Assignment Block VII

BLOCK 7

Musculoskeletal
System
Topics

STUDENT GUIDE BOOK

BRAWIJAYA UNIVERSITY
FACULTY OF MEDICINE
MALANG
2010
 Topic 1 : Anatomy and Physiology

Topic overview

This topic have four subtopics present anatomy and physiology aspect related to
patology problem and basic knowledge prior to medical student.
Subtopic 1 : Osteology and arthrology
Subtopic 2 : Anatomy of upper extremity
Subtopic 3 : Anatomy of lower extremity and spine
Subtopic 4 : Physiology

HUMAN ANATOMY AND OSTEOLOGY

Overview

The study of human Anatomy is a kind of science considers the structure and organs
which make up human body. Human Anatomy is one of the fundamental subjects in medical
study, and one third of the medical terminology used by medical worker come from
anatomy.

Learning objective
1. To master the common terms of anatomy
2. To manage the classification of bones
3. To manage the structure and function of bones
4. To understand the recent progress in anatomy scientific research
5. To master the important role of human Anatomy in clinical medicine

ARTHROLOGY

Overview
Arthrology is the study of joints.Joints are places where the components of the
skeleton meet. Often it is bone to bone (ex; humerus to scapula) but it can also be bone to
cartilage (ex; ribs to costal cartilage) or tooth to tooth socket. Joints are classified by two
criteria: structure and function.

Learning objective
1. To manage the classification of synovial joints
2. To master the structure of synovial joints
3. To master the accessory of synovial joints
4. To manage the movement of joints
5. To manage the type of synovial joints
UPPER EXTREMITIES

Overview

The superior extremities is associated with the lateral aspect of the lower portion of
the neck. It is suspended from the trunk by muscles and the sternoclavicular joint. Based on
the position of its major joints and component bones, it is divided into some region , those
are pectorals, deltoid, and scapulars region which also known as the shoulder, brachii region
(arm), antebrachii region (forearm), and manus region (wrist and hand).
The superior extremities is used for a broad range of both powerful and subtle actions. It
therefore has an especially complex array of muscle. According to their functional
relationships, muscles of the superior extremities divided into muscles that act on the
shoulder girdle, those that act on the humerus and shoulder joint, those that act on the
forearm and elbow joint, extrinsic (forearm) muscles that act on the wrist and hand, and
intrinsic (hand) muscles that act on the fingers.
Besides the muscles, in this sub module we also learned about the nerves that give
innervations to the muscle, the blood supplies , the lymphatic system and several special
structures which has a clinical importance such as the axilla, the fossa cubiti, and the carpal
tunnel.

Learning Objectives :

Upon completion of this module this module, the students should be able to :

1. Name the muscles with their nerves that act on the shoulder girdle, shoulder, elbow,
wrist, and hand.
2. Relate the actions of these muscles to the joint movements
3. Describes the structure of the shoulder and the elbow joint.
4. Explain the innervations of the superior extremities
5. Explain the blood supply of the superior extremities
6. Explain the lymphatic system of the superior extremities
7. Explain the structure and contents of the axilla
8. Explain the structure and contents of the fossa cubiti
9. Explain the structure and contents of the carpal tunnel

LOWER EXTREMITY

Overview

The Extremitas inferior (lower limb) is the part of human body that connected to the
trunk by the girdle. It is separated from the abdomen, back, and perineum by a continuous
line.
The Extremitas inferior have the function to support the body weight, with minimal
expenditure of energy. When standing erect, the weight of body is transmitted to the limb
via pelvis, where the center of gravity is anterior to the edge of of the SII in the pelvis. A
second major function of the extrimitas inferior is to move the body through space. This
involves the integration of movement of all joints in the extremitas inferior, the movement
of these joint are, flexion, extension, abduction, adduction, rotation, circumduction,
eversion and inversion.All this movement make possible by contraction of the muscle that
moves the bones, that is why in this module we will learn all about bone, muscle, nerve,
blood and lymphatic vessel of extremitas inferior. The function of nerve to maintained
muscle we called innervations, and the function of blood vessel to maintained muscle we
called vascularisation.
Some specials structure will discuss in this modul ie. foramen ischiadicum, femoral sheath,
trigonum femoralis, canalis adductorius, fossa poplitea, etc.
The Extremitas inferior is divided into the regio glutea, regio femoralis regio cruris and the
regio pedis.

Learning Objectives

After finish to learn this module the student should be able to :

1. Describes the margins of extremitas inferior

2. Explains the structure of nerve system that innervates the extremitas inferior.
3. Explains the blood supply of extremitas inferior.
4. Explains the lymphatic drainage of extremitas inferior.
5. Understand structure and the course of fascia lata and their derivatives.
6. Explains the structure and topography of regio glutea.
7. Explains the structure and topography of regio femoralis.
8. Explains the structure and topography of regio cruris.
9. Explains the structure and topography of regio pedis
10. Understand surface anatomy of extremitas inferior.

PHYSIOLOGY

Overview

Body movements are mostly occurred as a result of skeletal muscle activity which
consists of contraction and relaxation. About forty percent of human body is skeletal
muscle. Muscle contraction was initiated by nerve impulse, a traveler action potential, of
motor nervous system which through neuromuscular junction reach muscle fibers.
Student should be able to explain the route of this nerve impulse than initiate the
excitation-contraction coupling, a muscle contraction followed by relaxation stimulated by
action potential when it reach muscle fibers.
There are two types of muscle contraction, isotonic and isometric contraction.
However, skeletal muscle can contract against increasing load by involving more motor unit
called summation of motor unit.
The velocity of body movement can be fast but it is usually occurred in a short time,
because this activity was done by fast twitch muscle which be supplied by anaerobe energy,
while slow movement can stand longer because slow twitch muscles that support this
activity are supplied by aerobe energy.
 Topic 2 : General concept of Musculoskeletal injury
and Upper Extremity Injury

A. Topic overview
This topic presents common upper extremity injury therein fractures and
dislocations in adults and will help you develop a conceptual framework that can be applied
to most musculoskeletal injuries. You will learn principles of management to guide your
decision-making as you assess and treat fractures and dislocation

B. Learning objective

Upon completion of this topic, the student will be able to:

1. Describe a general approach to fracture treatment in chronological order,

2. Differentiate primary and secondary trauma surveys and explain the sequence of
eventsin a primary survey,
3. Assess and classify a musculoskeletal injury,
4. List different methods of fracture treatment and give examples
5. Identified common upper extremity fracture
6. Recognize and anticipate common complications associated with fractures and
dislocations

C. Overview Lecture

Principles of Fracture Management

It is important to understand the biology and stages of fracture healing in order to

planmanagement of bony injuries. In general, the assessment and treatment of fractures
and dislocations can be organized in fivestages:

1. Initial assessment of the whole patient to identify any immediate concerns. This
isparticularly important when treating a patient who has been involved in multiple
trauma(motor vehicle accident or fall from a height). In this setting this assessment is
called theprimary survey.
2. Specific assessment of the injury including imaging studies and documentation
ofassociated skin integrity and neurovascular status.
3. Reduction (re-alignment) of the fracture or the dislocation.
4. Immobilization of the bone or joint (can be done with internal or external means).
5. Rehabilitation of the injury: includes range of motion of joints and strengthening
ofadjacent muscles.

Multiple Trauma – Primary Survey

 Patients who have been multiply traumatized (two common mechanisms are motor
vehicleaccidents and falls from a height) should be rapidly assessed using the Advanced
Trauma LifeSupport (ATLS) algorithm developed by the American College of Surgeons. Full
discussion ofATLS is beyond the scope of this module as it requires knowledge of cardiac,
respiratory,neurological and gastrointestinal systems.
It is important, however, to understand the basic ATLS framework as you are learning
aboutskeletal injuries. This will be described briefly.

During the Primary Survey, the patient is assessed for:

A - Airway patency. Any airway obstruction is corrected. This may involve

simplerepositioning of the jaw, intubation or creation of a surgical airway. The
cervical spine iscontrolled during any airway manipulation to avoid any damage to
the spinal cord.
B - Breathing. Major chest injuries are identified and treated. Chest tubes are
commonlyrequired to drain trapped air (pneumothoraces) or blood collection
(hemothoraces).
C - Circulation. Hemodynamic stability is assessed on an ongoing basis. Hypovolemia
iscorrected with infusion of intravenous fluid and/or blood products.
D - Disability. The central nervous system is assessed using the Glasgow Coma Scale,
a15-point rating system based upon pupillary reaction, best verbal and motor
responses.
E - Exposure/Environmental control. The patient is fully exposed to alow
furtherassessment. The body temperature is monitored and corrected (fluid
warmers, warmsheets) as necessary.

Multiple Trauma – Secondary Survey

If possible, take an AMPLE medical history from the patient/family/paramedics:

A: Allergies
M: Medications
P: Past Medical History
L: Last meal (time of)
E: Events surrounding the injury

Complete a full head to toe, front to back assessment of the patient. Remember: "A
finger and atube in every orifice". Trauma can be sneaky: you don't want to miss a perineal
laceration in a pelvic fracture thus creating a (potentially lethal) open injury. Beware of
healthy youngpeople who maintain an apparently normal blood pressure despite a
tachycardia. Theirhaemodynamic system may collapse in a hurry once they lose the ability
to compensate forhypovolemia with tachycardia and good vascular tone. In a Multiple
Trauma situation, musculoskeletal injury may take a back seat to life threateninginjuries.
However, always be vigilant for the following limb threatening emergency situations:
 open fracture
vascular compromise
compartment syndrome

Assessment of Fractures

When assessing a fracture, it is helpful to classify the fracture in several different

ways. Alsoconsider whether the injury results from a high or low energy force. Review the
case outlinedbelow and think about how you would describe the injury based on the four
categories listedbelow:

Anatomic location
Fracture pattern
Fracture displacement
Associated soft tissue injury

History:

25-year old roofer fell from the top of a ladder while working. He recalls catching his leg
betweentwo of the rungs. He complains of severe pain in his right lower leg.

Physical examination:

An initial assessment in the Emergency room identifies that he has stable vital signs and
aGlasgow coma scale of 15. A head-to-toe assessment reveals tenderness and swelling in
thearea of the right mid-tibia. The skin is intact with no lacerations noted. Although he is
tender in thecalf, the muscles are soft. Distal pulses are palpable and the toes are pink and
warm. He isunable to flex and extend his toes secondary to pain but has normal sensation to
light touch onthe dorsal and plantar aspect of his foot.

Assessment of fractures - anatomic location

Diaphysis
Metaphysis
Epiphysis
Intra/extraarticular
Assessment of fractures – fracture pattern

The fracture pattern is dictated by the type and direction of force that the bone has
been subjected to. High energy injuries (motor vehicle accidents) often cause several
fracture linesresulting in comminuted fractures. Under these circumstances, there is often
considerable softtissue disruption and extensive devascularization of bone which may lead
to delayed healing. Thedirection of the fracture line may be described as transverse, oblique
or spiral.

Assessment of fractures – fracture displacement

Significant fracture displacement will cause deformity that may be obvious on clinical
examination.Displacement is quantified using x-rays. Consider how the fracture has changed
the normalanatomy in terms of the following descriptors:

• Translation
• Changes in length
• Angulation
• Rotation
Fracture displacement – translation

The translation of the two broken ends of the bone is described as a percentage of
normalalignment. This is often termed "apposition". A fracture that is 100% apposed has no
translationwhile a fracture that is 0% apposed has no contact between the proximal and
distal end.

Fracture displacement – changes in length and angulation

A long bone may be abnormally short ( or even absent ), or it may be abnormally

long. When the deformity involves only one of a pair of limbs, the result is limb length
discrepancy

Fracture displacement – rotation

Rotation maybe difficult to assess radiologically, however there are often clinical
clues. Even inchildren, there is little remodeling potential for rotational displacement, so it is
important to identifyand correct early on.

Assessment of fractures – associated soft tissue injury

This is an extremely important feature to assess and document as it will guide
treatment andsometimes establish an urgent timeline. Determine (and document) the
status of the followingstructures early on in your patient assessment:

1. Skin
2. Blood vessels
3. Nerves
Be aware of (or look up) the important neurovascular relationships in the vicinity of the
fractureor dislocation you are assessing. Always perform and document a complete
neurovascularexamination prior to any manipulation of the fracture.

Fracture treatment – general principles

Fracture treatment starts with immediate splinting to avoid further damage to soft
tissues. Thismay be achieved using prefabricated splints or by binding the injured limb to a
pillow or againstanother body part. Fracture treatment involves:

1. Reduction of deformity
2. Maintenance of reduction
3. Rehabilitation

Fracture treatment – reduction

Fracture malalignment and displacement can often be corrected by simple traction

andmanipulation. This is called 'closed reduction'. Open reduction involves surgical incision
anddirect manipulation of the bone ends.
Fracture treatment – maintenance of reduction

Reduction can be maintained in a variety of ways:

Cast

Casts must fit well and be appropriately molded to maintain fixation of a fracture. A
cast may beused to provide definitive maintenance of a closed reduction or to protect a
surgical repair. As theinitial injury-related swelling subsides in the first 10-14 days, a fracture
may redisplace.

Traction

Formerly this was the treatment of choice for femoral fractures requiring long
periods of bedrest inhospital. Traction is rarely used now. traction for treatment of a
femoral fracture.

Percutanous pinning

This child's lateral condylar humeral fracture was treated with open reduction and
insertion ofpercutaneous pins. Pins are used to provide extra stability for a fracture that
may have atendency to displace; they are usually supplemented with a cast.
Internal fixation - plates and screws

AP xray of an ankle fracture internally fixed with plate and screws.

Internal fixation - intramedullary devices

Some long bone fractures are treated by inserting a metal rod into the
intramedullary cavity.Rotation is controlled with the addition of screws. These are preferred
for biomechanical reasonsand because their insertion can often be done without a large
surgical dissection at the fracture site.
External fixation

External fixation may be chosen in an open fracture to minimize implanted metal (which may
perpetuate any deep infection by providing an avascular home for bacteria) while allowing access to
the skin for wound care.

Fracture treatment – rehabilitation

Rehabilitation is an important part of fracture care. The immobilization required to

achievefracture union may cause secondary joint stiffness and muscle atrophy. In extreme
cases,tendons may shorten if casts or splints are applied in an extreme position or
maintained for anexcessive period of time.
Therapeutic exercise must be prescribed and therefore a therapist trained in this
area is usuallyrequired. In the case of injury rehabilitation, the following progression is
usually followed:

1. Range of motion
2. Strengthening
3. Endurance
 4. Task specific activities

Range of motion (ROM) exercise

For a biomechanical system to functional optimally, full joint and soft tissue range of
motion isrequired. This type of exercise is indicated to maintain existing range and to
recover lost rangefollowing immobilization. Stretching is facilitated by tissue heating by
warm up or by the localapplication of heat. Slow sustained stretching overcomes muscle
stretch reflexes and allowscollagen to lengthen permanently. This biomechanical property is
called 'creep'.
Positioning isimportant to prevent contractures when a patient is immobilized.

Strengthening exercise

Strength is defined as the maximum force generated by muscle under certain

specifiedconditions. In general, strengthening is achieved when exercise is performed with
higherresistance and fewer repetitions. Strengthening may be accomplished using isometric
(muscle contraction but no change in muscle length), isotonic (muscle contraction with
constant tension and change in muscle length) or isokinetic (muscle contraction with change
in muscle length at constant velocity) exercies. Isometric exercise is useful when pain is
associated with exercise(arthritis, tendinitis); isotonic exercise is the most widely used
training regime; isokinetic exerciseis often used by athletes who have access to the
specialized training equipment required.

Endurance

Endurance is the ability to produce work over time or the ability to sustain effort. In
general,endurance is achieved with lower resistance and higher repetitions. Endurance
training isindicated for functional task involving many repetitions or sustained activity. This
sort of exerciseresults in increased strength of tendons and ligaments.

Complications of fractures and dislocations

Immediate/Early complications

Complications may occur soon after the fracture ('early') or occur several weeks to months
later('late'). Those identified at the time of the injury are termed 'immediate'. Several
immediateproblems have been alluded to in the section on fracture assessment: injuries to
the skin and softtissues (open fractures) and injuries to the neurovascular structures.
Every patient with a fracture or dislocation should have a detailed examination of these
relatedstructures with early documentation of the findings. Small skin wounds may be
missed if they arecovered with bandages or splints.
Compartment syndrome

Serious early complication associated with long bone fractures orcrush injuries of
any part of an extremity. The calf and forearm are commonly affected. In theselocations,
groups of muscles are encased in thick, restrictive fascia creating distinctcompartments. In
situations of injury, swelling and hemmorhage may increase theintercompartmental tissue
pressure to a level that impairs venous outflow and eventually arterialinflow. Ischemia
results followed by muscle death and fibrosis. Pain out of proportion with theinjury is an
early sign. The pain is made acutely worse by passive stretch of the musclecompartment.
The affected muscle compartment is hard to palpation. Late signs include pallor,paresthesia
and pulselessness. It is important to diagnose compartment syndrome at an earlystage
before these occur. If the diagnosis is suspected, all circumferential casts and
bandagesshould be removed. If symptoms persist, surgical release of the compartment is
done emergentlyin the operating room.
Late complications

If fractures fail to heal in the expected time course (approximately 6 weeks for
typical injuries,recognizing that some anatomic areas such as the tibia routinely take longer)
the injury may betermed a delayed union. If the fracture has not healed by six months it is
termed a non-union.
Non-unions may be the result of insufficient new bone formation (atrophic) or may
exhibitexuberant callus with persistence of the fracture line. The latter (hypertrophic non-
union) is oftencaused by inadequate immobilization of the bone. In situations of delayed or
non-union it isimportant to determine the likely cause.
Healing to identify patient and disease factors which may slow the healing of bone.
A malunion is diagnosed if a fracture heals with significant angular, translational or
rotational

Specific fracture and dislocation of the upper extremity

Colles’ fracture

Defined as a fracture through the flared out distal metaphysis of the radius, more
common in women over 50 years old cause by weakened of the bone by a combination of
senile and post-menopausal osteoporosis.
There is typical mechanism of injury, slip while walking and felldown with open hand with
the forearm pronated.

Clinical Features

The clinical deformity frequently referred to as a “dinner fork deformity” is typical. In

addition to swelling there is an obvious jog just proximal to the wrist due to the posterior tilt
of the distal radial fragment. The hand tends to be radially deviated and the wrist appears
supinated in relation to the forearm.

Radiographic Features

Two main types of Colles fracture can be differentiated radiographically. In stable

type there is one main transverse fracture line with little cortical comminution. In unstable
type there is gross comminution and also marked crushing of the cancellous bone.

Treatment

Undisplaced fracture require only immobilization in a below elbow cast for four
weeks. Displaced fracture can usually be well reduced by closed manipulation under
anaesthesia, but the major problem is maintenance of reduction. Some case external fixator
needed to maintain reduction.

Complication
 Finger stiffness
Malunion
Residual displacement
Reflex Sympathethic Distrophy of Suddeck

Smith’s fracture

Much less common than the colles fracture, which is referred to as a “reverse colles
fracture”. Occuring predominantlyin young men, this fracture caused by a fall or blow on the
back of the flexed wrist and hence is a pronation injury.
The fracture line is transverse and may enter the wrist join. Distal fragment
dispalaced anteriorly. Reduction requires strong supination of the wrist and an above elbow
cast is usually required during the six week immobilization to maintain the position of
supination.

Fractures of the shaft of the radius and ulna

The shaft of radius and ulna have a relatively small cross section, are composed of
dense cortical bone and covered by rather thin periosteum. For this reason fractures of the
forearm bones are much more likely to be displaced in adult than in children, consequently
they tend to be more unstable and they heal much more slowly than children.
Closed reduction of both fractures may be possible using traction and varying
degrees of pronation or supination. In general, fractures of the distal third are most stable
in pronation, those in middle third are most stable in the mid position and those in the
proximal third are most stable in supination.
Open reduction is usually required for fractures of both bones of the forearm in adults,
either as primary treatment or as a secondary treatment after failure of closed reduction.

Galeazzi fracture dislocation

Displaced fracture of the distal third of of the radial shaft are not common but when
they occur they are associated with complete disruption and dislocation of the distal
radioulnar joint. In this injury, which is usually sustained by young adults, the distal
fragment of the radius is tilted posteriorly.
The optimum form of treatment for the Galeazzi fracture dislocation is open
reduction and internal fixation of the radius. When the radius is perfectly reduced so also
dislocation of the distal radioulnar joint.
Most complication occur are malunion and delayed union.

Monteggia fracture dislocation

An angulated fracture of the proximal half of the ulna is invariably accompanied by a

dislocation of the proximal radioulnar joint. Thus, radiographic examination for fracture in
the forearm should always include both the wrist and elbow lest a fracture dislocation be
overlooked.
 In the common type of Monteggia fracture dislocation, a hyperextension and
pronation injury produce a fracture of a proximal half of the ulna with anterior angulation
and anterior dislocation of the proximal radioulnar joint.
Monteggia fracture dislocation in adults are best treated by open reduction and
internal fixation. In addition its usually necessary to perform repair of the annular ligament.

Posterior dislocation of the elbow

There are two possible mecahism of this fairly common injury : a fall on the hand
with the elbow slightly flexed or a severe hyperextension of the elbow. The distal of the
humerus is driven forward through anterior capsule as the radius and ulna dislocate
posteriorly. The brachial artery and median nerve may also be struck by distal end of the
humerus.

Clinical Features

The grossly swollen is held in position of semi flexion, the olecranon is readily
palpable posteriorly. Radiographic examination is essential, however, not only to confirm
the clinical diagnosis but also to detect any associated fractures.

Treatment

Reduction of the dislocation is readily accomplished by applying traction to the

flexed elbow through the forearm, which is then brought forward. The reduced elbow is
then flexed above the right angle to reduce tension on the torn anterior soft tissue and
immobilized in cast for three weeks.

Complication

Elbow stiffness
Median nerve injury
Brachial artery injury

Fractures of the shaft of the humerus

The common mechanism of injury is a direct blow, in which case the fracture tends
to be transverse or communitive. Indirect blow is more likely to produce a spiral fracture.
Must be remembered that the humeral shaft is a common site for metastases in the adult.
The humerus like the femur being surrounded by muscle, has a fairly thick
perioteum, and consequently fractures of the humerus usually unite well and rapidly unless
the racture has been overdistracted. The proximity of the radial nerve as its winds around
the midshaft of the humerus accounts for the high incidence of radial nerve injury
associated with fracture at this level.

Cinical Features
 Flail arm which the patien tries to support with the opposite hand. A radial nerve
lesion should always be sought and its presence or absence recorded at the time of the
initial asessment. The arm should be splinted before radiographic examination is carried
out.

Treatment

Fracture of the shaft of the humerus respond well to closed treatment, the aim of
which is to obtain and maintain reasonable alignment without rotational deformity. The
reduction does not need to be perfect and even side to side apposition with slight
shortening is acceptable. One indication for open reductionand internal fixation is
coexistent injury to the brachial artery.

Complication

Radial nerve injury

Delayed union
Non union

Dislocation of the glenohumeral joint

The shoulder joint depedent for its stability on the joint capsule and surrounding
muscles. The glenoid cavity, being small in relation to the head of the humerus, provides
little bony stability. The most sequela after injury of the shoulder is instability. Type of
dislocations are anterior dislocation, medial dislocation (subcoracoid) and rarely posterior
dislocation.

Anterior dislocation

An injury predominantly of young adults, caused by forced external rotation and

extension of the shoulder. The humeral head is driven forward and frequently avulses the
cartilaginous glenoid labrum (Bankart lesion)
Patient is immediately aware that something has “given away” and is unable to use
his arm which he tends to support with his opposite hand

Treatment

The dislocation should be reduce as soon as possible by any one of three manuever.

1. Stimpson manuever that patient lying down at the edge of the table and injured arm
hanging over the padded table edge.
2. Hippocrates manuever that surgeon apply longitudinal traction to the injured arm
and put local pressure with his unshod foot in the patient axilla
3. Kocher manueverthat patient reduce under general anaesthesia with exo and endo
rotation manuever of the patient shoulder.

Complication
 Recurent dislocation
Axillary nerve injury

Clavicle fracture

The common site is the middle third of clavicle and the lateral fragment is usually
pulled inferiorly and medially by weight of the shoulder and upper limb

Treatment

Since fracture of the clavicle heak well and perfect reduction is not essential, closed
manipulation is usually satisfactory. Both shoulder are pull back as far as possible.
Topic 3 : Lower extremity and spine injury

A. Topic overview
This topic presents common lower extremity injury therein fractures and dislocations
in adults and will help you develop a conceptual framework that can be applied to most
musculoskeletal injuries. You will learn principles of management to guide your decision-
making as you assess and treat fractures and dislocation

B. Learning objective

Upon completion of this module, the student will be able to:

Describe a general approach to spinal injury management in chronological order,

Assess and classify a spinal injury,
List different methods of treatment and give examples
Identified common spinal column and spinal cord injury
Recognize and anticipate common complications associated with spinal injury
Describe a general approach to fracture treatment in chronological order
Identified common lower extremity fracture
Assess and classify fracture and dislocation of lower extremity
List different methods of fracture treatment and give examples
Recognize and anticipate common complications associated with fractures and
dislocations of lower extremity.

C. Overview Lecture

PELVIC FRACTURE

The pelvis is a ring structure made up of three bones: the sacrum and two
innominate bones. The three bones and three joints composing the pelvic ring have no
inherent stability without vital ligamentous structures. The strongest and most important
ligamentous structures occur in the posterior aspect of the pelvis. These ligaments connect
the sacrum to the innominate bones. The stability provided by the posterior ligaments must
withstand the forces of weight bearing transmitted across the sacroiliac joints from the
lower extremities to the spine ( Browner 2003, Koval 2006 )
The pelvis is the key link between the axial skeleton and the major weight-bearing
locomotive structures, the lower extremities. The forces resulting from activities such as
sitting and ambulating are transferred through its bony structure to the spine. Major
structures of the vascular, neurologic, genitourinary, and gastrointestinal systems pass
through or across its ring ( Koval 2006).
Fig.1a. Pelvic Ring Fig.1b. major structure inside pelvic cavity (Browner 2003)

Fig. 1c. Young and Burgess classification. ( Young, J.W.R.; Burgess, A.R. 1987.)
A, Lateral compression force. This injury is stable.
B, Anteroposterior (AP) compression fractures. This fracture is rotationally unstable.
C, A vertically directed force or forces at right angles to the supporting structures of the pelvis leading to
vertical fractures in the rami and disruption of all the ligamentous structures. This injury is vertically and
rotationally unstable .
( from Young, J.W.R.; Burgess, A.R. Radiologic Management of Pelvic Ring Fractures. Baltimore, Munich, Urban
& Schwarzenberg, 1987.)

Physical examination ( Browner, 2003, Koval, 2006, Bucholz , 2006 )

Initial evaluation of pelvic trauma patients should follow guidelines established by

the American College of Surgeons and begins with the ABCs (airway, breathing, and
circulation). The goal of this primary survey is to identify and begin treatment of
immediately life-threatening injuries .
The secondary survey, the pelvis is assessed by palpation at the anterior superior
iliac spines. The examiner gently compresses the iliac wings together to expose instability in
internal rotation, and then gently pulls the wings apart to expose instability in external
rotation. This examination should be performed only once, because fracture motion can
disturb the pelvic hematoma and may lead to further bleeding.
 The skin, including the perineum, should be examined for lacerations. Scrotal or
labial hematomas are often noted.
All trauma patients should undergo digital rectal examination and, in females, an
examination of the vagina. In patients with a pelvic fracture these examinations are critically
important, because bony fragments may lacerate through the rectal or vaginal walls,
creating an open fracture that cannot be appreciated externally.
The urethral meatus should be inspected for gross blood. If blood is seen, the urinary
tract must be explored radiographically for injury ordinarily with a retrograde urethrogram,
followed by a cystogram if no urethral trauma is found.
Neurologic examination must included in pelvic fracture.

Imaging

- Plain X-Rays
An anteroposterior (AP) x-ray of the pelvis should be included in the initial
radiographic examination of patients with multi trauma . The clinician must be aware
that the pelvic ring as seen on the initial x-ray is simply a snapshot of one moment in
time. Fractures noted on the AP x-ray should prompt further investigation of the
pelvis with inlet and outlet views .
- Computed TomographyComputed tomography (CT) is used to gather more
information about fracture anatomy and may also reveal the size and location of a
pelvic hematoma.

Fig 2. Plain x-ray of pelvis AP, and CT of pelvis

Treatment ( Browner 2003, Koval 2006, Bucholz 2006 )

Treatment should be start at the prehospital phase. Paramedics must be able to

recognize the potential for an unstable pelvic ring injury from the history, characteristics of
the crash, and physical examination. If such injury is present in the prehospital situation,
application of a stabilization splint such as a pneumatic antishock garment (PASG), vacuum
splint, or the newer pelvic stabilization belts may be lifesaving.
Stabilization of a disrupted pelvis can be handled in several ways.

1. PASG.This inflatable garment is placed over the lower extremities and around the
abdomen and inflated until blood pressure is stabilized. The garment works by
increasing peripheral vascular resistance. Once the garment is applied in the
emergency situation, it should not be removed until the patient is receiving fluids
in the operating room so that the bleeding can be controlled surgically.
 2. Pelvic C-clamps. These clamps can be applied by a trained physician in the
emergency department. A pelvic C-clamp is applied to the posterior of the pelvis
at the level of the sacroiliac joints

Fig 3a . Application of in Pelvic C-clamps pelvic fracture

3. Anterior external fixation frame.

Beside act as a temporary pelvis stabilizer, C-clamps and external fixation decrease
the volume of pelvic cavity and give ‘tamponade effect’ to reduced intrapelvic
haemorrhage.

Fig 3b . Application of external fixation in pelvic fracture

For definitive stabilization of pelvic fracture, shoud be done several days later , after
the patient’s condition are stable .

Complication ( Browner 2003, Koval 2006 )

1. Hemorrhage is the most dangerous condition associated with pelvic fractures .

Bleeding after pelvic fracture can be life threatening. Sources of hemorrhage include
bleeding fracture surfaces, torn small arteries and veins, and disrupted major vessels
2. Deep vein thromboses
3. Injury to the gastrointestinal tract can occur from laceration caused by fracture
fragments at the moment of injury. These injuries usually involve the anus or
rectum, and often have extension into the perineum
4. Urologic trauma is more common in men than in women, because of the longer
male urethra, which is thus more susceptible to injury
5. Neurologic Injury. Lower-extremity motor function, sensory function, bladder and
bowel control, and sexual function can all be affected .
Hip Dislocation

Hip dislocations result from high-energy trauma, most commonly in a traffic

accident. Usually occurs when someone seated in a vehicle are thrown forward, striking
knee against the dashboard or static object. Severe associated injuries are common and
usually involve the craniofacial, chest, abdominal, or musculoskeletal systems.
Hip dislocations are classified according to the direction of dislocation: posterior,
anterior and central types. Anterior hip dislocations result from abduction and external
rotation. Posterior hip dislocation is resulted from an axial force applied to the flexed knee.
Approximately 90% of hip dislocations are posterior. Central type is result from direct blow
over greater trochanter.
In a posterior dislocation, the leg is short and lies adducted, internally rotated and
slightly flexed. In anterior dislocation, the leg is abducted, externally rotated and slightly
flexed without shortening. In central type, the leg lies in normal position. However, if the
ipsilateral femur is fractured, the clinical features can be missed.
The hip dislocation can be diagnosed on an anteroposterior (AP) pelvic radiograph.
With an anterior dislocation, the femoral head appears larger in diameter than the
contralateral side because of the increased distance of the femoral head from the
radiographic cassette; with a posterior dislocation, the femoral head will appear smaller
than the contralateral side. In central dislocation, the head of femur displaced medially , and
the acetabular floor are fractured.
Femoral artery and nerve injuries are uncommon and are associated with anterior
dislocations. Sciatic nerve injury occurs in approximately 10% of posterior dislocations.
Osteonecrosis (ON) can occur up to 5 years after injury(OKU). The risk of ON will increase
with a delay of more than 6 to 12 hours before reduction are 40 % (Appley). Bone
weakening occurs as result from ON, and the head of femur will collapse. After collapse of
head of femur, hip joint surface become incongruent and the secondary osteoarthritis
followed. Beside ON, secondary arthritis also is due to cartilage damage at the time of
injury, and presence of retained fragment in the joint.
For posterior and anterior dislocation prompt reduction under general anesthesia is
mandatory. In the vast majority, the reduction usuallystable. In central dislocation, closed
reduction should be attempted closed. But in presence of large displaced acetabular
fractures, the operative treatment must be considered.
Fig. 4. Anterior dislocation of hip with proximal femur fracture associated with proximal femoral fracture( left
), posterior dislocation of hip (right )

Hip fracture ( femoral neck and intertrochanteric fracture )

The incidence of hip fracture increases with increasing age, doubling for each decade
beyond 50 years of age. Women are more commonly affected by a ratio of 2.5 to 1. The
proximal femur are also a common site for metastatic lesions. For this reason, in eldery
patients with hip fracture, tumors work up must be a part of investigation.

Imaging Studies

Most hip fractures can be identified on standard pelvic radiographs, but occult hip
fractures require additional imaging studies like MRI .

Treatment Principles

The primary goal of fracture treatment is to return the patient to the prefracture
level of function. There is near universal agreement that in patients who sustain a hip
fracture, this can best be accomplished with surgery. Non surgical management resulted
excessive rate of medical morbidity and mortality, as well as malunion and nonunion.

Femoral Neck Fractures

The blood supply to the proximal end of the femur, dividing it into three major
groups: (1) an extracapsular arterial ring located at the base of the femoral neck, (2)
ascending cervical branches of the arterial ring on the surface of the femoral neck, and (3)
arteries of the ligamentum teres. Fracture of the neck femur will interfere the head femur
vascularization, and the head prone to get osteonecrosis (ON).

Fig 5. Head femur vascularization

Impacted and nondisplaced femoral neck fractures should be internally stabilized

using multiple screws. Treatment of displaced femoral neck fractures remains controversial.
Most authors advocate closed or open reduction and internal fixation in younger active
patients, and primary prosthetic replacement in older or in less active patients.
Nonunion and osteonecrosis (ON) are the most common complication. Non union
are caused by lack of periostium at neck of femur, and in other side, presence of synovial
fluid which can prevent haematoma formation. ON is due to impairment of blood supply to
the head of femur.

Fig 6 : fracture neck of femur after internal fixation ( right ), and after prosthetic replacement
Intertrochanteric Fractures

Intertrochanteric fractures occur with approximately the same frequency as femoral

neck fractures. This fracture is extracapsular, so the capacity of healing are better compared
to neck of femur fracture.
The leg is shorter and externally rotated and patient cannot lift her or his leg. Pelvis
x-ray can prove this fracture. The fracture line run along intertrochanteric line.
Malununion in varus and external rotation are common in patient are treated non
operatively. Open reduction and internal fixation using dynamic hip screw are the prefered
method in treatment of this fracture.

Fig 7: Intertrochanteric fracture (left), open reduction and internal fixation using Dynamic Hip Screw (
right)

Femoral Shaft Fractures

In most cases, patients with a femoral shaft fracture have sustained high-energy
trauma. Associated occult injuries are not uncommon. Therefore, examination of the
musculoskeletal and other system should be included. The Advanced Trauma Life Support
evaluation sequence must be performed at first time, and resuscitation must be done if the
life threatening problems are present.
 The leg is rotated externally and may short and deformed. The thigh is swollen and
bruised. Sometimes patient come with splint at injured limb. Reassesment of fracture and
its complication must be performed by removing the splint; and more convenient splint
must be reapplied soon after the diagnosed is established.
Early complication of femoral fracture are fat embolism, thromboembolism, and
vascular injury; and late complication are delayed or non union, malunion and joint stiffness.

Treatment

Nonsurgical Treatment. ( 3R : Reduced-Retain-Rehabilitation)

The fracture must be reduced first if displacement are unacceptable. Reduction
usually maintain by traction ( skin or skeletal traction ). The period of traction usually until
clinical union ( 4 – 6 weeks ), and followed by hemispica cast or cast brace application.
Although this treatment method has a high fracture union rate, it has long list of problems,
such as prolonged recumbency and hospital stay, knee stiffness, and fracture malunion,
preclude its general use.

Fig 8. Buck’s skin traction

Fig.9 Skeletal traction

Fig 10. Hemispica

Some residual deformity is almost inevitable in non operative treatment, but up to 2

cm of shortening, 10 degrees of angulation and 15 degrees of anterior bowing can be
toletated without significant loss of function.
The traction is used mainly for the temporary stabilization if definitive surgical
fixation must be delayed. Nowadays the using of traction as a definitive treatment is very
few. These include the lack of equipment or expertise to perform surgical fixation, systemic
contraindications to anesthesia, or a local contraindication, such as infection at the surgery
site.

Surgical treatment.
Nowadays, surgical treatment are more popular in treatment of femoral fracture.
With surgical treatment, the fracture fragment can be reduced properly. And then stable
fixation can be applied by using plate and screw or ( locked ) intramedullary nail. In some
cases with severe soft tissue damage or in multitrauma patients , the external fixation can
be considered as a temporary or definitive treatment . For open fracture, surgical
debridement, antibiotic and anti tetanus administration must be perform early. Internal
fixation or external fixation must be applied based on fracture personality.

Supracondylar fractures

The supracondylar fracture of femur occur in a bimodal age distribution. In the

younger, predominantly male patient group, the fractures result from high-energy trauma
with a greater incidence of intra-articular damage and associated systemic or skeletal
injuries. Fractures in the elderly, predominantly female group are low-energy injuries, often
preceded by radiographic evidence of generalized osteopenia or other "age-related
fractures" of the hip, spine, or pelvis.
Knee stiffness and osteoarthrosis are common sequelae of this injury. Fracture
management depends on many factors, including the fracture type, bone quantity, and the
patient's overall medical condition. Although treatments vary, both patient groups will
benefit from restoration of joint congruity and the institution of early knee motion.

a. b. c.

Fig 11: a. Supracondylar fracture, b. condyle fracture, c. intercondylar fracture

Treatment
It must be understood that these fractures are difficult to manage in traction and
require constant vigilance to minimize the significant risks of malunion and knee stiffness as
well as the potential complications of recumbency.Patients with displaced fractures who
present with contraindications to surgical intervention are the main candidates for this
treatment method. A variable period of traction is usually followed by mobilization using a
cast brace.
Surgical treatment must be considered in supracondylar fracture, especially fracture
with intra articular extention. The goal of surgery for this fracture are to get anatomical
reduction of intraarticular fracture, which can reduced the risk of post traumatic arthritis ;
and to provide early knee joint exercise to prevent knee stiffness because of intraarticular
adhesion.

Knee Ligament and Meniscal Injuries

The anterior cruciate ligament (ACL) is the primary restraint to anterior translation.
Approximately 50% of patients with ACL tears also have meniscal tears. The lateral meniscus
is torn more frequently than the medial meniscus in acute ACL injuries, but in chronic ACL
tears the medial meniscus is more commonly involved.
 MCL injury remains the most common isolated knee ligament injury, and it also is the
injury most commonly associated with ACL injury. Fortunately, it does not require surgical
treatment in most patients.
The posterior cruciate ligament (PCL) is a vertically oriented ligament that is
approximately 1.5 times as strong as the ACL. It is the primary restraint to posterior
translation of the knee and is important in knee proprioception.

History and Physical Examination

The history remains a key factor in diagnosing knee ligament injuries through
identification of the mechanism involved. Most ACL injuries are associated with a
hemarthrosis that occurs within the first few hours after injury. An audible pop is noted by
approximately half of the patients sustaining an ACL injury.
Mechanisms of PCL injury include a fall onto the ground with the foot plantarflexed
(striking the tibial tubercle), a direct posterior blow to a flexed knee (such as a dashboard
injury), hyperflexion, hyperextension, severe varus or valgus loads after failure of the
collaterals, or knee dislocations.
The examination of the knee with acute ligament injury often is difficult within the
first several hours, because swelling and pain cause guarding by the patient.
Special test for investigating the knee ligament injury are :
1. ACL injury : Lachman test, Pivot shift test and anterior drawer test
2. PCL injury : posterior drawer test, posterior shagging.
3. MCL injury : valgus tests in extention ; and 30 degree flexion.
4. LCL injury : varus test in extention ; and 30 degree flexion.

Imaging

Routine radiographs are indicated in all patients with a traumatic hemarthrosis or

chronic ligamentous deficiency. Knee anteroposterior (AP) and lateral views are performed
to identify a tibial spine fracture , avulsion of ACL or PCL. But plain x-ray unable to define the
ligament rupture
Magnetic resonance imaging (MRI) can be helpful to define of knee soft tissue injury,
especially when the clinical examination is limited because of pain and swelling and to
identify associated injuries to the menisci and articular cartilage.

Treatment

The main problem in knee ligament injury are joint instability, that can lead to early
joint osteoarthritis. The treatment of ligament injuries should be tailored to the individual
patient’s. Factors to be considered in determining treatment include activity level, amount
of time involved with high demand activities, willingness of the patient to modify these
activities, laxity of the joint, and presence of associated ligament, articular cartilage, or
meniscal injuries.
Tibial Plateau Fractures

Injuries to the tibial plateau result from a medially or laterally directed force or an
axial compressive load. The resulting fracture pattern is a reflection of the forces involved.
When a plateau fracture is suspected, the physical examination should thoroughly
document the neurovascular status, especially in suspected cases of fracture-dislocation.
Plateau fractures associated with fracture extension into the tibial diaphysis may
also be associated with acute compartment syndrome secondary to hemorrhage and edema
of the involved compartments. Severe contusion and internal degloving occur particularly
in high-energy injuries. Even in the absence of open fractures, the contused soft tissues may
be in jeopardy because of fracture instability or associated severe swelling.
Routine radiographic evaluation consists of AP and lateral views supplemented with
2 oblique projections and a "plateau view." CT scansprovide additional information
regarding the cross-sectional anatomy of the fracture. The use of magnetic resonance
imaging (MRI) has been shown to be superior in assessing associated soft-tissue injury, such
as meniscal and ligamentous disruptions, but is not routinely used on an emergent basis.
Arteriography should be considered for those high-energy fracture patterns in which an
intimal tear is suspected by clinical presentation.
The Schatzker classification is used to group fracture. Schatzker types I, II, and III are
typically the result of a lower energy mechanism of injury, as opposed to the more complex
Schatzker types IV, V, and VI fractures, which result from a high-energy mechanism of injury.

Fig 12: Schatzker classification for tibial plateu

Treatment

Tibial plateu is an intra articular fracture, Any attempt, should be directed to get the
anatomical reduction of joint surface ; to prevent early joint degeneration. For this purpose,
in displaced fracture, operative treatment are the best way to restore the joint surface and
to get stable fracture. In the same time , any meniscal injury can be treated . For
undisplaced fracture, non operative treatment should be considered, by applying long leg
cast.

Tibial Shaft Fractures

The tibia is the most commonly fractured long bone; frequently, these injuries are
caused by high-energy trauma. The tibia is subcutaneous throughout its length, with a
relatively poor blood supply.
Fractures can be classified by anatomic location, described as either proximal, mid or
distal third ; or based on fracture configuration such as simple, butterfly and comminuted.
The extent of soft-tissue injury is a predictor of outcome. As the severity of the soft-
tissue injury increases so does the incidence of nonunion, malunion, infection, and the
likelihood of a limited functional outcome.
Fracture of distal third fractures have demonstrated a higher incidence of delayed
union, malunion, and nonunion. It is evident that simple fractures have the best prognosis.
Comminuted or crush injuries have a significantly worse prognosis.

Treatment

It is generally accepted that the treatment standard for stable closed tibial shaft
fractures is closed reduction with the application of a long leg cast followed by functional
bracing ( Sarmiento patellar-tendon bearing cast ) with early weightbearing. Following
closed reduction, alignment should be maintained such that there is < 1 cm of shortening
with angulation < 5° and rotational deformity limited to 5° or less.
Internal fixation for tibia can be used for tibia are intramedullary (IM) nailing, plate.
Internal fixation after severe soft-tissue injury should be cautiously considered because of
possible complications, such as tissue loss and infection. Relative indications for plate
fixation include those tibial shaft fractures that have fracture extension into the ankle or
knee joint,
For open tibial fractures, external fixation can provide stabilization and adjunctive
wound care without foreign-body implantation. The relative indication are in multitrauma
cases. External fixation minimizes additional disruption of the soft-tissue envelope or the
vascularity of the fracture fragments
 a. b.
Fig. 13a. Tibial and fibular fracture with non operative treatment ( closed reduction and immobilized with long
leg cast ) . b. Sixth month after reduction.

a. b.
Fig 14a. Tibial fracture treated with long leg cast . b. Sarmiento patellar-tendon bearing cast

Ankle Fractures

Ankle trauma accounts for between 3% and 12% of all emergency room visits.
Although most patients with ankle injuries have radiographic examinations, fractures are
diagnosed in only 7% to 36%. The Ottawa clinical decision rule was developed to guide
physicians in their use of radiographs for evaluation of acute ankle injuries. This rule states
that an ankle radiograph is needed only if the patient has pain near the malleoli and one or
more of these findings: (1) age 55 years or older, (2) inability to bear weight immediately
after the injury and for 4 steps in the emergency department, or (3) bony tenderness at the
posterior edge or tip of either malleolus. The rule does not apply in the presence of
deformity with a clinically obvious fracture, and it may be unreliable in patients with altered
mental status, intoxicated patients, or those with language difficulties.
Stable, nondisplaced bimalleolar and trimalleolar fractures can be treated with cast
immobilization ( below knee cast ). Weekly radiographs are necessary for atleast 4 weeks to
detect loss of reduction in the cast. Weightbearing depends on the surgeon's judgment, but
usually can begin at 4 to 6 weeks.
Ankle fractures are intraaticular fracture. For this reason, in displaced fractures - of
both the medial and lateral malleoli - are best treated with open repair to reestablish a
congruent joint surface.
Fig. 15. Ankle fracture with dislocation.

ADULT SPINE TRAUMA

Introduction

In Syaiful Anwar Hospital there are approximately 50 – 70 new spinal injuries

reported yearly. Of these injuries, half are located in the cervical region, and approximately
75 % will result in a spinal cord injury with some degree of neurologic deficit.
There is a bimodal age distribution, in young adult, the spinal injury mostly caused by
high energy trauma , for this reason the associated injuries (such as intra abdominal organs,
intra thoracal haemorrhage ) must be considered. In elderly, because of bone weakening
(osteoporosis, malignancy ) fracture mostly result from low energy trauma.
Trauma in spine will produced spinal column or spinal cord or combined injuries. So
treatment must be addressed to reconstruct spinal alignment and stability , to protect
neural element and prevent further injury.

Anatomy

The spine is a mechanical entity. Its most important function is to protect the spinal
cord from damage while allowing physiologic motions at each vertebral level. Many times,
especially in disease states or in the case of trauma, vertebral motion may produce
impingement on the spinal canal, resulting in elevated pressure on the spinal cord.
Fig 1. Spine and its surrounding structure at thoracic level

Spinal Column Injury

In 1984 Denis developed a three-column concept in thoracolumbar injuries .

- The anterior column contains the anterior longitudinal ligament, the anterior half of
the vertebral body, and the anterior portion of the annulus fibrosus.
- The middle column consists of the posterior longitudinal ligament, the posterior half
of the vertebral body, and the posterior aspect of the annulus fibrosus.
- The posterior column includes the neural arch, the ligamentum flavum, the facet
capsules, and the interspinous ligaments (Posteroligamentous Complex-PLC ).

Supraspinosus
Superior endplate
Interspinosus ligament

Procesus spinosus
Inferior endplate
Posterior longitudinal ligament
Posterior wall

Annulus fibrosus
Anterior
Longitudinal
Intervertebral disc Ligament

Fig 2. Three Column Theory

According to Dennis, mechanical instability in vertebral column will happened if two or

more column are failed.
White and Panjabi define clinical instability of vertebral column as the loss of the ability
of the spine under physiologic loads to maintain its pattern of displacement so that there is
no initial or additional neurological deficit, no major deformity, and no incapacitating pain.

( Browner BD, Jupiter JB,Levine A M , Trapton PG, Skeletal Trauma, 1998, p. 967, W.B.Saunders Company)
Based on these theory, Dennis defined 4 major type of vertebral column injury.

1. Compression Fractures
Compression fractures involved of anterior column of the vertebral body. Unlike
burst fractures, there is no involvement of the posterior vertebral body wall. Most
compression fractures are thought to be stable.

Fig 4a.

Anterior column
fracture

Fig. 4b 4c.

Fig. 4a. Anterior column fracture

Fig. 4b. Classification of compression fracture. Type A involves both endplates, type B involves
the superior endplate, and type C involves the inferior endplate. In type D fractures,
there is a compression fracture of the anteriovertebral body.
th
Fig 4c. X-ray of compression fracture of Lumbar 4

1. Burst Fracture

This fracture are typically a result of an axial compressive force with or without a
flexion/distraction component. Burst fractures show comminution of the vertebral
body with involvement anterior and middle column ( including the posterior wall
 cortex). Most of these fractures (but not all) will show some degree of fracture
fragment retropulsion, and produced spinal canal stenosis (narrowing of spinal
canal).

Anterior Column
fracture
Posterior
wall fracture
Middle Column
fracture

Fig 5 a.

Fig. 5b. 5c.

Fig. 5a. Anterior and middle column ( with posterior wall fracture )
Fig 5b. Classification of burst fracture : Type A involves fractures of both endplates, type B involves
fractures of the superior endplate, and type C involves fractures of the inferior endplate.
Type D is a combination of a type A fracture with rotation. Type E fractures exhibit lateral
translation.
th
Fig.5c. Lateral X-ray of Thoracal 12 Burst Fracture. Posterior wall fracture ( black arrow )

3. Flexion-Distraction (Seat Belt or Chance Type) Injuries

The characteristic feature of a flexion-distraction injury is primarily tensile failure of
the PLC, facet capsules, and intervertebral disc or bone itself ( posterior and middle
columnsinjury). Injuries may occur through bone alone, soft tissue alone or combined.
Combined lesion are the most common lesion .
 Fig 6a.

Fig 6b.

Fig 6c.

Fig. 6a. Posterior and middle column failure

Fig. 6b. Types A and B occur at one level, either through bone (A) or ligament (B). Type C and D
occur at two levels (motion segments). Type C denotes that the middle column failed
through bone. Type D denotes that the middle column failed through ligament and
disc.
rd
Fig. 6c. Plain x-ray of 3 lumbar fracture ( flexion-distraction injury )

4. Fracture-Dislocations

Fracture-dislocations of the thoracolumbar spine are highly unstable injuries. All

three column are involved, the unique feature of this injury is translational deformity,
which can occur in the sagittal and/or coronal planes.
 Fig 7. Fracture dislocation

Clinical Finding

The conscious patient who is hemodynamically stable may be examined in greater

detail. But it is difficult to assess sensory and motor function in the unconscious or
intoxicated patient.
Inspection and palpation of the entire spine should be performed. The patient is
asked to report the location of any pain on her or his back and all the extremities. and to
move the upper and then the lower extremities to help localize any gross neurologic
deficit. Theextremities are examined for motor and sensory function by nerve root level.
The strength of each muscle is also graded. Physiologic reflex examination also must be
done.
A digital rectal examination for voluntary or reflex(bulbocavernosus) anal sphincter
contraction.
The conus medullaris (upper motor neurons) and cauda equina (lower motor
neurons) sign must be seek in this patient, because this syndrome are emergency in
spine surgery field.

Imaging

Plain radiographs form the basis of examination in all patients, at least

anteroposterior and lateral views are required. Visualization of all seven cervical are
mandatory, because C-7 fractures make up approximately 10% of the fractures of the
cervical spine. Applying traction to the arms in a caudal direction or obtaining a
swimmer's view may be necessary for adequate visualization of C7 or the
cervicothoracic junction.
CT and MRI may be useful together in determining the presence and extent of spinal
column injury. MRI is superior in demonstrating spinal cord pathology and
intervertebral disc herniation. CT is superior to MRI in demonstrating osseous injury (
Levitt )
 Fig 8. CT Scan of vertebral body with burst fracture. Protrution of the fracture fragment are noted (black
arrow )

Fig 9. MRI of thoracacal show the compression of the myelum due to disc prolapse.

Treatment for the vertebral fracture

Non Operative Treatment

The objectives of care of the spinal-injured patient areto have a stable, pain-free
spine, toprevent increasedneurological deficit, and to provide conditions for
theimprovement of neurological deficit. The neurologicaland biomechanical goals are
separate but interrelatedand must be thought of in a parallel rather thana sequential
fashion. Rehabilitation of the patient willbe optimal if these objectives can be met ( R
Hu , Rationale )
Closed treatment options are bed rest, halo apparatus, external orthosis, or cast
(Ersmak). Bed rest for the initial few weeks preceding bracing is an option for severely
unstable injuries. The level of injury serves as a guide for the category of external
orthosis. Casts can be applied in hyperextension to improve kyphosis. Bracing is
continued until bone healing is sufficient for load bearing: 8 weeks in cervical injuries
and 12 weeks in thoracolumbar injuries.
 Fig 9a. 9b.

Fig. 9a. Body cast for thoracolumbar fracture

9b. Minerva cast ( cervico-thoracic cast ) for cervical fracture or high thoracic fracture

Operative Treatment

Operative treatment only considered in unstable fracture. Vertebral fracture are

considered unstable :
1) fracture involved 2 column or more
2) Loss of body height> 50 %
3) Kyphotic angle > 30° 4
4) Multilevel fracture
With operative treatment, the decompression of neural structure and internal fixation can
be performed at the same time. (Garfin S, Blair B, Eismont F, Abitbol J.)

Fig 10 : female 30 years old, with burst fracture with bony compression to the neural structure at
thoracolumbar junction ( left ), decompression laminectomy and posterior stabilization had been performed.

Complication (Fletcher DJ, Taddonio RF, Byrne DW)

1. Urinary tract infection

2. Pneumonia
3. Respiratory failure
 4. Cardiac
5. Decubitus ( pressure sore )
6. Mortality
7. Late kyphotic deformity

Spinal Cord Injury

Anatomy

The spinal cord occupies approximately 35% of the canal at the level of the atlas (C1)
and 50% of the canal in the lower cervical spine and thoracolumbar segments. The
remainder of the canal is filled with epidural fat, cerebrospinal fluid, and dura mater.
The conus medullaris represents the caudal termination of the spinal cord. It
contains the sacral and coccygeal myelomeres and lies dorsal to the L1 body and L1-
2 intervertebral disc.
The cauda equina (literally translated means horse’s tail) represents the motor and
sensory roots of the lumbosacral myelomeres. These roots are less likely to be
injured because they have more room in the canal and are not tethered to the same
degree as the spinal cord..
A reflex arc is a simple sensorimotor pathway that can function without using either
ascending or descending white matter, long-tract axons. A spinal cord level that is
anatomically and physiologically intact may demonstrate a functional reflex arc at
that level despite dysfunction of the spinal cord cephalad to that level.

The bulbocavernosus, a reflex arc that is a simple sensorimotor pathway, can function without using
ascending or descending white matter long tract axons.

Primary spinal cord injury

Primary injury refers to physical tissue disruption caused by mechanical forces.

Contusion: This sudden, brief compression by a displaced structure affects central

tissues primarily and accounts for the majority of primary injuries and is thus
responsible for the majority of neurologic deficits. Contusion injuries are potentially
 reversible, although irreversible neuronal death occurs along with vascular injury
with intramedullary hemorrhage.
Compression: Injury results from decreased size of the spinal canal; it may occur with
translation or angulation of the spinal column, as with burst injuries, or with epidural
hematomas. Injury occurs by:
o Mechanical deformation interrupting axonal flow.
o Interruption of spinal vascularity resulting in ischemia of neurologic
structures.
Stretch: Injury results in longitudinal traction, as in the case of a flexion-distraction
injury. Injury occurs as a result of capillary and axonal collapse secondary to tensile
distortion.
Laceration: This is caused by penetrating foreign bodies, missile fragments, or
displaced bone.

Secondary spinal cord injury

Secondary injury refers to additional neural tissue damage resulting from the
biologic response initiated by the physical tissue disruption. Local tissue elements undergo
structural and chemical changes. These changes, in turn, elicit systemic responses. Changes
in local blood flow, tissue edema, metabolite concentrations, and concentrations of
chemical mediators lead to propagation of interdependent reactions. This pathophysiologic
response, referred to as secondary injury, can propagate tissue destruction and functional
loss.

Neurologic injury classification

Complete spinal cord injury :

- No sensation or voluntary motor function caudal to level of injury in the presence
of an intact bulbocavernosus reflex ( indicating intact S2-S3 and resolution of
spinal shock ).
- Prognosis is extremely poor.
Incomplete spinal cord injury
- Some neurologic function persists caudal to the level of injury after return of the
bulbocavernosus reflex
- The greater the function distal to lesion and the faster the recovery, the better
the prognosis.
It is very important to know anatomy and function of spinal cord, to understand the
clinical symptoms of spinal cord injury.
Many different grading systems are available for describing the degree of spinal cord
injury. There are impairment-based scores (Frankel Scale, ASIA scale, Yale Scale, Motor
index scale) and function-based scales (Modified Barthel Index). The ASIA (American Spinal
Injury Association) impairment scale, which is a modification of the Frankel scale or
classification, is one of the most commonly used scales for evaluating spinal cord injury in
orthopaedic field.
Level of Injury

According to ASIA definitions, the neurologic injury level is the most caudal segment of the
spinal cord with normal motor and sensory function on both sides: right and left sensation,
right and left motor function.

Fig. ASIA chart

ASIA impairment scale :
A. Complete = No motor or sensory function is preserved in the sacral
segment S4-S5
B. Incomplete = Sensory but not motor functions preserved below the
neurological level and includes the sacral segment S4-S5
C. Incomplete = Motor functions is preserved below the neurological level
and more then half key muscles below the neurological level have a
muscle grade less than 3.
D. Incomplete = Motor functions is preserved below the neurological level
and more then half key muscles below the neurological level have a
muscle grade of 3 or more.
E. Normal = motor and sensory normal

An incomplete spinal cord syndrome describes a constellation of neurologic findings

determined by the anatomic location of tissue injury. These include a central cord
syndrome, an anterior cord syndrome, a posterior cord syndrome, and the Brown-Séquard
syndrome .

The central cord syndrome is the most common type of spinal cord injury seen. Patients
with this syndrome usually have motor weakness or paralysis in the upper extremities with
relative sparing in the lower extremities. Functional recovery usually is poor to fair.

The anterior cord syndrome there is damage to the anterior two thirds of the spinal cord
with sparing of the posterior third. Damage to the pyramidal tracts results in loss of motor
function below the level of injury. If the spinothalamic tracts are injured there is loss of
touch, pain, and temperature sensation. Because the posterior cord is undamaged, there is
preservation of vibration and position sense. Functional prognosis depends on the degree of
neurologic deficit (complete or incomplete) as well as the level of injury.

The Brown-Séquard syndrome is a rare spinal cord injury that results in damage to half the
spinal cord. This results in ipsilateral motor weakness and loss of proprioception with
contralateral loss of pain and temperature sensation as well as light touch. This syndrome
has an excellent prognosis for ambulation.
The posterior cord syndrome is the least common spinal cord injury. Because the posterior
columns carry vibration and proprioception, this syndrome is characterized by loss of
vibration sensation and positional sense. There may be sparing of crude touch because of
the anterior location of the anterior spinothalamic tracts. Functional outcome in patients
with posterior cord syndrome is fair.

Imaging Studies
A complete radiologic survey including an anteroposterior (AP) and lateral
radiograph of the entire spine is essential so as not to miss a noncontiguous spinal injury. It
is mandatory to examine all 7 cervical vertebrae as well as the top of the T1 vertebral body
because approximately 10% of cervical spine fractures occur at the C7 level.
At present, magnetic resonance imaging (MRI) has supplanted conventional
myelography with or without computed tomography (CT) as a diagnostic tool in evaluating
cervical cord compression after trauma. MRI allows optimal visualization of cervical soft
tissues and demonstrates intra- or extramedullary and epidural hemorrhage or the presence
of intervertebral disk herniation.
Fig. Plain x-ray of cervical are not showed significant pathology, but from MRI multiple compression of spinal
cord caused by degenerative cervical spondylosis are noted.

Initial Management

The initial management of a patient with a spine and/or spinal cord injury begins at
the scene of the accident. There are 5 generally accepted stages in the initial management
of a spinal trauma patient:
(1) evaluation, (2) resuscitation, (3) immobilization, (4) extrication, and (5) transport.

Patient Evaluation

Evaluation of the accident patient includes a primary and a secondary survey. A

primary survey is undertaken to evaluate for life-threatening injuries as well as injury to the
spinal column. The secondary survey involves a more complete head to toe examination.

Resuscitation and Oxygenation

The resuscitation stage ensures adequate oxygenation of the patient in light of a

possible injury to the spinal cord. Excessive manipulation or hyperextention of the c-spine
shoul be avoided. Chin lift or jaw thrust in the best method for securing airway. Once an
airway is established, ventilation with oxygenation is begun.

Immobilization and Extrication

Proper immobilization is essential to prevent additional spinal column and/or spinal

cord injury. At the accident scene, initial in-line manual traction is recommended before
moving the spinal injured patient, and hard cervical collar should be applied. The collar
should have a manufactured opening in the front in case an emergency cricothyroidotomy is
needed. After the cervical collar is in place, the patient is moved to a firm spine board for
transportation.
Transport

In modern country, the general guidelines for means of transportation are (1) an
ambulance for distances < 50 miles, (2) a helicopter for distances of 51 to 150 miles or heavy
traffic patterns and severe injuries, and (3) a fixed-wing aircraft for distances > 150 miles.

Hospital Management

Reassesment of ABC should be performed soon after patient arrived at hospital.

Resuscitation must be continue, once life threatening problem are established.
Hypotension and bradycardia may be a sign of spinal shock. It is critical to distinguish
neurogenic shock from hypovolemic shock, as overly aggressive fluid administration in the
former could lead to intravascular overload and pulmonary edema.

Strict spinal precautions should be maintained until a full and thorough evaluation
can be performed on each suspected patient.
The initial treatment of a patient in neurogenic shock consists of placing the patient
in the Trendelenburg position with judicious administration of intravenous fluids. If blood
pressure instability persists, cardiac pressors along with atropine may be used.

Pharmacologic Therapy

Extensive research has been undertaken in the evaluation of various pharmacologic

agents regarding their ability to modify or lessen the secondary injury cascade that occurs
after an injury to the spinal cord. Such agents include but are not limited to corticosteroids,
21-aminosteroids, antioxidants, gangliosides, opioid antagonists, thyrotro-releasing
hormone, prostacyclin analogs, and calcium channel blockers.
Steroid Protocol for SCI.

The steroid protocol for giving methylprednisolone after SCI is controversial as to

whether any benefits outweigh the potentially significant side effects. Steroid treatment, if
given, is dependent on time from injury to treatment:

0 to 3 hours: 30 mg/kg loading dose, then 5.4 mg/kg for 23 hours

3 to 8 hours: 30 mg/kg loading dose, then 5.4 mg/kg for 48 hours
8 hours: no methylprednisolone

Penetrating wounds, pregnancy, age younger than 13 years, significant infection, or

unstable diabetes are all relative contraindications to the use of high-dose corticosteroids.

Complication (Fletcher DJ, 1995)

1. Urinary tract infection

2. Pneumonia, atelectasis
3. Respiratory failure
4. Cardiac
5. Decubitus ( pressure sore )
6. Mortality
7. Late kyphotic deformity

References

1. White, A.A.; Panjabi, M.M. Clinical Biomechanics of the Spine. Philadelphia, J.B.
Lippincott, 1978, pp. 236–251.
2. Levitt MA, Flanders AE. Diagnostic capabilities of magnetic resonance imaging and
computed tomography in acute cervical spinal column injury
3. ASIA. Standards for Neurological Classification of Spinal Injury. Chicago: American
Spinal Injury Association; 1996.
4. Ersmark H, Dalen N, Kalen R. Cervical spine injuries: a follow-up of 332 patients.
Paraplegia 1990;28(1):25-40.
5. Garfin S, Blair B, Eismont F, Abitbol J. Thoracic and upper lumbar spine injuries. In:
Browner B, Jupiter JB, Levine A, Trafton P, editors. Skeletal trauma. 2nd ed.
Philadelphia: W.B. Saunders Company; 1998. p 967--981.)
6. Fletcher DJ, Taddonio RF, Byrne DW, et al. Incidence of acute care complications in
vertebral column fracture patients with and without spinal cord injury. Spine
1995;20(10):1136-46.
 Topic 4 : Basic Rheumatology

A. Topic overview

This topic contents four topics introduce the student to understand of

principle and basic knowledge and clinical situation of rheumatology problem.
Subtopic 1 : Inflamation
Subtopic 2 : Autoimmunity
Subtopic 3 : Infection
Subtopic 3 : Bone and cartilage metabolism
Subtopic 4 : Approach to the patient with joint problem

B. Learning objective

Upon completion of this module, the student will be able to :

1. To understand the inflammation process in rheumatic diseases.

2. To understand the autoimmun mechanism in the pathogenesis of rheumatic
diseases.
3. To understand the bone and cartilage metabolism.
4. To define common rheumatic problems including joint pain, joint stiffness,
oligoarthritis, polyarthritis, and low back pain.

C. Lecture overview

Subtopic 1 : Inflammation

Inflammation is one of the most important and most useful of our host
defensemechanisms, and without an adequate inflammatory response none of us or
ourpatients would be living. Ironically it is also one of the most common means whereby our
own tissues are injured.

Definition:

Inflammation is the reaction of vascularized living tissues to local injury. Inflammation

comprises a series of changes in the terminal vascular bed,
in blood and in connective tissues with the purpose of eliminating the
offending irritant and to repair the damaged tissue.

Roles of Inflammation:
 1. Protection, under ideal conditions the source of the tissue injury is eliminated, the
inflammatory response resolves and normal tissue architecture and physiologic
functions are restored
2. Contain and isolate the injury ; The nature of the acute inflammatory reaction is
intense and the affected area is walled-off by the collection of inflammatory cells.
This process results in destruction of tissue by products of polymorphonuclear
leucocytes and formation of an abcess.
3. Destroy invading organism and inactive toxins ; failure to eliminate the pathologic
insult results in persistence of the inflammatory reaction.
4. Achieve healing and repair n ; chronic inflammation often keads to scar formation.

ACUTE INFLAMMATION
is early, immediate, response of vascularized living tissue to local injury
is nonspecific, may be evoked by all types of cell injury
its purpose is to localise and eliminate the injurious agent and then to
restore the tissue to normal function and to normal structure

SIGNIFICANCE OF INFLAMMATION
1. to destroy injurious agent
2. to reconstitute a damaged tissue (healing), repair already begins during early phases
of inflammation, during repair the injured tissue is replaced by regeneration of
parenchymal cells, by filling defects with fibroblastic scar tissue = scarring

CAUSES OF INFLAMMATION

Almost all possible causes of cell injury may stimulate inflammatory response

 microbial infections: bacteria, viruses, fungi, etc

 hypersensitivity reactions
 physical agents: burns, UV light, radition, trauma
 chemical agents: acids, alkalis, oxidising agents, toxins, endotoxins
 tissue necr osis: ischemia

MAIN CLINICAL SIGNS AND SYMPTOMS OF INFLAMMATION

Acute inflammation is characterized by five major signs described by Celsus and

Virchow
- rubor= redness from dilatation of blood vessels
- calor = increased heat and fever- redness and heat -due to an increased
rate and volume of blood flow because of vasodilatation, release of
pyrogens
- tumor=swelling from edema
- dolor =pain form edema and histamine release, pain is said to be due to
an accumulation of acid metabolits that stimulate nerve endings
- functio laesa = loss of function form pain and swelling
MORPHOLOGIC AND FUNCTIONAL CHANGES IN ACUTE INFLAMMATION
Acute inflammation is defined as the early inflammatory response to an injurious
agent which is characterized by the presence of neutrophils, and later macrophages. Acute
infl. last for a few hours or days.The early acute response is characterized by the presence of
edema fluid, fibrin, and neutrophilic leukocytes. This is caused by:
arteriolar dilatation and opening up of capillary channels
increased vascular permeability (exudate formation)
emigration of neutrophils from vessels
two main processes invovlved in acute infl. response are:
microcirculatory response (vascular)
cellular response

1. Microcirculatory response
Vascular response is characterized by an increased blood flow in an affected area, and
an increased permeability of blood vessels
active vasodilatation = hyperemia
First step in microcirculation in infl. area is transient vasocontriction, that is rapidly
followed by marked active vasodilatation of capillaries, small arteries and venules.
Vasodilatation leads to hyperemia(= increased amount of blood in infl. area )- heat and
redness
increased permeability of blood vessels- next event typical of acute inflammation-
associated with slowing of the circulation- called stasis
in normal tissuue - blood vessel walls permeability is a function of the intercellular
junctions between endothelial cells - these small gaps-pores normally permit passage of
only small molecules
in acute inflammation, immediate increase of permeability of venules and capillaries
(caused by active contraction of actin microfilaments in endothelial cells) - results in
widening of pores (intercellular junctions)- followed by an increase of amount of fluid
and high-molecular-weight proteins can pass through abnormally permeable vessels into
the extravascular space
increased passage of fluid out of microcirculation because of increased permeability in
acute inflammation –results in formation of inflammatory exudate- exudation of fluid
Vascular leakage, loss of protein-rich fluid from blood vessels results in a reduction of
osmotic pressure within blood vessels and in and increase within the interstitium-
accumulation of fluid out of blood vessels-passage of large amounts of fluid from
capillaries into the interstitium is associated withinflammatory edema- major feature of
acute inflammation
Composition of inflammatory exudate
Exudate is a fluid rich in plasma proteins, such as albumins, immunoglobulins, parts of
complement, fibrinogen-when extracapillary it is rapidly converted into fibrin by tissue
tromboplastin
 Fibrin can be recognized microscopically-pink fibers or clumps, macroscopically- most
easily seen on acute infl. of serosal surfaces-acute fibrinous pericarditis- „bread and
butter„ appearance.
in contrast Transudation= increased passage of fluids (very low level of plasma proteins,
and no cells) through blood vessels with normal permeability- cause either increased
hydrostatic pressure or decreased plasma osmotic pressure -composition similar to
ultrafiltrate of plasma
Significance of the process of exudation
Exudation helps to destroy infectious agent by its diluting, by flooding the area with
blood rich in immunoglobulins and other important defensive proteins, by increasing
lymphatic flow (helps to remove agents out of area)
Lymphatic drainage may be however harmful, helps to spread infectious agents and
acute inflammation is complicated by :

acute inflammation of lymphatics= lymphangitis

acute inflammation of lymph nodes=lymphadenitis

2. Cellular response
Acute inflammation is characterized by an active emigration of inflammatory cells
from the blood into the area of injury.
Two most important cellular events in acute inflammatory response are:
1. active emigration to inflammed area
2. phagocytosis

Active emigration of cells from the blood

early phase (first 24 hours): neutrophilic leukocytes
later phase (after first 24-48 hours): macrophages, lymphocytes and plasma cells

Leukocytes :
Neutrophilic leukocytes remain predominant cell type for several days in acute
inflammation.Major events affecting leukocytes in inflammation.
margination of neutrophils - in normal blood stream, the leukocytes are mostly confined to
axial stream (separated from the endothelial surface by plasma)
in dilated vessel in inflammation- the rate of blood flow decreases- erytrocytes form
aggregates that displace leucocytes from the centre of axial stream, in combination with a
decrease of amount of plasma due to exudation- leukocytes adhere to endothelial surface
-pavementing of neutrophils -dilated vessels in acute inflammation are lined by numerous
adherent leukocytes (increased adhesiveness of endothelial cells in inflammation)- probably
due to activity of chemical mediators of inflammation-process of leukocyte-endothelial cell
adhesion is followed by
-emigration of neutrophils -leukocytes actively leave the blood vessel by moving through
dilated intercellular junctions, pass through basement membrane and reach the
extracellular space
chemotactic factors- process of active emigrating of leukocytes is governed by
chemotactic factors (including C5 complement and various bacterial products),
leukocytes have cell surface receptors for chemotactic factors
movements of other cells:
emigration of 2.) MACROPHAGES and 3.) LYMPHOCYTESis similar to that of neutrophils-
chemotactic mediators for macrophages- complement factor C5 and lymphokines (secreted
by lymphocytes)
different process - 4.) ERYTHROCYTES enter extracellular space passively - RBCs are pushed
out from the blood vessel by hydrostatic pressure- the process is called erythrodiapedesis
when large numbers of erythrocytes enter the inflammed area= hemorrhagicinflammation

PHAGOCYTOSIS
Major mechanism by which leukocytes and macrophages inactivate noxious agents
Major events in phagocytosis
- recognition and attachmentof bacteria by the phagocytic cells - either directly
(large inactive particles) or after opsonization (antigen is coated by opsonins)
opsonins-
Fc fragment of IgG
C3b fragment of complement -for both molecules there are specific receptors on
the surface of leukocytes
engulfment- extensions of cytoplasm (pseudopods) flow around the particles -
formation of phagocytic vacuole, this vacuole fuses with membrane of lysosomal
vacuoles-degranulation of leukocytes
bacterial killing and degradation-killing of bacterial organisms is accomplished by
activities of reactive oxygen species
Failure of oxidative metabolism during phagocytosis - leads to a severe disorder of
immunity = in chronic granulomatous disease of childhood

CHEMICAL MEDIATORS OF INFLAMMATION

1. Mediators originate from plasma or from cells, plasma-derived mediators: are
present in plasma in precursor forms and must be activated to acquire their
biologic activity. Cell-derived mediators: are normally within intracellular
granules (histamine in mast cells) and must be secreted or even synthesized de
novo - due to response to specific stimulus
 2. When activated or released from the cell, most mediators are quickly inactivated.
Important for balanced and controlled mediator activity, the activity is rapid,
specific but short
3. almost all mediators perform their biologic activities by binding to specific
receptor on specific cells

MAJOR CLASSES OF MEDIATORS OF INFLAMMATION

Can be divided to the following groups according to their activities

1. Vasoactive mediators: histamine and serotonine
2. Plasma proteases: kinin system (bradykinin-kalikrein), complement systém, and
coagulation-fibrinolytic system
3. So called AA metabolites (arachidonic acid metabolites): include
endoperoxidases, prostaglandins, thromboxane
4. Lysosomal components ( proteases)
5. Oxygen-derived free radicals
6. Platelet activating factors (PAFs)
7. Cytokines
8. Growth factors

Vasoactive mediators: „H-substances“

Histamine and serotonin are believed to mediate an immediate active phase of an

increase of vessel permeability. In human, histamine is widely distributed (stored in granules
of mast cells and blood basophils, in platelets).
Different agents can release histamine from mast cells:
physical agents- such as cold, trauma
immunologic reactions, through well known mechanism involving the receptors on
the mast cell for IgE
fragments of complement that can induce icrease of permeability of blood vessels
(anaphylatoxins)
histamine-releasing factors of leukocytes and platelet, interleukin-1

Function of vasoactive substances:

-Histamine- causes dilation of arterioles and in increase of permeability of venules

histamine -is rapidly inactivated by histaminase, thus histamine is important mainly in early
inflammatory response and in immediate IgE -mediated hypersensitivity
-Serotonin- second vasoactive mediator, main source of serotonin- platelets, release
of serotonin from platelets is stimulated when platelets aggregate after their contact with
complex antigen-antibody, with collagen etc.

Plasma -derived mediators:

a variety of phenomena in acute inflammatory response are mediated by three interrelated
systems- kinins, complement, and the clotting system
 -kinin system -activation of kinin system leads to a release of bradykinin-causes
arterial dilatation and increase of permeability of venules, rapidly inactivated by kinases
there is multi-step pathway to activate kinin system-system of activation is related to
clotting systeme, key role of Hagemann factor XII of coagulation
-complement system -consists of several plasma proteins and plays a role both in
inflammation and immunity.
Complement components ( C1-C9 ) are present in plasma in inactive form
„complement cascade“- most important is C3
activation may start either complex antigen-antibody (IgG and IgM)= classic pathway
or bacterial polysaccharids and endotoxins= alternative pathway
complement system influences:
-vascular changes in inflammation
-chemotactic effect for monocytes, neutrophils
-acts as opsonin-helps in phagocytosis
clotting system (coagulation cascade )
coagulation is iniciated by activation of factor XII- Hagemann factor XII - cause activation of
series of plasma proteins - the final step is change of fibrinogen to fibrin

Platelet-activating factor (PAF)

is a mediator derived from antigen-stimulated basophils that had been sensitized by

IgE and cause aggregation of plateles and release of their active constituents, such as
histamine and serotonin
PAFs are not stored, they are rapidly generated after cell stimulation
PAF causes - increase of vessel permeability, increase of leukocyte aggregation and adhesion
to endothelium
PAFs appear to act directly on target cells but they can also stimulate the synthesis of other
mediators, particularly prostaglandins and leukotriens
Cytokines-are certain polypeptide products of activated lymphocytes and macrophages
refered to as lymphokines and monokines
-are involved in cellular response in immune processes, such as lymphocyte proliferation - it
has been known for long time, but recently it has become clear that cytokines are involved
also in inflammatory response
the most important cytokines in inflammation are
interleukin I
tumor necrosis factor (TNF) = cachectin
-because it is thought to be involved also in the cachexia in chronic inflammation and
cancer
their most important actions in inflammation are
-1) local effects on endothelium, such as stimulation of increased adhesion of
leukocytes and lymphocytes to endothelium and stimulation of synthesis of PAFs
-2) induce the systemic acute inflammatory responses, such as induction of fever,
release of ACTH and corticosteroids, release of neutrophils to the circulation, etc.

MORPHOLOGIC PATTERNS OF ACUTE INFLAMMATION

 -Basic patterns of acute inflammatory response depend on severity of noxious agent,
severity of reaction, type of tissue involved, site, local circumstances, composition of
exsudate etc.

Serous inflammation
-is characterized by abundant serous fluid (exudate) that is derived either from the
blood stream or from the secretory activity of mesothelial cells lining peritoneal, pleural or
pericardial cavities, serous exudate is easily removed.
Fibrinous inflammation
-with more serious injuries, the permeability of blood vessel is greater and more
proteins including large molecules of fibrinogen pass the vascular wall.
Fibrinous inflammation develops if highly permeable wall let pass the fibrinogen- lots of
fibrin in the inflammatory fluid.
Fibrin- histologically-eosinophilic meshwork or it may be amorphous.
Fibrinous exsudate may be removed-this process is called resolution. When fibrinous
exsudate is not removed-fibrin may stimulate the ingrowth of fibroblasts into the blood
vessel wall, thus leading to scarring- this process is called organization.
Fibrinous exsudate may have more serious consequencies than the serous exsudate.
Suppurative or purulent inflammation
-is characterized by production of large amounts of purulent exsudate (= pus ).
Localized suppuration- caused mainly by staphylococci- pyogenic bacteria
acute suppurative appendicitis- common example of purulent inflammation.
-Abscess= localized collections of purulent exsudate
pyogenic inflammation in the skin-folliculitis (furuncle)
-Ulcer = is a local defect in the tissue, mainly in the mucosal or cutaneous surfaces
examples: include inflammatory necrosis in mouth, stomach intestines, genitourinary tract
or, peptic ulcer of stomach or duodenum, ulcers of the lower extremites due to vascular
disorders
acute ulcer- intense leukocyte infiltrate and vascular dilatation in the margins
chronic ulcer-more developed fibroblastic reaction, scarring and infiltration of lymphocytes,
macrophages and plasma cells.

SYSTEMIC CLINICAL SIGNS OF ACUTE INFLAMMATION

1. fever- is one of the most prominent features of acute inflammation

Fever results either of direct activity of cytokines or through local activity of
prostaglandins
2. changes in the peripheral white blood cells
leucocytosis- the total number of neutrophils in the peripheral blood is increased
-is common feature especially in bacterial infections
-under these circumstances, peripheral blood leukocytes tend to be of the less mature
forms with fewer nuclear lobes ( so called „ band forms“) and they often contain large
cytoplasmic granules ( so called „ toxic granulation“)
the term „ shift to the left“means the change to increased number of immature neutrophils
in peripheral blood
Leukocyte count-may reach levels of about 15 or 20 thousands cells per mm3- extreme
levels (more than 40 thousand)- referred to as leukemoid reaction
Leukocytosis occurs initially because of accelerated release from bone marrow, later
proliferation of precursors in bone marrow appears, caused by stimulation by cytokines
(colony-stimulating factors). On the other hand- viral infections tend to produce
neutropenia (decreased number of leukocytes) with lymphocytosis- excess of lymphocytes
in the blood
3) changes in plasma protein levels
elevated levels of acute phase reactants, including C-reactive protein, alfa-1-antitrypsin,
fibrinogen, ceruloplasmin, etc.incresed erythrocyte sedimentation rate

DIAGNOSIS OF ACUTE INFLAMMATION:

1) local cardinal signs of acute inflammation (rubor, calor, dolor, tumor)- enable a correct
diagnosis when process involves surface structures (skin, mouth mucosa, etc)
2) acute inflammation of internal organs, such as lungs, kidney, liver may first manifest with
systemic changes, such as fever, blood cell changes, etc.

Further Reading

1. Inflammation. AM Abeles, MH Pillinger, SB Abramson. Rheumatology,4 th ed. MC

Hochberg, AJ Silman, JS Smolen, et al. Mosby Elsevier,2008:161-176.

Subtopic 2 : Autoimmunity

Immunologic tolerance is specific unresponsiveness to an antigen induced by exposure

of lymphocytes to that antigen. All individuals are tolerant of (unresponsive to) their own
(self) antigens. These mechanisms are responsible for one of the cardinal features of the
immune system, namely, its ability to discriminate between self and nonself (usually
microbial) antigens. If these mechanisms fail, the immune system may attack the
individual's own cells and tissues. Such reactions are called autoimmunity, and the diseases
they cause are called autoimmune diseases.
Central tolerance (negative selection) is induced by the death of immature
lymphocytes that encounter antigens in the generative lymphoid organs (bone marrow and
thymus). Peripheral tolerance results from the recognition of antigens by mature
lymphocytes in peripheral tissues.
Central tolerance (negative selection) of T cells is the result of high-affinity recognition
of antigens in the thymus, which tend to be widely disseminated self antigens. Central
tolerance may eliminate the potentially most dangerous T cells, which express high affinity
receptors for disseminated self antigens. This process of central tolerance affects self-
reactive CD4+ T cells and CD8+ T cells, which recognize self peptides displayed by class II
MHC and class I MHC molecules, respectively.
Peripheral tolerance of T cells is induced when mature T cells recognize self antigens in
peripheral tissues, leading to functional inactivation (anergy) or death, or when the self-
reactive lymphocytes are suppressed by regulatory T cells (immune supression). Anergy
(functional inactivation) results from the recognition of antigens without costimulators
(second signals) or when T cells use inhibitory receptors to recognize costimulators. Deletion
(death by apoptosis) occurs when T cells repeatedly encounter self antigens.
In В lymphocytes, central tolerance is induced when immature В lymphocytes interact
strongly with self antigens in the bone marrow, the В cells are either killed (negative
selection) or they change their receptor specificity (receptor editing). While peripheral
tolerance is induced when mature В lymphocytes that encounter high concentrations of self
antigens in peripheral lymphoid tissues and do not receive T cell help (because helper T cells
are absent or tolerant), become anergic and cannot again respond to that self antigen
Autoimmune diseases result from a failure of self-tolerance. Multiple factors
contribute to autoimmunity, including immunologic abnormalities, susceptibility genes, and
environmental triggers such as infections.
Multiple genes predispose to autoimmune diseases, the most important of these being
MHC (HLA) genes. Particular MHC alleles may contribute to the development of
autoimmunity because they are inefficient at displaying self antigens, leading to defective
negative selection of T cells, or because peptide antigens presented by these MHC alleles
may fail to stimulate regulatory T cells. There are some other genes that have role in
autoimmunity such as: complement, Fas and FasL, AIRE.
Infections predispose to autoimmunity, by induce a local innate immune response, and
this may lead to increased expression of costimulators and cytokines by tissue APCs. As a
result, these activated tissue APCs may be able to stimulate self-reactive T cells that
encounter self antigens in the tissue (break T cell anergy). The second mechanism is by
cross-reactions between microbial and self antigens (molecular mimicry). Infections may
also injure tissues and release antigens that are normally sequestered from the immune
system.

Subtopic 3 : Infection

This topic presents the most common infections of musculoskeletal system including
osteomyelitis, septic arthritis, and gangrene. You will learn the causative agents,
pathogenesis and general diagnosis approaches of such infectious cases. It will help you to
develop a conceptual framework that can guide your decision-making as you assess and
manage the infections on musculoskeletal system.

Overview

Introduction

A small number of microbes cause disease of muscle, bone, and joints system.
Invasion of these sites is generally from the blood, but the reason for localization to
particular tissues is often obscure. Circulating microbes tend to localize in growing or
damaged bones (acute osteomyelitis) and in damaged joints.
Some of parasites can invade the muscle. The parasites are Taenia solium and Trichinella
spiralis. Infection occur if human eat the infective form of this parasites (the egg of Taenia
solium and the larvae of Trichinella spiralis)
Osteomyelitis

Bone can become infected by adjacent infection or hematogenously

Infection can be by the direct route (e.g. from a nearby focus of infection, after fractures,
after orthopedic surgery) or from circulating microbes. The commonest cause of
hematogenous osteomyelitis is Staphylococcus aureus, but when infection is from a
neighboring site it is generally mixed, with Gram negative rods and occasionally anaerobes
also present.
Acute osteomyelitis typically involves the growing end of a long bone, where sprouting
capillary loops adjacent to epiphyseal growth plates promote the localization of circulating
bacteria. It therefore tends to be a disease of children and adolescents, and may follow non-
penetrating injury to the bone.
Osteomyelitis results in a painful tender bone lesion and a general febrile illness.
Osteomyelitis is treated with antibiotics and sometimes surgery
The infection is diagnosed from blood cultures taken before the start of antimicrobial
therapy or, if there is an open lesion, from a bone biopsy. Periosteal reaction and bone loss
may be visible radiologically. Treatment is begun on a ‘most likely’ basis as soon as
microbiologic samples have been taken.
Osteomyelitis can become chronic, especially when there are necrotic bone
fragments to act as a continued source of infection. Surgical intervention for debridement
and drainage, as well as prolonged courses of antibiotics, may be necessary.
Tuberculosis may affect the spine, the hip, the knee and the bones of hands and feet.

Fig 4.1 Acute staphylococcal osteomyelitis in the femur of a 24-year old woman. There is a
well defined periosteal reaction in relation to the midshaft of the femur and an underlying
lucency (Courtesy of AM Davies in Mims C., et al, 2004)
Fig 4.2 A, Gram stain of Staphylococcus aureus ; B, Culture of Staphylococcus aureus on
blood agar medium

Septic arthritis

Joints can become infected by the hematogenous route or directly following trauma
or surgery, but in many cases the condition is immunologically mediated rather than due to
microbial invasion of the joint. The microbe responsible is at a distant site in the body and
causes a ‘reactive arthritis”. Reactive arthritis and arthralgia occur after certain enteric
bacterial infections, and the arthralgia in rubella and hepatitis B infections is of similar
origin. In this type arthritis more than one joint is usually affected.
Circulating bacteria sometimes localize in joints, especially following trauma.
Such bacterial localization can then cause a suppurative (septic) arthritis. Generally a
single joint is involved. Joints are very susceptible, particularly if they are already damaged,
for instance by rheumatoid arthritis, or if a prosthesis has been inserted. Knees are most
commonly affected, followed by hips, ankles, and elbows. Signs include a fever, joint pain,
limitation of movement and swelling, and usually a joint effusion. Bacteria can be isolated
from the joint fluid or seen in the centrifuged deposit, and the commonest organism is
Staphylococcus aureus. Sometimes the source of the circulating bacteria is obvious (e.g. a
septic skin lesion), but often no source is apparent.

Gas gangrene

Gas gangrene or clostridial myonecrosis can be caused by several species of

clostridia, but Clostridium perfringens is the most common. The organism and its spores are
found in the soil and in human and animal feces, and can therefore gain access to
traumatized tissues by contamination from these sources. Infection develops in areas of the
body with poor blood supply (anaerobic), and the buttocks and perineum are common sites,
particularly in patients with ischemic vascular disease or peripheral arteriosclerosis. The
organisms multiply in the subcutaneous tissues, producing gas and an anerobic cellulites,
but a characteristic feature of clostridial infection is
Figure 4.3 Septic arthritis of the ankle with marked erythema and swelling of the ankle and
leg (Courtesy of TF Sellers, Jr in Mims C., et al., 2004)

that the organisms invade deeper into the muscle, where they cause necrosis and produce
bubble gas, which can be felt in the tissue and sometimes seen in the wound. The infection
proceeds very rapidly and causes acute pain. Much of the damage is due to the production
by Clostridium perfringens of a lecithinase (also known as alpha toxin), which hydrolyzes the
lipids in cell membranes resulting in cell lysis and death. The presence of dead and dying
tissue further compromises the blood supply, and the organisms multiply and produce more
toxin and more damage. Other extracellular enzymes may also play a role in helping the
clostridia to spread. If the toxin escapes from the affected area and enters the bloodstream,
there is massive hemolysis, renal failure and death.
Amputation may be necessary to prevent further spread of clostridial infection.
Because of the rapid progression and fatal outcome of this type of clostridial infection,
gangrenous areas require immediate surgery to excise all the affected tissue, and
amputation may be necessary. Anti-alpha toxin may help if given early enough, and
treatment in a hyperbaric oxygen chamber has also been recommended to improve the
oxygenation of the tissue.
Antibiotics (e.g. penicillin) are adjuncts to, not replacements for, surgical
debridement.
Prevention of infection is of foremost importance. Wounds should be cleansed and
debrided early to remove dead and poorly perfused tissue, which the anaerobes favor.
Prophylactic antibiotic should be given preoperatively to patients having elective surgery of
body sites liable to contamination with fecal flora.

Cysticercosis of muscle

The larval stage of Taenia solium has been found in practically every organ and tissue of the
body. The symptoms produced vary according to the number of the cysticerci present and
their location. The most frequent location is in the subcutaneous and intermuscular tissues.
Figure 4.4 Gas gangrene caused by Clostridium perfringens. Organisms from the fecal flora
may contaminate a wound and grow and multiply in poorly perfused (anaerobic)
tissue. Infection spreads rapidly, and gas can be felt in the tissue and seen on
radiographs (Courtesy of J Newman).

Figure 4.5 The Nagler reaction. Clostridium perfringens produces alpha toxin, which is a
lecithinase. If the organism is grown on a medium containing egg yolk (lechitin),
enzyme activity can be detected as opacity around the line of growth (right). If
anti-alpha toxin is applied to the surface of the plate before inoculation of the
organism, the action of the toxin is inhibited (left). This test can be used to confirm
the identity of the clostridial isolates (Mims C., et al., 2004)

The presence of growing larva provokes a typical sequence of local cellular reaction,
including infiltration of neutrophils and eosinophils, lymphocyte and plasma cells, followed
by fibrosis and necrosis of the capsule, with eventual caseation or calcification of the larva.

Diagnosis.

Diagnosis usually awaits excision of the larva and its microscopic examination. Its
invaginated scolex, with its four suckers and anterior circle of hooks, is exactly the same as
that of the adult worm.

Treatment
 Excision is indicated wherever possible an as soon as possible.

Prevention

1. Personal hygiene

2. General sanitary measures.

People must understand that eating raw pork may expose them to pork tapeworm (as well
as trichinosis) and that fecal contaminations make it possible to acquire cysticercosis

References :

1. Brooks GF., Butel JS., Morse SA., 2004, Jawetz, Melnick & Adelberg’s Medical
rd
Microbiology 23 ed, The Mc Graw-Hill Companies Inc., USA
2. Kasper DL., Fauci AS., Longo DL., Braunwald E., Hauser SL., Jameson JL., 2005,
th
Harrison’s Principles of Internal Medicine 16 ed, The McGraw-Hill Companies, Inc.,
USA
3. Mims C., Dockrell, HZ., Goering RV., Roitt I., Wakelin D., Zuckerman M., 2004,
rd
Medical Microbiology 3 ed, Mosby, Spain
4. Ryan KJ., 1994, Sherris Medical Microbiology An Introduction to Infectious Diseases
rd
3 ed, Prentice Hall International Inc., USA
5. Tortora GJ., Funke BR., Case CL., 2005, Microbiology An Introduction, The
Benjamin/Cummings Publishing Company Inc., USA

Subtopic 4 : Bone and cartilage metabolism

Types of Bone

There are two types of bone namely cortical (compact) and cancellous (trabercular)
bone. Bone consists of a dense outer cortical layer which encloses the cancellous bone.
Cancellous bone consists of trabecular plates which interconnect with each other and with
the inner aspects of the cortical bone. These trabecular plates are orientated along lines of
stress.
Composition of bone
Bone consists of an organic matrix, bone cells and a mineral element. The matrix is
composed of collagen fiibres (mainly type I collagen) and which are laid down by
osteoblasts. Collagen contains hydroxyproline which is released during collagen breakdown
and can be measured in the urine as an index of bone activity. Other important proteins
include osteocalcin which can also be measured to indicate the rate of bone turn over (see
later).The mineral element of bone is calcium and phosphate in the form of hydroxqapatite
crystals. Individual crystals are very small and are orientated along the lines of the collagen
fibres.
Metabolic activity takes place on the surface of bone. The surface area of cortical bone is 10
fold less than the surface area of cancellous bone. This is one reason that osteoporosis
presents earlier ad is more marked in cancellous than cortical bone.
All bony surfaces are covered by endosteal cells. Bone remodelling starts with the
attraction of a number of mononuclear (macrophage) cells from the blood to a bone
surface. These cells then differentiate into osteolasts which are then responsible for bone
resorption. This occurs roughly every 10 seconds somewhere on a bony surface. What
controls this activation is unknown but fatigue fractures, parathyroid and thyroid hormones
play a role. The gonadal hormones and calcitonin are inhibitors. Later a second cell, the
osteoblast, replaces the osteoclast and is responsible for new bone formation and
mineralisation.

Erosion of bone

A group of activated osteoclasts excavate an erosion cavity to a depth of 40-60um

over 4-12 days, first by lowering the Ph under the osteoclast. This solubilizes the mineral
phase of the bone (calcium etc.). Then the production of acid proteases allows the
enzymatic degradation of the remaining organic components including the collagen. Over
the next 7-10 days a layer of a cement substance is deposited which is rich in acid
phosphatase, glycoproteins and proteoglycans. This is called the reversal phase. Once this
has taken place a process called coupling attracts osteoblasts to the eroded surface where
they form a sheet of cells over the eroded surface and excrete layers of osteoid matrix. A
few days later this osteoid undergoes mineralisation.
Alkaline phosphatase is actively excreted by the osteoblasts at this stage. Osteocalcin
(bone gla protein) is another mineralisation protein exclusively excreted by osteoblasts. This
process is called a bone structural unit (BSU) and takes about 6 months to complete. About
l0% of the bone surfaces are remodelling at any one time. In cancellous bone a BSU is 40-
60um thick 0.5-1mm². in diameter. With oestrogen deficiency this cellular activity is
increased 2 to 3 fold. Also the number of osteoclasts per BSU is increased 2-3 fold. The
importance of this is that the depth of the erosion is increased and can penetrate the full
thickness of the trabecula. If this happens it cannot be replaced. Further the osteoblasts
that follow have a suboptimal performance. They have oestrogen receptors which must be
activated for optimal osteoblast activity. In osteoporosis each remodelling sequence is
associated with a small but finite deficit in bone.
In postmenopausal osteoporosis and with immobilization there is a marked loss of
trabecular numbers whereas in steroid induced osteoporosis the trabeculae are reduced in
thickness but a scaffolding of bone remains.

Subtopic 5 : Approach to the patient with joint problem

Evaluation of patients with joint problem should focus on clinical patterns and
symptom complexes. The history taking and physical examination are the cornerstones of
diagnosis of rheumatic disease. Joint pain is the most common symptom that most often
will lead to a clinic visit. It is important to differentiate between a subjective symptom of
joint pain (arthralgia) and an objective finding of joint inflammation revealed on physical
examination (arthritis). Cardinal sign of inflammation include heat, redness, pain, swelling,
and loss of function. These sign, which may not all be present, are helpful in differentiating
an inflammatory arthritis from other joint pain. Pain is a key symptom in patient with
arthritis. Description of pain should include the perception, location, distribution, duration,
and quality of pain. Joint stiffness in rheumatoid arthritis is typically generalized joint
stiffness that characteristically occurs in the morning, last longer than 30 minutes, and
resolves with mobilization of the joint. In contrast with osteoarthritis, this is localized to
involved joints and usually last less than 30 minutes.

The musculoskeletal examination

To obtain clues to the origin of a patient’s pain, medical students should closely
observe patients, noting their gait and movement on rising from a sitting position. Patients
should undergo a general physical examination focusing on information elicited during the
history. It is important to understand the anatomy of a particular area and the features of a
normal joint. Initially, joints should be inspected for such obvious signs as enlargement,
malalignment, or deformity. Next, joint should be palpated to help determine whether
there is capsule tenderness, warmth, or swelling. Joint swelling may be secondary to fluid
accumulation, bony growth, or synovial proliferation. Both active and passive range of
motion should be determined. Joint crepitus can be elicited during the joint movement.
Arthritis involving more than 3 joints is called polyarthritis, 3 joints or less is called
monoarthritis or oligoarthritis.

Laboratory and imaging examination

Laboratory studies should confirm a diagnosis suggested by history and physical

examination. Baseline laboratory studies include a complete blood count, serum chemistry
studies, and urinalysis. Additional studies such as acute phase reactants and serum
antibodies, should be ordered when appropriate. Diagnostic imaging is not indicated in
most patients for diagnosis confirmation. But, radiography is becoming an increasingly
important method for evaluating disease activity and joint damage in patients with
rheumatic disease.
Reference :

1. Current Rheumatology Diagnosis & Treatment. J Imboden, DB Hellmann, JH Stone.

McGraw Hill,2005.
 Topic 5 : Clinical Rheumatology

A. Topic overview

This topic presents common rheumatology problem based on local index

clinical situation and clinical egibility prior for medical student standardized by Indonesian
Medical council. Contents of this modul divided into eight topics :
Topic 1 Rheumatoid arthritis
Topic 2 Osteoarthristis
Topic 3 Spondyloarthropathy
Topic 4 Sistemic lupus erythematosus
Topic 5 Gouty arthristis
Topic 6 Septic arthritis
Topic 7 Osteoporosis

B. Learning objective

Upon completion this module, the students will be able to :

1. To understand the pathogenesis of major rheumatic diseases including

osteoarthritis, rheumatoid arthritis, systemic lupus erythematosus,
spondyloarthropathy, gouty arthritis, septic arthritis and osteoporosis.
2. To understand the differential diagnosis for common rheumatic problems (acute and
chronic arthritis, monoarthritis and polyarthritis).
3. To understand the diagnosis of major rheumatic diseases including osteoarthritis,
rheumatoid arthritis, systemic lupus erythematosus, spondyloarthropathy, gouty
arthritis, septic arthritis, and osteoporosis.
4. To understand the treatment principles of major rheumatic diseases including
osteoarthritis, rheumatoid arthritis, systemic lupus erythematosus,
spondyloarthropathy, gouty arthritis, septic arthritis, and osteoporosis.

C. Lecture overview

Rheumatoid arthritis

Rheumatoid arthritis (RA) is a systemic inflammatory autoimmune disease that

affects approximately 1% of the population. The mean age of onset of RA is 52 years, mainly
affects patients between 40 and 70 years of age. RA has a 3 to 5:1 female predominance.

Pathogenesis

RA is associated with presence of a shared epitope on small regions of the HLA-

DRB1*0401 and HLA-DRB1*0404 alleles. In the presence of the antigen HLA-DR and the as
yet unidentified RA-inciting antigens, macrophages produce cytokines and present the
putative RA-inducing antigen to T cells. The cytokines, such as tumor necrosis factor (TNF)-α,
cause many of the systemic features of RA. TNF-α and interleukin-1 also induce the
proliferation of T cells and the activation of B cells, and develop into plasma cells. Plasma
cells produce autoantibodies, such as rheumatoid factor.

Clinical manifestation and diagnosis

RA is a symmetrical polyarthritis that involves the small joints of the hands and feet,
as well as other joints throughout the body, result in joint damage and progressive
functional limitation. RA frequently associates with systemic symptoms such as fatigue, mild
fever or anemia. These features may include subcutaneous nodules or rheumatoid
vasculitis. Diagnosis of RA can be made based on American College of Rheumatology (ACR)
criteria including morning stiffness, symmetric polyarthritis, hand arthritis, large joint
arthritis, rheumatoid nodule, rheumatoid factor and joint eriosion on radiograph. The
presence minimal 4 of 7 criteria confirms diagnosis of RA.

Figure 1. Hand arthritis in early rheumatoid arthritis

(Source : Rheumatology Clinic Dr.Saiful Anwar Hospital slide collection)
 Figure 2. Typical hand deformities in advanced rheumatoid arthritis

Treatment : Early and aggressive disease control is indicated in RA to stop development of

joint damage and functional limitation. In very early RA, nonsteroidal anti-inflammatory
drugs and short courses of low dose corticosteroid are indicated. In patients with well-
defined RA who do not achieve remission or an optimal response to this therapy, initiation
of disease modifying anti-rheumatic drugs (DMARD) therapy is crucial. DMARD that
frequently prescribed for RA-patients are methotrexate, hydroxychloroquine, and
sulfasalazine. Adjunctive therapy with a TNF-α antagonist is indicated if the disease
continues to be active and progressive despite the use of methotrexate and other DMARDs.

References

1. MKSAP14. Medical Knowledge Self-Assessment Program. Rheumatology. American

College of Physicians, 2006.
2. Current Rheumatology Diagnosis and Treatment. Imboden J et al. The McGraw-Hill
Companies, International Edition, Boston, 2005.

Osteoarthritis

Osteoarthritis (OA) is a heterogeneous group of disorders in which biomechanical,

biochemical, and genetic factors cause a common clinical presentation.. Prevalence of OA
increases with age in men and women. 30% Of people between 45 and 65 years of age have
OA and more than 80% of people 80 years of age or older have OA.

Pathogenesis

Joint cartilage degradation is considered to be the most important event in the

pathogenesis of OA. OA involve the entire joint component, including subchondral bone.
Recognition of the role inflammation including cytokines and mvetalloproteinases in the
synovium and cartilage in OA has recently increased. Therefore, OA is no longer considered
only a degenerative disease. Age is the most important risk factor for developing OA.
Additional risk factors include genetics, obesity, and trauma-induced mechanical joint
instability.

Figure 3. Joint abnormalities in knee osteoarthritis

Clinical manifestation and diagnosis

Pain is the most common symptom associated with OA, which usually worsens
during activity and is relieved by rest. Patients may also have morning joint stiffness, which
commonly lasts less than a half hour. Stiffness after periods of inactivity also may develop.
As the disease progresses, joints may appear “bony” as the joint space becomes narrower
and bony hypertrophy develops. The joint most commonly involve in OA are weight-bearing
joints. Findings on physical examination typically include bony enlargement and
malalignment. Joint effusions may occur in patients with OA, but erythema and warmth are
usually absent or minimal. There may be pain on range of motion of the affected joints.
Joint crepitus is frequently detected with motion of large joint. There are no routine
laboratory findings specific for OA. The classic radiographic findings of OA are bony spurs at
the joint margins, joint space narrowing, subchondral sclerosis and cyst formation.

Treatment

Goals in the treatment of OA are symptomatic relief, functional improvement, and

disability prevention. Management of OA includes nonpharmacologic and pharmacologic
therapeutic components. Nonpharmacologic therapy includes exercise, weight control,
other lifestyle modification, and physical interventions. Pharmacologic therapy include
topical agents (eg: capsaicin), oral agents (analgesic and NSAIDs), and intraarticular therapy
(corticosteroid, hyaluronic acid). Several agents are being studied for structure/disease
modifying agents, such as doxycycline and glucosamine. Surgical interventions include
removal of loose bodies, stabilization of joints, redistribution of joint forces, relief of neural
impingement, and joint replacement.
References

1. MKSAP14. Medical Knowledge Self-Assessment Program. Rheumatology. American

College of Physicians, 2006.
2. Current Rheumatology Diagnosis and Treatment. Imboden J et al. The McGraw-Hill
Companies, International Edition, Boston, 2005.

Seronegative spondyloarthropathies

The seronegative spondyloarthropathies (SSA) are a group of systemic inflammatory

joint disorders that share distinct clinical, radiographic, and genetic features. These
disorders include ankylosing spondylitis, reactive arthritis (Reiter’s syndrome), psoriatic
arthritis, and enteropathic arthritis. Characteristic feature of SSA include inflammatory spine
and sacroiliac disease, asymmetrical inflammation in four or less peripheral joints,
inflammation at the site of ligament and tendon insertion (enthesitis), the presence of HLA-
B27, and extra-articular conditions, such as uveitis, colitis, urethritis, aortitis, and psoriasis.

Pathogenesis

The SSA most likely are caused by the interplay between genetic and environmental
factors. These disorders frequently occur in patients with HLA-B27. Exposure to infectious
stimuli may precipitate the expression of the SSA. TNF is a mediator of inflammation in the
synovium, enthesis, and bone. This findings suggest that TNF is crucial to the pathogenesis
of SSA.

Figure 4 A. Limited spinal mobility in patient with ankylosing spondylitis.

Figure 4B. Bilateral sacroiliitis on radiograph in ankylosing spondylitis
(Source : Rheumatology Clinic Dr.Saiful Anwar Hospital slide collection)
Clinical manifestation

The SSA are characterized by spondylitis and sacroiliitis. Clinical criteria for
spondyloarthropathy include significant and persistent lower back morning stiffness and
limited spinal mobility and chest expansion. Back pain in spondyloarthropathy is associated
with morning stiffness. Clinical criteria for the SSA also include radiographic findings of
sacroiliitis, spinal inflammation, and ligamentous ossification.

Treatment

NSAIDs are used to treat joint inflammation, may be accompanied by short course of
low-dose prednisolone. DMARDs that used in RA are also prescribed for patients with SSA
such as sulfasalazine, and methotrexate. Recently, anti-TNF has been associated with
significant clinical and radiologic benefits in patient with SSA.

References

1. MKSAP14. Medical Knowledge Self-Assessment Program. Rheumatology. American

College of Physicians, 2006.
2. Current Rheumatology Diagnosis and Treatment. Imboden J et al. The McGraw-Hill
Companies, International Edition, Boston, 2005.

Systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is a chronic multisystem autoimmune disease of

unknown cause. Manifestation of this heterogeneous syndrome range from mild to severe
and life threatening.

Pathogenesis

The pathogenesis of SLE is not yet well defined. Expression of this condition involves
genetic and environmental factors. Susceptibility to SLE may involve 40 or more genes.
Defects in apoptosis and impaired removal of apoptotic cells may contribute to an overload
of autoantigens that may initiate an autoimmune response. Insusceptible patients, this
response includes antibody-mediated tissue damage. Environmental factors that may be
associated with expression of SLE include infectious agents, medications, ultraviolet
exposure, and stress. Because SLE has a female predominance, it has bees suggested that
sex hormones, which have immunomodulatory properties, also may affect disease
pathogenesis.

Clinical manifestation and diagnosis

SLE most commonly involves the skin and musculoskeletal system. Cutaneous
manifestations of this condition include malar rash, papulosquamous or annular polycyclic
rash, or discoid lesions. Joint pain in SLE is usually polyarticular, affects both large and small
joints, and is not erosive. Glomerulonephritis is the most frequent renal manifestation that
develops in SLE. Neuropsychiatric involvement in SLE patients includes various
manifestation of the central, peripheral, and autonomic nervous systems, as well as
psychiatric syndromes. These conditions may be life threatening and may include seizures,
encephalitis, stroke, transverse myelitis, or psychosis. Immune-mediated inflammation
associated with SLE may develop anywhere within the cardiopulmonary system. Anemia of
inflammatory disease is the anemia most likely develop in patients with SLE. Immune-
mediated destruction may affect all cell lines, and up to 15% of patients with SLE develop
Coombs antibody-positive hemolytic anemia. The production of autoantibodies that
recognize numerous cellular antigens is a hallmark of SLE. Approximately 99% of these
patients have high titers of antinuclear antibodies (ANA).

Figure 7. Typical malar rash in patient with systemic lupus erythematosus

(Source : Rheumatology Clinic Dr.Saiful Anwar Hospital slide collection)

Therapy

Mild symptoms of SLE such as arthralgia, myalgia, and fatique may response to
NSAIDs, low-dose corticosteroid, or hydroxychloroquine. Methotrexate is frequently
prescribed for arthritis associated with SLE. In patients with moderate to severe
manifestations of SLE (including glomerulonephritis, pneumonitis, central nervous system
disease, or severe cytopenias), high-dose or intravenous pulse corticosteroids,
cyclophosphamide, azathioprine, or mycophenolate mofetil may be indicated.

References

1. MKSAP14. Medical Knowledge Self-Assessment Program. Rheumatology. American

College of Physicians, 2006.
2. Current Rheumatology Diagnosis and Treatment. Imboden J et al. The McGraw-Hill
Companies, International Edition, Boston, 2005.
Gouty arthritis

Gout is the most prevalent inflammatory arthritis in men. Hyperuricemia is a risk

factor for this condition, and risk for developing gouty arthritis correlates with the degree of
elevation in urate levels. Gout and hyperuricemia are strongly associated with the metabolic
syndrome (insulin resistance), hypertension, and coronary artery disease.

Pathogenesis

Gout is caused by inflammation reaction to monosodium urate crystals deposition in

synovial tissue, bursae, and tendon sheath. The solubility of urate at physiologic pH is
approximately 6.7 mg/dL. If the urate concentration increases above this concentration,
urate deposits may develop in these tissues. Gout attacks accur when urate crystals are
released from preexisting tissue deposits. Urate crystal deposition in tissue is called tophi.
Tophaceus deposits may occur in joints and other soft-tissue structure, such as under the
skin at points of trauma, and in the olecranon bursa.

Figure 5. Large tophy on feet in patient with chronic tophaceus gout

(Source : Rheumatology Clinic Dr.Saiful Anwar Hospital slide collection)

Clinical manifestation and diagnosis

Initially, gout has a predilection for joints of the distal lower extremities. However,
over time, involvement of additional joints may occur, including the fingers, wrist, and
occasionally, axial joints. Diagnosis of gout is definitely established by arthrocentesis or
aspiration of a tophus and should not be based solely on the disease course or the presence
of hyperuricemia. Radiographic diagnosis is relatively reliable, but classic findings of gout
develop very late in the disease course.

Treatment
 Effective treatment of acute attack of gout involves high-dose therapy with NSAID,
corticosteroids, or colchicine. Oral colchicine, 0.6 mg hourly until symptoms are relieved or
side effects prevent additional use. Intra-articular corticosteroid therapy is effective, but
joint infection should be excluded before initiation of this treatment. Chronic low-dose
colchicine therapy effectively decreases the frequency of future attacks. During an acute
attack of gout, manipulation of uate levels usually is not indicated. On resolution of an
attack, hypouricemic therapy may be initiated.
References

1. MKSAP14. Medical Knowledge Self-Assessment Program. Rheumatology. American

College of Physicians, 2006.
2. Current Rheumatology Diagnosis and Treatment. Imboden J et al. The McGraw-Hill
Companies, International Edition, Boston, 2005.

Septic arthritis

Bacterial infection accounts for less than 20% of all cases of acute arthritis. However,
septic arthritis is life and limb threatening. Therefore, the possibility of infection should
determine the sequence and pace of a patient’s evaluation. Septic arthritis affects men and
women equally, and the mean age of patients with this condition is 55 years.

Pathogenesis

Most bacteria reach the joint via the vasculature of the synovium, which has no
basement membrane. Risk of infection is increased in damaged joints. Infection may occur
with traumatic inoculation, such as cat bite.

Clinical manifestation and diagnosis

Septic arthritis should be considered in patients with acute arthritis and a sudden
increase in pain in a chronically damaged joint. Several conditions may associate with septic
arthritis include prodromal systemic symptoms, comorbid immunosuppression, a history of
intravenous drug use or intravenous catheterization, sexually transmitted disease or
diabetes mellitus. Sudden articular or periarticular pain should always be evaluated,
especially if pain occurs when the joint is at rest or is passively moved.
 Figure 6. Septic arthritis following joint operation in immunocompromised patient
(Courtesy : Arthritis Care and Research Foundation of the Philippines)

Synovial fluid analysis include leukocyte count, Gram stain, culture, and examination by
polarized light microscopy are initially indicated when there is any clinical suspicion for
septic arthritis. The utility of radiography is extremely limited in the early diagnosis of acute
joint infection. However, imaging studies are useful in diagnosing chronic arthritis or
osteomyelitis.

Therapy

Septic arthritis typically is treated with drainage and parenteral antibiotics guided
initially by Gram stain but ultimately by culture findings and short-term joint immobilization
to alleviate pain. A 4- to 6-week course of parenteral antibiotics generally is administered.
Acetaminophen and NSAIDs are not indicated until microbiologic identification or
documented clinical improvement with antibiotic therapy confirms the diagnosis.

References

1. MKSAP14. Medical Knowledge Self-Assessment Program. Rheumatology. American

College of Physicians, 2006.
2. Current Rheumatology Diagnosis and Treatment. Imboden J et al. The McGraw-Hill
Companies, International Edition, Boston, 2005.

Osteoporosis

Osteoporosis is a systemic skeletal disorder characterized by low bone mass,

microarchitectural disruption of bone tissue, and a compromised bone strength leading to
an increased risk fracture. Hip fractures are the most devastating osteoporotic fractures in
terms of medical, psychosocial, and financial consequences.
Pathogenesis

Bone loss in women begins before the onset of menopause. Typically, women lose
bone mass beginning in the late third and early fourth decades. The process accelerates for
the 5 to 10 years around the menopause. Postmenopausal osteoporosis results from
estrogen deficiency-induced changes in the production of several key cytokines. Ultimately,
this leads to an imbalance between bone formation and resorption so that resorption is
favored over formation. The pathogenesis of glucocorticoid-induced osteoporosis is
complex. Glucocorticoid antagonize the actions of vitamin D especially in the intestine,
leading to reduced calcium absorption. Glucocorticoid also promote calcium excretion by
the kidney. Long-term glucocorticoid result in deleterious effects on the lifespan and
functional capacity of osteoblasts and osteocytes.

Clinical evaluation and diagnosis

Osteoporosis is often clinically silent until a fragility fracture occurs. The evaluation
of osteoporosis begins with the clinical assessment. This include the medical history and
history of medication use especially glucocorticoid, smoking, alcohol intake, dietary calcium
intake, and family history of osteoporosis and fractures. The physical examination is focused
on signs of bone pain or deformity, anemia, hyperthyroidism, hypercortisolism,
malnutrition, or disorders that cause secondary form of osteoporosis (such as systemic
inflammation in RA, SLE, or SSA). Osteoporosis can be diagnosed clinically with bone
densitometry or by the presence of fragility fractures in patient at risk for the disease. Dual-
energy x-ray absorptiometry (DXA) method is the best standardized technique for
diagnosing osteoporosis and monitoring responses to therapy.

Therapy

The essentials of management for most forms of osteoporosis include lifestyle

modification, nutritional interventions, and pharmacologic therapies. Patients should be
encouraged to discontinue smoking and alcohol consumption. Exercise improves well-being
and neuromuscular coordination, which can help condition reflexes to respond better to
falls. Nutritional interventions include increase calcium intake to 1000 mg elemental calcium
per day and vitamin D intake 400-800 IU per day. Pharmacologic therapies have been
intensively researched in recent years. Agents that are effective in preventing and treating
osteoporosis are hormone replacement therapy (HRT), selective estrogen response
modulators (SERM), calcitonin, bisphosphonates, and parathyroid hormone.
 Figure 8. Radiograph of multiple spine fracture associated with osteoporosis
(Source : Rheumatology Clinic Dr.Saiful Anwar Hospital slide collection)

References

1. MKSAP14. Medical Knowledge Self-Assessment Program. Rheumatology. American

College of Physicians, 2006.
2. Current Rheumatology Diagnosis and Treatment. Imboden J et al. The McGraw-Hill
Companies, International Edition, Boston, 2005.