7) Lower Extremity Manifestations Of The Autonomic Nervous System Flashcards
1
Q
Hypothalamus main function
A
- Homeostasis
2
Q
Hypothalamus afferent input
A
- Visceral sensory – blood pressure, gut distention
- Reticular formation – skin temperature
- Intrinsic receptors – temperature and ionic balance
3
Q
Hypothalamus efferent input
A
- Vagal – heart rate, vasoconstriction, digestion
- Pituitary regulation
4
Q
Wernicke’s syndrome
A
- Nutritional deficiency in thiamine
- Often occurs in chronic alcoholics
5
Q
Wernicke’s syndrome triad
A
- Mental status changes (short term memory loss, maintain cognitive function)
- Ataxia (Broad based gait)
- Ophthalmoplegia (cranial nerve IV palsy, gaze-evoked nystagmus)
6
Q
Role of thiamine
A
- Co-factor in carbohydrate catabolism
- Areas with highest metabolic rate at greatest risk
- Paraventricular hemorrhages occur
7
Q
Wernicke’s syndrome treatment
A
- 100 mg thiamine along with magnesium
- Repeat until symptoms subside
- Symptoms may lessen but persist → Korsakoff’s Syndrome
8
Q
Autonomic nervous system
A
- Regulates glands, smooth and cardiac muscle
9
Q
ANS sympathetic component
A
- Fight or flight
- Catabolic
- Thoracolumbar
10
Q
ANS parasympathetic component
A
- Rest and digest
- Anabolic
- Caudocranial
11
Q
Sympathetic nervous system preganglionic fibers
A
- Arise within intermediolateral columns of spinal cord
- Course from T1 – L2
- Exit column to enter paravertebral chain (sympathetic chain)
- May travel up or down prior to synapsing
- First synapse – cholinergic
12
Q
Sympathetic nervous system postganglionic fibers
A
- Second synapse – adrenergic
- Exception – sweat ducts - cholinergic
13
Q
Parasympathetic nervous system nerves originate in the medulla oblongata
A
- Cell bodies within intermediolateral columns from S2 – S4
- Cranial nerves III, VII, IX and X
- Synapses lie close to or within viscera
- First and secondary synapses – cholinergic
- Exceptions – some secondary synapses use nitric oxide
14
Q
Autonomic neuropathy CVS manifestations
A
- Resting tachycardia
- Vagal nerve dysfunction
- Fail to do valsalva maneuver
15
Q
Diagnosing CVS manifestations of autonomic neuropathy
A
- Valsalva maneuver – normally 4 phases
- Phase 1 – transient HR
- Phase II – ↑ HR
- Phase III – further ↑ HR
- Phase IV – transient ↓ HR
- With neuropathy – no transient changes in HR
16
Q
Postural hypotension
A
- Fall of systolic pressure
- From supine to standing
- Drop >30 mm/Hg significant
- Fall in diastolic pressure
- “isometric” test
- Maintain hand grip
- Drop >10 mm/Hg significant
17
Q
Painless of silent MI
A
- Greater general anesthesia risk
- Damages afferent innervation
- Risk greatest in the morning
18
Q
Diurnal variation
A
- BP normally declines at night
- BP increases at night with neuropathy
19
Q
Established acute MI ECG readings
A
- Prominent Q wave
- Elevated ST segment
- Inverted T waves
20
Q
Esophageal symptoms (autonomic neuropathy)
A
- Dysphagia – uncommon
- Occasional heartburn
21
Q
Gastric dysfunction (autonomic neuropathy)
A
- Gastroparesis
- Early satiety
- Nausea and vomiting (undigested food)
- Emesis of undigested food
- Abdominal bloating and epigastric pain
22
Q
Complications with GI autonomic neuropathy
A
- Compromised nutrient delivery to small bowel
- Interferes with glucose absorption
23
Q
Autonomic neuropathy GI treatment
A
- Good glucose control aids gastric motor function
- Eat multiple small meals
24
Q
Neurogenic bladder
A
- ↓ Bladder sensation due to afferent nerve damage
- Bladder enlarges up to 3x
- Inability to void completely
- Increased risk of urinary infection
25
Neurogenic bladder treatment
- Parasympathomimetics
- Alpha-1 blocker
- Self catheterization
26
Autonomic neuropathy sexual dysfunction
- Erectile dysfunction
- Retrograde ejaculation
- Female dysfunction
27
Sudomotor symptoms of autonomic neuropathy
- Disturbances with thermal regulation
- Hyperhidrosis – upper body
- Anhidrosis - lower body
- Dry, brittle skin
- Increase risk of ulceration
28
Sudomotor symptoms palliative treatment
- Emollients (helps exfoliate)
| - Patient education
29
Charcot joint disease hypertrophic form
- Proliferative dense osseous reaction
- Coalescence resulting in “healing”
- Results in significant deformity
30
Hypertrophic charcot joint disease etiology
- Neurotraumatic theory
| - Neurovascular theory”
31
Neurotraumatic theory (charcot joint)
- Loss of pain and proprioception
- Unable to recognize joint subluxation
- Presence of periarticular fragmentation
- Seen Radiographically
- Repetitive microtrauma
- Glycosylated collagen
- Abnormal weight bearing load distribution
32
Autonomic neuropathy (CJD)
- Increased osseous circulation
- Periarticular osteopenia
- Decreased mineralization
33
Motor neuropathy (CJD)
- Intrinsic minus foot
- Abnormal distribution of weight bearing load
- Micro stress fracture
- Non-enzymatic glycosylation of collagen
- Weakened ligaments
- Decreased capsular strength
34
CJD stage 0
- Clinical
| - Erythema, edema, and increased temperature
35
CJD stage I
- Development
- Generalized demineralization
- Periarticular fragmentation
- Loose body formation
- Joint dislocation
36
CJD stage II
- Coalescence
- Organization and early healing of fragments
- Periosteal new bone formation
- Resorption of bony debris
37
CJD stage III
- Reconstruction/consolidation
- Greater definition of bony spurs
- Reconstruction or ankylosis of bones
38
CJD anatomic classification (Brodsky)
- Type 1 = midfoot = rare instability, symptomatic plantar prominences
- Type 2 = hindfoot = grossly deformed and unstable, longer immobilization
- Type 3a = ankle = leads to more severe instability
- Type 3b = calcaneal fracture = leads to pes planus, creates Achilles insufficiency
39
CJD midtarsus deformity classification (Schon)
- Type 1 = met-cuneiform/met-cuboid joints = plantar medial process
- Type 2 = nav-cun/met-cub = plantar lateral prominence
- Type 3 = perinavicular region = plantar central prominence, plantar lateral prominence
- Type 4 = transverse tarsal = variable prominences
40
CJD clinical recognition
- Bounding pedal pulses
- Red, hot, swollen foot
- Generally painless
41
CJD differential diagnosis
- Osteomyelitis
- Bone tumor
- Cellulitis
- Deep venous thrombosis
42
CJD diagnosis
- Clinical presentation
- Radiographic findings
- Osseous shards with synovial biopsy
43
CJD treatment
- Early recognition!!!
- Prevention of additional trauma
- Wide distribution of weight bearing load
44
CJD surgical intervention indications
- Chronic ulceration from deformity
- Joint instability that cannot be braced
- Recurrent ulceration from bony prominences
- Acute displaced fractures – good circulation
45
CJD surgical intervention timing
- Avoid acute and subacute phases – fixation failure
- Simon et al* – good results with early arthrodesis
- He did this during Stage I
- Heal all ulcers if possible
46
Tendo-Achilles off-loading techniques
- Limited ankle joint dorsiflexion increases forefoot plantar pressures
- Tendon thickening may occur secondary to glycosylation
47
Tendo-Achilles lengthening
- Benefits: temporary relief of forefoot pressures
| - Downfalls: increased rearfoot pressures
48
CJD midfoot surgical intervention
- Most common area for neuropathic arthropathy
| - Exostectomy
49
CJD midfoot exostectomy
- Stable midfoot
- Consideration of ulcer location if present
- Consideration of rotational flap
50
CJD midfoot surgical intervention arthrodesis
- Importance of restoring lateral arch
- Unstable midfoot
- May require multiple multi-planar osteotomies
- Plate is stronger construct that cannulated screws
- Consider external fixation if ulcer present
51
CJD hindfoot and ankle surgical intervention
- Maintain weight bearing alignment
- Prevent progression of deformity
- Fixation may be a challenge
52
CJD hindfoot and ankle surgical intervention considerations
- Tendo Achilles lengthening
- Anatomic alignment of rearfoot to leg with restoration of calcaneal inclination angle
- Restoration of the forefoot to rearfoot relationship
- Use of bone stimulator
- Many options available – internal and external
53
CJD sequelae
- Rocker bottom foot
- Bony abnormalities
- Neurotrophic ulcerations
54
CJD treatment
- Insensate foot measures
- Accommodative shoe gear
- Surgical intervention
55
Diabetic osteolysis
- Less common variety
- Occurs in response to hyperemia
- Tubular bones develop atrophic bone changes
- Classic “penciling” of metatarsal heads
- Hourglass resorption of phalanges
56
Clinical signs of sympathetic nervous dysfunction
- Visible color changes
- Temperature alterations
- Hydration changes
57
Sympathetic nervous system dysfunction with overactivity
- Vasoconstriction and hyperhidrosis
| - Cyanotic, cool and clammy extremity
58
Sympathetic nervous system dysfunction with underactivity
- Vasodilation and anhidrosis
| - Bounding pulses, erythema and anhidrosis
59
Hyperhidrosis
- Increased SNS activity
| - Hands affected more than feet
60
Hyperhidrosis predilection for
- Tinea
- Cutaneous diphtheroid infections
- Bromhidrosis
61
Hyperhidrosis treatment
- Glutaraldehydes
| - Anti-perspirant creams
62
Anhidrosis
- Complete loss of sympathetic input
| - Total loss of sweating with lesion above T7
63
Prolonged anhidrosis leads to
- Decreased muscle bulk
- Demineralization of bone
- Significant xerosis
64
Anhidrosis treatment
- Emollients
| - Physical therapy
65
Raynaud's Disease
- Vasomotor instability
| - Tri-phasic color response (pallor, cyanosis, rubor)
66
Raynaud's incidence
- Females > males
| - May co-exist with several collagen vascular diseases
67
Raynaud's Disease symptoms
- Paresthesias
- Digital stiffness
- Exacerbated by cold
68
Raynaud's Disease diagnosis
- Rule out underlying disorders
- CBC with differential
- Rheumatoid profile
- ESR
69
Raynaud's management
- Medical management of underlying etiology – if present
- Minimize stress and anxiety (Yoga)
- “insulate” the digit
70
Digit insulation for Raynaud's
- Multiple layers of socks
- Petroleum jelly on digits
- Nitroglycerin paste
- Drug therapy to reduce peripheral vasoconstriction
71
Acrocyanosis
- SNS overactivity
- Etiology unknown
- Persistence of cyanosis
- Females > males
72
Acrocyanosis symptoms
- Swelling
- Decreased sensory perception
- Paresthesias
- Hyperhidrosis
73
Acrocyanosis treatment
- Minimize cold exposure
74
Erythromelalgia characterized by
- Erythema and swelling
- Pain or “itching”
- Triggered by a “critical temperature” (hotter climate exacerbates it)
75
Erythromelalgia etiology
- Unknown but may be due to congenitally small vessels
- Unable to dissipate heat
- Males > females
76
Erythromalalgia diagnosis
- Itching or burning with triggering temperature
- Intact pedal pulses
- Symptomatic relief with aspirin?
- May have concomitant polycythemia vera
77
Erythromelalgia treatment
- Patient education
- Elevation with cold compresses
- Lumbar sympathectomy
78
Complex regional pain syndrome
- Occurs secondary to vasomotor instability mediated by the SNS
- Pain out of proportion to injury
79
Type I CRPS
- Formerly known as Reflex Sympathetic Dystrophy
- Sequalae of “minor” trauma
No identifiable nerve lesion
80
Type II CRPS
- Formerly known as Causalgia
Identifiable nerve lesion
- Sympathetically maintained pain
- Pain restricted to the distribution of a single nerve
81
CRPS short circuit theory
- Nociceptor efferent pathways lose insulation
- Normal impulses are disrupted
- Impulses are misdirected and cross stimulate afferent pain fibers
82
CRPS internuncial neurons
- Act as “liaisons” between afferent and efferent stimulus which governs reflex responses
- Internuncial neurons are overstimulated by afferent input of irritated nerve
- In turn overstimulate motor and smooth muscle efferent nerves
83
Early CRPS diagnosis
- Swelling (comes and goes)
- Temperature (hot)
- Agony (pain out of proportion)
- Redness/purple discoloration
- Tremors (sometimes w/ weakness)
84
CRPS treatment
- Nerve meds (gabapentin, pregabalin, duloxetine)
- Opioids
- Work outs (PT as well)
85
CRPS Type I acute stage
- Lasts 2-3 months
- Presence of severe burning pain
- Increased warmth, swelling and joint stiffness
- Symptoms involve an entire region
- Exacerbated by limb dependency, emotional stress of physical contact
- Radiographs: maybe early demineralization
86
CRPS Type I dystrophic stage (phase 2)
- Several months
- Warm edematous phase subsides
- Extremity becomes firm, cyanotic and cool
- Pain becomes constant and unrelenting
- Symptoms exacerbated by any stimulus (hypersensitive to anything that can exacerbate their pain)
- Radiographic Findings: diffuse osteoporosis (Sudeck’s atrophy), flexion contractures of digits begin to develop
87
CRPS Type I atrophic stage (phase 3)
- Irreversible
- Pain may subside or become intractable
- Skin and subcutaneous tissues become atrophic
- Flexion contractures become irreversible
- Radiographic findings: ground glass appearance of bone, advanced osteoporosis
88
CRPS Type I incidence
- Individuals of all ages
- Female to male – 3:1
- Psychological profile: “Type A” personalities, anxious, inquisitive
- Minor trauma – especially crush injuries!
89
CRPS diagnosis
- Early recognition and treatment essential
- Changes on radiographs
- Triphasic technetium scan (intense, focal peri-articular uptake in phase 3)
- Thermography
- Symptomatic relief to sympathetic nerve block
90
CRPS Type I imaging
- Periarticular
- Osteopenia
- Diffuse midfoot uptake in phase 3
91
CRPS treatment
- Aggressive physical therapy (prevent joint contracture and muscle wasting)
- Sympathetic nerve blocks (biweekly administration, break aberrant nerve impulses)
- Pain management (Bier blocks, tricyclic anti-depressants, anticonvulsants, surgical sympathectomy)
