diagnosis of Central Pontine Myelinosis
MRI
Shows symmetric area of abnormal high signal intensity within the basis pontis
Therapeutic guidelines for restoration of severe hyponatremia
= 10mmol/L (10meq/L) within 24 hours
AND
20mmol/L (20meq/L) within 48 hours
Common and preventable disorder due to deficiency of thiamine occuring mostly in alcoholics
Wernicke’s disease
Which in the symptoms of Wernicke’s disease improves FIRST after thiamine administration?
Ocular palsy (within hours)
An amnestic state with impairment in recent memory and learning frequently persistent as symptoms of Wenicke’s disease recede
Korsakoff’s psychosis
T or F:
Wernicke’s disease is a medical emergency
True
Treatment of Wernicke’s Disease
Thiamine 100mg IV or IM stat then DAILY until patient resumes normal diet to be given PRIOR to IV glucose solution
When is intubation considered in patients with peripheral nervous system (PNS) involvement?
Maximal inspiratory force falls to
General principles of respiratory evaluation in patients with PNS involvement
- Assessment of pulmonary mechanics [Maximal Inspiratory Force(MIF) and vital capacity (VC)
- Evaluation of strength of bulbar muscles
Most common PNS complication related to critical illness
Critical illness polyneuropathy
Electrophysiology of critical illness polyneuropathy
Diffuse, symmetric, distal axonal sensorimotor neuropathy; axonal degeneration
Decreases the risk of critical illness polyneuropathy
Aggressive glycemic control with insulin infusion
Treatment of critical illness polyneuropathy
Supportive.
Treat the underlying illness.
Recovery period in critical illness polyneuropathy
Weeks to months
Needs long-term ventilatory support and care even after underlying critical illness has resolved
Early signs of foodborne botulism
Diplopia
Dysphagia
Treatment for botulism
Supportive.
Antitoxin early in course may limit duration of neuromuscular blockade
Overall term describing several different discrete muscle disorders (muscle weakness and wasting) that may occur in critically ill patients
Critical illness myopathy
An asthmatic patient required high-dose glucocorticoids and nondepolarizing neuromuscular blocking agents (pancuronium, veruconium, rocuronium, cisatracurium) to facilitate mechanical ventilation. What type of myopathy can occur?
Thick-filament myopathy
Good prognosis.
Takes weeks or months for recovery.
Prevention: Avoid nd neuromuscular blocking agents
Most common cause of SAH
Rupture of saccular aneurysm
Excluding head trauma
Rate of rebleeding if patient survives the aneurysm
First 2 weeks : 20%
First month : 30%
Per year afterward: 3%
Annual risk of rupture for aneurysms <10 mm and >/=10mm in size
<10mm : 0.1%
>/= 10mm: 0.5-1%
3 most common locations of anuerysms
- Terminal internal carotid artery
- Middle cerebral artery bifurcation
- Top of the basilar artery
Aneurysms from infected emboli due to bacterial endocarditis usually located distal to first bifurcation of major arteries of the circle of Willis.
Mycotic aneurysm
Location of saccular aneurysms
Bifurcations of large to medium-sized intracranial arteries
85% of aneurysms occur in anterior circulation, mostly on circle of Willis
Factors increasing the risk of rupture of aneurysm
- > 7mm diameter
- Top of basilar artery
- Origin of posterior communicating artery
Hallmark of aneurysmal rupture
Sudden headache + absence of focal neurologic symptoms
Focal neurologic symptoms occur if hematoma produce mass effect
Variant of migraine that stimulates SAH
Thunderclap headache
Hunt-Hess scale Grade that presents with severe headache and normal mental status
Grade 2
Hunt-Hess scale Grade presents with stupor, moderate to severe motor deficit, and may have intermittent reflex posturing
Grade 4
Grade 4 and 5 have 80% mortality rate
4 major causes of delayed neurologic deficits
- Rerupture
- Hydrocephalus
- Vasospasm
- Hyponatremia
Incidence of rerupture of UNTREATED aneurysm following SAH
First month : 30% peak in first 7 days
60% mortality rate, poor outcome
T or F:
Hyponatremia in SAH should be treated with free-water restriction
False.
This can increase the risk of stroke.
Clears over 1-2 weeks.
Contraindicated in pt at risk for vasospasm
Hallmark of aneurysmal rupture
Blood in CSF
Xanthochromic spinal fluid is caused by conversion of hemoglobin to bilirubin that stains the spinal fluid yellow within 6-12 hours and lasts for how long?
1 - 4 weeks
When is lumbar puncture indicated in patients suspected with SAH?
Only if CT scan is not available
Imaging for suspected SAH
Noncontrast CT scan within 72h
Once SAH is confirmed:
Four-vessel conventional xray angiography
Alternative: CT angiography
Structural myocardial lesions produced by catecholamines and excessive discharge of sympathetic neurons occur after SAH. Reversible cardiomyopathy causes shock or CHF.
ECG findings in SAH:
- ST segment and T wave changes similar to ischemia
- prolonged QRS complex
- increased QT interval
- prominent “peaked” or deeply inverted symmetric T waves
*Asymptomatic troponin elevation is common
Leading cause of morbidity and mortality following aneurysmal SAH
Vasospasm
Treatment: Nimodipine 60mg PO every 4h
T or F:
All patients should have pneumatic compression stockings applied to prevent pulmonary embolism
True
T or F:
Unfractionated heparin can be administered SC for DVT prophylaxis following endovascular treatment (craniotomy + surgical clipping) of SAH
True
