3. Neurocritical Care Flashcards
Types of cerebral edema?
Vasogenic.
Cytotoxic.
Interstitial.
Example of interstitial edema?
The edema seen in acute obstructive hydrocephalus, as the CSF is forced by hydrostatic pressure to move from the ventricular spaces to the interstitium of the parenchyma.
Transependymal edema is another term used for this type of edema.
Vasogenic edema?
Alteration of the blood–brain barrier with movement of water from the intravascular to the interstitial space, and accumulation of fluid in the extracellular space. Also leading to the extravasation of fluid out of the intravascular space.
Vasogenic edema is usually seen surrounding neoplastic lesions.
Factors play a role in extravasation of fluid in vasogenic edema?
- Hydrostatic forces.
- Inflammatory mediators.
- Endothelial permeability, leading to the opening of the endothelial tight junctions and subsequent formation of the edema.
Cytotoxic edema?
Intracellular accumulation of fluid.
Most commonly seen in hypoxic-ischemic insult, in which there is a lack of energy to the cells, leading to depletion of ATP and subsequent failure of the Na+ K+ ATPase, causing an alteration in the selective permeability of cellular membranes.
Also seen with alterations in systemic osmolality, leading to intracellular edema.
Therapeutic hypothermia improves neurologic outcomes in unconscious survivors after cardiac arrest. Rhythms?
The evidence supports the use of hypothermic therapy in cardiac arrest from ventricular fibrillation (VF).
Limited evidence in the setting of non-VF rhythms, including pulseless electrical activity or in asystole.
Hypothermia targeted a temperature?
32° to 34°C for 12 to 24 hours.
Temperatures lower than 32°C may not provide additional benefit and may be harmful.
Regarding higher temperature targets, a study comparing a target temperature of 33°C and 36°C in unconscious survivors after cardiac arrest irrespective of initial rhythm demonstrated no significant differences in these two groups, suggesting that temperature control up to 36°C may also be effective in these patients.
Hypothermic therapy complications?
Coagulopathy.
Arrhythmias.
Electrolyte abnormalities.
Risk of infections.
Uncal herniation? Compressed structures? Manifestations?
- The ipsilateral midbrain, affecting the ipsilateral CN III nucleus and nerve. The mass effect compresses parasympathetic fibers that mediate miosis, resulting in mydriasis. A fixed dilated pupil localizes the side of the uncal herniation.
- Distortion of the ascending arousal system in the brainstem impairs consciousness.
- The ipsilateral cerebral peduncle including the corticospinal tract that has not decussated at the level of the midbrain, causing contralateral hemiparesis.
- Occasionally, the uncal herniation will lead to displacement of the midbrain against the contralateral Kernohan’s notch, resulting in a contralateral compression of the corticospinal tract, and therefore an ipsilateral hemiparesis.
- Compression of the PCA in the tentorial notch, causing infarction in this territory.
Conditions associated with cerebral edema?
Hyponatremia.
Prolonged cardiac arrest.
Rapid ascent into high altitude.
Lead intoxication.
Liver failure.
Mechanism of cerebral edema in hyponatremia?
There is a decrease in the osmolarity of the extracellular fluid, and by osmotic gradient there is entry of water into the cells, especially when hyponatremia develops rapidly.
Hyperosmolar agents for the treatment of cerebral edema; mechanism?
In hypernatremia, water moves from the intracellular space to the extracellular space.
Hyponatremia in prolonged cardiac arrest; mechanism?
Prolonged cardiac arrest leading to hypoxic-ischemic encephalopathy is associated with diffuse cytotoxic edema, likely caused by the lack of energy supply and failure of the Na+ K+ ATPase pumps in cellular membranes.
ICP-measuring devices?
Intraventricular catheters.
Parenchymal devices.
Epidural devices.
Subarachnoid bolts.
ICP-measuring device indications?
May be used in patients with head injury and a GCS score of 7 or less, if the following conditions are met:
- A condition leading to ICP elevation amenable to treatment.
- The ICP measurement will have an impact on the decisions made for the treatment of the patient.
- The benefits of the device outweigh the risks.
Intraventricular catheters?
Provides the capability to transduce the ICP and allowing the possibility of CSF drainage, which can help decrease the ICP, hence preferred if there is a need for ventricular CSF drainage.
Indicated in setting of SAH with hydrocephalus.
Up to 6% risk of hemorrhage and up to 22% risk of infection.
Parenchymal devices?
Inserted into the brain parenchyma and provide pressure measurements.
Do not allow CSF drainage.
May be susceptible to pressure gradients across the parenchyma.
Epidural devices?
Placed between the dura and the calvarium.
Have lower rates of hemorrhage and infection, but their accuracy is low.
Subarachnoid bolts?
Placed through a burr hole and in communication with the subarachnoid space.
Their placement may be easier and the risks of infection and hemorrhage are not as high as with intraventricular devices, however, the accuracy is not optimal, it does not allow CSF drainage, and the device tends to get occluded.
Normal ICP range?
Between 5 and 15 mm Hg (7.5 to 20 cm H2O).
Intracranial hypertension; mechanism of brain injury?
It produces a decrease in the cerebral perfusion pressure and therefore reduced cerebral blood flow, resulting in cerebral ischemia.
The general measures in every patient with increased ICP?
- Head position (elevated above 30 degrees).
- Maintenance of normothermia (avoid fever).
- Glucose control.
- Blood pressure control.
- Adequate nutrition.
- Prevention of complications.
Specific interventions to reduce ICP?
- Hyperventilation.
- Use of osmotic agents.
- Use of hypertonic solutions.
- Use of corticosteroids in select cases.
CSF drainage. - Surgical decompression in select cases.
Specific interventions to reduce ICP in refractory cases?
Barbiturate coma.
Pharmacologic paralysis.
Hypothermia
Hyperventilation to lower ICP? Mechanism? Target pCO2?
Produces a reduction in partial pressure of CO2 (pCO2), and this hypocapnia leads to cerebral vasoconstriction, reducing cerebral blood volume and therefore reducing ICP. Does not act by changing the CSF osmolarity.
Has a rapid effect; however, it lasts for 10 to 20 hours and subsequently a rebound phase with increased ICP may be seen.
This therapy should be used to target a reduction of pCO2 by 10 mm Hg, and/or to a target of approximately 30 mm Hg, and should be reversed slowly.
Mannitol mechanism in lowering ICP?
An osmotic agent and acts by raising the serum osmolarity and producing an osmotic gradient, driving water from the interstitium to the intravascular compartment.
Mannitol: dosing? Monitoring? Target osmolarity?
It is usually given in boluses of 0.5 to 1.5 g/kg and not as a continuous infusion.
While on this medication, serum osmolarity should be checked at regular intervals targeting a level no higher than 320 mOsm/L.
Mannitol adverse effects?
Produces diuresis, and may lead to hypotension and hypovolemia.
Depletion of potassium, magnesium, and phosphorus.
If there is damage to the blood–brain barrier, mannitol can leak into the interstitium, worsening vasogenic edema.
Mechanism of hypertonic saline to reduces the ICP? Monitoring?
By drawing water out from brain cells via an osmotic gradient.
It can be used as a continuous infusion targeting a serum sodium concentration of 150 mmol/L. Serum sodium concentration should be monitored closely during administration of hypertonic saline, and changes should occur very gradually.
Barbiturates coma to lower ICP?
May be used when the ICP is elevated and refractory to other measures.
Reduce the ICP by lowering cerebral metabolic activity, leading to a decrease in cerebral blood flow and blood volume.
Patients should have continuous EEG monitoring to titrate to burst suppression.
Pentobarbital is the barbiturate of choice and is usually started with a bolus followed by a continuous infusion.
Its discontinuation should be gradual.
Barbiturate coma has multiple complications: hypotension, myocardial depression, predisposition to infections and hypothermia.
Propofol half-life?
Short half-life. It produces sedation within a few minutes, it has a drug effect that lasts between 5 and 10 minutes, and awakening may occur 10 to 15 minutes after discontinuation (depending on the baseline neurologic function).
Propofol effect on ICP?
Reduces the ICP in patients with normal intracranial dynamics and preserved cerebral perfusion pressure, which makes this attractive in the care of patients with increased ICP.
Propofol side effects?
- Hypotension.
- Respiratory depression.
- Hypertriglyceridemia.
- Infections.
- Propofol infusion syndrome.
Propofol infusion syndrome?
- Lethal complication.
- Seen rarely, mainly in patients on high doses for long periods of time.
- Manifests with hypotension, bradycardia, lactic acidosis, hyperlipidemia, and rhabdomyolysis.
Stupor definition?
State of pathologically reduced consciousness from which the patient can be aroused only with strong and continuous stimulation.
Even after being aroused, the cognitive function may be impaired.
When not disturbed, the patient goes back to the poorly responsive state.
Coma definition?
State of unresponsiveness, in which the patient cannot be aroused even with vigorous stimulation.
There may be a grimace response or stereotyped withdrawal movement of the limbs to noxious stimulation, but the patient does not localize to the stimulus.
Locked-in state definition?
Occurs in brainstem lesions, in which the patient is awake and conscious, but quadriplegic, with paralysis of the lower cranial nerves, and with horizontal gaze palsy.
The patient can typically blink and move his eyes vertically (because of sparing of the vertical gaze centers) and may be able to communicate with vertical eye movements and blinking.
Unresponsive wakefulness definition?
New name for “vegetative state” which avoids the negative connotations of the prior terminology.
It is characterized by return of sleep–wake cycles in an unresponsive patient (usually previously comatose), with lack of cognitive neurologic function.
These patients have no awareness of themselves or the environment, do not interact with others, and do not have purposeful or voluntary behavioral responses.
Predictors of malignant cerebral edema in MCA strokes?
- High NIHSS score (greater than 15 in nondominant hemisphere infarcts, or greater than 20 in dominant hemisphere infarcts).
- Early hypodensity of more than 50% of the MCA territory on CT.
- Younger age.
Malignant cerebral edema in complete MCA infarctions, seen in strokes with occlusions at?
The ICA terminus and most proximal (M1) segment of the MCA.
Malignant cerebral edema in complete MCA infarctions, mortality rate?
Up to 80% mortality with conservative therapy.
PRES & RPLS; stand for?
Posterior reversible encephalopathy syndrome (PRES), aka reversible posterior leukoencephalopathy syndrome (RPLS).
PRES on neuroimaging?
Vasogenic edema predominantly in the posterior cerebral region, especially in the occipital and parietal lobes (though more anterior areas can also be involved in PRES).
Risk factors and causative factors associated with PRES?
- Hypertension.
- Renal failure.
- Organ transplantation.
- Autoimmune diseases.
- Immunosuppressive drugs (particularly cyclosporine).
- Cancer chemotherapy.
- Septic shock.
- Preeclampsia, and eclampsia.
Clinical manifestations of PRES?
- Headache.
- Nausea.
- Visual changes.
- Focal neurologic symptoms.
- Altered mental status.
- Coma.
- Seizures.
PRES pathophysiology?
- Not well understood.
- It is thought to be related to a disruption in autoregulation of the posterior circulation, which associated with hypertension and hyperperfusion may result in alteration of the blood–brain barrier and vasogenic edema.
- Endothelial injury and dysfunction also may play a role.
Picture?
PRES.
Sodium nitroprusside? Effect? Use?
A vasodilator that produces arterial and venous dilation and reduces blood pressure rapidly.
It is used in a continuous infusion; while it is not the first line of treatment for hypertension, it may be indicated in severe hypertension.
Sodium nitroprusside MOA?
Nitric oxide and cyanide are produced in the circulation. Nitrous oxide then increases cGMP and produces vasodilation.
Effect of Sodium nitroprusside on ICP?
Causes vasodilation in both cerebral and systemic vessels, causing an increase in cerebral blood flow and volume, and increasing the ICP, which along with a decrease in the mean arterial pressures can compromise cerebral perfusion pressure. Therefore, it should be used cautiously in patients with increased ICP.
Cyanide and thiocyanate toxicity with continuous and prolonged infusion of sodium nitroprusside?
- Cyanide originates from the nitroprusside molecule and can be cleared by binding to methemoglobin, or when thiosulfate donates a sulfur group, transforming the cyanide into thiocyanate.
- Cyanide toxicity should be suspected when tachyphylaxis occurs.
- The accumulation of cyanide can be treated with sodium thiosulfate, which provides sulfur groups favoring the conversion to thiocyanate, which can be cleared by the kidneys. However, thiocyanate is also toxic. Risk of thiocyanate intoxication is increased in patients with renal disease; therefore, sodium nitroprusside should not be used in this patient population.
- Manifestations of thiocyanate toxicity include anxiety, confusion, pupillary constriction, tinnitus, hallucinations, and seizures. This intoxication can be treated with dialysis.
Picture?
Subdural hematoma.
The most common cause of subdural hematoma?
Trauma, by producing an acceleration force, thereby tearing and causing rupture of the cerebral surface bridging veins that drain into the dural venous sinuses.
SDH management?
Surgical evacuation is indicated if the subdural hematoma is more than 1 cm or if there is midline shift.
If the subdural hematoma is small it may be observed without the need for surgical evacuation.
Mechanism of epidural hematoma?
Most commonly caused by head trauma, leading to rupture of the middle meningeal artery, which passes through the foramen spinosum.
Complications of SAH?
- Acute hydrocephalus.
- Rebleeding.
- Vasospasm.
- If a hematoma forms, it can produce mass effect and lead to uncal herniation.
The leading cause of morbidity and mortality in patients who survive initial SAH?
Vasospasm causing ischemia and delayed infarcts.
Vasospasm after SAH timeline?
Occur between 3 and 15 days from the onset of the bleeding, with a peak between days 6 and 8.
Rebleeding after SAH timeline?
Usually occurs early on, when the aneurysm has not been secured.
Epidural hematoma clinical presentation?
A brief loss of consciousness followed by a lucid interval and subsequent deterioration hours later.
Diffuse axonal injury; mechanism?
Occurs from disruption of intracerebral axons and is caused by the effect of angular forces and shear injury, but not from direct contusion or penetrating trauma.
Most commonly seen in severe head injuries, such as MVA, and in which the brain is subject to rotational or stretching forces within the confines of the skull, or in which the head suffers severe and rapid acceleration and deceleration.
At the time of the injury, the axons may not be transected, but the microtubules and neurofilaments may be disrupted, leading to axonal transport impairment, with subsequent swelling of the axons appearing as bulb like or balloon like, subsequently separating and becoming disconnected.
DAI clinical presentation?
Alteration of consciousness or loss of consciousness, progress to coma, and if they survive, they may remain unconscious, in unresponsive wakefulness, or severely disabled.
DAI location of damage?
Widespread damage of axons involving cerebral hemispheres (gray–white junction), corpus callosum, brainstem, and cerebellum.
DAI; macroscopically?
Small hemorrhages in the corpus callosum, superior cerebellar peduncle, deep nuclei, and throughout the hemispheric white matter.
Picture?
Head trauma with coup and contrecoup injury. Shows a left frontal lobe hematoma from direct contusion (coup) as well as a right occipitotemporal hematoma (contrecoup injury).
Picture?
SAH, which seems to be denser in the left Sylvian fissure, likely associated with rupture of a left MCA aneurysm.
Picture?
Central pontine myelinolysis.
Picture?
Subdural hematoma and a subfalcine herniation.
