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

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)

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2
Q

What condition occurs as a result of compartment syndrome?

A

Rhabdomyolysis

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3
Q

What is the pathophysiology of compartment syndrome?

A

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.

The resulting reducion in venous drainage causes a further rise in interstitial tissue pressures with the formation of tissue eodema. Only in the late stages is arterial flow comprimised.

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

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4
Q

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

A

Oedema or haemorrhage

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5
Q

Causes of compartment syndrome

A
  • Decrease in comparment size
    • Closure of fascial defects
    • Tight plaster casts
    • Localised external pressure (lying on limb
    • Pneeumatic antishock garments/burns
  • Increase in comparment content
    • Haemorrhage following soft tissue injury/fracture
    • Post op swelling and oedema
    • Post ischaenia swelling
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6
Q

What are signs that someone might have compartment syndrome?

A
  • Swelling
  • Redness
  • Mottling
  • 6 Ps - pain, paralysis, pallor, pulselesness, parasthesia, perishingly cold,
  • Loss of muscle function
  • Pain on passive muscle stretching - disproportionate to injury

PAIN IS OUT OF PROPORTION TO INJURY, NOT IMPROVING WITH SIMPLE ANALGESIA

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7
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
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8
Q

How would you manage someone with compartment syndrome?

A

ABCDE

  • Dressing release
  • Hold the limb at the level of the heart (not above) to promote arterial flow
  • Analgesia
  • IV fluids
  • GOLD STANDARD:
    • Surgical - fasciotomy/Amputation
  • Consider haemodialysis - if severe AKI from Rhabdo
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9
Q

What is involved in compartment pressure reading?

A

Measure compartment pressure and compare to diastolic BP

DBP - compartment pressure

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10
Q

How long have you got to save the limb?

A

From onset of ischaemia:

  • 4 hours - muscle and nerves will tolerate and functionally survive
  • 6 hours - variable injury to muscle and nerve
  • 8 hours - ischaemia yields permanent damage to both nerve and muscle.
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11
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

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12
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
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13
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

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14
Q

What are causes of fat embolism?

A

Long bone fratures - typically after pelvis or femur

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15
Q

What are features of a fat embolism?

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

Respiratory

  • Early persistent tachycardia
  • Tachypnoea, dyspnoea, hypoxia usually 72 hours following injury
  • Pyrexia

Dermatological

  • Red/brown impalpable petichial rash
  • Subconjunctival and oral haemorrhage/petechiae

CNS

  • Confusion and agitation
  • Retinal haemorhages and intra-arterial fat globules on fubdosocopy
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16
Q

Where are petechial rashes found in fat ambolism syndrome?

A
  • Axillary region
  • Conjunctivae
  • Oral mucosa
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17
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

Imaging may be normal - fat emboli tend to lodge distally and therefore CTPA may not show any vascular occlusion, a ground glass appearance may be seen at the periphery

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18
Q

What is the mortality rate for fat embolism syndrome?

A

15%

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19
Q

How would you manage someone with fat embolism syndrome?

A

Supportive management in ITU

  • Mechanical ventilation to support respiratory failure

Prompt fixation of long bone fractures needed

DVT prophylaxis

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20
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

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21
Q

What is the defintion of an open fracture?

A

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

22
Q

What classification system is used to classify open fractures?

A

Gustilo classification system

23
Q

What is gustilo type I open fracture?

A
  • Low-energy wound < 1cm long
  • Clean
  • Simple fracture pattern
24
Q

What is gustilo type II open fracture?

A
  • Low-energy wound > 1cm long
  • Moderate soft tissue damage
  • Simple fracture pattern
  • Adequate skin coverage
25
Q

What is gustilo type IIIa open fracture?

A
  • High energy injury
  • Extensive soft tissue damage
  • Complex fracture pattern
  • Adequate periosteal coverage
26
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
27
Q

What is gustilo type IIIc open fracture?

A
  • High energy injury
  • Extensive soft tissue damage
  • Complex fracture pattern
  • Vascular injury requiring repair
28
Q

How would you grade the following fracture?

A

Gustilo type I

29
Q

How would you grade the following fracture?

A

Gustilo type II

30
Q

How would you grade the following open fracture?

A

Gustilo IIIa

31
Q

How would you grade the following open fracture?

A

Gustilo IIIb

32
Q

How would you grade the following fracture?

A

Gustilo IIIc

33
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
34
Q

What antibiotics would you consider using when managing open fractures?

A

Cefuroxime / Augmentin / Clindamycin - Gent at time of fixation

35
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.

36
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
37
Q

What defines CRPS type I?

A

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

38
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
39
Q

How would you confirm the diagnosis of CRPS type I?

A

Usually clinical diagnosis, but can consider

  • X-ray
  • Bone scintigraphy
40
Q

How would you manage someone with CRPS type I?

A
  • Refer to OT/PT - intense physiotherapy
  • Analgesia for neuropathic pain - Amitryptilline +/- NSAIDs, Morphine
41
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.

42
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.

43
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
44
Q

What are the mechanisms of renal failure in rhabdomyolysis?

A
  • Renal vasoconstriction
  • Intraluminal cast formation
  • Direct haem-protein induced cytotoxicity
45
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
46
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
47
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

48
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
49
Q

What’s crush syndrome?

A

Typically found during rescue of trapped victims eg traumatic rhabdomylosis.

Defined as compression of extremeties or other parts of the body that cause muscle swelling/neurological disturbances.

The features fo rhabdomylosis come on acutely.

Victims should therefore be extricated very careully, with aggressive IV fluid hydration to manage the abrupt release of potassium and their intracellular electrolytes when they are freed.

50
Q

Complications of prolonged recumbancy

A
  • Hypostatic pneumonia
  • Pressure sores
  • DVT and PE
  • Muscle wasting and stiffening of joints, making mobilisation more difficult
  • Skeletal decalcification and formation of urinary tract calculi
  • UTI
  • Neurological complications
    • Common peroneal nerve (where external rotation leads to pressure in fibular neck region)
    • Ulnar neuropathy (when the patient repeatdly tries to change position using downwards pressure of the elbows against the bed)
  • Cardiac complications
    • ​Weaking of cardiac muscles due to poor venous return
  • Psychaitric problems