3. Neurocritical Care Flashcards
(162 cards)
1
Q
Types of cerebral edema?
A
Vasogenic.
Cytotoxic.
Interstitial.
2
Q
Example of interstitial edema?
A
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.
3
Q
Vasogenic edema?
A
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.
4
Q
Factors play a role in extravasation of fluid in vasogenic edema?
A
- Hydrostatic forces.
- Inflammatory mediators.
- Endothelial permeability, leading to the opening of the endothelial tight junctions and subsequent formation of the edema.
5
Q
Cytotoxic edema?
A
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.
6
Q
Therapeutic hypothermia improves neurologic outcomes in unconscious survivors after cardiac arrest. Rhythms?
A
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.
7
Q
Hypothermia targeted a temperature?
A
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.
8
Q
Hypothermic therapy complications?
A
Coagulopathy.
Arrhythmias.
Electrolyte abnormalities.
Risk of infections.
9
Q
Uncal herniation? Compressed structures? Manifestations?
A
- 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.
10
Q
Conditions associated with cerebral edema?
A
Hyponatremia.
Prolonged cardiac arrest.
Rapid ascent into high altitude.
Lead intoxication.
Liver failure.
11
Q
Mechanism of cerebral edema in hyponatremia?
A
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.
12
Q
Hyperosmolar agents for the treatment of cerebral edema; mechanism?
A
In hypernatremia, water moves from the intracellular space to the extracellular space.
13
Q
Hyponatremia in prolonged cardiac arrest; mechanism?
A
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.
14
Q
ICP-measuring devices?
A
Intraventricular catheters.
Parenchymal devices.
Epidural devices.
Subarachnoid bolts.
15
Q
ICP-measuring device indications?
A
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.
16
Q
Intraventricular catheters?
A
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.
17
Q
Parenchymal devices?
A
Inserted into the brain parenchyma and provide pressure measurements.
Do not allow CSF drainage.
May be susceptible to pressure gradients across the parenchyma.
18
Q
Epidural devices?
A
Placed between the dura and the calvarium.
Have lower rates of hemorrhage and infection, but their accuracy is low.
19
Q
Subarachnoid bolts?
A
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.
20
Q
Normal ICP range?
A
Between 5 and 15 mm Hg (7.5 to 20 cm H2O).
21
Q
Intracranial hypertension; mechanism of brain injury?
A
It produces a decrease in the cerebral perfusion pressure and therefore reduced cerebral blood flow, resulting in cerebral ischemia.
22
Q
The general measures in every patient with increased ICP?
A
- Head position (elevated above 30 degrees).
- Maintenance of normothermia (avoid fever).
- Glucose control.
- Blood pressure control.
- Adequate nutrition.
- Prevention of complications.
23
Q
Specific interventions to reduce ICP?
A
- Hyperventilation.
- Use of osmotic agents.
- Use of hypertonic solutions.
- Use of corticosteroids in select cases.
CSF drainage. - Surgical decompression in select cases.
24
Q
Specific interventions to reduce ICP in refractory cases?
A
Barbiturate coma.
Pharmacologic paralysis.
Hypothermia
25
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.
26
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.
27
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.
28
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.
29
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.
30
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.
31
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).
32
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.
33
Propofol side effects?
- Hypotension.
- Respiratory depression.
- Hypertriglyceridemia.
- Infections.
- Propofol infusion syndrome.
34
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.
35
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.
36
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.
37
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.
38
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.
39
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.
40
Malignant cerebral edema in complete MCA infarctions, seen in strokes with occlusions at?
The ICA terminus and most proximal (M1) segment of the MCA.
41
Malignant cerebral edema in complete MCA infarctions, mortality rate?
Up to 80% mortality with conservative therapy.
42
PRES & RPLS; stand for?
Posterior reversible encephalopathy syndrome (PRES), aka reversible posterior leukoencephalopathy syndrome (RPLS).
43
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).
44
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.
45
Clinical manifestations of PRES?
- Headache.
- Nausea.
- Visual changes.
- Focal neurologic symptoms.
- Altered mental status.
- Coma.
- Seizures.
46
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.
47
Picture?
PRES.
48
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.
49
Sodium nitroprusside MOA?
Nitric oxide and cyanide are produced in the circulation. Nitrous oxide then increases cGMP and produces vasodilation.
50
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.
51
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.
52
Picture?
Subdural hematoma.
53
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.
54
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.
55
Mechanism of epidural hematoma?
Most commonly caused by head trauma, leading to rupture of the middle meningeal artery, which passes through the foramen spinosum.
56
Complications of SAH?
- Acute hydrocephalus.
- Rebleeding.
- Vasospasm.
- If a hematoma forms, it can produce mass effect and lead to uncal herniation.
57
The leading cause of morbidity and mortality in patients who survive initial SAH?
Vasospasm causing ischemia and delayed infarcts.
58
Vasospasm after SAH timeline?
Occur between 3 and 15 days from the onset of the bleeding, with a peak between days 6 and 8.
59
Rebleeding after SAH timeline?
Usually occurs early on, when the aneurysm has not been secured.
60
Epidural hematoma clinical presentation?
A brief loss of consciousness followed by a lucid interval and subsequent deterioration hours later.
61
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.
62
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.
63
DAI location of damage?
Widespread damage of axons involving cerebral hemispheres (gray–white junction), corpus callosum, brainstem, and cerebellum.
64
DAI; macroscopically?
Small hemorrhages in the corpus callosum, superior cerebellar peduncle, deep nuclei, and throughout the hemispheric white matter.
65
DAI; microscopically?
Swollen (“bulb like”), disconnected and injured axons throughout the brain. These dystrophic axons are seen on hematoxylin–eosin after 18 to 24 hours of survival, but can be seen as early as 2 hours after the injury with beta-amyloid precursor protein immunostaining.
66
Lundberg A waves or “plateau waves”; ICP monitor tracing?
Pathologic and associated with decreased intracranial compliance and intracranial hypertension, with the risk of cerebral ischemia.
These waves are sustained with duration between 5 and 20 minutes.
Their amplitude is high, in the range of 50 to 100 mm Hg.
67
B waves; ICP monitor tracing?
Normal.
Duration: 1 to 2 minutes.
Amplitudes in the range of 20 to 50 mmHg.
68
C waves; ICP monitor tracing?
Are of no pathologic consequence.
Last for 4 to 5 minutes.
Less than 20 mm Hg of amplitude.
69
Signs of skull fracture?
- Periorbital ecchymoses or hematoma (raccoon eyes).
- Postauricular ecchymosis (Battle’s sign).
- CSF rhinorrhea, and otorrhea.
>> Nasogastric tubes should be avoided.
70
Fat embolism, mechanism?
Results from fat droplets entering the circulation usually in the setting of surgery or trauma, and especially after fractures of long bones such as the femur. Fat microparticles from the bone marrow can travel in the venous system to the lungs and may be compliant to access the arterial circulation and spread systemically.
71
Fat embolism, clinical presentation?
Hypoxia and respiratory distress, followed by agitation, delirium, and/or coma. A petechial rash is characteristic, often seen over the thorax, axillary region, and conjunctiva. Multiple petechial hemorrhages can be seen in the gray and white matter of the brain on autopsy.
72
Respiratory parameters in GBS?
Frequent evaluations of negative inspiratory force and vital capacity.
ABGs are not accurate predictors of the need for intubation and mechanical ventilation, since hypoxia and hypercapnia occur late in the course of respiratory failure, once the patient is decompensating.
73
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).
74
The contrecoup injury; most common locations?
A result of injury that occurs distant from the site of initial impact and is usually seen in the frontal or temporal lobes, as these are in close relationship with the frontal bone and the sphenoid ridge, respectively.
75
Picture?
SAH, which seems to be denser in the left Sylvian fissure, likely associated with rupture of a left MCA aneurysm.
76
The most common cause of nontraumatic subarachnoid hemorrhage?
Rupture of an intracranial aneurysm.
77
Risk factors for aneurysmal SAH?
- Hypertension and smoking are the most important.
- Family history of a first degree relative with SAH.
- Heavy alcohol use.
- Cocaine use.
78
Sensitivity of brain CT for SAH?
Demonstrates the hemorrhage in more than 95% of the cases when the scan is performed within 48 hours.
A negative CT scan does not rule out SAH.
79
Next step if the CT scan is negative in suspected SAH?
LP should be performed in order to detect blood in the subarachnoid space, evidenced by CSF RBC count that does not decrease in subsequent tubes or the presence of xanthochromia.
The appearance of xanthochromia requires the presence of RBCs in the CSF for some time; therefore, it may not be present in the first few hours following the hemorrhage.
80
Hunt and Hess scale for SAH?
1. Asymptomatic or minimal headache and slight nuchal rigidity.
2. Moderate–severe headache, nuchal rigidity, no neurologic deficit other than cranial nerve palsy.
3. Drowsiness, confusion, or mild focal neurologic deficit.
4. Stupor, moderate–severe hemiparesis, possible early decerebrate rigidity and vegetative disturbances.
5. Deep coma, decerebrate rigidity, moribund appearance.
81
The World Federation of Neurological Surgeons Scale for SAH?
1. GCS of 15 with no motor deficit.
2. GCS 13–14 with no motor deficit.
3. GCS 13–14 with motor deficit.
4. GCS 7–12 with or without motor deficit.
5. GCS 3–6 with or without motor deficit.
82
The Fisher grading scale for SAH?
Based on admission CT scan, and characterized according to the presence of blood:
1. No SAH on CT.
2. Diffuse or thin vertical layer of blood <1 mm thick.
3. Localized clot and/or vertical layer of blood ≥1 mm thick.
4. Intracerebral or intraventricular clots with diffuse or no SAH.
83
Central pontine myelinolysis (CPM) causes?
- Rapid and aggressive correction of hyponatremia.
- Severe alcoholism.
- Chronic liver disease.
- Liver transplantation.
- Extensive burns.
84
Areas affected by CPM?
>> The pons.
>> Extrapontine myelinolysis in:
- Cerebellum.
- Thalamus.
- External and extreme capsules.
- Basal ganglia.
- Deep layers of the cerebral cortex and adjacent white matter.
>> Sometimes even in:
- Fornix.
- Subthalamic nucleus.
- Amygdala.
- Optic tract.
- Spinal cord.
85
The rate of correction of hyponatremia to avoid CPM?
No more than 12 mEq/L per day, or 0.5 mEq/L per hour.
86
CPM manifestations?
Are evident within 3 to 10 days.
Progressive paraparesis or quadriparesis.
Pseudobulbar palsy.
Dysphagia.
Dysarthria.
Altered mental status.
May lead to locked-in syndrome.
87
Pathohistology CPM?
Bilateral symmetric focal destruction of myelin in the ventral pons, sparing axons and neuronal cell bodies.
88
Cholinergic crisis in patients with myasthenia gravis; cause?
Taking excessive amounts of acetylcholinesterase inhibitors such as pyridostigmine may be at risk for a cholinergic crisis.
89
Cholinergic crisis manifestations?
- Small and even pinpoint pupils.
- Excessive secretions.
- Diarrhea.
- Sweating.
- Bradycardia.
- Muscle weakness and fasciculations.
> The symptoms will subside with cessation of the acetylcholinesterase inhibitor.
90
Cholinergic crisis vs myasthenic crisis?
The presence of pinpoint pupils and increased cholinergic activity suggest a cholinergic crisis and not a myasthenic crisis.
91
Adrenergic crisis or thyrotoxicosis vs Cholinergic crisis?
> Adrenergic crisis or thyrotoxicosis may have similar manifestations but will have mydriasis and tachycardia.
92
Triple H therapy for the treatment of vasospasm in SAH?
Hypervolemia, hypertension, and hemodilution.
This is achieved by expanding the intravascular volume using isotonic fluids, and sometimes colloids such as albumin.
Risks: rebleeding from an unsecured aneurysm, pulmonary edema, CHF, and cerebral edema.
93
Picture?
Central pontine myelinolysis.
94
Respiratory rhythm control?
An intrinsic function of a group of neurons in the ventrolateral medulla, but under the control of a pontine cell group that integrates breathing with other functions, reflexes, and metabolic input.
95
Apneustic breathing?
-A respiratory pause after inspiration alternating with end-expiratory pause.
-Occurs from bilateral pontine lesions.
96
Cheyne–Stokes respiration?
-A pattern of periodic breathing in which hyperpnea alternates with apnea and the depth of breathing increases and decreases gradually. -Seen in forebrain impairment with intact brainstem respiratory reflexes but also seen in severe cardiopulmonary disease.
97
Hyperventilation caused by CNS lesions?
-Reported in patients with midbrain lesions.
-Also in metabolic encephalopathies such as uremia and hepatic encephalopathy.
98
Ataxic breathing?
-An irregular respiratory pattern (gasping respiration).
-Seen with lesions damaging the respiratory rhythm generator in the upper medulla.
99
Warfarin MOA?
Coagulation factors II, VII, IX, and X and the anticoagulant proteins C and S require γ-carboxylation in the liver for their activation, and this process requires the reduced form of vitamin K. Warfarin is a vitamin K antagonist.
100
Vitamin K for Warfarin reversal?
-The IV route is preferred for urgent reversal of anticoagulation.
-Requires new synthesis of coagulation factors, which takes time, 6-24 hours to reverse the coagulopathy even with IV vit. K.
-IV route has a rare risk of anaphylaxis.
101
Fresh frozen plasma (FFP) for Warfarin reversal?
Pros:
-Provides many coagulation factors, including those depleted by warfarin.
-Faster way to reverse coagulopathy from warfarin as compared to vitamin K.
Cons:
-Delays due to the process of compatibility testing and administration.
-May lead to fluid overload, allergic reactions, and transfusion-related complications.
-Reversal of warfarin with FFP may be only transient.
102
Prothrombin complex concentrates (PCC) for Warfarin reversal?
-Plasma derived factor concentrates which can provide high concentration of coagulation factors in small volumes, allowing for rapid administration and rapid normalization of the INR.
-PCCs correct warfarin-related coagulopathy faster than FFP.
-There are several formulations of PCCs with various concentrations of the required factors II, VII, IX, and X.
103
Heparin reversal agent?
Protamine sulfate.
104
Dabigatran MOA?
A direct thrombin inhibitor.
105
Dabigatran reversal agent?
Idarucizumab is a monoclonal antibody fragment that binds free and thrombin-bound dabigatran neutralizing its activity.
106
Indications for intubation in GBS?
-Clinical evidence of fatigue.
-Severe oropharyngeal weakness.
-VC < 15 to 20 mL/kg, or < 1 L, or a reduction of more than 30% from the baseline.
-Maximal inspiratory pressure < 30 cm H2O.
-Maximal expiratory pressure < 40 cm H2O.
-Hypoxemia with pO2 of <70 mm Hg on room air. However, pO2 and pCO2 are not sensitive, and are not good predictors of the need for early intubation, since abnormalities in these parameters occur late and when the patient is already decompensating.
107
Other parameters associated with the possible need for intubation in GBS?
-Bulbar weakness.
-Presence of cranial nerve palsies.
-Autonomic dysfunction.
-Short period from onset to peak of symptoms.
-Abnormalities on chest x-ray, such as infiltrates or atelectasis.
108
Critical illness polyneuropathy and myopathy; risk factors?
-Sepsis.
-Systemic inflammatory response syndrome.
-Use of neuromuscular blocking agents.
-Use of steroids.
-Poor nutrition.
-Abnormal glucose levels.
-Low albumin levels.
109
Critical illness polyneuropathy; affected fibers and locations?
Axonal sensory–motor polyneuropathy that affects the limbs and respiratory muscles.
110
Critical illness polyneuropathy; NCS?
-Reduced CMAPs and SNAPs.
-Normal or mildly reduced conduction velocities.
111
Critical illness polyneuropathy; Needle EMG?
Fibrillation potentials and positive sharp waves.
112
Critical illness polyneuropathy; Histopathology?
Axonal degeneration of motor and sensory fibers, and denervation atrophy.
113
Critical illness myopathy?
A primary myopathy not secondary to denervation.
114
Critical illness myopathy; NCS?
-SNAP >80% of the lower limit of normal.
-Low amplitude CMAPs.
115
Critical illness myopathy; Needle EMG?
Fibrillation potentials and positive sharp waves [seen in both critical illness polyneuropathy and myopathy].
116
Critical illness myopathy; Histopathology?
-Loss of thick myosin filaments and varying degrees of necrosis.
117
Critical illness polyneuropathy and myopathy. Which one improves earlier and faster?
Critical illness myopathy improves earlier and faster than critical illness polyneuropathy.
118
Predictors of poor outcome after cardiac arrest?
-No pupillary response at 24 to 72 hours from the cardiac arrest.
-No corneal reflexes and eye movements at 72 hours after the cardiac arrest.
-EEG showing burst suppression or generalized suppression.
-Somatosensory-evoked potentials with median nerve stimulation showing bilaterally absent N20 responses at days 1 to 3.
-Elevated neuron-specific enolase.
119
Death by neurologic criteria (or brain death) definition?
The irreversible cessation of function of the brain, including the brainstem.
This diagnosis requires the presence of a catastrophic CNS condition leading to irreversible damage, examination findings of absent brainstem reflexes, and the presence of apnea on the apnea test.
120
How to perform an apnea test?
-The patient should be preoxygenated for 10 minutes with FiO2 of 100%. A baseline arterial blood gas is obtained, and pCO2 should be between 35 and 45 mm Hg.
-The patient is then disconnected from the ventilator but should receive oxygenation at a rate of 6 L/minute.
-The patient is then observed for 10 minutes for any chest or abdominal rise suggesting an inspiratory attempt.
-After this time, an arterial blood gas is obtained. If the patient had not demonstrated any respiratory movements and the pCO2 has risen to at least 60 mm Hg, then the test is positive, supporting a diagnosis of brain death.
>To perform the apnea test, the patient should not be hypotensive (SBP should be 90 mm Hg or above), and the patient’s core temperature should be 36.5°C or above.
121
The following is required for the diagnosis of brain death?
-Absence of intoxication, neuromuscular blockade, pharmacologic sedation, or a medical condition that may obscure the clinical picture.
-A normal or near-normal core body temperature (>36°C).
-SBP > 90 mm Hg, or MAP > 60 mm Hg.
122
Brain death; confirmatory tests?
-EEG showing electrocerebral silence in a recording of at least 30 minutes.
-Transcranial Doppler showing no flow signals, or abnormal signals including oscillating flow or short and low amplitude spikes in systole without diastolic flow.
-Nuclear medicine scan showing no isotope uptake in the brain parenchyma or no intracranial flow.
-Angiography demonstrating no flow in the circle of Willis.
123
Decorticate posture?
-Flexion of the upper extremities at the elbow.
-Extension of the lower extremities.
124
Decorticate posture localization?
Seen in lesions involving the forebrain down to the level of the rostral midbrain, and 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).
125
Decerebrate posture?
-Extension and hyperpronation of the upper extremities.
-Extension of the lower extremities.
126
Decerebrate posture localization?
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, enhancing extensor tone, and without the influence from the red nuclei.
> Lesions below the vestibular nucleus will abolish a posture response, and are generally associated with flaccid limbs.
127
Picture?
Subdural hematoma and a subfalcine herniation.
128
Subfalcine herniation?
The cingulate gyrus herniates under the falx cerebri. The pericallosal and callosomarginal arteries may be compressed against or herniate under the falx cerebri.
129
Uncal herniation?
Occurs from expansion of a lesion in a cerebral hemisphere, pushing the medial temporal lobe to herniate medially and downward over the tentorial edge. The medial temporal lobe will push against the midbrain and manifest with a fixed dilated pupil. Along with this finding, patients have altered level of consciousness, and a hemiparesis, which is most often contralateral; however, the hemiparesis may be ipsilateral if the temporal lobe pushes the midbrain against Kernohan’s notch on the contralateral side, therefore affecting the contralateral corticospinal tract. Uncal herniation may also produce a posterior cerebral artery compression resulting in an infarct in this territory.
130
Central transtentorial herniation?
Occurs from an expanding lesion in the diencephalon, leading to a downward displacement, which may put pressure on the midbrain.
131
Tonsillar herniation?
Occurs when the cerebellar tonsils are displaced through the foramen magnum, compressing the medulla and occluding the fourth ventricle outflow.
132
Transcalvarial herniation?
Occurs when a patient with brain edema undergoes hemicraniectomy, and brain tissue herniates through the skull defect.
133
The Monro–Kellie doctrine?
The adult brain is encased in a nonexpansible bony cavity that also contains blood and CSF. The intracranial volume, pressure, and cerebral blood flow are intimately related. The Monro–Kellie doctrine dictates that the volume in the intracranial cavity is constant, and an increase in the volume of any of the components of this cavity will produce a displacement of the other components. Initially, the system is compliant, with only small increases in the ICP as the volume increases. However, this compliance is limited, and as the volume continues to increase, the pressure will rise exponentially (not linearly).
134
Cerebral perfusion pressure calculations?
CPP = MAP − ICP
CPP: ideally >70 mm Hg, lower limit of 50 mm Hg.
ICP: normal 5 to 15 mm Hg.
135
Vascular autoregulation range?
Permits optimal cerebral blood flow and is effective at MAP ranges between 60 and 150 mm Hg; however, this range is variable and may be altered in patients with chronic hypertension.
136
CO2 effect on ICP?
Increases in pCO2 cause vasodilatation resulting in increased ICP.
137
Effect of hematocrit on cerebral blood flow?
Lower hematocrit and lower blood viscosity are associated with increased cerebral blood flow.
138
Changes occur after seizure onset?
-First few milliseconds to seconds: release of neurotransmitters, ion channel activity, and protein phosphorylation.
-Seconds to minutes: alterations in receptor trafficking with reduction of certain GABA inhibitory receptor subunits and increase in excitatory NMDA and AMPA receptors. This contributes to resistance to benzodiazepines.
-Minutes to hours: alteration in neuropeptide expression of excitatory and inhibitory substances, leading to a hyperexcitable state.
-Days to weeks of ongoing seizures: changes in gene expression contributing to epileptogenicity and neuronal damage.
139
Malignant hyperthermia; pathogenesis?
An excessive release of calcium from the sarcoplasmic reticulum in the skeletal muscle in response to halogenated inhaled anesthetics and depolarizing muscle relaxants (more commonly succinylcholine).
140
Malignant hyperthermia; genetics?
-Autosomal dominant disorder.
-A mutation in the ryanodine receptor gene.
141
Malignant hyperthermia; clinical manifestations?
-Initial rise in the end-tidal partial pressure of carbon dioxide (PCO2) during anesthesia.
-mMuscle rigidity.
-Increased body temperature.
-Altered consciousness
-Autonomic instability.
-Rhabdomyolysis occurs, leading to myoglobinuric renal failure.
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Malignant hyperthermia, treatment?
-The culprit anesthetics should be stopped and alternative anesthetics not associated with malignant hyperthermia should be used instead.
-Ventilatory support and oxygenation should be optimized.
-Intravenous fluids should be increased.
-Physical measures to reduce the temperature should be attempted.
-Dantrolene is a specific treatment that blocks release of calcium from the sarcoplasmic reticulum and should be administered early on.
143
NMS; clinical manifestations?
-Increased body temperature.
-Muscle rigidity.
-Altered mental status.
-Autonomic instability.
144
NMS; cause and treatment?
-It is induced by antipsychotics, but other drugs that inhibit dopaminergic transmission may also be implicated.
-Management includes discontinuation of the antipsychotic and use of dantrolene and bromocriptine.
145
Serotonin syndrome; clinical manifestations? And treatment?
-Starts abruptly.
-Mental status changes.
-Hyperthermia.
-Autonomic hyperactivity.
-Hyperkinesis.
-Hyperactive deep tendon reflexes, clonus, and muscle rigidity.
> The treatment is supportive, along with benzodiazepines and discontinuation of the causative drug.
146
The ICH score for 30-day mortality after ICH?
-GCS (2 points for GCS 3–4, 1 point for GCS 5–12, 0 points for GCS 13–15).
-ICH volume (1 point if ≥30 cc).
-Intraventricular hemorrhage (1 point).
-Infratentorial origin of the hemorrhage (1point).
-Age (1 point for ≥80 years of age).
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Dexmedetomidine?
-Alpha-2 receptor agonist.
-Causes sedation, amnesia, and mild analgesia without respiratory depression.
-Can be helpful in the treatment of delirium and during the transition from mechanical ventilation to spontaneous breathing.
-Can cause bradycardia and hypotension.
148
Propofol MOA and effects?
-A strong sedative that also has amnestic effects without analgesia.
-It binds to GABA receptors and is very lipophilic.
149
Lorazepam vs. Midazolam; onset of action and duration?
-Lorazepam is a benzodiazepine with rapid onset of action (in status epilepticus onset of action is within 2 minutes, and effect can last 12 hours).
-Midazolam is a rapid onset and short-acting benzodiazepine, causing sedation within 2 minutes, and lasting 1 to 2 hours.
150
Neurologic worsening in SAH with unsecured aneurysm?
Suspect rebleeding.
151
Neurologic worsening in sAh with secured aneurvsm. and between 3 and 15 days?
Suspect vasospasm.
152
Pinpoint pupils, apneustic breathing pattern?
Pontine lesion.
153
Ataxic breathing pattern?
Medullary lesion.
154
Decorticate posture?
Lesion above the red nucleus.
155
Decerebrate posture?
Lesion between the red nucleus and the vestibular nucleus.
156
Petechial hemorrhages in the brain after trauma with bone fractures?
Consider fat embolism.
157
Brain injury and anisocoria?
Consider uncal herniation.
158
State of pathologically reduced consciousness from which the patient can be aroused to purposeful response only with external stimulation?
Stupor.
159
"Deep sleep" cannot be aroused, may grimace or have stereotyped movements but does not localize to the stimulus?
Coma.
160
Awake and conscious, but quadriplegic,
paralysis of lower cranial nerves and horizontal gaze. Preserved vertical gaze and blinking?
Locked-in state.
161
Previously comatose, but with return of the sleep-wake cycles. Lack cognitive function?
Unresponsive wakefulness.
162
Alteration of consciousness with poor attention, and fluctuation?
Delirium
