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MS/Rheum > MSk Disease in the ER > Flashcards

MSk Disease in the ER Flashcards

1
Q

Most Common Musculoskeletal Symptoms

in the ER

A
  1. Pain
  2. swelling
  3. other
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2
Q

Joints Most Commonly = The Issue in the ER

A
  1. ankle
  2. wrist
  3. knee
  4. hip
  5. shoulder
  6. elbow
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3
Q

Most common type of ankle injury

A

lateral sprain due to inversion, while walking or running

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4
Q

Trx of ankle sparain

A

PRICE

Protection, Rest, Ice, Compression, Elevation

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5
Q

Common ankle frx epidemiology

A

Equally common in men and women, but

young men and late middle-aged women

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6
Q

“Vast majority” of ankle frx are:

“Majority” of ankle frx are:

A

malleolar fractures

unimalleolar fractures

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7
Q

Complications of ankle frx

A 
joint space disruption
dislocation
soft tissue/skin necrosis
nerve injury
arterial disruption
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8
Q

What ankle fracture complication is a srx emergency?

A

Loss of arterial blood supply

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9
Q

Why should an ankle dislocation be treated ASAP?

A

pressuring skin&raquo_space; necrosis of overlying skin

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10
Q

Most common type of wrist injury:

A

fracture of radius (or ulna or carpal bones) due to fall on outstretched hand

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11
Q

Wrist injury causes fracture far (more/less) commonly than ankle injury

A

more

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12
Q

Most common wrist fracture

A

Colles fracture, at the distal radial metaphysis, with proximal and dorsal displacement, creating “dinner fork” deformity

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13
Q

Most common type of knee injury?

A

ACL injury (100,000 per year in the US)

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14
Q

How do you dx ACL rupture (often)?

A

history: pain + audible pop at time of injury (70% of the time)

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15
Q

Any knee injury associated with an effusion or haemarthrosis ought to be assessed by:

A
  1. an appropriately trained clinician (ASAP)

2. XR –mandatory to exclude frx and ligamentous avulsion frx

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16
Q

Epidemiology of hip fractures?

Average age in M and F?

A

elderly, F>M (2:1), 1/3 more common in whites vs blacks

female 77
male 72

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17
Q

Hip Fractures: Pathophysiology

A

Weakening of bone with aging

(*90% in the elderly associated with simple fall from standing position or fall because femoral neck breaks)

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18
Q

Hip Fractures: Symptoms

A

sudden onset of hip pain, before or after fall, and inability to bear weight

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19
Q

Hip Fractures: Signs

A

leg shortened and externally rotated if fracture displaced

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20
Q

Hip Fractures: Risk

A

leg DVT

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21
Q

85% of episodes of low back pain are:

A

idiopathic

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22
Q

Non-idiopathic causes of low back pain:

A 
intervertebral disc herniation
spinal metastases
spinal infection
epidural abscess
hemorrhage,
spinal fracture 
ankylosing spondylitis
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23
Q

Lumbar Intervertebral Disc Herniation: Epidemiology

A

middle-aged adult, 30 to 50 years old

*Typically, with recurring episodes of low back pain

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24
Q

Only 1% of patients with back pain have:

95% of patients with back pain due to a herniated disc have:

A

sciatica

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25
Q

What is sciatica?

A

Syndrome of sharp pain in lower back, buttock and leg, commonly in a single dermatome
+/- sensorimotor symptoms
+/- leg weakness
+/- numbness or tingling, typically unilateral

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26
Q

90% of cases of sciatica are due to:

A

herniation of lower lumbosacral intervertebral disc

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27
Q

Test for lower lumbar intervertebral disc herniation?

A

Straight leg raise, between 30 and 70 degrees above level
(+) = pain in distribution of sciatic nerve (90% sen, 25% sp)

*If raising opposite leg causes pain, 25% sen and 90% sp

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28
Q

What is cauda equina syndrome, and what does it cause?

A 
Compression of cauda equina, causes some combo of:
low back pain
sciatica
leg weakness
bladder dysf
saddle hypo- or anesthesia
fecal incontinence
sexual dysf
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29
Q

Key feature of cauda equina syndrome:

A

Bladder dysfunction

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30
Q

Incomplete cauda equina syndrome:

A

altered urinary sensation
loss of desire to void
poor urinary stream
need to strain to be able to micturate

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31
Q

Complete cauda equina syndrome:

A

painless urinary retention
overflow incontinence
inability to pass urine spontaneously

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32
Q

CAUDA EQUINA SYNDROME: Signs

A 
bladder distention
decreased anal tone
absent ankle, knee or bulbocavernosus reflexes 
saddle anesthesia 
bilateral sciatica
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33
Q

All patients with cauda equina syndrome have:

A

> 500 ml urinary retention

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34
Q

Most important thing to know about cauda equina syndrome:

A

“Cauda equina syndrome is a neurosurgical emergency”

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35
Q

Most important risk factors for a spinal epidural abscess:

A 
spinal surgery or recent trauma
immunosuppression 
distal site of infection 
IV drug use
DM
alcoholism 
**20% = no predisposing factor
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36
Q

2 important manifestations of spinal epidural abscess that are missed in the ER:

A

Back pain

fever

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37
Q

Up to __% (estimate) of ER patients are seeking

drugs to misuse, especially opioid narcotics.

A

10

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38
Q

What now accounts for more overdose deaths than cocaine and heroin combined?

A

Opioid pain relievers

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39
Q

What is necrotizing fasciitis?

A

rare acute progressive destructive infection of muscle fascia and overlying subcutaneous fat

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40
Q

Why does necrotizing fasciitis spreads along muscle fascia?

A

relatively poor blood supply of fascia, whereas Muscle frequently spared (good blood supply

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41
Q

Why is necrotizing fasciitis difficult to dx without surgery?

A

Overlying tissue can seem unaffected initially

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42
Q

Necrotizing fasciitis: signs/symptoms

A

Area of erythema (without sharp margins),swelling and warmth, shiny, exquisitely tender

*pain out of proportion to physical findings

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43
Q

What causes type 1 necrotizing fasciitis?

What causes type 2 necrotizing fasciitis?

A

Type 1 = polymicrobial (aerobes + anaerobes)

Type 2 = group A strep (or MRSA) [or both]

44
Q

Necrotizing fasciitis: Risk factors

A

diabetes, vascular disease, immunosuppression, trauma, surgery

45
Q

Necrotizing fasciitis: Microscopic pathology

A

coagulative necrosis w/ acute inflamm (neuts and fibrin exudation) starting at edge

+/- aggregates of bacteria (but not where neutrophils are)

+/- nuclear dust (debris primarily from neutrophil breakdown)

+/- hemorrhage

46
Q

Necrotizing fasciitis progresses over ___ days

A

3-7

47
Q

Skin color changes associated with necrotizing fasciitis?

A

red to purple to purple with patches of blue-gray

48
Q

What occurs within the first 3-5 days of necrotizing fasciitis?

A

skin breaks down with bullae, containing thick pink or purple fluid

49
Q

What are the final symptoms of necrotizing fasciitis?

A
  • -frank cutaneous gangrene

- -anesthetic area, resulting from thrombosis of small blood vessels and destruction of superficial nerves

50
Q

What may precede skin necrosis in necrotizing fasciitis?

A

anesthesia

51
Q

Necrotizing fasciitis:
Most common site =
Second most common =

A

legs

perineum

52
Q

Which type of necrotizing fasciitis presents with subcut gas?

A

1

53
Q

What are the signs/symptoms of advanced necrotizing fasciitis infections?

A 
fever of 38.9 to 40.5 C (102 to 105 F)
tachycardia
hypotension
malaise
myalgias
anorexia 
diarrhea
54
Q

Treatment of necrotizing fasciitis?

A

surgical debridement of necrotic tissue
broad spectrum empirical abx
hemodynamic support

55
Q

Prognosis of necrotizing fasciitis?

A

bad (up to 40% mortality)

56
Q

Compartment syndrome occurs when…

A

increased pressure within a compartment compromises the circulation within that space

57
Q

Acute compartment syndrome occurs following…

A

trauma

58
Q

Chronic compartment syndrome occurs most often in what patient population?

A

athletes (presents with insidious pain)

59
Q

Pathophys of compartment syndrome?

A
  1. Inadequate venous drainage = tissue edema and increased interstitial pressure
  2. increased compartment pressure = decreased venous outflow = increased venous pressure
  3. this decreases arteriovenous pressure gradient
60
Q

What is the initial problem in compartment syndrome?

A

fascial enclosure preventing adequate expansion of tissue volume to compensate for increase in fluid

61
Q

What decreases the arteriovenous pressure gradient in compartment syndrome?

A
  1. Inadequate venous drainage&raquo_space; tissue edema + increased interstitial pressure
  2. Increased compartment pressure = decreased venous outflow + increased venous pressure rises
  3. When tissue pressure > end-arteriolar pressure, arterioles collapse
62
Q

Why is blood ultimately shunted away from compartmental tissues (compartmental syndrome)?

A

Ultimately arteriolar pressure is insufficient to overcome compartment pressure and blood is shunted away from compartmental tissues

63
Q

When is acute compartment syndrome most likely?

A

soon after significant trauma, particularly with long bone fractures

particularly in leg (tibial diaphysis) or forearm (distal radius)

64
Q

What are nontraumatic causes of acute compartment syndrome? (7)

A
  1. bleeding
  2. thrombosis
  3. vascular disease
  4. nephrotic syndrome
  5. extravasation of IV fluids
  6. injection of recreational drugs
  7. prolonged limb compression (e.g., following severe drug or alcohol intoxication)
65
Q

Acute Compartment Syndrome Symptoms :

A
  1. Pain out of proportion to apparent injury
    (early and common finding)
  2. Persistent deep ache or burning pain
  3. Paresthesias (onset within one half-2 hours)
66
Q

Acute Compartment Syndrome Signs :

A
  1. Pain with passive stretch of muscles in the affected compartment (early finding)
  2. Tense compartment with a firm “wood-like“ feeling
  3. Diminished sensation
  4. Muscle weakness (onset within 2-4 hours)
67
Q

Nml compartment pressure?

Compartment pressure when pain develops?

A

0 to 8 mmHg

20 to 30 mmHg

68
Q

When does capillary blood flow becomes compromised (as a result of rising tissue pressure)?

A

when tissue pressure increases to within 25 mmHg of mean arterial blood pressure

69
Q

When does ischemia occur (as a result of rising tissue pressure)?

A

when tissue pressures approach diastolic pressure

70
Q

At what perfusion pressure should you treat compartment syndrome?

A

A perfusion pressure (diastolic – compartment) of less than 30 mmHg

71
Q

What is the trx for acute compartment syndrome?

A

Fasciotomy

72
Q

How are compartment pressure measurements problematic as a diagnostic test?

A

poor specificity for compartment syndrome in the traumatized limb

73
Q

What is Clostridial myonecrosis (gas gangrene)?

A

life-threatening necrotizing muscle infection

74
Q

What are 2 causes of Clostridial myonecrosis (gas gangrene)?

A
  1. infection from contiguous area of trauma

2. hematogenous muscle seeding from GI tract

75
Q

What are 2 major forms of Clostridial myonecrosis (gas gangrene)? What causes each/

A
  1. Traumatic; most commonly C. perfringens

2. Spontaneous; most commonly C. septicum

76
Q

What are the effects of alpha toxin?

A
  1. platelet aggregation
  2. adherence of neutrophils to endothelium,
  3. inhibiting cardiac pump function (negative inotrope)
77
Q

What enzymatic actions does alpha-toxin have?

A

phospholipase
sphingomyelinase
(also hemolytic)

78
Q

What is theta-toxin?

A

cholesterol dependent cytolysin

*aka perfringolysin O, PFO

79
Q

alpha- and theta-toxin are virulence factors produced by what bacteria?

A

C. perfringens

80
Q

Pathophysiology of Clostridial myonecrosis (gas gangrene)?

A
  1. Trauma introduces Clostridia (bacteria or spores) into deep tissue
  2. If trauma impairs blood supply = optimal for growth of Clostridia (anaerobic, low red-ox potential, acidic pH)
81
Q

What is the main problem caused by Clostridial myonecrosis (gas gangrene)?

A

severe muscle necrosis

82
Q

What is absent from infected tissues in Clostridial myonecrosis (gas gangrene)? Why?

A

neutrophils

Arrive at site of infection, adhere to + accumulate along endothelium of arterioles/capillaries/venules, but do NOT cross endothelium into infected tissue.

83
Q

What is seen microscopically in Clostridial myonecrosis (gas gangrene)?

A
  • -Necrotic muscle with gas bubbles
  • -No neutrophils
  • -Large boxcar-shaped gram-positive rods (which may be gram-negative in tissue)
84
Q

How does alpha toxin cause damage?

A

forms of occlusive intravascular masses of activated platelets leukocytes and fibrin =
causes potent rapid irrev decline in muscle blood flow and ischemic necrosis

85
Q

What receptors does alpha toxin-induction activate?

A

platelet fibrinogen receptor glycoprotein IIb/IIIa

86
Q

What is a potential drug therapy for Clostridial myonecrosis (gas gangrene)?

A

platelet glycoprotein inhibitors (e.g. eptifibatide, abciximab); block alpha-toxin activation of platelets = maintain blood flow

87
Q

How does traumatic gas gangrene present?

A

sudden onset of severe pain at the site of trauma, <24h following trauma

88
Q

What causes pain associated with traumatic gas gangrene?

A

toxin-mediated ischemia

89
Q

What skin symptoms are associated with gas gangrene?

A
  1. skin over infected area goes from pale, to bronze, to purple/red
  2. skin becomes tense and “exquisitely” tender
  3. bullae +/- arborizing pattern of distended blood vessels (full of hemolyzed blood)
  4. gas in soft tissue that may be palpated
90
Q

What systemic signs are associated with gas gangrene?

A

tachycardia and fever, followed by shock and multiorgan failure

91
Q

Definitive diagnosis of traumatic gas gangrene?

A

demonstration of large Gram stain-variable rods

at the site of injury

92
Q

Histopathology of gas gangrene?

A

characteristic absence of acute inflammatory cells

93
Q

Treatment of traumatic gas gangrene?

A
  1. aggressive and thorough surgical debridement 2. antibiotics (clindamycin and penicillin)
94
Q

Prognosis of traumatic gas gangrene?

A

~20% mortality, primarily with shock at

presentation

95
Q

Risk factors for fatality associated with spontaneous gangrene?

A

underlying malignancy and immunocompromised state

96
Q

What is rhabdomyolysis?

A

muscle necrosis + release of intracellular muscle constituents into the circulation

97
Q

Symptoms of rhabdomyolysis?

A
  • -classic triad = muscle pain, weakness and dark urine
  • -also: muscle stiffness and cramping
  • > 50% of patients have no muscular symptoms
  • *degree of symptoms varies widely, and some patients are asymptomatic.
98
Q

In rhabdo, where is muscle pain most prominent?

A

proximal muscles (thighs and shoulders), lower back, calves

99
Q

Symptoms of rhabdomyolysis in severely affected patients?

A

malaise, fever, tachycardia, nausea/vomiting, abd pain

100
Q

Signs of rhabdomyolysis?

A 
Reddish-brown urine (50% of cases)
\+/- Muscle swelling with rehydration
\+/- Muscle tenderness
\+/- Muscle weakness 
OR no physical signs
101
Q

Causes of rhabdomyolysis: (3 categories)

A
  1. Trauma (e.g., crush syndrome)
  2. Exertion (e.g., extreme exertion, hyperthermia, metabolic myopathies)
  3. Miscellaneous (e.g., toxins, meds, infections)
102
Q

The hallmark of rhabdomyolysis?

A

elevation in serum muscle enzymes

–CK up to 5x nml

103
Q

What urine abn is associated with rhabdomyolysis?

A

Myoglobinuria (+ blood urine test, but no RBC microscopically)

104
Q

How can rhabdo cause renal failure?

A

Myoglobin can clog the renal tubules

105
Q

Know them because they are common:

A

Lumbar disc herniation
Ankle sprain
Hip fracture
ACL tear

106
Q

Know them because they are surgical emergencies:

A

Necrotizing fasciitis
Cauda equina syndrome
Acute loss of arterial supply
Acute compartment syndrome

MS/Rheum (23 decks)

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