ortho

CC Huevos, Haziel
FUNCTIONS OF
CLAVICLE
Clavicle
■ The clavicle (collarbone) extends between the manubrium of the sternum and the
acromion of the scapula.
■ It is classed as a long bone and can be palpated along its length. In thin individuals,
it is visible under the skin.
■ The main function of the clavicle is as a strut to position the scapula in its correct
location. Since the scapula is the base upon which the arm and hand function, a
malunion or nonunion of the clavicle alters the position of the scapula such that the
mechanical advantage of the associated muscles is affected.
■ The clavicle has other functions:
– Attaches the upper limb to the trunk as part of the ‘shoulder girdle’.
– Protects the underlying neurovascular structures supplying the upper limb.
– Transmits force from the upper limb to the axial skeleton
Clinical relevance of clavicle
■ The clavicle acts to transmit forces from the upper limb to the axial skeleton. Given
its relative size, this leaves it particularly susceptible to fracture. The most common
mechanism of injury is a fall onto the shoulder or onto an outstretched hand.
■ The clavicle is arbitrarily divided into thirds:
– 15% of fractures occur in the lateral third
– 80% occur in the middle third
– 5% occur in the medial third
■ The majority of clavicular fractures (80% to 85%) occur in the midshaft of the bone
because:
– The bone is narrowest
– The enveloping soft tissue structures (which may help dissipate injury force)
are most scarce.
Clinical relevance of clavicle
■ After a fracture, the lateral end of the clavicle is displaced inferiorly by the weight of
the arm and displaced medially by the pectoralis major. The medial end is pulled
superiorly by the sternocleidomastoid muscle.
■ Management of a clavicular fracture can be conservative (e.g. sling immobilisation)
or operative (e.g. open reduction and internal fixation). The supraclavicular
nerves lie in close proximity to the clavicle and are occasionally sacrificed during a
surgical repair – resulting in a numb patch over the upper chest and shoulder.
CLAVICLE AGENESIS
(CLEIDOCRANIAL
DYSPLASIA)
Cleidocranial dysplasia
■ Cleidocranial dysplasia is a rare skeletal dysplasia characterized by short stature,
distinctive facial features and narrow, sloping shoulders caused by defective or
absent collarbones (clavicles).
■ Major symptoms may include premature closing of the soft spot on the head
(coronal), delayed closure of the space between the bones of the skull (fontanels),
narrow and abnormally shaped pelvic and pubic bones and deformations in the
chest (thoracic region).
■ Delayed eruption of teeth, moderately short stature, a high arched palate, a wide
pelvic joint, failure of the lower jaw joints to unite, and fingers that are irregular in
length may also be present.
Cleidocranial dysplasia
■ Cleidocranial dysplasia is usually caused by mutations in the RUNX2 gene. This gene
provides instructions for making a protein that is involved in the development and
maintenance of teeth, bones, and cartilage. Cartilage is a tough, flexible tissue that
makes up much of the skeleton during early development. Most cartilage is later
converted to bone (a process called ossification), except for the cartilage that
continues to cover and protect the ends of bones and is present in the nose,
airways, and external ears.
■ The RUNX2 gene reduce or eliminate the activity of the protein produced from one
copy of the RUNX2 gene in each cell, decreasing the total amount of functional
RUNX2 protein. This shortage of functional RUNX2 protein interferes with the normal
development of bones, cartilage, and teeth, resulting in the signs and symptoms of
cleidocranial dysplasia.
Cleidocranial dysplasia
■ The main skeletal deformity is hypoplasia
of clavicle bone, affecting mostly lateral
portion. In 10% of cases, clavicle is totally
absent. This allows hypermobility of the
shoulders resulting in the ability to touch
them in front of the chest.
CORACOCLAVICULAR
(CC) LIGAMENT
Coracoclavicular Ligament
■ The CC ligament is a very strong, heavy ligament whose fibers run from the outer,
inferior surface of the clavicle to the base of the coracoid process of the scapula.
■ The CC ligament has two components: The conoid and the trapezoid ligaments

Measurement
■ The trapezoid ligament measures from 0.8 to 2.5 cm in length and from 0.8 to 2.5
cm in width.
■ The conoid ligament varies from 0.7 to 2.5 cm in length and from 0.4 to 0.95 cm in
width.
■ The distance from the lateral clavicle to the most lateral fibers of the trapezoid
ligament may measure as little as 10 mm.
Coracoclavicular Ligament
■ Attachment
– The conoid ligament, the more medial of the two ligaments, is cone shaped, with
the apex of the cone attaching on the posteromedial side of the base of the
coracoid process. The base of the cone attaches onto the conoid tubercle on the
posterior undersurface of the clavicle. The conoid tubercle is located at the apex of
the posterior clavicular curve, which is at the junction of the lateral third of the
flattened clavicle with the medial two-thirds of the triangular shaft.
– The trapezoid ligament arises from the coracoid process, anterior and lateral to the
attachment of the conoid ligament. This is just posterior to the attachment of the
pectoralis minor tendon. The trapezoid ligament extends superiorly to a roughline
on the undersurface of the clavicle.
■ Function
– The coracoclavicular ligament serves to connect the clavicle and the coracoid
process of the scapula. Its two-component structure allows for proper apposition of
the acromion and the clavicle while preventing vertical displacement of the scapula
with respect to the clavicle. The angled space between the trapezoid and conoid
ligaments allows for some rotation of the scapula with respect to the clavicle.
Although not an intrinsic component of the AC joint, it adds stability to the AC joint.
ACROMIOCLAVICULAR
(AC) LIGAMENT
Acromioclavicular ligament
■ The AC joint is stabilized by the two sets of ligaments:
– A pair of intrinsic ligaments found within the articular capsule; the superior
and inferior acromioclavicular ligaments
– A single extrinsic ligament found outside the joint capsule; the coracoclavicular
ligament.
■ The superior acromioclavicular ligament connects the superior surfaces of the
acromion and acromial end of clavicle. A part of the trapezius muscle fibers fuse
with this ligament, supporting the joint capsule from its superior side. Similarly, the
inferior acromioclavicular ligament connects the inferior surfaces of the acromion
and the acromial end of clavicle.
Measurement
■ The acromioclavicular joint space measures 1-6 mm (females) and 1-7 mm (males),
decreasing with age
Acromioclavicular ligament
Function
■ The function of this joint is to enable the pectoral girdle to follow the movements of
the shoulder joint, particularly after the sternoclavicular joint has reached its
maximal range of motion. In addition, the AC joint also allows for transmission of
forces from the upper limb to the clavicle.
– controls horizontal motion and anterior-posterior stability
– has superior, inferior, anterior and posterior components
– posterior and superior AC ligaments are most important for stability
SPIRAL FRACTURE
■ Spiral fractures are complete fractures of
long bones that result from a rotational or
twisting force applied to the bone. Spiral
fractures are usually the result of high
energy trauma and are likely to be
associated with displacement.
■ Spiral fractures often occur when the
body is in motion while one extremity is
planted.
MUSCLE COMPARTMENTS
OF THE UPPER EXTREMITY
Anterior compartment

■ The anterior compartment of the arm is also known as the “flexor compartment” of
the arm as its main action is that of flexion.
■ The muscles in the anterior compartment of the arm flex the arm at the shoulder or
flex the forearm at the elbow and are innervated by the musculocutaneous nerve
which arises from the fifth and sixth and seventh cervical spinal nerves.
■ The muscles of the anterior compartment of the forearm are wrist and digital flexors
and pronators innervated by either the median nerve or the ulnar nerve.
■ The blood supply is from the brachial artery.
Posterior compartment

■ The posterior compartment of the arm is also known as the "extensor

compartment", as its main action is extension.
■ The muscles of the posterior compartments of the arm and forearm extend the
elbow and wrist, respectively. These muscles, plus the supinator and brachioradialis
(developmentally posterior compartment muscles), are all innervated by branches
off the radial nerve.
■ Functionally, the supinator supinates the forearm, and the brachioradialis, which
crosses the anterior side of the elbow, acts as a forearm flexor.
■ Their blood supply is from the profunda brachii.
ARM
ANTERIOR COMPARTMENT
■ Muscles: Biceps brachii, coracobrachialis, and brachialis
Blood supply: Brachial artery (Fig. 9.42)
Nerve supply to the muscles: Musculocutaneous nerve
Structures passing through the compartment: Musculocutaneous, median, and
ulnar nerves; brachial artery and basilic vein. The radial nerve is present in the lower
part of the compartment.
POSTERIOR COMPARTMENT
■ Muscle: The three heads of the triceps muscle
Nerve supply to the muscle: Radial nerve
Blood supply: Profunda brachii and ulnar collateral arteries
Structures passing through the compartment: Radial nerve and ulnar nerve
FOREARM
ANTERIOR COMPARTMENT
■ Muscles: A superficial group, consisting of the pronator teres, the flexor carpi radialis, the
palmaris longus, and the flexor carpi ulnaris; an intermediate group consisting of the
flexor digitorum superficialis; and a deep group consisting of the flexor pollicis longus,
the flexor digitorum profundus, and the pronator quadratus
Blood supply to the muscles: Ulnar and radial arteries
Nerve supply to the muscles: All the muscles are sup- plied by the median nerve and its
branches, except the flexor carpi ulnaris and the medial part of the flexor digitorum
profundus, which are supplied by the ulnar nerve.
MOBILE COMPARTMENT
The lateral fascial compartment may be regarded as part of the posterior fascial
compartment.
■ Muscles: Brachioradialis and extensor carpi radialis longus
Blood supply: Radial and brachial arteries
FOREARM
POSTERIOR COMPARTMENT
■ Muscles: The superficial group includes the extensor carpi radialis brevis, extensor
digitorum, extensor digiti minimi, extensor carpi ulnaris, and anconeus. These
muscles possess a common tendon of origin, which is attached to the lateral
epicondyle of the humerus. The deep group includes the supinator, abductor pollicis
longus, extensor pollicis brevis, extensor pollicis longus, and extensor indicis.
Blood supply: Posterior and anterior interosseous arteries
Nerve supply to the muscles: Deep branch of the radial nerve
Hand compartments
10 compartments in total:
■ hypothenar
■ thenar
■ adductor pollicis
■ dorsal interosseous (x4)
■ volar (palmar) interosseous (x3)
MUSCLE COMPARTMENTS
OF THE THIGH
The thigh has three muscle
compartments:
■ Anterior compartment (pink)
– Sartorius and quadriceps muscles (rectus femoris, vastus lateralis, vastus
intermedius, vastus medialis).
– The femoral nerve and superficial femoral artery supply these muscles.
■ Medial compartment (green)
– Pectineus, obturator externus, gracilis, and adductor muscles (longus, brevis,
magnus, minimus).
– The obturator nerve innervates the medial compartment.
■ Posterior compartment (blue)
– Biceps femoris, semimembranous, and semitendinous muscles.
– The sciatic nerve innervates the posterior compartment. The deep femoral
artery supplies the posterior compartment.
MUSCLE COMPARTMENTS
OF THE LEG
Compartments of the leg:
■ Anterior compartment (blue):
– Tibialis anterior, extensor muscles of the foot, and fibularis (peroneus) tertius muscles.
– The anterior tibial artery and deep fibular (peroneal) nerve supply the anterior compartment.
■ Lateral compartment (green):
– Fibularis (peroneus) longus and fibularis (peroneus) brevis muscles.
– The superficial fibular (peroneal) nerve and branches from the anterior tibial artery supply
these muscles.
■ Superficial posterior compartment (purple):
– Gastrocnemius, soleus, and plantaris muscles.
– Tibial nerve branches supply these muscles. The arteries that supply these muscles descend
from the popliteal artery. The sural arteries (medial, lateral) supply the gastrocnemius. The
soleus is variably supplied by the popliteal artery, posterior tibial artery, and fibular
(peroneal) artery.
■ Deep posterior compartment (pink):
– Tibialis posterior, flexor muscles of the foot, and popliteus muscles.
– The deep posterior compartment is innervated by the tibial nerve and supplied by the
posterior tibial and fibular (peroneal) arteries.
MUSCLE COMPARTMENTS
OF THE FOOT
Compartments of the foot
■ Interosseous compartment
Dorsal interossei muscles
Plantar interossei muscles
Plantar lateral artery, vein and nerve
■ Medial compartment
Abductor hallucis
Flexor hallucis brevis
Tendon of flexor hallucis brevis
Medial plantar arteries, veins and
nerves
■ Lateral compartment:
Abductor digiti minimi/quinti
Flexor digiti minimi
Opponens digiti minimi
Branches of the lateral plantar artery
vein and nerve
■ Central compartment (3 levels)
First level: Adductor hallucis
Second level: Quadratus plantae;
lumbrical muscles; tendons of flexor
digitorum longus
Third level: Flexor digitorum brevis
All levels of the central compartment
contain (deep) branches of the plantar
lateral artery, vein and nerve
COMPARTMENT
SYNDROME
Compartment syndrome
■ Acute compartment syndrome
– occurs when pressure rises within a confined space in the body, resulting in a
critical reduction of the blood flow to the tissues contained within the space.
– defined as the elevation of intracompartmental pressure (ICP) to a level and for
a duration that without urgent decompression will cause tissue ischemia,
necrosis, and functional impairment.
– should be differentiated from other related conditions, so awareness of the
different definitions associated with compartment syndrome is important.
■ Exertional compartment syndrome
– elevation of intracompartmental pressure during exercise, causing ischemia,
pain, and rarely neurologic symptoms and signs. It is characterized by
resolution of symptoms with rest but may proceed to acute compartment
syndrome if exercise continues.
Compartment syndrome
■ Volkmann ischemic contracture
– is the end stage of neglected acute compartment syndrome with irreversible
muscle necrosis leading to ischemic contractures.
■ Crush syndrome
– is the systemic result of muscle necrosis commonly caused by prolonged
external compression of an extremity. In crush syndrome muscle necrosis is
established by the time of presentation, but ICP may rise as a result of
intracompartmental edema, causing a superimposed acute compartment
syndrome.
Signs and symptoms
■ Pain
– considered to be the first symptom of acute compartment syndrome
– pain experienced by the patient is by nature ischemic and usually severe and
out of proportion to the clinical situation
– May be absent in acute compartment syndrome associated with nerve injury or
minimal in the deep posterior compartment syndrome
– Pain with passive stretch of the muscles involved
– As ACS progresses, the extremity becomes edematous and tense.
– There is increased pressure placed on nerve fibers and injured components
within the compartment.
Signs and symptoms
■ Pressure
– Pressure, swelling, and tenseness may be the only objective findings of early
compartment syndrome; however, these findings also tend to be unreliable
physical markers of compartment syndrome
■ Pallor
■ Paresthesia
– Paresthesia and hypoesthesia may occur in the territory of the nerves
traversing the affected compartment and are usually the first signs of nerve
ischemia, although sensory abnormality may be the result of concomitant
nerve injury
Signs and symptoms
■ Paralysis
– Paralysis of muscle groups affected by the acute compartment syndrome is
recognized as being a late sign
– This sign has equally low sensitivity as others in predicting the presence of
acute compartment syndrome, probably because of the difficulty of interpreting
the underlying cause of the weakness, which could be inhibition by pain, direct
injury to muscle, or associated nerve injury
– As ICP increases, neuronal tissues become ischemic and this contributes to
nerve dysfunction and paresthesia, paresis, and ultimately paralysis.
Paresthesia may occur within 30 minutes following injury to nerves
Signs and symptoms
■ Pulselessness
– Peripheral pulses and capillary return are always intact in acute compartment
syndrome unless there is major arterial injury or disease or in the very late
stages of acute compartment syndrome when amputation is inevitable
– A late finding is pulselessness which is a poor indicator of ACS, whereas pallor
is a less common finding.
– Arterial insufficiency is atypical in the early stages of ACS thus both dorsalis
pedis and posterior tibial pulses are palpable; capillary refill is brisk and the
extremity is typically pink.
– However, as ICP rises, loss of limb pulses and pallor indicates compression of
arterial perfusion
Signs and symptoms
■ Pedia (3 A’s)
*Children may not be able to express the severity of their pain, so restlessness,
agitation, and anxiety with increasing analgesic requirements should raise the suspicion
of the presence of an acute compartment syndrome
– Anxiety (restlessness)
– Agitation (crying)
– Analgesia (increasing requirement)
Diagnosis of Acute Compartment Syndrome
■ The Signs and Symptoms (6Ps) are used for clinical diagnosis
– The clinical finding of paresis is a late finding.
■ Compartment Pressure Monitoring
– Because raised tissue pressure is the primary event in acute compartment
syndrome, changes in ICP will precede the clinical symptoms and signs.
■ Needle manometer method, uses a needle introduced into the compartment and
connected to a column filled partly with saline and partly with air. A syringe filled with air
is attached to this column, as is a pressure manometer or transducer. The ICP is the
pressure that is required to inject air into the tubing and flatten the meniscus between
the saline and the air. This method was modified to allow infusion of saline into the
compartment. The ICP is the pressure resistance to infusion of saline.
– ICP is usually monitored in the anterior compartment because this is most
commonly involved in acute compartment syndrome and is easily accessible. If the
anterior compartment alone is monitored, the surgeon must be aware of the small
chance of deep posterior acute compartment syndrome and measure the deep
posterior compartment pressures if there are unexplained symptoms in the
presence of anterior compartment pressures with a safe difference between the
diastolic pressure and the tissue pressure (ΔP). It is important to measure the peak
pressure within the limb, which usually occurs within 5 cm of the level of the
fracture.
Treatment
■ The single most effective treatment for acute compartment syndrome is fasciotomy,
which if delayed can cause devastating complications
■ Fasciotomy
– The basic principle of fasciotomy of any compartment is full and adequate
decompression.
– Skin incisions must be made along the full length of the affected
compartment. There is no place for limited or subcutaneous fasciotomy in
acute compartment syndrome.
– It is essential to visualize all contained muscles in their entirety to assess their
viability and any muscle necrosis must be thoroughly debrided to avoid
infection. Subcutaneous fasciotomy is contraindicated for these reasons and
also because the skin may act as a limiting boundary.
Complication
■ Reperfusion Injury
– The reperfusion syndrome is a group of complications following re-establishment of
blood flow to the ischemic tissues
– It can occur after fasciotomy and restoration of muscle blood flow in the ACS
– Reperfusion is followed by an inflammatory response in the ischemic tissue that
can cause further tissue damage. The trigger for the inflammatory response is
probably the breakdown products of muscle.
■ Some breakdown products are procoagulants that activate the intrinsic clotting system.
This results in increasing microvascular thrombosis, which in turn increases the extent
of muscle damage.
– If there is a large amount of muscle involved in the ischemic process, the
inflammatory response may become systemic.
– In acute compartment syndrome this is most likely to occur in the crush syndrome.
■ Procoagulants escape into the systemic circulation and produce systemic coagulopathy
with parallel activation of inflammatory mediators. These then damage the vascular
endothelium, leading to increased permeability, transcapillary fluid leakage and
subsequent worsening of intracompartmental pressure, and eventually multiple organ
failure.
■ Systemic clotting and the breakdown products of dead and dying cells also lead to
activation of white blood cells, with the release of additional inflammatory mediators
such as histamine, interleukin, oxygen free radicals, thromboxane, and many others.
ENTRANCE VS
EXIT WOUND
Entrance wounds
■ Entrance wounds, as a rule, is oval or circular with inverted edges except in near
shot or in grazing wounds. As the bullet approaches the skin, there is an identation
of the skin surface but later on account of the extreme pressure, the skin tissues
give away. The rough surface of the bullet produces a contusion or abrasion collar.
The wound of entrance is smaller than the caliber of the wounding bullet due to
retraction of the connective tissue.
Exit wounds
■ The exit wound, on the other hand, is larger
than the wound of entrance. It may be
stellate and slit like, cruriform or markedly
lacerated. The deformity of the bullet in its
course in the body, lack of support beyond
the skin and velocity of the missiles are
responsible for the increase in size of the
wound.
 HIGH VELOCITY VS
LOW VELOCITY BULLET
In terms of design:
■ Low velocity bullets are made of low melting point lead alloys. If fired from high
velocity, they melt secondary to friction - they deform and change missile ballistics.
■ High velocity bullets are coated or jacketed with harder metal (high temperature
coating) and have less deformity when fired.
In terms of firearm type:
■ Low Velocity Firearm
– firearms with muzzle velocity of not more than 1,400 feet per second
– e.g. revolver, pistols
■ High Power Firearm
– firearms with muzzle velocity of more than 1,400 feet per second; usual
muzzle velocity is 2,200 to 2,500 feet per second or more
– e.g. military rifle
In terms of velocity:
■ Velocity of a projectile or bullet is usually measured in ft/s or m/s. The two most
common descriptions of velocity are high and low velocity relating to rifle (>2,500
ft/s) or handgun (<1,000 ft/s). These two arbitrary numbers cover the majority of
handgun and rifle calibers but leave projectiles traveling in the 1,000–2,500 ft/s
open for interpretation as to whether they are truly low or high velocity by definition.
In terms of wounding power:
■ In ballistics, the wounding power of a bullet is due to the mass (weight) and its
velocity, with the velocity playing a very important role
■ Tissue damage of a bullet of a very high velocity is very much greater than those
with much less velocity.
■ The damage caused by a bullet with impact velocity similar to muzzle velocity is
greater than when the impact occurred at a reduced speed after the bullet has
travelled a distance.
■ Low velocity, less severe
– Less than 1000 ft/sec
– Less than 230 grams
■ High velocity, very destructive
– Greater than 2000 ft/sec
– Weight less than 150 grams