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24 Physical & Health Assessment > Neuro Disease Assessment COPY > Flashcards

Neuro Disease Assessment COPY Flashcards

1
Q

What factors modulate cerebral blood flow (CBF)?

A

Cerebral metabolic rate
CPP (MAP-ICP)
PaCO2 and PaO2
drugs, pathologies

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2
Q

What is the approximate cerebral blood flow with autoregulation?

A

50 mL/100g brain tissue/min
~750mL/min

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3
Q

What does the intracranial and spinal vault contain?

A

Neural tissue
blood
CSF

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4
Q

What is the normal combined volume of brain tissue, intracranial CSF, and intracranial blood combined?

A

1200-1500mL

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5
Q

What is the normal intracranial pressure (ICP) range?

A

5-15 mmHg

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6
Q

What is the Monro-Kellie hypothesis?

A

Increase in one component must be offset by a decrease in another to prevent elevated ICP

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7
Q

How do homeostatic mechanisms compensate for increased ICP?

A

By increasing MAP to support CPP

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8
Q

What can happen if compensatory mechanisms for increased ICP fail?

A

Result in cerebral ischemia

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9
Q

What reflection of the dura separates the two cerebral hemispheres?

A

falx cerebri

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10
Q

What reflection of the dura lies rostral to the cerebellum and marks border between supratentorial and infratentorial spaces?

A

tentorium cerebelli

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11
Q

What is subfalcine herniation?

A

Hemispheric contents herniate under the falx cerebri.

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12
Q

What artery is compressed in subfalcine herniation?

A

Anterior cerebral artery

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13
Q

What is transtentorial herniation?

A

Supratentorial contents herniate past the tentorium cerebelli.

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14
Q

What is the consequence of transtentorial herniation?

A

Brainstem compression

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15
Q

What is the result of brainstem compression in transtentorial herniation?

A

AMS, gaze and ocular reflex defects, hemodynamic and respiratory compromise, and death

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16
Q

What is uncal herniation?

A

Subtype of transtentorial herniation where the uncus (medial temporal lobe) herniates over the tentorium cerebelli.

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17
Q

What are the manifestations of uncal herniation?

A

Pupillary dilatation, ptosis, lateral eye deviation, brainstem compression and death

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18
Q

What are the symptoms of herniation of the cerebellar tonsils?

A

Medullary dysfunction, cardiorespiratory instability

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19
Q

What are the types of brain herniation are indicated in 1-4?

A
  1. Subfalcine
  2. Transtentorial
  3. Cerebellar contents through foramen magnum
  4. traumatic hernation out of cranial cavity
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20
Q

How do tumors cause increased ICP?

A
  • Directly due to size
  • indirectly by causing edema in surrounding brain tissue
  • obstructing CSF flow
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21
Q

How do intracranial hematomas cause increased ICP?

A

Similar to mass lesions

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22
Q

How can blood in the CSF lead to increased ICP?

A

Obstruct CSF reabsorption

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23
Q

What effect can infections like meningitis/encephalitis have on ICP?

A

Lead to edema or obstruction of CSF reabsorption

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24
Q

What positioning method encourages jugular venous outflow to decrease ICP?

A

Elevation of the head

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25
Q

How does hyperventilation help decrease ICP?

A

Lowers PaCO2 ⇒ vasoconstriction

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26
Q

How does using external ventricular drain (EVD) to decrease ICP?

A

CSF drainage

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27
Q

How do hyperosmotic drugs help decrease ICP?

A

Increase osmolarity, drawing fluid across BBB

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28
Q

What do diuretics do to help decrease ICP?

A

Induce systemic hypovolemia

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29
Q

How do corticosteroids help decrease ICP?

A

Decrease swelling and enhance BBB integrity

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30
Q

What is the role of cerebral vasoconstricting anesthetics like propofol in decreasing ICP?

A

Decrease CMRO₂ and CBF

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31
Q

What is a surgical intervention to decrease ICP?

A

Surgical decompression

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32
Q

What components are considered in a neurological assessment?

A

History, symptoms, baseline neuro-deficits

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33
Q

What should be included in pre-op documentation for a neurological assessment?

A

Factors considered and rationale for chosen plan

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34
Q

What is multiple sclerosis (MS)?

A

Progressive autoimmune demyelination of central nerve fibers

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35
Q

What are some risk factors for MS?

A
  • Female (onset age 20-40)
  • Epstein-Barr Virus
  • other AI disorders
  • smoking
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36
Q

What are some exacerbation triggers for MS?

A
  • Stress
  • elevated temps
  • postpartum period
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37
Q

What are the symptoms of MS?

A
  • Motor weakness
  • sensory disorders
  • visual impairment
  • autonomic instability
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38
Q

How is MS managed?

A

Corticosteroids
immune modulators
targeted antibodies

No cure

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39
Q

What is close temperature management critical for patients with Multiple Sclerosis?

A

increase in body temp can cause exacerbation of MS

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40
Q

Why might a stress-dose of steroids be necessary for an MS pt?

A

Long term steroids cause adrenal suppression

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41
Q

Why is it important to monitor glucose and electrolytes in MS patients?

A

Steroids impact levels

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42
Q

Why should Succinylcholine be avoided in MS patients?

A

May induce hyperkalemia from upregulated nAChRs

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43
Q

What is Myasthenia Gravis?

A

Autoimmune disorder characterized by production of antibodies that attack nAchR’s

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44
Q

Which muscle type is affected in Myasthenia Gravis?

A

Skeletal muscle (not smooth or cardiac 😃)

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45
Q

What exacerbates muscle weakness in Myasthenia Gravis?

A

Exercise

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46
Q

What are common symptoms of Myasthenia Gravis?

A

Ocular
Diplopia
ptosis

Muscle weakness (general)

bulbar
Laryngeal/pharyngeal weakness
respiratory insufficiency
risk of aspiration

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47
Q

What surgical procedure can improve 90% of patients with Myasthenia Gravis?

A

thymectomy

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48
Q

What can exacerbate symptoms of Myasthenia Gravis?

A

stress 😵‍💫
Pain
Insomnia
Infection
surgery

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49
Q

What are the treatment options for Myasthenia Gravis?

A

Ach-E inhibitors, immunosuppressive agents, steroids, plasmapheresis, IVIG

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50
Q

Preanesthetic Considerations for Myasthenia Gravis

A

Assess deficits, consider pulmonary function tests

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51
Q

MG Management During Anesthesia

A

Reduce paralytic dosage, caution with opioids

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52
Q

MG Labs

A

CBC, BMP, LFT (if on Azathioprine)

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53
Q

MG Steroid Considerations

A

Monitor glucose/electrolytes, consider pre-op steroids for long-term use

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54
Q

MG Post-Anesthesia respiratory considerations

A

Increased risk of resp support/ventilation until recovery

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55
Q

What is Eaton-Lambert Syndrome?

A

Autoantibodies against VG Calcium chnls ⇒ decreased release of ACh presynaptically

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56
Q

What is the most common associated cancer with Eaton-Lambert Syndrome?

A

Small cell lung carcinoma

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57
Q

What are the symptoms of Eaton-Lambert Syndrome?

A
  • Progressive limb-girdle weakness that improves with repeated use
  • dysautonomia
  • oculobulbar palsy
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58
Q

What are treatment options for Eaton-Lambert Syndrome? (6)

A
  • Selective K⁺ channel blocker (3-4 diaminopyridine)
  • AChE inhibitors
  • immunologics (azathioprine)
  • steroids
  • plasmapheresis
  • IVIG
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59
Q

How consideration should be made with neuromuscular blocking agents and LEMS?

A

LEMS pts are VERY sensitive to ND-NMBs and D-NMBs

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60
Q

What should patients be counseled on regarding post-operative respiratory support?

A

Risks for needing it until fully recovered

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61
Q

What is Muscular Dystrophy?

A

Hereditary disorder of muscle fiber degeneration from dystrophin genetic abnormalities

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62
Q

What is the most common and severe form of Muscular Dystrophy?

A

Duchenne MD

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63
Q

What population is affect by Duchenne’s MD?

A
  • Only in boys
  • Onset 2-5yo
  • avg lifespan ~20-25yr
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64
Q

What are symptoms of Duchenne Muscular Dystrophy? (5)

A

Progressive muscle wasting
long bone fragility
kyphoscoliosis
respiratory weakness
frequent Pneumonia

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65
Q

What is a key characteristic seen in Duchenne MD laboratory tests?

A

Elevated serum creatine kinase from muscle wasting (20-100x 🤯)

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66
Q

What cardiac evaluations should be performed pre-operatively?

A

Pre-op EKG, echocardiogram. Evaluate for cardiomyopathy

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67
Q

What syndrome is similar to MH and can be seen with Succinylcholine and volatile anesthetics with muscular dystrophy?

A

Hypermetabolic Syndrome

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68
Q

What complications can hypermetabolic syndrome lead to?

A

rhabdomyolysis
hyperkalemia
Vfib
cardiac arrest

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69
Q

What muscle relaxant and anesthesia approach is recommended for patients with MD?

A

low dose rocuronium and TIVA

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70
Q

Why is regional anesthesia preferred over general anesthesia in at-risk patients with MD?

A

To avoid triggers and cardiopulmonary complications

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71
Q

What is myotonia?

A

Prolonged contraction after muscle stimulation

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72
Q

What are the symptoms of myotonic dystrophy?

A

Muscle wasting, may affect various muscles including face, airways and cardiac muscles

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73
Q

20% of individuals with myotonic dystrophy may have ___?

A

mitral valve prolapse (MVP)

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74
Q

How are myotonias triggered in these disorders?

A

By stress and cold temperatures

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75
Q

What is myotonia congenita?

A

milder form of myotonic dystrophy involving skeletal muscles but not smooth or cardiac muscles

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76
Q

What is central core disease?

A

disorder where core muscle cells lack mitochondria enzymes ⇒ proximal muscle weakness and scoliosis

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77
Q

What is the treatment approach for these myotonia disorders?

A

Symptom management with Quinine, Procainamide, Steroids

no cure

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78
Q

Why should Succinylcholine be avoided in myotonia disorders?

A

Fasciculations trigger myotonia

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79
Q

What should be assessed in pre-anesthetic considerations for myotonia disorders?

A

Cardiac and pulmonary abnormalities
endocrine abnormalities

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80
Q

What poses an increased risk of aspiration in myotonia?

A

GI hypomotility

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81
Q

What caution should be taken with opioids in these myotonia patients?

A

To avoid post-op respiratory depression

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82
Q

What are the 3 major dementia syndromes?

A

Alzheimer’s (70%)
Vascular dementia(25%)
Parkinson’s (5%)

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83
Q

What type of anesthesia should be considered to reduce the risk of post-op delirium?

A

Consider TIVA

84
Q

Why should opioid use be minimized in dementia pts?

A

avoid exacerbating delirium

RA preferred to decrease opioid requirements

85
Q

What is the pathology & cause of Parkinson’s Disease?

A

Degeneration of dopaminergic fibers of basal ganglia
Unknown cause; Advanced age is a risk factor

86
Q

How does dopamine play a role in Parkinson’s Disease?

A

Regulates extrapyramidal motor system (inhibits excess stimulation)

87
Q

What is the triad of symptoms of Parkinson’s Disease?

A

Tremor, rigidity, akinesia, (postural instability)

TRAP

88
Q

What are some signs of Parkinson’s Disease?

A

rhythmic Pill rolling
facial rigidity
slurred speech
dysphagia
dementia
respiratory difficulty

89
Q

What are some treatment options for Parkinson’s Disease?

A

Levodopa
Anticholinergics
MAOIs
Deep brain stimulator

90
Q

What should be assessed in patients with Parkinson’s disease before anesthesia?

A

Assess severity and degree of pulmonary compromise

91
Q

Why is it important to review the patient’s home medications before anesthesia in Parkinson’s disease?

A

Many may interact with anesthetics (MAOIs)

92
Q

Which medications should be avoided in patients with Parkinson’s disease before anesthesia?

A

Avoid: Reglan, Phenothiazines, Butyrophenones
Avoid Demerol if on MAOI

93
Q

Why is PO Levodopa continued before anesthesia in Parkinson’s disease?

A

To avoid unstable extreme extrapyramidal effects (chest wall rigidity)

94
Q

What type of cautery is recommended if used in patients with Parkinson’s disease? Why?

A

Bipolar cautery- reduces scattering of electrocurrent

if pt has deep brain stimulator

95
Q

What are common symptoms of brain tumors?

A

↑ICP
Papilledema
Headache
AMS
Mobility impairment
Vomiting
Autonomic dysfunction
Seizures

96
Q

What can the mass effects of a brain tumor cause?

A

Neurologic deficits

97
Q

Which CNS glial cells are the most common?

A

Astrocytes

98
Q

Which tumors are primary tumors, least aggressive astrocytomas?

A

Gliomas

99
Q

Which tumors are usually found in young adults with new onset seizures?

A

gliomas

100
Q

Which tumors are mostly benign, good outcomes if resectable?

A

Pilocytic astrocytomas

101
Q

Which tumors usually evolve into glioblastoma multiforme?

A

Anaplastic astrocytomas

102
Q

Which tumors carry a high mortality (weeks) and usually require surgical debulking and chemo?

A

Glioblastoma Multiforme

103
Q

What is the general prognosis for meningiomas?

A

(Arise from dura or arachnoid tissue)
Usually benign, Good prognosis with surgical resection

104
Q

What surgical methods are typically used for the removal of pituitary adenomas?

A

Transsphenoidal or open craniotomy usually curative

105
Q

What is the typical prognosis for acoustic neuromas?

A

Good prognosis with resection +/- radiation

106
Q

What are characterized by benign schwannomas involving the vestibular component of CN VIII within the auditory canal?

A

acoustic neuromas

107
Q

Why are patients often on steroids before surgery for brain tumors? Should they be continued?

A

Minimize cerebral edema
will need to continue

108
Q

What are common medications used for brain tumor patients closer to the motor cortex?

A

(Supratentorial lesions, close to motor cortex)
Anticonvulsants

109
Q

What is often used to reduce intracranial volume and pressure in brain tumor patients?

A

Mannitol

110
Q

How may autonomic dysfunction manifest in brain tumor patients?

A

manifest on EKG, labile HR & BP’s

111
Q

What are strokes characterized by?

A

Sudden neurological deficits from Ischemia (88%) or hemorrhage (12%)

112
Q

What is the leading cause of death and disability globally?

A

Stroke

113
Q

Where is blood supplied to the brain from?

A

Internal carotid arteries & vertebral arteries

114
Q

What are the joining vessels on inferior brain surface?

A

circle of willis

115
Q

What does the circle of Willis provide during ideal circumstances?

A

Collateral circulation to multiple areas of the brain

116
Q

What are the clinical features of an anterior cerebral artery occlusion?

A

Contralateral leg weakness

117
Q

What are the clinical features of a middle cerebral artery occlusion?

A
  • Contralateral hemiparesis and hemisensory deficit
  • Aphasia
  • contralateral visual field defect
118
Q

What are the common clinical features of posterior cerebral artery occlusion?

A
  • contralateral visual field defect
  • contralateral hemiparesis
119
Q

What are the common clinical features of penetrating artery occlusion?

A
  • Contralateral hemiparesis
  • contralateral hemisensory deficits
120
Q

What are the clinical manifestations of vertebral artery occlusion?

A

lower cranial nerve deficits and/or ataxia

121
Q

What deficits may occur with basilar artery occlusion?

A

Oculomotor deficits and/or ataxia with crossed sensory and motor deficits

122
Q

What is an ischemic stroke?

A

Occlusion of a vessel in the brain causing cellular ischemia

123
Q

What is a transient ischemic attack (TIA)?

A

Sudden neurologic deficit resolving in 24 hrs

124
Q

Why is a non-contrast CT needed in suspected stroke cases?

A

To distinguish ischemic from hemorrhagic stroke

125
Q

___ of pts who experience TIA will subsequently suffer a stroke

A

1/3

126
Q

What is often the recommended initial treatment for acute ischemic stroke?

A

PO Aspirin

127
Q

What is essential in the pre-anesthetic evaluation for revascularization in ischemic stroke treatment?

A

Baseline neuro assessment, ability to lay flat, cardiovascular function

128
Q

What CV risk factors do patients with ischemic stroke frequently have?

A

HTN, DM, CAD, Afib, valvular disease

129
Q

How is stroke revascularization usually performed?

A

performed in IR, and angiographic and radiographic guidance during administration of thrombolytics or thrombectomy

130
Q

What is an acute hemorrhagic stroke and its effect?

A

Bleeding inside cranial vault impairing brain perfusion

131
Q

What are the two most reliable predictors of outcome in hemorrhagic strokes?

A

Estimated blood volume & change in LOC

132
Q

What are the subtypes of hemorrhagic stroke based on the location of blood?

A

Intraparenchymal
epidural hematoma
subdural hematoma
subarachnoid hemorrhages
intraventricular hemorrhage

133
Q

What does conservative treatment for hemorrhagic CVA focus on?

A

Reduction of ICP, blood pressure control, seizure precautions

134
Q

What is a key aspect of surgical treatment for hemorrhagic CVA?

A

Evacuation of the hematoma

135
Q

New anticoagulant for thrombus=No elective cases within ____

A

3 months

136
Q

What is required when there is a need to discontinue anticoagulants for regional anesthesia (RA)?

A

For RA planned, d/c anticoagulants for sufficient time to safely perform block

137
Q

What assessments should be conducted for a patient with cerebrovascular disease pre-op?

A

(Mini neuro exam)
Orientation
pupils
grip strength
LE strength

138
Q

What symptoms should be asked about in a patient with cerebrovascular disease pre-op?

A

Headaches, tinnitus, vision/memory loss, bathroom issues

139
Q

What should be examined regarding the root cause of cerebrovascular accident?

A

Vascular disease, embolic causes

140
Q

What imaging studies are recommended for a patient with cerebrovascular disease pre-op?

A

Carotid U/S, CT/MRI head & neck, echocardiogram

141
Q

What tests should be performed preoperatively on a patient with cerebrovascular disease?

A

EKG, CBC, BMP, possible T & C

142
Q

What vascular access measures should be considered pre-op?

A

A-line, 2 IVs and/or CVC

143
Q

What is the recommended timeframe for intervention in cerebral aneurysms post-rupture?

A

Within 72 hours

144
Q

What are some risk factors for cerebral aneurysms? (5)

A

HTN
smoking
female
oral contraceptives
cocaine use

145
Q

What are the common symptoms of cerebral aneurysms? (5)

A

Headache
photophobia
confusion
hemiparesis
coma

146
Q

What imaging techniques are used for diagnosing cerebral aneurysms?

A

CT/angio, MRI, Lumbar puncture with CSF analysis if rupture suspected

147
Q

What are some pre-anesthesia assessments needed for a patient with a cerebral aneurysm?

A

CT/MRI, EKG, Echo, CBC, BMP, T&C with blood available

148
Q

What are the surgical treatment options for cerebral aneurysms?

A

Coiling, stenting, trapping/bypass for very large aneurysms

149
Q

What does anesthesia management generally entail?

A

Avoid rupture
BP control (mannitol)
Seizure prophylaxis

150
Q

Why is glucose monitoring important in patients with cerebral aneurysms?

A

May be on Steroids, may lead to hyperglycemia

151
Q

When does the risk for vasospasm typically occur post SAH?

A

3-15 days post SAH

152
Q

What triggers inflammatory mediators in post-SAH vasospasms?

A

Free hgb

153
Q

What does free hgb trigger that reduces nitric oxide availability and increases endothelin 1?

A

Inflammatory mediators => vasoconstrictor/vasospasms

154
Q

What does Triple H therapy stand for in managing post-SAH vasospasms?

A

Hypertension
Hypervolemia
Hemodilution

155
Q

What is the initial main treatment to avoid complications of hypervolemia in managing post-SAH vasospasms?

A

HTN

156
Q

What interventional treatments can relieve vasospasm in post-SAH cases?

A

Balloon dilation, direct injection of vasodilators (CCB)

157
Q

What is the main aneurysm grading scale used for prognosis?

A

Hunt and Hess Classification
ranges from

  • 0: unruptured aneurysm: 0-2% mortality
  • 1: ruptured w/ minimal s/s
  • 2: headache 🤕
  • 3: drowsiness & AMS
  • 4: stupor, hemiparesis, early decerebrstion
  • 5: deep coma, decerebrate: 40-50% mortality
158
Q

What is an Arteriovenous Malformation (AVM)?

A

Arterial to venous connection without intervening capillaries

159
Q

What symptoms can Arteriovenous Malformations present with?

A

Range from mass-effects to hemorrhage

160
Q

AVM create an area of ___ flow, ___ resistance shunting

A

high flow
low resistance

161
Q

How are Arteriovenous Malformations diagnosed?

A

Angiogram, MRI

162
Q

What are the treatment options for Arteriovenous Malformations?

A

Radiation
angio-guided embolization
surgical resection

163
Q

What interventions may be needed for patients with Arteriovenous Malformations before anesthesia?

A

BP control
seizure prophylaxis
CVC or 2 large bore IV’s
A-line

164
Q

How is a Spetzler-martin arteriovenous malformation grading system scored?

A
165
Q

What are congenital brain abnormalities?

A

Defects in development or structure of CNS, often hereditary

166
Q

What is Chiari Malformation?

A

Congenital displacement of cerebellum

167
Q

What are the different types of Chiari Malformation?

A
  • Type 1: downward displacement of cerebellum
  • Type 2 (Arnold Chiari): downward displacement of vermis
  • Type 3: occipital encephalocele, downward cerebella displacement
  • Type 4: cerebellar hypoplasia, w/o displacement (not compatible with life)
168
Q

What are the symptoms of Chiari Malformation?

A

Headache
visual disturbances
ataxia

169
Q

How is Chiari Malformation treated?

A

Surgical decompression

170
Q

What pre-anesthesia considerations should be taken for Chiari Malformation?

A

may hyperventilate to ↓ICP
2 large bore IV or CVC
A-line

171
Q

What is another name for Tuberous Sclerosis?

A

Bourneville Disease

172
Q

What type of disease is Tuberous Sclerosis?

A

Autosomal dominant disease causing benign hemartomas, angiofibromas and other malformations

173
Q

What are some brain lesions seen in Tuberous Sclerosis?

A

Cortical tumors, giant-cell astrocytomas

174
Q

Which organs can be affected by Tuberous Sclerosis tumors?

A

Face
oropharynx
heart
lungs
liver
kidneys

175
Q

What are common presentations associated with Tuberous Sclerosis?

A

Mental retardation and seizure disorders

176
Q

What must be considered during anesthesia for Tuberous Sclerosis patients?

A

Airway compromise, cardiac/kidney involvement

177
Q

What is Von Hippel-Lindau Disease characterized by?

A

Autosomal dominant disease causing tumors of the CNS, eyes, adrenals, pancreas, kidneys

178
Q

What should be considered in anesthesia management for patients with Von Hippel-Lindau Disease and pheochromocytoma?

A

Exaggerated HTN

179
Q

Why may neuraxial anesthesia be limited in Von Hippel-Lindau Disease patients?

A

Co-existing spinal cord tumor

180
Q

What is neurofibromatosis characterized by?

A

genetic disorder of nervous system causing tumors to form on the nerves in the body

181
Q

What are the three types of neurofibromatosis?

A

Type 1 (most common)
Type 2
Schwannomatosis (rare)

182
Q

What are some anesthesia considerations for patients with neurofibromatosis?

A

Increased ICP
Airway issues
Scoliosis
Possible pheochromocytoma

183
Q

Why should neuraxial blockade be avoided in patients with neurofibromatosis?

A

High likelihood of spinal tumors

184
Q

What is hydrocephalus?

A

Disorder of CSF accumulation causing increased ICP and ventricular dilation

185
Q

What causes the accumulation of CSF in hydrocephalus?

A

Imbalance between CSF production and absorption

186
Q

What are some possible causes of hydrocephalus?

A

congenital or acquired: Meningitis, tumors, head injury, stroke

187
Q

What are the main treatment options for hydrocephalus?

A

Diuretics
Serial LPs
Ventriculoperitoneal (VP) shunt
Endoscopic Third Ventriculostomy (ETV)

188
Q

What is a VP shunt in the treatment of hydrocephalus?

A

Drain placed in ventricle draining into peritoneum

189
Q

What is a ETV in the treatment of hydrocephalus?

A

Drain placed in lateral ventricle of brain and empties into peritoneal space, R atrium, or pleural space

190
Q

When does VP shunt malfunction most frequently occur?

A

First year after placement

191
Q

What are the two categories in which Traumatic Brain Injury (TBI) can be classified?

A

Penetrating or non-penetrating depending on breach of the dura

192
Q

How is the severity of TBI categorized?

A

Glasco-Coma Scale

193
Q

What are some examples of secondary injuries in TBI?

A

Neuroinflammation
cerebral edema
hypoxia
electrolyte imbalances
neurogenic shock

194
Q

When is intubation required in severe TBI?

A

GCS <9
AW trauma
resp distress

195
Q

Why might mild hyperventilation be recommended for TBI?

A

To control ICP

196
Q

What imaging is recommended ASAP for TBI patients?

A

CT of head/neck

197
Q

What should be done before emergent surgery?

A

C-spine stabilization
adequate IV access, CVC
a-line
Possible uncrossmatched blood

198
Q

What labs and medications should be considered intra-op?

A

ISTAT labs, Pressors, Bicarb, Calcium, Blood products

199
Q

Why should NGT/OGT be avoided?

A

Potential for basal skull fx

200
Q

What is a seizure?

A

Transient, paroxysmal, synchronous discharge of neurons in the brain

201
Q

What are some possible transient abnormality causes of seizures?

A

hypoglycemia
hyponatremia
hyperthermia
intoxication

202
Q

What is epilepsy?

A

Recurrent seizures due to congenital or acquired factors

203
Q

What is the action of antiepileptic drugs?

A

Decrease neuronal excitability/enhance inhibition

204
Q

What are important pre-anesthesia considerations in regard to seizure history?

A
  • Determine seizure source (if known) and how well controlled
  • Have antiseizure drugs on board before incision
205
Q

Which medications are enzyme-inducers for seizures?

A

Phenytoin, Tegretol (carbamezapine), Barbiturates

206
Q

What may be required for hepatically-cleared medications in patients actively taking seizure medications?

A

Likely higher doses required

207
Q

What action may be needed post-seizure in some cases?

A

RSI intubation with cricoid pressure

24 Physical & Health Assessment (33 decks)

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