Complex fractures/Complications of Fractures (Open Fractures, Dislocations, Acute Compartment Syndrome, Fat Embolism syndrome, Complex regional Pain Syndrome Type 1, Crush Syndrome) Flashcards Preview

MSK > Complex fractures/Complications of Fractures (Open Fractures, Dislocations, Acute Compartment Syndrome, Fat Embolism syndrome, Complex regional Pain Syndrome Type 1, Crush Syndrome) > Flashcards

Flashcards in Complex fractures/Complications of Fractures (Open Fractures, Dislocations, Acute Compartment Syndrome, Fat Embolism syndrome, Complex regional Pain Syndrome Type 1, Crush Syndrome) Deck (50)
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1
Q

What is compartment syndrome?

A

A pathological condition characterised by elevated interstitial pressure in a closed osseofascial compartment that results in microvascular compromise (restriction of capillary blood flow)

2
Q

What condition occurs as a result of compartment syndrome?

A

Rhabdomyolysis

3
Q

What is the pathophysiology of compartment syndrome?

A

Elevated interstitial pressure in a closed osseofascial compartment may be secondary to several different factors. Haemorrhage within the compartment or direct trauma to the muscles with subsequent oedema can lead to increased pressure to above the capillary level, which restricts capillary flow. This results in tissue necrosis secondary to oxygen deprivation. There is evidence that muscle necrosis can occur even in the face of apparently normal circulation, if the intracompartmental pressure is >30 mmHg for >8 hours

4
Q

What is increased pressure in compartment syndrome most commonly caused by?

A

Oedema or haemorrhage

5
Q

What are signs that someone might have compartment syndrome?

A
  • Swelling
  • Redness
  • Mottling
  • Pulseless
  • Paraesthesiae
  • Paralysis
  • Loss of muscle function
  • Pain on passive muscle stretching - disproportionate to injury
6
Q

If you suspected someone had compartment syndrome, what might you do to investigate?

A
  • Examine them
  • Bloods - Serum CK, U+E’s
  • Specific - compartment pressure metre, Urine myoglobin
7
Q

How would you manage someone with compartment syndrome?

A

ABCDE

  • Dressing release
  • Analgesia
  • IV fluids
  • Surgical - fasciotomy/Amputation
  • Consider haemodialysis - if severe AKI from Rhabdo
8
Q

What is involved in compartment pressure reading?

A

Measure compartment pressure and compare to diastolic BP

DBP - compartment pressure

9
Q

What is diagnostic on compartment pressure monitoring of compartment syndrome?

A

Differential pressure within 20-30 mmHg of the diastolic pressure (delta pressure) is considered a strong indicator for fasciotomy

A compartment pressure of > 30 mmHg is considered critical

10
Q

What differential would you consider in someone with suspected compartment syndrome?

A
  • Deep vein thrombosis
  • Cellulitis
  • Peripheral vascular disease/ischaemic limb
  • Septic Arthritis
  • Rhabdomyolysis
11
Q

What is fat embolism?

A

Type of embolism in which the embolus consists of fatty material. They are often caused by physical trauma such as fracture of soft tissue trauma, and burns

12
Q

What are causes of fat embolism?

A

Long bone fratures - typically after pelvis or femur

13
Q

What are features of a fat embolism?

A
  • Altered mental state
  • Pyrexia
  • SOB/hypoxia
  • Tachycardia
  • Petechial rash
14
Q

Where are petechial rashes found in fat ambolism syndrome?

A
  • Axillary region
  • Conjunctivae
  • Oral mucosa
15
Q

How would you approach investigating someone for fat embolism syndrome?

A
  • Examination
  • Bedside - temperature
  • Bloods - ABG, FBC
  • Specific - urine for fat globules, sputum for fat globules
16
Q

What is the mortality rate for fat embolism syndrome?

A

15%

17
Q

How would you manage someone with fat embolism syndrome?

A

Supportive management in ITU

  • Mechanical ventilation to support respiratory failure
18
Q

What measures can be taken to prevent fat embolism?

A

Early fracture stabilization (within 24 hours) of long bone fracture - most important factor in prevention of FES

19
Q

What is the defintion of an open fracture?

A

There is a direct communication between the external environment and the fracture

20
Q

What classification system is used to classify open fractures?

A

Gustilo classification system

21
Q

What is gustilo type I open fracture?

A
  • Low-energy wound < 1cm long
  • Clean
  • Simple fracture pattern
22
Q

What is gustilo type II open fracture?

A
  • Low-energy wound > 1cm long
  • Moderate soft tissue damage
  • Simple fracture pattern
  • Adequate skin coverage
23
Q

What is gustilo type IIIa open fracture?

A
  • High energy injury
  • Extensive soft tissue damage
  • Complex fracture pattern
  • Adequate periosteal coverage
24
Q

What is gustilo type IIIb open fracture?

A
  • High energy injury
  • Extensive soft tissue damage
  • Complex fracture pattern
  • Tissue loss requiring soft tissue coverage procedure
25
Q

What is gustilo type IIIc open fracture?

A
  • High energy injury
  • Extensive soft tissue damage
  • Complex fracture pattern
  • Vascular injury requiring repair
26
Q

How would you grade the following fracture?

A

Gustilo type I

27
Q

How would you grade the following fracture?

A

Gustilo type II

28
Q

How would you grade the following open fracture?

A

Gustilo IIIa

29
Q

How would you grade the following open fracture?

A

Gustilo IIIb

30
Q

How would you grade the following fracture?

A

Gustilo IIIc

31
Q

How would you manage an open fracture?

A
  • Full ATLS assessment and treatment
  • Tetanus and antibiotic prophylaxis
  • Repeated examination n/v status - Wounds only handled to remove gross contamination, photograph, cover (saline swabs) and stabilise limb
  • No provisional irrigation / exploration
  • Radiographs - orthogonal views including joint above and below
  • Surgical debridement and fixation, followed by assessment for skin coverage
32
Q

What antibiotics would you consider using when managing open fractures?

A

Cefuroxime / Augmentin / Clindamycin - Gent at time of fixation

33
Q

What is complex regional pain syndrome?

A

Defined as continuing (spontaneous and/or evoked) regional pain out of proportion to the severity of the inciting event and beyond the normal time frame expected following the event. The pain is usually regional (not in a specific nerve territory or dermatome) and has a distal predominance of abnormal sensory, motor, sudomotor, vasomotor, and/or trophic findings with variable progression over time.

34
Q

What are causes of CRPS type I?

A
  • Carpal tunnel release
  • Ops for Dupuytrens
  • Tendon release procedure
  • Mastectomy
  • Knee surgery
  • Crush injury
  • Amputation
  • Fracture
  • MI
35
Q

What defines CRPS type I?

A

CRPS in the absence of an identifiable nerve lesion (previously known as reflex sympathetic dystrophy)

36
Q

What are features of CRPS type I?

A

Initial trauma, followed by:

  • Pain/Allodynia/hyperalgesia - burning in nature
  • Sensory abnormalities
  • Abnormal blood flow - may have cold and cyanosed limb
  • Sweating
  • Tissue oedema +/- Trophic changes
  • Worse after exercise - clumsiness, spasms, dystonia, allodynia
37
Q

How would you confirm the diagnosis of CRPS type I?

A

Usually clinical diagnosis, but can consider

  • X-ray
  • Bone scintigraphy
38
Q

How would you manage someone with CRPS type I?

A
  • Refer to OT/PT - intense physiotherapy
  • Analgesia for neuropathic pain - Amitryptilline +/- NSAIDs, Morphine
39
Q

What is rhabdomyolysis?

A

Rhabdomyolysis may result from any traumatic or medical injury to the sarcolemma (the myocyte cell membrane). The subsequent release of intracellular ions, myoglobin, CK, and urates into the circulation results in electrolyte disturbances, disseminated intravascular coagulation (DIC), renal failure, and multi-organ failure.

40
Q

What is the pathophysiology of rhabdomyolysis?

A

Release of intracellular contents - Contents include myoglobin, CK, potassium, magnesium, phosphorus, and uric acid. Cellular integrity and function is dependent on the strict maintenance of low intracellular sodium and calcium ion concentrations regulated by ATPase-dependent cation exchange mechanisms. Direct physical injury such as trauma or toxic injury allows disruption of ionic homeostasis across the sarcolemma and cellular swelling with subsequent lysis. Because homeostasis is also ATP-dependent, any process impairing its production by skeletal muscle also causes myocyte destruction.

41
Q

What are causes of rhabdomyolsysis?

A
  • Metabolic and endocrine - thyroid storm, phaeochromocytoma, myxoedema, DKA, HONK
  • Ischaemia - compartment syndrome, prolonged immobilisation (e.g. coma, drug overdose), prolonged tourniquet use, post aortic clamp operations, reperfusion injuries.
  • Trauma - crush injury, burns, electrocution
  • Excessive physical activity - prolonged exertion, prolonged seizures
  • Infection - viral (e.g. severe influenza), clostridium, persistent high fever
  • Autoimmune - polymyositis, dermatomyositis
  • Electrolytes - hypokalaemia, hypophosphataemia
  • Hyperthermia and hypothermia
  • Drugs and toxins
42
Q

What are the mechanisms of renal failure in rhabdomyolysis?

A
  • Renal vasoconstriction
  • Intraluminal cast formation
  • Direct haem-protein induced cytotoxicity
43
Q

What are complications of rhabdomyolysis?

A
  • Hyperkalemia
  • Hypocalcemia - due to phosphate release
  • AKI - due to myoglobin
  • DIC - due to release of thromboplastins
  • Shock - due to “third space” losses from extravasation of fluid from extensively damaged muscle
44
Q

What are features of rhabdomyolysis?

A
  • Muscle pain (~50%); can be painless
  • Dark discolored urine (myoglobinuria)
  • Evidence of complications - Hyperkalaemia, hypoclaemia, DIC, Shock, AKI
45
Q

What investigations might you consider doing in someone with suspected rhabdomyolysis?

A
  • Bedside - NEWS score, ECG, dipstick (for blood)
  • Bloods - CK, ABG, FBC, U+Es, Coag screen
  • Specific - urine myoglobin (dipstick may indicate presence of blood)

Further investigations as appropriate to determine underlying cause and detect susepcted complications

46
Q

How would you manage someone with rhabdomyolysis?

A

ABCDE

  • Monitoring
  • IV Fluids - aim for hypervolaemia to haemodilute blood being presented to the glomerulus
  • Treat Hyperkalaemia
  • Treat hypocalcaemia
  • Consider RRT - helps with hyperkalaemia and acidosis
  • Consider urine alkalinisation - prevent myoglobin precipitation
47
Q

What is the classic triad of rhabdomyolysis?

A
  • Myalgia
  • Generalized weakness
  • Darkened urine (red to brown)
48
Q

What are features of crush syndrome?

A

Features of rhabdomyolysis, plus

  • Hypovolaemia
  • Shock
49
Q

What bloods would you do if you suspected rhabdomyolysis?

A
  • FBC
  • CK
  • U+E’s
  • Phosphate
  • Calcium
  • Myoglobin
50
Q

What would you look for in the urine in someone with suspected rhabdomyolysis?

A

Myoglobinurea