Compartment syndrome: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
Cycle: Increased pressure-->impaired perfusion-->disruption of cellular metabolism-->cytolysis with release of osmotically active contents into compartment-->additional fluid drawn into compartment-->increased pressure | Cycle: Increased pressure-->impaired perfusion-->disruption of cellular metabolism-->cytolysis with release of osmotically active contents into compartment-->additional fluid drawn into compartment-->increased pressure | ||
==Presentation== | ==Presentation== | ||
#5 Ps: pain, paresthesias, pallor, poikilothermia, pulselessness | |||
##NB: pain, paresthesias are NOT reliable | |||
##Pain at rest or with passive ROM | |||
##Sensory nerves are first to lose conductive ability | |||
==Etiology== | |||
#Most often develops soon after significant trauma (particularly involving long bone fractures of the lower leg or forearm) | |||
#May also occur following minor trauma or from nontraumatic causes: | |||
##ischemia-reperfusion injury | |||
##coagulopathy | |||
##certain animal envenomations and bites | |||
##extravasation of IV fluids | |||
##injection of recreational drugs | |||
##prolonged limb compression | |||
Etiology== | |||
Most often develops soon after significant trauma (particularly involving long bone fractures of the lower leg or forearm) | |||
May also occur following minor trauma or from nontraumatic causes: | |||
==Diagnosis== | ==Diagnosis== | ||
#Non-invasive tests are NOT reliable | |||
#Striker | |||
##Normal = 0-8mm Hg | |||
##Capillary blod flow starts to be compromised at 20mmHg | |||
###-Symptoms and signs may develop with pressures above approximately 20 mmHg | |||
##Muscles and nerve fibers at risk at >30-40mmHg | |||
#interpret in light of SBP | |||
#The pressure necessary for injury varies | |||
#Higher pressures may be necessary with systemic hypertension | |||
#May develop at lower pressures in those with hypotension or peripheral vascular disease | |||
#A single normal compartment pressure reading, early in the course of the disease, does NOT rule out comp sy. | |||
#Serial or continuous measurements are important when patient risk is moderate to high or clinical suspicion exists. | |||
==Specific Syndromes== | ==Specific Syndromes== | ||
===Forearm (<5%)=== | |||
(most frequent injuries associated with comp sy in forearm are supracondylar humerus fractures in children and distal radius fractures in adults) | (most frequent injuries associated with comp sy in forearm are supracondylar humerus fractures in children and distal radius fractures in adults) | ||
# deep volar | |||
##at highest risk for comp sy | |||
##contains the digital flexors | |||
##decreased wrist extension | |||
##includes flexor digitorum profundus (responsible for distal interphalangeal joint flexion) and the flexor pollicis longus (responsible for interphalangeal joint flexion of the thumb) | |||
# superficial volar | |||
# dorsal | |||
##contains the digital extensors | |||
# lateral | |||
===Lower (Leg 2-12% tibia)=== | |||
# Anterior | |||
##most common site compartment sy | |||
##contains the four extensor muscles of the foot, the anterior tibial artery, and the deep peroneal nerve | |||
##sx include loss of sensation between the 1st and 2nd toes and weakness of foot dorsiflexion | |||
##late sequelae include foot drop, claw foot, and deep peroneal nerve dysfunction | |||
# Lateral | |||
##contains muscles for foot eversion and some plantar flexion (ie, peroneus brevis, peroneus longus), the peroneal artery, the superficial peroneal nerve, and the proximal portion of the deep peroneal nerve | |||
##sx include deep peroneal nerve deficit (weakness in dorsiflexion and inversion of the foot and sensory loss in the web space between the great toe and the adjacent toe) | |||
##superficial peroneal nerve also travels through this compartment and supplies sensation to the lower leg and foot | |||
# Deep posterior | |||
##muscles that aid in foot plantar flexion, as well as the posterior tibial artery, peroneal artery, and the tibial nerve | |||
##sx include plantar hypesthesia, weakness of toe flexion, and pain with passive extension of the toes | |||
# Superficial posterior | |||
##the major muscles of plantar flexion (ie, gastrocnemius, soleus) | |||
##no major arteries or nerves in this compartment. | |||
##least likely to develop ACS in lower leg | |||
##sx include pain and a palpably tense and tender compartment | |||
==Treatment== | ==Treatment== | ||
#Raise limb to level of heart | |||
#AVOID ice (will further compromise microcirculation) | |||
Raise limb to level of heart | #Bivalve or remove cast if present | ||
#Surgery consult | |||
AVOID ice (will further compromise microcirculation) | #Definitive: Fasciotomy | ||
#Goal: < 6hours | |||
Bivalve or remove cast if present | |||
Surgery consult | |||
Definitive: Fasciotomy | |||
Goal: < 6hours | |||
==Source== | ==Source== | ||
Adapted from KajiQuestions and Donaldson; Perron (ACEP '09) | Adapted from KajiQuestions and Donaldson; Perron (ACEP '09) | ||
[[Category:Ortho]] | [[Category:Ortho]] | ||
Revision as of 05:50, 31 March 2011
Pathophysiology
Cycle: Increased pressure-->impaired perfusion-->disruption of cellular metabolism-->cytolysis with release of osmotically active contents into compartment-->additional fluid drawn into compartment-->increased pressure
Presentation
- 5 Ps: pain, paresthesias, pallor, poikilothermia, pulselessness
- NB: pain, paresthesias are NOT reliable
- Pain at rest or with passive ROM
- Sensory nerves are first to lose conductive ability
Etiology
- Most often develops soon after significant trauma (particularly involving long bone fractures of the lower leg or forearm)
- May also occur following minor trauma or from nontraumatic causes:
- ischemia-reperfusion injury
- coagulopathy
- certain animal envenomations and bites
- extravasation of IV fluids
- injection of recreational drugs
- prolonged limb compression
Diagnosis
- Non-invasive tests are NOT reliable
- Striker
- Normal = 0-8mm Hg
- Capillary blod flow starts to be compromised at 20mmHg
- -Symptoms and signs may develop with pressures above approximately 20 mmHg
- Muscles and nerve fibers at risk at >30-40mmHg
- interpret in light of SBP
- The pressure necessary for injury varies
- Higher pressures may be necessary with systemic hypertension
- May develop at lower pressures in those with hypotension or peripheral vascular disease
- A single normal compartment pressure reading, early in the course of the disease, does NOT rule out comp sy.
- Serial or continuous measurements are important when patient risk is moderate to high or clinical suspicion exists.
Specific Syndromes
Forearm (<5%)
(most frequent injuries associated with comp sy in forearm are supracondylar humerus fractures in children and distal radius fractures in adults)
- deep volar
- at highest risk for comp sy
- contains the digital flexors
- decreased wrist extension
- includes flexor digitorum profundus (responsible for distal interphalangeal joint flexion) and the flexor pollicis longus (responsible for interphalangeal joint flexion of the thumb)
- superficial volar
- dorsal
- contains the digital extensors
- lateral
Lower (Leg 2-12% tibia)
- Anterior
- most common site compartment sy
- contains the four extensor muscles of the foot, the anterior tibial artery, and the deep peroneal nerve
- sx include loss of sensation between the 1st and 2nd toes and weakness of foot dorsiflexion
- late sequelae include foot drop, claw foot, and deep peroneal nerve dysfunction
- Lateral
- contains muscles for foot eversion and some plantar flexion (ie, peroneus brevis, peroneus longus), the peroneal artery, the superficial peroneal nerve, and the proximal portion of the deep peroneal nerve
- sx include deep peroneal nerve deficit (weakness in dorsiflexion and inversion of the foot and sensory loss in the web space between the great toe and the adjacent toe)
- superficial peroneal nerve also travels through this compartment and supplies sensation to the lower leg and foot
- Deep posterior
- muscles that aid in foot plantar flexion, as well as the posterior tibial artery, peroneal artery, and the tibial nerve
- sx include plantar hypesthesia, weakness of toe flexion, and pain with passive extension of the toes
- Superficial posterior
- the major muscles of plantar flexion (ie, gastrocnemius, soleus)
- no major arteries or nerves in this compartment.
- least likely to develop ACS in lower leg
- sx include pain and a palpably tense and tender compartment
Treatment
- Raise limb to level of heart
- AVOID ice (will further compromise microcirculation)
- Bivalve or remove cast if present
- Surgery consult
- Definitive: Fasciotomy
- Goal: < 6hours
Source
Adapted from KajiQuestions and Donaldson; Perron (ACEP '09)
