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Pod Med > Lump > Flashcards

Lump Flashcards

1
Q

Background

A

 First described by Weir Mitchell, a civil war surgeon, in the 1860’s

 Coined the term causalgia after describing the chronic burning pain his soldiers endured after sustaining nerve injuries

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2
Q

Epidemiology

A

 Described in both adults and children
- The majority of young patients have unusual stress in 1 or more aspects of their life
- Example: family dysfunction
 Majority of adult patients are Caucasian
 Female predominant
 Average age of onset is in the 6th to 7th decades.

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3
Q

Classification

A

 In the past, prior classifications were unclear and confusing
 In 1994, the International Association for the Study of Pain ( IASP) established standardized diagnostic criteria for CRPS
 Based on description rather than pathophysiology. . . since the etiology is still unclear

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4
Q

Diagnostic Criteria

1. CRPS can be divided into 2 groups:

A

 Type 1- absence of peripheral nerve injury . . . initial event may or may not have been traumatic
- Majority of cases

 Type 2- presence of an identifiable nerve injury

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5
Q

Diagnostic Criteria

A
  1. Spontaneous pain, allodynia, hyperalgesia occurs, is not limited to the territory of a single peripheral nerve, and is disproportionate to the inciting event.
  2. History and evidence of edema, skin blood flow abnormalities, or sudomotor abnormalities in the painful region since the inciting event.
  3. No other concomitant conditions account for the degree of pain and dysfunction.
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6
Q

Pathophysiology

A

 Numerous theories exist, but the exact mechanism remains unclear
 Over the years, many theories have tried to explain CRPS’s clinical picture
- sympathetic dysfunction
- central nervous system dysfunction
- peripheral nervous system dysfunction - exaggerated inflammatory response
- genetic predisposition

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7
Q

Pathophysiology

A

The most popular theory focuses on sympathetic dysfunction!

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8
Q

Pathophysiology

A

 “Vicious Circle” hypothesis
- sympathetic impulses do not shut off, triggering a constant cycle of the inflammatory response
- Consequently, this leads to a continual release of neurotransmitters resulting in increased pain and tissue destruction

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9
Q

Diagnosis

A

 Complex and challenging task
 Must have a high index of suspicion
 No specific diagnostic test or pathognomonic
symptom associated with an exact diagnosis
 Must rely on focused clinical history, physical examination, laboratory tests, and diagnostic modalities

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10
Q

Clinical History

A

 May or may not be able to remember an identifiable traumatic event
- minor as an ankle sprain
- severe as major nerve trauma Most prevailing symptom is pain
- most often described as a burning that can spread beyond the area of initial injury

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11
Q

Clinical History

A

 Pain resulting from a non-noxious stimulus
- allodynia
- example: pressure from bed sheets
 Pain that is disproportionate to a noxious stimuli
- hyperalgesia

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12
Q

Physical Examination

A

 May have taken on a guarded posture (dont even let me touch) to shield the affected area
 Clinical Manifestations
- vasomotor and sudomotor instability of the affected limb due to sympathetic dysfunction

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13
Q

Physical Examination

A

Symptoms can range from a warm and erythematous extremity to one that is cool and mottled in appearance
Common manifestations. . . - hyperhidrosis
- edema
- color changes
- temperature changes

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14
Q

Physical Examination
Patient may also experience . . . - muscle weakness

A
  • muscle atrophy
  • tremors
  • muscle spasms
  • decreased ROM
  • muscle contractures
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15
Q

Physical Examination
 Later in the course of CRPS . . .

A

Trophic changes to the affected limb can occur including:
- atrophy of the skin - loss of hair growth - hypertrophic or
atrophic nails

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16
Q

Laboratory Tests

A

 Lab tests are important because they can exclude other etiologies
 For example: A patient is experiencing vasomotor instability. . .
- blood tests: ESR, CBC, C-reactive protein, RA factor, and ANA
- rule out inflammatory conditions

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17
Q

Stages Stage 1 (days to weeks)

Burned ca ra’s music

A

 Burning throbbing pain with vasomotor instability
 Muscle spasms
 Radiographs are usually normal
 Can be self limiting at this point

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18
Q

Stages Stage 2 (3-6 months)

E M R

Chronic edema pt get’s thick skin

A

 Progression of edema with development of brawny skin (thickening of skin and soft tissue) and toenail changes

 Muscle atrophy
 Radiographs can begin to reveal spotty osteoporosis

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19
Q

Stages
 Stage 3 (after 6 months)

Most co tra limited to na ra

A

 Limitation of movement
 Contractures
 Trophic skin changes…fat atrophy
 Nails become severely dystrophic
 Radiographs reveal significant demineralization
 Most severe stage

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20
Q

The longer the patient is in stage 3, the more difficult it is to reverse the clinical course of the disease with any type if intervention!!

A

The longer the patient is in stage 3, the more difficult it is to reverse the clinical course of the disease with any type if intervention!!

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21
Q

Diagnostic Modalities Radiographs
 Rule out bone pathology

A

 Can detect osteopenia or “patchy de- mineralization”
 Most likely due to disuse of the limb
 Known as Sudeck’s atrophy

22
Q

Diagnostic Modalities
 Bone density testing
- evaluate the extent of bone loss

A

 Technetium bone scan
- images the metabolic activity of the
skeleton with a radioactive tracer
- relatively non-specific

 EMG/NCV
- rule out nerve entrapment, peripheral neuropathy, or nerve injury- Need neurology consultation!

23
Q

Diagnostic Modalities Continued

A

 Thermography
- asymmetric difference between limbs
- downside: temperature is dynamic

 Resting sweating output and quantitative sudomotor axon reflex test (QSART)
- measure sweat output between limbs
 Other tests . . .

24
Q

Differential Diagnosis

A

Many disorders can mimic the signs and symptoms of CRPS . . .
- post herpetic neuralgia

  • entrapment neuropathy
  • cellulitis
  • lymphedema
  • stress fractures
  • bone tumors
  • rheumatic and inflammatory arthritis
  • connective tissue diseases
  • malignancy
  • factitious conditions
  • many more . . .
25
Q

Treatment
The primary goal of treatment therapy focuses on restoring limb function.

A

Treatment
The primary goal of treatment therapy focuses on restoring limb function.
This can be accomplished with physical therapy and pain control
modalities.

26
Q

Treatment

Successful treatment seems to depend on 5 separate principles . . .

A
  1. Patient awareness and commitment
  2. Capable multidisciplinary team
  3. Timely diagnosis
  4. Positive family support
  5. Sound therapeutic measures
27
Q

Conservative Treatment Options

A

 Physical therapy is the foundation of treatment
 The patient undergoes a series of phases that build upon each other . . .
1. Desensitization and mobilization
2. Regaining flexibility and controlling
edema
3. Isotonic strengthening and stress loading 4. Restoring normal limb function

28
Q

Conservative Treatment Options Continued

A

 Trancutaneous electrical nerve stimulation (TENS)
 Mild electrical current stimulation helps block pain messages short- term

29
Q

Pharmacological Options

 Topical agents
- EMLA
- Lidoderm patch (24h)
- Capsaicin( for diabetes)

A

 Corticosteroids (antidepressant, antiinflamm)
- may suppress ectopic neural
discharges in addition to anti-inflammatory effects

 Tricyclic antidepressants (amitriptyline) - inhibits NE and serotonin uptake - unknown mechanism of pain relief

30
Q

Pharmacological Options Continued

 Antiepileptic agents (Gabapentin)-diabetes
- helps prevent the spread of excitation
from a focus of irritability

A

 Opioids
- used sparingly when pain is not
controlled with other medications

 Others medications
- muscle relaxants . . .

31
Q

Procedural Options

A

 Sympathetic nerve blocks
- lumbar block spares motor and
sensory function
- can allow patient to participate in physical
therapy

 Sympathectomy
- suppress sympathetic NS activity to affected
area

 Electrical stimulation of spinal cord

 Implantable pain pump

32
Q

Prognosis

A

The prognosis for CRPS varies from person to person.
Spontaneous remission from symptoms occurs in certain individuals.
Others can have unremitting pain and crippling with irreversible changes in spite of treatment.

33
Q

LUMPS & BUMPS

A

Ganglionic Cyst - bigger needle is better
Rheumatoid Nodule
Gouty Tophi
 Fibroma
 Lipoma
Epithelial Inclusion Cyst

34
Q

Ganglionic Cyst Characteristics** u will see all the time

A

Freely movable subcutaneous cystic lump or bump… can change size
Well-circumscribed and soft to firm in nature
Fluid filled – consistency of honey/jelly
Generally painless unless nerve
involvement or repetitive trauma
 Transilluminate (if it’s cystic, if it’s soluble, wont transilluminate)

35
Q

Ganglionic Cyst Characteristics continued . . .
 Seen over joints or tendons

A

 Involves a flaw in the joint capsule or tendon sheath that allows the joint tissue to bulge out

 Multiple small cysts can give the appearance of more than one cyst, but a common stalk within the deeper tissue usually connects them

36
Q

Ganglionic Cyst
Treatments

A

Smash☺
Aspirate, inject &compress
Surgical excision

    • very high reoccurrence rate
    • pink-18gazes, blue-25gazes
    • u need bigger needle
    • as most proximal as you can get to prevent reoccurence
37
Q

Rheumatoid Nodule Characteristics

Firm non-tender lump or bump over bony prominences or areas subject to pressure
Often seen under metatarsal heads

A

Develop in approximately 25% of patients with
rheumatoid arthritis (RA)
Associated with a more rapidly progressive and
destructive disease process
Can ulcerate or become secondarily infected

38
Q

Rheumatoid Nodule ****

A

Immune-mediated granulomas with necrotic center
Palisaded histiocytes immediately adjacent to the necrosis
Layer of chronic inflammatory cells

39
Q

Rheumatoid Nodule

Treatment

A
  • Padding to accommodate
  • Shoegear modifications
  • Steroid injection
  • Excision
40
Q

Gouty Tophi– 1st mpj
Characteristics

** it can also be in organs

A

 Firm lump or bump over bony prominences

 Seen in chronic tophaceous gout
- The development of tophaceous deposits is a function of duration and severity of hyperuricemia

 Monosodium urate crystal deposits
 Occur in subcutaneous tissues, joints, viscera
 May erode bone or ulcerate & drain. . . chalky
in nature

41
Q

Gouty Tophi
Treatment

A

-Refer to PCP to lower serum uric acid
-Rarely may need to excise

42
Q

Plantar Fibroma Characteristics

A

Firm to hard lump or bump corresponds to a subcutaneous thickening of the plantar fascia
Moves with the fascia/aponeurosis
Most often affects the medial and central
bands
Single or multiple/Unilateral or bilateral
Can become painful on weightbearing
Also called Ledderhose’s disease

43
Q

Plantar Fibroma
Treatment

A
  • Padding/accommodation with orthotics
  • Want orthotics to achieve two things:
  1. Decrease tension on the plantar fascia
  2. Decrease pressure on the lump in your arch
44
Q

Plantar Fibroma
Treatment

A
  • Topical transdermal verapamil
    • Calcium channel blocker
    • Inhibits fibroblast activity
    • No concrete evidence!
  • Injection with corticosteroids
  • Wide excision is recommended due to the high reoccurrence rate
45
Q

Lipoma Characteristics

A

 Subcutaneous lump or bump composed of mature fat cells
 Rubbery or doughy consistency
 Often lobulated
 Most often asymptomatic **

46
Q

Lipoma
Treatment

A
  • Simple surgical excision - Liposuction!!
47
Q

Epithelial Inclusion Cyst
Characteristics

A

Firm subcutaneous lump or bump
Other name: epidermoid cyst
Grossly appears like a cocktail onion
Filled with foul-smelling whitish cheesy (caseous) like material. . . keratin
Caused by epithelial cells driven deep into dermis
-surgery -trauma -congenital

48
Q

Epithelial Inclusion Cyst

A

 The source of this epidermis is nearly always the upper segment of the hair follicle

 Inflammation is mediated in part by the horny material/keratinized material contained in epidermoid cysts.
** Extracts of this material have been shown to be chemotactic for poly-
morphonucleocytes.

49
Q

Epithelial Inclusion Cyst
Treatment

A

-Incision and drainage
- Excision
- Incomplete excision will lead to reoccurrence

50
Q

Complex Regional Pain Syndrome
Reflex Sympathetic Dystrophy Syndrome (RSDS)

A

Other Names  Causalgia
 Sympathetically maintained pain

 Sudeck’s atrophy
 Post-traumatic dystrophy
 Shoulder-Hand syndrome
 Many more names…

51
Q

Complex Regional Pain Syndrome
Reflex Sympathetic Dystrophy Syndrome (RSDS)

Other Names

A

 Causalgia
 Sympathetically maintained pain

 Sudeck’s atrophy
 Post-traumatic dystrophy
 Shoulder-Hand syndrome
 Many more names…

Pod Med (8 decks)

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