Patho Ii, Exam 2

Front 1

When caring for pts with diseases affecting the brain, they may undergo anesthesia for surgery ____ or ____ to their disease condition, and its important to consider underlying ____ when forming anesthetic plan.

Back 1

related, unrelated, diseases

Front 2

For individuals with CNS or brain disorders, ____ protection is paramount.

Back 2

cerebral brain protection

Front 3

Anesthetists often have to manipulate intracranial volume and pressure through control of ...

Back 3

vasodilation and CO2 monitoring and manipulation

Front 4

Cerebral blood flow is ____ Regulated, and normal CBF is _____/100 g brain tissue.

Back 4

autoregulated,
50

Front 5

What governs CBF?

Back 5

1. CMRO2 (measured as a rate of O2 consumption, nomral is 3-3.8 mL/100g brain tissue, can be incr by incr temp and seizures, decr by temp reductions and some anesthetics)
2. cerebral perfusion pressure (MAP - ICP, want to see range between 50-150 mmHg)
3. Arterial CO2 (manipulate w hyperventilation)

Front 6

How do anesthetic drugs affect CBF?

Back 6

1. vasoconstriction of CBF is desirable in incr ICP, may be achieved with ketamine, barbs (Na thiopental), etomidate, propofol, opioids (Except meperidine d/t seizure potential)
2. IAs (iso, sevo, des) when given in concentrations > 1 MAC result in cerebral vasodilation, want to maintain MAC < 0.6
3. N20 and NMBs have little effect
4. Vasodilation from some anesthetics can lead to incr CBF, incr CBV, and incr ICP (Esp w halothane) -- can be offset by HYPOCAPNIA

Front 7

There are no ____ receptors located in the brain, so once the surgeon is in the intracranial vault, it is not a stimulating surgery. Therefore...

Back 7

keep pt paralyzed to tolerate ETT and avoid cough for herniation but go easy on opioids

Front 8

What constitutes ICP?

Back 8

pressure within cranial and spinal vault

Front 9

Under normal conditions, brain tissue, intracranial CSF, and blood have a volume of between ______ mL with a normal ICP of _____ mmHg.

Back 9

1200-1500 mL, 5-15 mmHg

Front 10

Any increase in one component fo the vault must be offset by decreasing _____ of another component.

Back 10

volume

Front 11

Normally, ____ and ___ are shifted to compensate for increases in ICP, however this is _____ compensation.

Back 11

blood and CSF,
self-limiting

Front 12

Alteration in CSF flow from ______ can lead to incr ICP.

Back 12

malabsorption back into villi and circulation

Front 13

CSF is normally produced at a constant rate of ____/day.

Back 13

500-600 mL

Front 14

Increases in ICP may ultimately lead to ____ and death.

Back 14

herniation

Front 15

What does the intracranial elastance curve depict?

Back 15

impact of incr intracranial volume on ICP -- as intracranial volume incr, initially ICP does not incr because CSF is shifted from cranium into spinal subarachnoid space -- then as curve continues to rise, pts can no longer compensate and ICP abruptly increases and pt becomes symptomatic

Front 16

At what ICP is the pt in danger of herniation?

Back 16

>40

Front 17

Where are the places that the brain can herniate into?

Back 17

incr in contents of supratentorial space by masses, edema or hematoma can herniate into:
1. cingulate gyrus under falx leading to subfalcine herniation
2. contents over tentorium cerebelli causing transtentorial herniation
3. herniation of cerebellar tonsils out through the foramen magnum
4. herniation of brain contents out of a traumatic defect in cranial cavity

Front 18

Herniation into the cerebellum will wipe out the pts ability to...

Back 18

maintain breathing, HR and BP

Front 19

A normal ICP wave is ____ and varies wtih _____.

Back 19

pulsatile,
varies w cardiac rhythm and spontaneous breathing

Front 20

Increases in ICP above 15 produce ____ waves.

Back 20

plateau

Front 21

Incr ICP from medullary dysfunction results in ____ and ____.

Back 21

cardiorespiratory instability and death

Front 22

What are the nonspecific signs of incr ICP?

Back 22

- headache
- N/V
- papilledema
- change in LOC

Front 23

Describe the ICP modality of neuro monitoring?

Back 23

- ICP monitor localized in brain ventricle (Brain tissue, subarachnoid, epidural or subdural space)
- 20-25 mmHg is treatment threshold
- treat elevations with hyperventilation, head elevation, sedation, CSF drainage, paralysis, barb-induced coma, surgery

Front 24

Describe the blood pressure modality of neuro monitoring?

Back 24

- Use A-line
- treatment threshold is to maintain MAP < 100 mmHg
- treat fluctuations from desired value with vasopressors, fluids, blood replacement

Front 25

Describe the CPP modality for neuro monitoring?

Back 25

- CPP=MAP-ICP
- treatment threshold is to maintain MAP > 70 mmHg
- treat w control of ICP and BP

Front 26

Describe the jugular bulb venous o2 saturation (SjvO2) modality of neuro monitoring?

Back 26

- catheter (often fiberoptic) inserted into jugular bulb
- treat if <50% saturation
- treat fluctuations with control of ICP and CPP

Front 27

Describe brain tissue O2 monitoring as a neuro monitoring modality?

Back 27

- microcatheter placed into frontal cerebral white matter
- treatment threshold is < 8.5 mmHg
- control with ICP and CPP

Front 28

What is the primary method to draining CSF?

Back 28

subdural bolt

Front 29

What are the intracranial measurement methods available?

Back 29

- ventriculostomy catheter
- intraparenchymal fiberoptic catheter
- epidural transducer
- subdural catheter
- subdural bolt

Front 30

When do you treat increases in ICP?

Back 30

> 20 or appearance of plateau waves on ICP monitoring

Front 31

What are the methods used to decr ICP?

Back 31

1. elevation of head
2. hyperventilation
3. CSF drainage
4. admin hyperosmotic drugs (mannitol)
5. diuretics (loop, lasix)
6. corticosteroids (Before, during and after case)
7. admin cerebral vasoconstricting agents
8. surgical decompression

Front 32

As heads up position is increased, ICP may be _____, but beyond 30 degrees heads up, _____ is likely compromised.

Back 32

reduced, CPP

Front 33

A-waves or plateau waves result when mean systemic blood pressure _____ from threshold, and thus CPP _____ from ischemic threshold. _____ will occur in response, and in the noncompliant cranium, this results in greatly ___ ICP.

Back 33

decreases below, falls below,
cerebrovasodilation, increased

Front 34

What is the first action to rapidly decr ICP?

Back 34

hyperventilation

Front 35

During hyperventilation to treat incr ICP, it is recommended to maintain PaO2 of _____, and ETCO2 is usually _____ higher than PaCO2.

Back 35

30-35, 3-5

Front 36

When hyperventilating to treat incr ICP, you should watch for ____ changes, and can optimize conditions w co-administration of _____.

Back 36

hemodynamic,
peripheral vasodilators or cerebral vasoconstrictors

Front 37

The effects of hyperventilation to control elevated ICP diminishes after ___ hrs.

Back 37

6-12 -- can see rebound incr in ICP following discontinuance from prolonged hyperventilation

Front 38

Low CO2 levels to control incr ICP illicits vasoconstriction by creating _______. Eventually when pH normalizes, vasodilation will occur and the pt is at risk for ______.

Back 38

cerebrospinal fluid alkalosis, reperfusion injury

Front 39

Mannitol

Back 39

- #1 hyperosmotic drug to control incr ICP
- 0.25-0.5 mg/kg IV over 15-30 min (larger doses can lead to rebound incr ICP)
- removes approx 100 ml of H20 from brain
duration: 6 hrs

Front 40

During mannitol administration, the provider must ensure maintenance of _____ to prevent adverse effects on ____ and ______.

Back 40

crystalloid infusion, electrolytes and intravascular volume

Front 41

Mannitol must be used with caution in pts with ___ compromise. Why?

Back 41

cardiac compromise
CHF- can be thrown into cardiac failure crisis

Front 42

What are the types of intracranial tumors?

Back 42

- astrocytoma- neuroglial cells
- oligodendroglioma- myelin producing cells
- ependymoma- cells lining ventricles and central canal of spinal cord
- primitive neuroectodermal tumor- blastomas
- meningioma- slow growing benign
- pituitary tumor
- acoustic neuroma- schwannoma CN 8
- CNS lymphoma-
- metastatic tumors- often lung or breast

Front 43

Describe the preop care for brain tumor pts?

Back 43

- directed toward identifying presence or absence of incr ICP
- may be sensitive to CNS depressant drugs
- hypoventilation can lead to incr PaCO2
- sedation can mask altered LOC
- sedation can unmask subtle neuro deficits that were not present
- anticholinergics or H2 antagonists usually safe
- sedate w extreme caution or avoid altogether esp if pt has decr LOC (establish baseline neuro fcn first)

Front 44

Describe the induction techniques used for brain tumor pts?

Back 44

- use propofol, thiopental or etomidate
- non-depol agent (succ leads to incr ICP due to fasciculations)
- hyperventilation before intubation (PaCo2 of around 35)
- blunt laryngoscopy w lidocaine 1.5 mg/kg (caution may cause seizures) and fentanyl 2-5 mcg/kg
- avoid PEEP

Front 45

_____ provide some level of cerebral protection from seizure activity.

Back 45

Benzos

Front 46

Describe anesthesia maintenance techniques for brain tumor pts?

Back 46

- IAs/opioids/NMBs
- can use all IAs (halothane w caution, N20 can be used but concerns w air embolism)
- all IV agents (except ketamine) decr ICP
- opioids are mainstay of maintenance, effective as long as hypotension avoided
- remifentanil and propofol TIVA most often used (need plan for analgesia when remi weaned at end of case)
- use non depol NMB
- all IAs incr ICP (Vary in magnitude, produce isoelectric EEG and may play role in cerebral protetion, sevo allows rapid treatment for decr decr depth and facilitates earlier neuro exam postop, smooth emergence w decr coughing
- all anesthetics decr CMRO2 but potency varies (induction agents > IAs > opioids and benzos)

Front 47

Describe the fluid plan for brain tumor surgery?

Back 47

- need to account for maint requirements and excessive urine losses d/t diuresis/mannitol
- ignore fluid deficit due to fasting in calculation -- goal to achieve mild negative balance 500-1000 mL
- use isotonic solns (NS or LR) -- avoid glucose-containing, avoid LR if large vol needed
- mannitol: monitor u/o, serum osmolality and lytes

Front 48

Describe the monitoring plan for brain tumor surgery?

Back 48

- standard monitors
- A-line if using peripheral vasodilators or entering cranial vault
- evoked potential monitoring/EEG

Front 49

What are the consideration for sitting position during brain tumor surgery?

Back 49

- observe for s/s of VAE
- doppler sonography over R chest or TEE
- incr ET N20 (preceded by decr ETCO2)

Front 50

How do you treat VAE?

Back 50

- flood operative site w fluid, apply occlusive material to bone edges nad attempt to identify where air is getting in
- aspirate air via R atrial cath and eliminate N20 use immediately
- apply PEEP
- treat symptomatically

Front 51

What are the considerations for vegetative brain function disorders?

Back 51

- coma
- maintain patent airway
- assess using GCS
- breathing patterns (Biot's, cheyne stokes)
- anesthesia mgmt for organ donation: maintain BP and O2 until harvest

Front 52

GCS scores range from ___ to ___, and pts within score of ____ are usually said to be in a coma.

Back 52

3 -15
3-8 coma

Front 53

GCS for eye opening, motor response, and verbal response:

Back 53

eyes:
4- spontaneous
3- to speech
2- to pain
1- nil
motor:
6- obeys
5- localizes
4- withdraws (flexion)
3- abnormal flexion
2- extensor response
1- nil
verbal:
5- oriented
4- confused
3- inappropriate words
2- incomprehensible sounds
1- nil

Front 54

Ataxic (biot's) breathing

Back 54

pattern: unpredictable sequence of breaths varying in rate and TV
site of lesion: medulla

Front 55

Apneustic breathing

Back 55

pattern: repetitive gasps and prolonged pauses at full inspiration
site of lesion: pons

Front 56

Cheyne-Stokes breathing

Back 56

pattern: cyclic crescendo-decrescendo TV pattern interrupted by apnea
site of lesion: cerebral hemispheres, CHF

Front 57

Central neurogenic hypoventilation

Back 57

pattern: hypocarbia
site of lesion: cerebral thrombosis or embolism

Front 58

Posthyperventilation apnea

Back 58

pattern: awake apnea following decr in PaCO2
site of lesion:Frontal lobes

Front 59

Diencephalon compression during transtentorial herniation presents with...

Back 59

pupils: small 2 mm but reactive to light
normal response to oculocephalic or cold caloric testing
motor: purposeful, semipurposeful, or decorticate (Flexor posturing)

Front 60

Midbrain compression during transtentorial herniation presents with....

Back 60

pupils: midsize 5 mm and unreactive to light
test response: may be impaired
motor: decerebrate (Extensor) posturing

Front 61

Pons or medulla oblongata compression during transtentorial herniation presents with...

Back 61

pupils: midsize 5 mm and unreactive to light
test response: absent
motor: no response

Front 62

How should anesthesia be managed for vegetative brain function disorders?

Back 62

- avoid incr ICP (may be draining CSF via bolt to decr ICP)
- avoid N20 - want to ensure good organ perfusion
- use Non depol NMB to intubate, avoids K release of depol that could damage organs
- Brain death/Organ donation: preservation of organs by treating hypotension but avoiding massive peripheral vasoconstriction, maintaining O2 and temp, avoiding hypovolemia (DI can be apparent, treat w vasopressin 0.04-0.1 u/hr or DDAVP 0.3 mcg/kg)

Front 63

What are the clinical features of anterior cerebral artery occlusion?

Back 63

contralateral leg weakness

Front 64

What are the clinical features of middle cerebral artery occlusion?

Back 64

- contralateral hemiparesis and hemisensory deficit (Face and arm more than leg)
- aphasia (Dominant hemisphere)
- contralateral visual field deficit

Front 65

What are the clinical features of posterior cerebral artery occlusion?

Back 65

- contralateral visual field defect
- contralateral hemiparesis

Front 66

What are the clinical features of penetrating arteries being occluded?

Back 66

- contralateral hemiparesis
- contralateral hemisensory

Front 67

What are the clinical features of basilar artery occlusion?

Back 67

- oculomotor deficits and/or ataxia with "Crossed" sensory and motor deficits

Front 68

What are the clinical features of vertebral artery occlusion?

Back 68

- lower cranial nerve deficits and/or ataxia with crossed sensory deficits

Front 69

This is the sudden loss of blood flow to a region of the brain, symptoms evolving over minutes to hours, most likely caused by a cardiac embolism:

Back 69

acute ischemic stroke

Front 70

TIAs usually resolve within ____, but may be a herald of impending ____.

Back 70

24 hrs, ischemic stroke

Front 71

What is the anesthesia management for acute ischemic stroke?

Back 71

- maintain airway, oxygenation, ventilation, SBP (Crucial to ensure adequate CPP to supply blood to ischemic area)
- prevent hypothermia (shivering will be detrimental (incr ICP and CMRO2)
- cerebral edema and incr ICP will complicate overall clinical course

Front 72

This is the bleeding into brain tissue due to weakened/diseased blood vessels rupturing, and is four times more lethal than ischemic strokes.

Back 72

acute hemorrhagic stroke, intracerebral hemorrhage

Front 73

It is helpful to sedate pts having acute hemorrhagic stroke with ________ and minimize _____.

Back 73

propofol, barbs, benzos,

minimize HTN

Front 74

Subarachnoid hemorrhage

Back 74

- bleeding into subarachnoid space
- most commonly due to rupture of an intracranial aneurysm
- classic "Worst headache of my life" complaint

Front 75

What are the goals of anesthesia management for pts with acute hemorrhagic stroke (intracerebral/subarachnoid)?

Back 75

- limit aneurysm rupture
- control BP and ICP w hyperventilation and HOB 30 deg, giving vasodilatory drugs
- prevent cerebral ischemia (same 3 mechanisms and ensuring adequate O2)
- facilitate surgical exposure (monitor for VAE while pt sitting upright)

Front 76

Intracerebral hemorrhage is more common in the ____ population due to ____.

Back 76

black population, due to HTN

Front 77

How is hemorrhagic stroke treated?

Back 77

- IV admin of recombinant activated factor 7a within 4 hrs of onset of symptoms results in decr of hematoma volume and clinical outcomes
- prompt ventricular drainage (CSF) and control of HTN (keep MAP < 130)

Front 78

How is hemorrhagic stroke treated?

Back 78

- IV admin of recombinant activated factor 7a within 4 hrs of onset of symptoms results in decr of hematoma volume and clinical outcomes
- prompt ventricular drainage (CSF) and control of HTN (keep MAP < 130)

Front 79

What is an epidural hematoma? What are the S/S and treatment?

Back 79

- arterial bleed into epidural space
- s/s: LOC then return of consciousness, variable lucidity, hemiparesis, mydriasis, bradycardia (uncal herniation)
- tx: prompt drainage

Front 80

What is intraparenchymal hematoma? How is it treated?

Back 80

- abnormal collection of blood located within brain tissue
- can be difficult to treat given location
- conservative mgmt often chosen unless size and pressure is likely to cause herniation
- tx: avoid vascular spasm w nimodipine, manage HD stability, GETA if surgery indicated with good relaxation

Front 81

A traumatic subarachnoid hemorrhage is from...
What is the incidence in head trauma pts?

Back 81

blood in the subarachnoid space from intracranial hemorrhage
seen in 40% of pts w moderate to severe head trauma

Front 82

How is traumatic subarachnoid bleed treated?

Back 82

- treat vasospasm w nimodipine (Ca channel blocker) 60 mg q4h for 21 days (30 mg if cirrhosis, avoid IV admin)

Front 83

Describe a subdural hematoma

Back 83

- torn bridging veins between dura and subarachnoid space
- CSF remains clear

Front 84

What are the S/S and treatment of subdural hematomas?

Back 84

- s/s: evolve over several days, slow venous bleed, headache universal, drowsy/obtunded, hemiparesis (1 sided weakness) and hemianopsia (1 sided vision disturbance), language problems
- treatment: drainage via burr holes under GETA or local with MAC

Front 85

What are the perioperative mgmt concerns for traumatic brain injuries?

Back 85

- optimize CPP
- minimize cerebral ischemia
- avoid drugs that incr ICP
- continue post op mech vent
- skeletal muscle paralysis

Front 86

This is the transient, paroxysmal and synchronous dischages of a group of neurons:

Back 86

seizure disorder

Front 87

The symptom of a seizure depend on...

Back 87

the location of the discharge

Front 88

Simple seizure

Back 88

no LOC

Front 89

Complex seizure

Back 89

loss of consciousness

Front 90

Partial seizure

Back 90

single hemisphere

Front 91

Generalized seizure

Back 91

both hemispheres

Front 92

Jacksonian seizure

Back 92

tremor marches up the arm, localized

Front 93

This degenerative brain disease increases with age, and is characterized by a loss of dopaminergic fibers in the basal ganglia...

Back 93

parkinsons disease

Front 94

What is the parkinson's symptom triad?

Back 94

1. skeletal muscle rigidity
2. tremor
3. akinesia

Front 95

What is the anesthesia mgmt of parkinsons dz?

Back 95

- abrupt withdrawal of levodopa can cause muscle rigidity -- makes ventilation dificult
- incr possibility of hypotension and cardiac arrhythmaias

Front 96

This neurodegenerative dz is autoimmune and is characterized by demyelination in the brain and spinal cord, with multifocal involvement. Symptoms depend on the location of lesions and the pt experiences periods of exacerbation and remission:

Back 96

multiple sclerosis

Front 97

What are the anesthesia mgmt techniques utilized for Multiple sclerosis pts?

Back 97

- surgical stress may exacerbate symtpoms (Give benzo before epidural placement)
- avoid hyperthermia (incr demyelination)
- changing and unpredictable neuro presentation mut be considered during regional (spinals can exacerbate symptoms, regional is a relative contraindication)
- GA is most frequently used technique due to minimal interactions between the drugs and dz.

Front 98

What is the #1 agent that causes seizure activity in the OR?

Back 98

- ethrane

LAs can also cause seizures, may want to avoid!

Front 99

What is the parkinson's symptom triad?

Back 99

1. skeletal muscle rigidity
2. tremor
3. akinesia

Front 100

What is the anesthesia mgmt of parkinsons dz?

Back 100

- abrupt withdrawal of levodopa can cause muscle rigidity -- makes ventilation dificult
- incr possibility of hypotension and cardiac arrhythmaias

Front 101

This neurodegenerative dz is autoimmune and is characterized by demyelination in the brain and spinal cord, with multifocal involvement. Symptoms depend on the location of lesions and the pt experiences periods of exacerbation and remission:

Back 101

multiple sclerosis

Front 102

What are the anesthesia mgmt techniques utilized for Multiple sclerosis pts?

Back 102

- surgical stress may exacerbate symtpoms (Give benzo before epidural placement)
- avoid hyperthermia (incr demyelination)
- changing and unpredictable neuro presentation mut be considered during regional (spinals can exacerbate symptoms, regional is a relative contraindication)
- GA is most frequently used technique due to minimal interactions between the drugs and dz.

Front 103

What is the #1 agent that causes seizure activity in the OR?

Back 103

- ethrane

LAs can also cause seizures, may want to avoid!

Front 104

What are the anesthesia considerations for pts with seizure disorders?

Back 104

- consider impact of antiseizure drugs on organ function and anesthetic drugs on seizure activity
- additive sedation from seizure drugs and anesthetics
- methohexital can activate a seizure focus
- most IAs can produce seizure actiity bc of halogen atoms in chemical structure
- avoid epileptogenic drugs
- barbs, opioids and benzos are preferred

Front 105

Chiari malformation

Back 105

congenital displacement of cerebellum
cant drain CSF causing incr ICP
typically young females
tx: surgical decompression by freeing adhesions and enlarging foramen magnum
significant intraop blood loss, esp in chiari II malformations

Front 106

Neurofibromatosis

Back 106

- caused by autosomal dominant mutation that is not limited to race/ethnic origin
- one common feature: progression of disease over time
- tx: antiepileptic drugs, surgical removal of cutaneous neurofibromas for disfiguring/functionally compromised pts, treat progressive kyphoscoliosis w surgical stabilization
- anesthesia: possible pheochromocytoma, incr ICP reflects expanding intracranial tumors, airway patency may be jeopardized by exapinding laryngeal neurofibromas, using regional could place pt at risk for future spinal neurofibromas in spinal cord, epidural recommended for L&D

Front 107

Von Hippel Landau Dz

Back 107

- retinal angiomas, hemagioblastomas, CNS (Cerebellar) and visceral tumors
- risk for pheochromocytoma
- cant use spinal if spinal cord hemangioblastoma
- epidural for c-section to avoid hyperventilation
- barb coma useful to control intracranial HTN
- assoc. lung injuries -- impair O2 and ventilation in these pts-- may neeed mech vent
- neurogenic pulm edema
- DIC following head trauma (d/t release of brain thromboplastin into systemic circulation)
- ANESTHESIA: optimize CPP (>70), minimize cerebral ischemia, avoid drugs and techniques that could incr ICP, dont hyperventilate unless temporary for control of ICP, avoid glucose-containing solns, potential hidden extracranial injuries (bone fx, pneumothorax -- can lead to excessive blood loss), avoid N20 to prevent pneumocephalus, if acute brain swelling occurs investigate and treat source (HTN, hypoxemia, hyperCO2, venous obstruction), maintain skeletal muscle paralysis postop to facilitate mech vent

Front 108

Tuberous Sclerosis (Bourneville's dz)

Back 108

- mental retardation, seizures, facial angiofibromas
- benign hamartomatous proliferative lesions and malformations in every organ
- prognosis depends on organs involved (no symptoms to life threatening)
- anesthesia: consider presence of MR, treat w antiepileptics, determine upper airway abnormalities preop, intraop cardiac arrhythmias if cardiac involvement, impaired renal fcn possible (dont use drugs that depend on renal clearance)

Front 109

The ____ spine is pariticularly vulnerable and injury to this area initially produces _____.

Back 109

cervical,
flaccid paralysis

Front 110

Acute spinal cord injuries have total absence of ____ below the level of injury, and the cord is not usually physically _____.

Back 110

sensation, transected (usually just bruised)

Front 111

The extent of physiologic effects of acute spinal cord injury depends on....

Back 111

level of injury
most severe - cervical
less severe moving caudally

Front 112

In acute spinal cord injury, there is a loss of ______ Regulation and _______ reflexes below the level of injury.

Back 112

temp regulation, spinal reflexes

(may not realize they have a full bladder --> HD instability)

Front 113

What are the anesthesia mgmt techniques for acute cervical spine injury?

Back 113

- establish secure airway
- minimize neck mvmt w intubation
- have assistant stabilize head until airway secured
- beward of dramatic hypotension (spinal shock)
- SKG abnormalities common in early phase
- breathing best managed mechanically
- maintain temp

Front 114

What are some of the complications associated with chronic spinal cord injuries?

Back 114

UTI
skeletal muscle spasticity
chills and fever
decubitus ulcer
autonomic hyperreflexia
skeletal muscle/joint pain
GI dysfunction
CV dysfunction
visual/hearing disorder
urinary retention

Front 115

What are some of the complications associated with chronic spinal cord injuries?

Back 115

UTI
skeletal muscle spasticity
chills and fever
decubitus ulcer
autonomic hyperreflexia
skeletal muscle/joint pain
GI dysfunction
CV dysfunction
visual/hearing disorder
urinary retention

Front 116

The systemic effects of chronic spinal cord injuries increase as the lesion site moves ______.

Back 116

rostrally (north)

Front 117

Transection of the spinal cord above ____ typically leads to apnea.

Back 117

C5

Front 118

2 Common syndomes in chronic spinal cord injury pts are...

Back 118

depression and chronic pain

Front 119

In chronic spinal cord injured pts, _____ can occur in areas of complete sensory loss.

Back 119

phantom body pain

Front 120

Anesthesia mgmt in chronic spinal cord injured pts is focused on...

Back 120

preventing autonomic hyperreflexia

Front 121

Most common complication in chronic spinal cord injured pts?

Back 121

UTI

Front 122

What is autonomic hyperreflexia?

Back 122

- appears in association with the return of spinal reflexes
- triggered by cutaneous or visceral stimulation below level of transection -- activation of pregang sympathetic nerves
- mostly likely to occur in transections above T6
- S/S: HTN, bradycardia, vasodilation above injury, nasal stuffiness, headache, blurred vision

Front 123

What is the anesthesia mgmt in pts exhibiting autonomic hyperreflexia?

Back 123

- prevent development of autonomic hyperreflexia if possible
-initiate anesthesia prior to noxious stimuli
- monitor for sudden HTN
- be prepared to treat sudden HTN w short acting vasodilators

Front 124

This is the disc cavitation of the spinal cord usually caused from spinal cord trauma or neoplastic conditions

Back 124

syringomyelia

Front 125

What are the 2 forms of syringomyelia?

Back 125

1. communicating: communication between cystic regions of SA space to the central canal of the cord (hx of basilar arachnoiditis or Chiari malformations)
2. non-communicating: cysts present w no connection to the CSF spaces (usually caused from trauma of spinal needle, arachnoiditis - toxicity, or neoplasms)

Front 126

What are the S/S of syringomyelia?

Back 126

- usually in 3rd or 4th decade of life w complaints of sensory impairment in upper extrem (pain and temp neuronal pathways that cross near central canal)
- can see destruction of lower motor neurons as disease progresses with LOC, thoracic involvement, paralysis of tongue, palate and vocal cords
- no tx except symptomatic

Front 127

What is the anesthesia mgmt of syringomyelia?

Back 127

- consider neuro deficits and document
- VQ deficits (Can see problems w extubation secondary to decr airway reflexes)
- avoid succ (hyperK)
- exaggerated response to non-depol NMBs