Neurologic Diseases (Exam III)-Mordekai Flashcards
1
Q
What factors affect cerebral blood flow?
A
- CMR (cerebral metabolic rate)
- CPP (cerebral perfusion pressure. MAP - ICP)
- ICP
- PaCO₂
- PaO₂
- Various drug and intracranial pathologies
2
Q
What vessels provide the blood flow to the brain?
A
- 80% via the carotid arteries
- 20% via the vertebral arteries
3
Q
What is the average cerebral blood blow?
A
50ml/100g/min
* Approx - 750mL/min total
4
Q
What percent of cardiac output goes to cerebral blood flow?
A
15%
5
Q
What structures are contained in the intracranial and spinal vault?
What 2 structures enclose these vaults?
A
- Neural tissue (brain and spinal cord)
- blood
- CSF
- Dura mater
- Bone
6
Q
Under normal conditions, what is the combined volume of brain tissue, intracranial CSF, and intracranial blood?
A
1200-1500mL
7
Q
What is the Monroe Kellie Doctrine?
A
Any increase in one component of the intracranial space (blood, brain tissue, CSF) must be offset with an equivalent decrease in another component to prevent an elevated ICP.
8
Q
Name the three components of the brain that form the Monroe-Kellie Doctrine.
A
- Brain 80%
- Blood 12%
- CSF 8%
9
Q
What mengial barriers seperate the brain contents?
A
- Falx cerebri - a reflection of dura that seperates the 2 cerebral hemispheres.
- Tentorium cereblli - a reflection of the dura that lies rostral to the cerebellum and marks the border between the supratentorial and infratentorial spaces.
10
Q
What happens when you hvae an increase in the contents of one region of the brain?
A
- This will cause regional increases in ICP, and in extreme cases, the contents will herniate into different compartments of the brain.
11
Q
What are herniation syndromes categorized by?
A
The region of the brain affected.
12
Q
What is subfalcine herniation?
A
Herniation of hemispheric contents under the falx cerebri, typically compressing branches of the anterior cerebral artery.
13
Q
What range is normal for ICP?
A
5 - 15 mmHg
14
Q
What is transtentorial herniation?
A
- Herniation of the supratentorial contents past the tentorium cerebelli, causing brain stem compression in a rostral to caudal direction.
15
Q
What are the S/S of transtentorial herniation?
A
- AMS
- Defects in gaze and ocular reflexes
- hemodynamic and respiratory compromise
- Eventual death
16
Q
What is Uncal herniation?
A
- A subtype of transtentorial herniation, where the uncus (medial portion of the temporal lobe) herniates over the tentorium cerebelli.
- This results in ipsilateral oculomotor nerve dysfunction.
17
Q
What are the signs and symptoms of uncal herniation?
A
- pupillary dilation
- ptosis
- lateral deviation of the affected eye.
- brain stem compression
- eventual death
18
Q
Why do the pupils become fixed and dilated with uncal herniation?
A
CN-3 (oculomotor) crosses near tentorium and is compressed by the herniation.
19
Q
What is herniation of the cerebellar tonsils?
A
- Occurs due to elevated infratentorial pressure, causing the cerebellar structures to herniate through the foramen magnum.
20
Q
What are the S/S of herniation of the cerebellar tonsils?
A
- Medullary dysfunction
- cardiorespiratory instability
- subsequently death
21
Q
What is the most common site of brain herniation?
A
Uncal
↑ICP forces temporal uncus into the infratentorial space (see 3 on the figure below).
22
Q
Label the sites of brain herniation
A
- Subfalcine
- Transtentorial
- Herniation of Cerebellar tonsils
- Traumatic event causing herniation out of cranial cavity
23
Q
What are causes of increased ICP?
A
- Tumors (directly because of their size, indirectly by causing edema in surrounding brain tissue, and by obstructing CSF flow as seen with tumors involving the 3rd ventricle)
- Intracranial hematomas (Cause increasedd ICP similar to mass lesions)
- Blood in the CSF (as seen in subarachnoid hemorrhage, which may lead to obstruction of CSF reabsorption, and granulations can further exacerbate increased ICP)
- Infections (such as meningitis or encephalitis can lead to edema or obstruction of CSF reabsorption)
- Aqueductal stenosis
24
Q
What symptoms are seen with abnormally high ICP?
A
- Headache
- N/V
- Papilledema
- ↓LOC
25
Q
How can elevated ICP be treated?
A
- Elevate HOB 30° (encourages jugular venous outflow)
- Hyperventilate (lowers PaCO2)
- Drain CSF (with an EVD, external ventral drain)
- Mannitol
- Diuretics (induce systemic hypovolemia)
- Corticosteroids (decreases swelling and enhances integrity of the BBB)
- Cerebral vasoconstricting anesthetics (propofol will decrease CMRO2 and CBF)
- Surgical decompression
26
Q
How can ICP be qualitatively assessed with ultrasound?
A
By measuring the optic nerve diameter.
↑ICP = ↑ optic nerve sheath
27
Q
What does Cushing’s Triad indicate?
What is the triad?
A
↑ICP
- ↑sBP
- ↓HR
- ↓RR (Cheyne-Stokes)
28
Q
Name 6 genetic neurological diseases.
A
- Multiple Sclerosis
- Myasthenia Gravis
- Lambert Eaton Syndrome
- Muscular dystrophy
- Myotonic dystrophy
29
Q
- What is multiple sclerosis?
- What is the onset age?
- What are the risk factors?
- What are the triggers?
- S/S
- Treatment
A
- A progressive autoimmune demylenation of central nerve fibers characterized by periods of exacerbations and remissions.
- Has an onset age of 20-40.
- Risk factors - being a female, Smoking, having a 1st degree relative with MS, Epstein-barre virus, having other autoimmune disorders.
- Triggers - stress, elevated temps, postpartum period
- S/S - motor weakness, sensory disorders, visual impairment, autonomic instability. S/S because of site demyelination.
- Treatment - no cure. Managed with corticosteroids, immune modulators, targeted antibodies, interferons, azatjioprine, and methotrexate.
30
Q
What are multiple sclerosis anesthesia considerations?
A
- Assess existing deficits
- If respiratory compromise, consider pulmonary funtion test.
- Labs - CBC, BMP, LFTs (LFT if pt on dantrolene and azithioprine because they cause bone marrow suppresion and liver function impairment. Pay close attention to glucose and electrolytes as steroids may impact levels)
- Preop stress dose steroids for anyone on longterm steroids (due to adrenal suppresion)
* Temperature managment (an increase in body temp can cause an exacerbation of MS symptoms). - Can use general anesthesia, regional, or peripheral nerve blocks with these patients.
* Avoid SUX as it may induce hyperkalemia from upregulated nACh receptors.
31
Q
- What is myasthenia gravis?
- What is it characterized by?
- S/S
- What are S/S exacerbated by?
- Treatment
A
- MG is an autoimmune diease where antibodies are generated against nACh receptors at skeletal motor endplates. It effects skeletal muscle only, not cardiac or smooth msucle.
- Characterized by muscle weakness that is exacerbated with exercise.
- occular symptoms such as diplopia and ptosis. Bulbar involvement includes laryngeal and pharyngeal wekaness, respiratory insufficiency, aspiration risk.. Thymic herplasia is common in 10% of MG patients which improves by 90% after thymectomy.
- S/S exacerbated by pain, insomnia, infection, and surgery.
- Treatment - ACh-E inhibitors (pyridostigmine), immunosuppresive agents, steroids, plasmapheresis, IVIG.
32
Q
What are myasthenia gravis anesthesia considerations?
A
- Assess existing deficits
- If respiratory compromise, consider pulmonary funtion test.
- Labs - CBC, BMP, LFTs (LFT if pt on dantrolene and azithioprine because they cause bone marrow suppresion and liver function impairment. Pay close attention to glucose and electrolytes as steroids may impact levels)
- Preop stress dose steroids for anyone on longterm steroids (due to adrenal suppresion).
-
Optimize respiratory function. counselpts on increased risk of needing post-op respiratory support/ventilation until fully recovered from anesthesia.
* Reduce paralytic doasge to avoid prolonged muscle weakness. - Use caution with opioids to avoid respiratory compromise.
- ACh-E inhibitors such as pyridostigmine may prolong SUX and ester local anesthetics**
33
Q
- What is Eaton Lambert syndrome?
- S/S
- Treatment
A
- A disorder causing the development of autoantibodies against voltage gated Ca++ channels (This reduces the Ca++ influx into the presynaptic Ca++ channel which decrease ACh release at the NMJ). Greater than 60% of cases are associated with small cell lung carcinoma (occurring as a paraneoplastic sydrome).
- S/S - progressive limb-girdle weakness, dysautonomia, oculobulbar palsy, proximal muscle weakness that improves with repeated use.
- Treatment - Selective potassium channel blocker 3-4 diaminopyridine, ACh-E inhibitors, immunologics such as azathioprine, steroids, plasmapheresis, IVIG
34
Q
What are Eaten Lambert syndrome anesthesia considerations?
A
- Assess existing deficits
- If respiratory compromise, consider pulmonary funtion test.
-
Optimize respiratory function. counselpts on increased risk of needing post-op respiratory support/ventilation until fully recovered from anesthesia.
* Reduce paralytic doasge to avoid prolonged muscle weakness.
*** Use extreme caution with opioids and paralytics. - Very sensative to nondepolarizing neuromuscular blockades and depolarizing neuromuscular blockades. significantly more sensative to ND-NMBDs than MG patients**
35
Q
- What is muscular dystrophy?
- What is Duchenne MD?
- S/S
A
- A hereditory disorder of muscle fiber degeneration caused by breakdown of the dystropin-glycoprotein complex that leads to myonecrosis, fibrosis, and skeletal muscle membrane permeability. There are 6 types of MD.
- Duchene MD - the most common and severe form of MD. Occurs only in boys with an onset between 2-5yo. Wheelchair bound by age 8-10. Average lifespan is 20-25yo due to cardiopulmonary complications.
- S/S - progressive muscle wasting without motor and sensory abnormalities, kyphoscoliosis, long bone fragility, respiratory weakness, frequent pneumonia, EKG changes, an elevated Serum creatine kinase caused by muscle wasting.
36
Q
What are muscular dystrophy anesthesia considerations?
A
- Assess existing deficits
- If respiratory compromise, consider pulmonary funtion test.
- Labs - CBC, BMP, and CK.
- Use caution with ND-NMBDs, use careful monitoring throughout.
*** Hypermetabolic syndrome can lead to rhabdo, hyperkalemia, vfib, and cardiac arrest. - Avoid SUX and volitiles as they exacerbate instability of muscle membrane.
- Consider low dose Roc and TIVA for general anesthesia. However, regional is preferred over GA to avoid cardiopulmonary complications.
- Have malignant hyperthermia cart available.**
37
Q
- What is myotonic dystrophy?
- What is myotonia?
- What is myotonia congenita?
- What is central core disease?
- What are myotonias triggered by?
- Treatment
A
- Myotonic dystrophy is the most common type of myotonia. Onset is 20-30s. S/S - muscle wasting on the face. masseter, hand, and pretibial muscles. May also affect pharyngeal, laryngeal, and diaphragmatic muscles. Cardiac conduction may be affected, 20% have mitral valve prolapse.
- Myotonia is a prolonged contraction after muscle stimulation which can be seen in several muscle disorders..
- Myotonia congenita is a milder form of Myotonic dystrophy involving the skeletal muscles only. Smooth and cardiac muscles are spared.
- Central core disease is rare. Core muscle cells lack mitochondrial enzymes. S/S = proximal muscle weakness and scoliosis.
- Myotonias are tiggered by stress and cold temperatures.
- Treatment = no cure. Symptoms managed with quinine, procainamide, and steroids.
38
Q
What are myotonic dystrophy anesthesia considerations?
A
- Assess the extent of cardiac and pulmonary abnormalities.
- Assess breath and heart sounds for abnormalities.
*** GI hypomotility puts them at increased aspiration risk. - High risk for endocrine abnormalities. Check thyroid and glucose levels.
- Keep patients warm to avoid flare ups
- Avoid SUX because fasciculations trigger myotonia.
- Pts are at increased risk for post-op respiratory weakness. **
- Caution with opioids to avoid post-op respiratory depression.
*
39
Q
Name 2 degenerative neurological disorders.
A
- Dementia
- Parkinsons
40
Q
- What are the 3 major dementia syndromes?
A
- Alzheimer’s 70%
- Vascular dementia 25%
- Parkinsons 5%
41
Q
What anti-cholinergic is best for Alzheimer’s patients?
Why is this?
A
Glycopyrrolate (doesn’t cross the BBB)
42
Q
What are the anesthesia considerations for dementia?
A
- Assess baseline level of cognitive dysfunction.
- Pt may not be able to give informed consent, look to MPOA.
- Potential aspiration risk from full stomach
- Review pre-op meds that may affect anesthetics such as ACh-E-I, MAOIs, and psych meds
- Increased risk for post op delerium, consider TIVA.
- Balance opioids to meet analgesic needs without exacerbating delerium.
- Regional anesthesia preferred to decrease opioid requirements.
43
Q
- What is Parkinsons disease?
- What is the cause?
- What will increase the risk of developing Parkinson’s?
- S/S
- Treatment
A
- Degeneration of dopiminergic fibers of basal ganglia. Dopamine regulates (inhibits excess stimulation) the extrapyramidal motor system, which is stimulated by ACh. IN parkinson’s, these motor neurons are overstimulated.
- Cause = unknown. advanced age is the biggest risk factor.
- Welding, herbacides, pesticides, and genetics will all increase the risk of getting Parkinson’s.
- S/S - triad of sx = skeletal muscle tremor, rigidity, and akinesia. Pill rolling, facial rigidity, slurred speech, difficulty swallowing, respiratory difficulty, depression and dementia.
- Treatment - Levodopa (crosses BBB), anticholinergics, MAOIs (inhibit dopamine degradation), deep brain stimulator.
44
Q
What drugs will counteract levodopa ans are contraindicated in parkinsons patients?
A
- Metoclopramide
- Haldol
- Droperidol
- Promethazine
45
Q
What are the anesthesia considerations for Parkinson’s disease?
A
- Assess severity with special attention to degree of pulmonary compromise.
- May need EKG, echo if indicated.
- Increased aspiration risk
- Avoid reglan, phenothiazines, and butyrophenes.
- Avoid demerol if on home MAOIs.
- PO levodopa must be continued to avoid unstable extreme EPS effects and chest wall rigidity.
- Deep brain stimulators may need to be disabled to avoid interaction with cautery.
- If cautery used, bipolar cautery recommended as it reduces scattering of electrocurrant.
46
Q
What does the mass effect of any tumor cause?
A
neurologic deficits
47
Q
What are common signs and symptoms of brain tumors?
A
- Increased ICP
- Papilledema
- Headache
- AMS
- Mobility impairment
- Vomitting
- Seizures
- Autonomic dysfunction
48
Q
Describe the function of each lobe of the brain
* Frontal
* Parietal
* Occipital
* Temporal
* Medulla
* Pons
A
- Frontal - controls personality, movement and sense of smell
- Parietal - Controls identification of objects, sense of pain and touch, body navigation, and spatial position.
- Occipital - controls vision.
- Temporal - controls memory, speech, and musical rhythm.
- Medulla - controls heart and lungs.
- Pons - controls eye and face movement.
49
Q
True/False
All brain tumors may either be primary or metastatic?
A
True
50
Q
Which is the most common CNS glial cell?
A
Astrocytes
51
Q
Decribe the following brain tumors:
* Gliomas
* Pilocyctic astrocytomas
* Anaplastic astrocytomas
* Glioblastoma multiforme
A
- Gliomas - Primary tumors. Least aggressive astrocytoma. Often found in young adults with new onset seizures
- Pilocyctic astrocytomas - Found in children and young adults. Mostly benign. Good pt outcomes id resectable.
- Anaplastic astrocytomas - Poorly differentiated. Usually evolve into a glioblastoma multiforrme.
- Glioblastoma multiforme - High mortality rate. Usually requires surgical debulking and chemo. Life expectancy is usually within weeks, even with treatment.
52
Q
Describe the following brain tumors:
* Meningiomas
* Pituitary adenomas
* Acoustic neuromas
* Metastatic carcinomas
A
- Meningiomas - Usually benign. Arise from dura or arachnoid tissue. Good prognosis with surgical resection.
- Pituitary adenomas - Noncancerous varying subtypes. Transsphenoidal or open craniotomy for removal is usually curative.
- Acoustic neuromas - Usually benign with schwannomas involving vestibular component of CN VIII within the auditory canal. Good prognosis with resection and radiation.
- Metastatic carcinomas - Can vary widely in origin and symptoms. Outcomes are generally less favorable.
53
Q
What are the anesthesia considerations for brain tumors?
A
- Ask about previous therapies, presenting symptoms, and neurological defects.
- Radiation damage may lead to lethargy and AMS.
- Chemotherapy may also have neurological effects.
- Consider CT, MRI, CBC, BMP (glucose), EKG (autonomic dysfunction may manifest on EKG).
- Pt may have labile HR and BP.
- Mannitol often used to reduce intracranial volume and pressure.
- Use pre-op steroids and antiseizure meds per surgeons request.
54
Q
Name 3 vascular neurological disorders.
A
- Cerebral vascular disease
- Aneurysms
- Arteriovenous malformation
55
Q
- What is a CVA?
- What percent are ischemic?
- What percent are hemorrhagic?
A
- A stroke that is characterized by sudden neurologic deficits resulting from ischemia or hemorrhage.
- Ischemic = 88% of cases
- Hemorrhagic = 12% of cases
56
Q
Globally, what is the leading cause of death and disability?
A
Stroke
57
Q
What is the difference between an ischemic and hemorrhagic stroke?
A
- Ischemic stroke is caused by an occlusion of a vessel that supplies a region of the brain resulting in cellular ischemia.
- Hemorrhagic stroke is caused by bleeding in the cranial vault that in turn impairs perfusion of the brain.
58
Q
What are the risk factors for Ischemic stroke?
A
- Hypertension
- cigarrettes
- hyperlipidemia
- Diabetes Mellitus II
- ETOH
59
Q
What are the risk factors for hemorrhagic stroke?
A
- Hypertension
- Cigarrettes
- Cocaine
- Being a female
60
Q
What is a TIA?
A
- A sudden focal vascular neurologic deficit that resolves within 24-hours.
- 1/3 of patients who experience a TIA will subsequently suffer a stroke.
- Stroke prognosis depends on the time from onset to thrombolytic intervention (needs to be done in under 90 minutes).
- If stroke suspected, get a stat CT without contrast to distinguish ischemic from hemorrhagic.
61
Q
What is the TOAST classification of causes of ischemic stroke?
A
- Large artery atherosclerosis (EX: carotid stenosis)
- Small vessel occlusion (EX: lacunar stroke)
- Cardioaortic embolus (EX: emboli from Afib)
- Other etiology (EX: stroke due to hypercoagulable states or vasculopathies)
- Undetermined etiology.
62
Q
What is the treatment for an ischemic stroke?
A
- PO Aspirin
- IV orintra-arterial recombinant tissue plasminogen activator (TPA)
- Thrombectomy devices have been used to stent vessels and remove clots
- Revascularization: performed in interventional radiology (IR), allowing for angiographic assessment and radiographic guidance during administration of thrombolytics or thrombectomy
63
Q
What are the anesthesia considerations for ischemic strokes?
A
- Pre-anesthetic evaluation should be concise & efficient, avoiding any delay in treatment.
- Focus on baseline neuro assessment,ability to safely lay flat, and cardiovascular function.
- Determine whether procedure could be done under sedation, or if a secure airway necessary
- Patients w/ischemic stroke frequently have CV risk factors, including HTN, DM, CAD, Afib, andvalvular disease, that could impact vasoactive drug choices and hemodynamic goal.
64
Q
What are the treatments for a hemorrhagic stroke?
A
- Tx depends on severity
- Conservative txis centered on the reduction of ICP,blood pressure control, seizure precautions, and vigilant monitoring
- Surgical treatment involves evacuation of the hematoma
- May remain intubated depending on cardiopulmonary stability
- ICU monitoring required postoperatively
65
Q
What are the 2 most reliable predictors of outcome for a hemorrhagic stroke?
A
- estimated blood volume
- change in LOC
66
Q
Wat are the subtypes of hemorrhagic strokes?
A
- Bloodwithin the brainis called an intraparenchymal hemorrhage
- Blood in the epidural, subdural, or subarachnoid spaces are referred to as epidural hematoma, subdural hematoma, and subarachnoid hemorrhages, respectively.
- Blood located in the ventricular system is an intraventricular hemorrhage, and usually occurs in conjunction with other types of hemorrhagic stroke
67
Q
What type of stroke is 4 times more likely to cause death than the other?
A
Hemorrhagic
68
Q
What are the overall anesthesia considerations for any kind of CVA?
A
- New anticoagulant for thrombus=No elective cases within 3 months
- Anticoagulants for CVA prophylaxis= consult prescriber to establish protocol
High risk pts for CVA that pause long acting anticoags (Warfarin) will need short acting anticoags (LMWH, IV unfractionated heparin) to bridge the gap - Close monitoring of coagulation status is required
If regional anesthesia planned, d/c anticoagulants for sufficient time to safely perform block - Assess orientation, pupils, bilateral grip strength, LE strength
- Ask about headaches, tinnitus, vision/memory loss, bathroom issues
- Look at route cause of CVA: Vascular disease, embolic (a-fib, prosthetic valve, right to left shunt/PFO)
- Imaging: Carotid U/S, CT/MRI head & neck, echocardiogram
- Preop EKG
- CBC, BMP,possible T & C
- Cerebral oximetry if possible
- Aline,2 IVs and/or CVC
69
Q
What is the circle of willis?
A
- Blood is supplied to the brain from the internal carotid arteries and vertebral arteries.
- These vessels join on the inferior surface of the brain to form the circle of willis, which, during ideal circumstances, provides collateral circulation to multiple areas of the brain.
70
Q
Name the pertinent vasculature of the circle of Willis.
This card is just to look at the picture on the other side.
A
71
Q
Name the clinical manifestations of regional stroke for each occluded artery.
* Anterior cerebral artery -
* Middle cerebral artery -
* Posterior cerebral artery -
* Penetrating arteries -
* Basilar artery -
* Vertebral artery -
A
- Anterior cerebral artery - contralateral leg weakness
- Middle cerebral artery - contralateral hemiperesis and hemisensory defecit (face and arm more than leg), aphasia, contralateral visual field defecit.
- Posterior cerebral artery - contralateral visiual field deficit, contralateral hemiperesis.
- Penetrating arteries - contralateral hemiparesis, contralateral hemisensory defecit.
- Basilar artery - Oculomotor defecits, and or ataxia with crossed sensory and motor deficits.
- Vertebral artery - Lower cranial nerve deficits and or ataxia with crossed sensory deficits.
72
Q
Where is bleeding located with an epidural hematoma?
A
Inbetween the dura and the skull
73
Q
Where is bleeding in subdural hematomas located?
A
Between the dura mater and the arachnoid mater.
74
Q
What intracranial bleed is characterized by:
lucidity → unconscious → conscious → unconscious
A
Epidural hematoma
75
Q
When are the majority of cerebral aneurysms diagnosed?
A
- After they rupture.
- Only 1/3rd of aneurysm patients have symptoms before rupture.
76
Q
Cerebral aneurysms:
* S/S
* Risk factors
* Diagnostic
* Intervention
* Treatment
* Anesthesia considerations
A
- S/S - headache, photophobia, confusion, hemiparesis, coma
- Risk factors - Hypertension, smoking, female, birth control, cocaine use.
- Diagnositc - CT/angiogram, MRI, lumbar puncture with/CSF analysis if rupture suspected.
- Intervention should be performed with 72 hours of rupture for best outcomes
- Treatment - surgical coiling, stenting, trapping/bypassing (for very large aneurysms). The neurosurgeon may be on standyby in case intra-op rupture/SAH.
- Anesthesia considerations - CT, MRI, EKG, echo, CBC, BMP, type and screen with blood available on standby, seizure prophylaxis, blood pressure cpntrol to avoid rupture, could possibly use mannitol.
77
Q
When is the risk for cerebral vasospasm post SAH?
A
3-15 days
78
Q
Post SAH vasospasm
* MOA
* What is triple H therapy?
* What is the initial main treatment?
* What are the Interventional treatments?
* What are the anesthesia considerations?
A
- Free hemoglobin from a SAH triggers inflammatory mediators, which reduce nitric oxide availability and increase endothelin-1, leading to vasoconstriction in the brain.
- Triple H therapy = hypertension, hypervolomeia, and hemodilution.
- Hypertension is the initial main treatment so that we avoid complications of hypervolemia.
- Interventional treatments include subarachnoid balloon dilation and direct injection of vasodilators to relieve the spasm.
- Anesthesia considerations - BP cpntrol to avoid rupture, seizure prophylaxis, CT, MRI, EKG, Echo, CBC, BMP, type and screen with blood available. Possible use of mannitol.
79
Q
What intracranial bleed is often characterized as the “worst headache of one’s life”?
A
Subarachnoid hemorrhage
80
Q
What location is often the site of bleeding in subarachnoid hemmorhaging?
A
Circle of Willis (usually aneurysmal rupture)
81
Q
How is cerebral vasospasm treated?
A
Triple “H” Therapy
- HTN
- Hypervolemia
- Hemodilution
82
Q
- What does a score of 0 mean on the aneurysm grading for prognosis?
- What does a score of 5 mean?
A
- 0 = unruptured aneurysm, 0-2% mortality rate, GCS of 15
- 5 = Deep coma, decerebrate rigidity, 40-50% mortality rate, GCS 3-6. Could have presence of major focal defecit.
83
Q
- What is an AV malformation?
- What does an AV malformation create?
- S/S
- How is it diagnosed?
- Treatment
- What are the anesthesia considerations?
A
- An AV malformation is an arterial to venous connection without intervening capillaries, that is believed to be congenital.
- It creates an area of high flow and low resistance shunting.
- S/S range from mass effects to hemorrhage. The majority of AVMs are supratentorial.
- It is diagnosed with MRI and angiogram.
- Treatment = radiation, angio-guided embolism, and surgical resection which has a higher mortality rate.
- Anesthesia considerations - MRI, CBC, BMP, BP control, possible use of mannitol, CVC, a-line, seizure prophylaxis, EKG, echo, type and screen with blood available.
84
Q
How is an AVM graded?
What is the surgical outcome based on number of points?
A
- Nidus size = small (<3cm)-1, medium (3-6cm)-2, large (>6cm)-3
- Eloquence of adjacent brain= noneloquent-0, eloquent-1
- Pattern of venous drainage = superficial only-0, deep only or deep and superficial-1
- Number of points = percent of patients with no post-op neurologic defeicit
- 1 = 100%
- 2 = 95%
- 3 = 84%
- 4 = 73%
- 5 = 69%
85
Q
Name 4 congenital neurological disorders.
A
- Chiari malformations
- Tuberous sclerosis
- Von-hippel-Lindau disease
- Neurofibromatosis
86
Q
What are congenital brain abnormalities?
A
- These result from defects in the development or structure of the CNS, and are often hereditary.
- Disease process may be diffuse or confines to specific neuronal structures.
87
Q
What is a chiari malformation and what are the different types?
A
- A congenital displacement of the cerebellum
- Type 1 - Downward displacement of cerebellum
- Type 2 - (arnold chiari) downward displacement of cerebellar vermis, often associated with myelomeningocele
- Type 3 - rare, occipital encephalocele with downward displacement of cerebellum
- Type 4 - Cerebellar hypoplasia without displacement of posterior fossa contents, and not campatible with life.
88
Q
A
89
Q
Chiari malformation
* S/S -
* Treatment -
* Anesthesia considerations -
A
- S/S - headache extending to arms and shoulders, visual disturbance, ataxia
- Treatment - surgical decompression
- Anesthesia considerations - good neuro assessment, assess defecits, may hyperventilate to decrease ICP, CBC, BMP, type and screen with blood available, MRI, a-line, CVC or 2 large bore IVs
90
Q
- What is tuberous sclerosis?
- What is another name for it?
- S/S -
- How does it often present?
- What are the anesthesia considerations?
A
- It is an autosomal dominant disease causing benign hematomas, angiofibromas, and other malformations that can occur anywhere in the body.
- AKA bourneville disease
- It often involves co-existing tumorsof the face, oropharynx, heart, lungs, liver, and kidneys. Lesions of the brain include cortical tumors, and giant cell astrocytomas.
- Presentation likely includes mental retardation and eizure disorders.
- Anesthesia consideration must take into account airway compromise, as well as cardiac and kidney involvement.
91
Q
- What is Von Hippel-Lindau Disease?
- What are the anesthesia considerations?
A
- An autosomal dominant disease that produces benign tumors in the CNS, eyes, adrenals, pancrease, and kidneys. Patients may present with pheochromocytoma.
- Anesthesia considerations take into account exagerated hypertension with pheo, and neuraxial anesthesia should be avoided if there is a co-existing spinal cord tumor.
92
Q
- What is neurofibromatosis?
- What are the 3 types?
- S/S
- treatment
- What are the anesthesia considerations?
A
- It is an autosomal dominant disease of the nervous system that causes tumors to form on the nerves in the body, anywhere, at any time.
- Type-1 = most common, type-2, schwannomatosis are the rarest.
- S/S - has many different disease presentation including tumors all over the skin.
- There is no cure at this time.
- Anesthesia considerations = acount for increased ICP, airway issues, scoliosis, and possibility of pheo. neuraxial anesthesia should be avoided if there is a co-existing spinal cord tumor.
93
Q
- What is a hydrocephalus?
- How do you get a hydrocephalus?
- S/S
- Treatment
A
- A disorder of CSF accumulation causing increased ICP, that results in ventricular dilation. The accumulation of CSF is due to an imbalance between CSF production and absorption.
- A hydrocephalus can be congenital or acquired due to meningitis, tumors, head injury, or stroke.
- S/S - acute, aubacute, or chronic
- Treatment - mainly diuretics (furosemide and acetazolamide decrease CSF production), VP shunt (drain placed in the ventricle of the brain that empties into the peritoneum) or endoscopic third ventriculostomy (catheter placed into the lateral ventricle of the brain that peritoneal space). Shunt malfunction usually occurs most frequently in the first year of placement (high failure rate).
94
Q
What are the two types of hydrocephalus? Which is more common?
A
- Obstructive (most common)
- Communicating
95
Q
- What is a TBI?
- How is a TBI categorized?
- Describe primary and secondary injuries in reference to S/S.
- What are the anesthesia considerations?
A
- Traumatic brain injury that is categorized as either penetrating or non-penetrating depending on breach of dura.
- severity is categorized by GCS scale.
- Primary injuries occur at the time of insult. Secondary injuries = neuroinflammation, cerebral edema, hypoxia, anemia, electrolyte imbalances, and neurogenic shock.
- Anesthesia considerations - intubation required in severe TBI with a GCS <9, and respiratory distress. Mild hyperventilation to control and lower ICP, CT of head and neck ASAP, gross neurologic exam but due not delay emergent surgery. C-spine stabilization, refrain from NG or OGT due to potential for basilar skull fracture. Pressors, bicarb, calcium, and blood products.
96
Q
What is a seizure disorder?
What is epilepsy?
What do antiepileptic drugs do?
What are the anesthesia considerations?
What kind of anesthesia would you do for post-seizure on the flow?
A
- Seizures are transient, paroxysmal, or synchronous discharge of neurons in the brain. Can be caused by transient abnormalties of hypoglycemia, hyponatremia, hyperthermia, and intoxication. In these cases, treating the underlying cause is curative.
- Epilepsy - recurrent seizure due to congenital or acquired factors.
- Antiepileptic drugs decrease neuronal excitability and enhance inhibition.
- Anesthesia considerations - determine the source of seizure if known and how well they are controlled, Give antiseizure meds before incision, if giving seizure meds such as tegritol, pheytoin or barbiturates patients will likely require higher doses of hepatically cleared meds.
- RSI with cricoid pressure.
97
Q
What induction agent is a good first-line agent for treatment of acute seizures?
A
Propofol
98
Q
What are the s/s of seizures whilst under anesthesia?
A
- ↑HR
- HTN
- ↑ ETCO₂
