mss(0).pptx

Musculoskeletal System
 COMPOSED OF :
Bones
Muscles
Cartilages
1
Ligaments
Joints
Tendons

Musculoskeletal system -------
 It is classified in to three main functional part
Skeletal system
Articular system
Muscular system
2

Musculoskeletal system----
 206 bones in the human body.
 Divided into four categories:-
Long bones (e.g. femur) .
Short bones (e.g. metacarpals).
Flat bones (e.g. sternum).
Irregular bones (e.g. vertebrae)
3

Muscular system
Muscle Types
There are three types of muscle tissue:
Visceral ( stomach, intestine, blood vessels)
Cardiac ( heart)
 Skeletal Muscle(bones, purely voluntary)
Skeletal Muscle are about ( 700 named )
4

Musculoskeletal system----
General functions :
 Support
 Locomotion
 Protection and leverage
 Hematopoiesis
 Mineral storage/internal equilibrium.
 Heat production
 Maintenance of posture
5

Articulations (joints)
Allow movement
Three types according to degree of movement
Synarthrosis—no movement (fibrous joint lacks
synovial cavity. Eg. Sutures
Amphiarthrosis—slight movement (tibia, fibula,
vertebral bone joints )
Diarthrosis—free movements
6

Types of joints ------
Hing joint -------elbow, knee, fingers
Ball and socket joint-----hip and shoulder
Gliding joint ----back bone , finger base
7

Musculosketal----
Three types of muscles exist in the body
Skeletal Muscles
Cardiac muscles
Smooth/Visceral muscles
8

Musculoskeletal ----
 The major bones in which redbone marrow located.
 Sternum
 Ileum
 Vertebrae
 Ribs
9

Musculoskeletal------
Bone is a type of connective tissue
Biochemically, it is defined by its special
blend/mixture of organic matrix (35%) and
 Inorganic elements(mineral deposits) (65%).
Bone contains inorganic components: calcium 99%,
phosphorus 85% , and sodium and magnesium 65%

The organic component includes:
 The cells of bone.
Proteins of the matrix.
 The bone-forming cells include:-
1.OSTEOBLASTS
Function in bone formation by secreting bone
matrix/surrounding substance .
 Located on the surface of bone & synthesize,
transport, & arrange many proteins of the matrix;
they also initiate mineralization
11

2.OSTEOCYTES:-
Are matured bone cells involved in bone-maintenance
functions.
 These are the most numerous bone-forming cells.
3. OSTEOCLASTS
Involved in destroying, resorbing, and remoulding
bone
12

OSTEOMYELITIS
 SEVERE INFECTION OF THE:
Bone.
Bone marrow.
Surrounding soft tissue.
Caused by a variety of microorganisms.
Most common infecting microorganism is
Staphylococcus aureus
13

Etiology
ORGANISM POSSIBLE PROBLEM
Staphylococcus aureus Pressure ulcer, penetrating wound,
open fracture, orthopedic infection,
vascular insufficiency disorder
Staphylococcus epidermidis Indwelling prosthetic device
Streptococcus viridans Abscessed tooth, gingival disease
Escherichia coli Urinary tract infection
Mycobacterium tuberculosis Tuberculosis of any tissue
Neisseria gonorrhoeae Gonorrhea of urinary system
Pseudomonas sp. Puncture wounds, intravenous
drugs
Salmonella sp. Sickle cell disease
Fungi, mycobacteria Immunocompromised host

WAYS OF INFECTION
Indirect Entry:
 Hematogenous through the blood stream.
 Contagious focus (Peripheral Vascular
disease-associated)
 Extension from adjacent tissue infection.
Indirect infection into the bone.

INDIRECT ENTRY-----
 Frequently affects growing bone in boys <12 yrs old.
 Associated with increased incidence of blunt trauma
Most common sites of indirect entry.
Distal femur ,Proximal tibia.
Humerus ,Radius.

Indirect Entry
 Adults with increased risk.
Vascular disorders
Genitourinary and respiratory infections
Spread infection from blood to bone
Vascular-rich bone sites infections.
Pelvis
Tibia
Vertebrae 17

Haematogenous
Predominantly occur in children, middle-aged, and
older adults .
There is usually a single organism that enters a bone
via the bloodstream from a site of infection (most
commonly S. aureus).
Common sources of infection: UTI, skin infection,
URTI, and acute otitis media.
18

Contagious Infection
Onset is insidious .
Infection spreads to adjacent bone through the
soft tissue .
Greater risk for clients with Diabetes Mellitus
and severe atherosclerosis
19

Direct Entry
Can occur at any age.
Open wound where microorganisms can gain
entry to body.
May also occur in presence of foreign body:
Implant.
Orthopedic prosthetic device.
20

CLASSIFICATIONS OF OSTEOMYELITIS
1.ACUTE OSTEOMYELITIS.
2. CHRONIC OSTEOMYLITIS
21

ACUTE OSTEOMYELITIS
DEFINITION:
Is an acute bacterial infection of the bone and its
medullary cavity.
It commonly affects children, boys more than
girls
22

CAUSES
Staphylococcus aurous is in 80% of cases
Gram negative rods & Staphylococcus in neonates
H. Influenza in children under 5 years of age
Trauma may predispose children to osteomyelitis
23

Clinical Manifestations-
 Systemic sign of :
Fever
Night sweats
Chills
Restlessness
Nausea
24

Clinical Manifestations---
 ACUTE OSTEOMYELITIS
 Local/Rooting symptoms
Constant bone pain that worsens with activity.
Swelling, tenderness, warmth at infection site
Restricted movement of affected part
Later signs: drainage from sinus tracts
25

DIAGNOSIS
History- Clinical Manifestations
Physical Examination - Localized bony tenderness
(most important)
Adjacent joint may contain effusion
 Lab. Investigation - Leukocytosis
 Raised ESR
Positive blood culture
26

Radiological investigation
 X-ray changes of bone: late to develop (10-15
days)
Is not helpful for diagnosis of acute osteomyelitis
27

TREATMENT
 ANTIBIOTICS:
IV antibiotic should be started empirically after
taking blood sample for culture
Choice of antibiotics depends on the age:
 Neonates:- E.g. Cloxacillin + Gentamycin
28

TREATMENT: depends on the age
 Children under 5 years:
e.g. Cloxacillin + Chloramphenicol
 Patients above 5 years:-
e.g. Cloxacillin
29

TREATMENT
 The duration of antibiotic treatment is 6 weeks.
 IV route is changed to oral after fever .
 Leukocytosis have disappeared (with in 7-14 days).
30

TREATMENT
 Surgery: to drain abscess is recommended if fever
and pain fail to subside after 48 hours of IV antibiotic
treatment or if there is evidence of pus collection.
 Analgesics and splinting: Analgesics and POP casts
splinting of the limb in functional position.
 skin traction: Also reduces pain in the acute phase.
31

CHRONIC OSTEOMYELITIS.
It is usually follows a delay or inappropriate
treatment of an acute stage.
 It may also follow direct infection of bone in
compound fracture.
It is bone infection lasting longer than a month.
Infection that has failed to respond to initial course of
antibiotic therapy.
32

Clinical manifestations .
Systemic signs fever ,bacterial toxicity may be
diminished.
Local signs of infection more common:
Constant bone pain
Swelling, tenderness, warmth at infection site
Wound discharges & dead bone (sequester) lies in an
abscess cavity 33

Chronic Osteomyelitis of the Femur
34

PATHOPHYSIOLOGY
After entry, microorganisms lodge in an area
of bone where circulation slows.
Microorganisms grow causing increased
pressure because most bone is nonexpanding
Increased pressure leads to ischemia and
vascular compromise of periosteum
35

PATHOPHYSIOLOGY-----
Eventually, infection passes through bone and
marrow cavity.
Results in bone devascularization and necrosis.
Once ischemia occurs, bone dies & Sequestrum
forms.
Sequestrum is devitalized bone tissue separates
from living bone .
36

Part of periosteum that continues to have a blood
supply forms new bone called involucrum
Sequestrum continues to be an infected island of
bone, surrounded by pus
Difficult for blood-borne antibiotics or white
blood cells (WBCs) to reach sequestrum.
Sequestrum can move out of bone and into soft
tissue.
37

Once outside bone.
Sequestrum may.
Revascularize and then undergo removal by
normal immune process.
Be surgically removed through debridement of
necrotic bone.
If necrotic sequestrum is not resolved, it may
develop a sinus tract resulting in chronic, purulent
cutaneous drainage.
38

Investigations
A newly formed bone (Involcrum) under the
elevated periosteum
 CBC: leucocytosis.
 ESR usually is elevated (90%) nonspecific.
 culture, test sensitivity.
39

Investigations-----
Blood culture :positive in only 50% of patients with
hematogenous osteomyelitis.
X-Ray:-
First sign is soft-tissue edema at 3-5 days after
infection.
Approximately 40-50% focal bone loss is necessary
to cause detectable damage on plain films.
40

X/ray -----
 MRI :Early detection and surgical localization of
osteo-myelitis.
Sensitivity ranges from 90-100%.
 Radionuclide bone scanning :-
Show increase activity but it is a non specific sign of
inflammation
41

Diagnostic criteria for os/m
 Requires 2 of the 4 following:-
A. Localized classic physical findings of bony
tenderness, with overlying soft-tissue erythema
or edema.
B. Purulent material on aspiration of affected bone.
C. Positive findings of bone tissue or blood culture.
D. Positive radiological imaging study.
42

Treatment of chronic os/m----
 Principles of treatment:-
 Analgesia as general supportive measures.
 Rest of the affected part.
 Antibiotic treatment.
 Surgical eradication of pus and necrotic
tissue(debridement)
43

Treatment……
Antibiotic treatment:-
Start with IV antibiotics for 1-2 weeks then oral for 3-
6 weeks.
Take cultures to detect the organism and its sensitivity
pattern.
Start empirical treatment before the results came back,
then modify it according to the results.
44

Antibiotic choices:-
Older children and adults (staph infection):-
fluloxacillin .
Children younger than 4 year-old or those with
gram negative organisms: 3rd generation
cephalosporin.
Heroin addicts and immuno-compromised
patients: more specific antibiotics after culture.
45

Treatment…..…
Sickle cell anemia and osteomyelitis:-
fluoroquinolone antibiotic (not in children)
A 3rd generation-cephalosporin (eg, ceftriaxone) is
an alternative choice.
Nail puncture (S aureus and Pseudomonas
aeruginosa): ceftazidime or cefepime. Ciprofloxacin
is an alternative treatment
46

Treatment…..…
Trauma (S aureus, coliform bacilli, Pseudomonas
aeruginosa):- Nafcillin , ciprofloxacin,vancomycin ,
cephalosporin
Drainage:-
 Subperiosteal abscess
 Pyrexia and local tenderness more than 24 hour after
adequate antibiotic treatment.
# Removal of prosthetic implants:-
If they become unstable after a trauma/
intractable infection following joint replacement.
47

Prevention for os/m
 Post-traumatic infection (regular wound dressing
for established infection.)
 Debridement of open fractures.
 Stabilization of fractures.
 Antibiotics.
 Closure of exposed bone surfaces
48

Postoperative infection
 Cleanest possible surgical environment.
 Careful haemostasis.
 Suction drainage.
 Prophylactic antibiotics in high risk surgeries
 Urinary catheters and drains removal as soon as
possible.
49

General Nursing care of Os/m
 Overall goals:
Have satisfactory pain and fever control.
Not experience any complications associated with
osteomyelitis.
Cooperate with treatment plan.
Maintain a positive outlook on outcome of
disease
50

Independent nursing care
 Health promotion:-
Control infections already in body
Susceptible adults.
Immunocompromised.
Wear orthopedic prosthetic devices.
51

Independent nursing care----
Have vascular insufficiencies.
Instruct susceptible adults and their families
on local and systemic manifestations
52

Independent-----
 Acute intervention:-
Some immobilization of affected limb will
↓ pain.
Limb should be handled carefully to avoid
excessive manipulation that ↑ pain.
Assess and manage patient’s pain level.
Dressings to absorb exudate from draining
wounds
53

Independent-----
 Acute intervention
Patient frequently positions affected extremity in a
flexed position to promote comfort.
Contracture may then progress to deformity.
Foot drop can develop quickly in lower extremity if
foot is not supported in a neutral position by a splint
or if there is excessive pressure from a splint
54

Acute intervention-----
Instruct patient to avoid activities that
↑ circulation and swelling and serve as stimuli to
spread infection.
Exercise, heat application.
Teach patient potential adverse and toxic reactions
with prolonged and high-dose antibiotic therapy
55

Acute intervention -------
Lengthy antibiotic therapy can result in an
overgrowth of Candida albicans .
Patient and family often frightened and discouraged
Continued psychologic and emotional support is an
integral part of nursing management
56

Independent care-----
 Ambulatory and home care .
IV antibiotics can be administered to patient in a
skilled nursing facility or home setting.
If at home:-
Patient and family must be instructed on proper
care and management of venous access device
and how to administer antibiotic.
57

Independent-----
 Ambulatory and home care :-
Importance of continuing antibiotics after
symptoms have subsided should be stressed.
Periodic nursing visits provide support and decrease
anxiety.
Frequent dressing changes for open wounds.
It may require supplies and instruction in technique
58

Collaborative Care
Vigorous and prolonged intravenous (IV) antibiotic
therapy.
Treatment of choice for acute osteomyelitis
as long bone ischemia has not been occurred
cultures or bone biopsy should be done.
if possible delaying antibiotic treatment may require
surgical debridement and decompression.
59

Collaborative------
Patients are often discharged to home care .
skilled nursing facility with IV antibiotics delivered
via
A central venous catheter.
Peripherally inserted central catheter
60

Collaborative------
Antibiotic therapy may be continued for at home for 4
to 6 weeks or as long as 3 to 6 months.
Variety of antibiotics may be prescribed.
Penicillin, nafcillin .
Neomycin, vancomycin.
Cephalexin ,Cefazolin
61

Collaborative------
Adults with chronic osteomyelitis ,prescribed oral
therapy + fluoroquinolone for 6 to 8 weeks instead
of IV antibiotics.
Oral antibiotics may be given after acute IV therapy
to ensure resolution of infection.
Patient’s response monitored through bone scans and
ESR tests for possible improvement.
62

Collaborative------
 Surgical treatment for chronic osteomyelitis
Removal of poorly vascularized tissue and dead
bone.
Extended use of antibiotics.
Antibiotic-impregnated polymethyl methylcylate
bead chains.
63

Collaborative------
After debridement, wound may be closed and a
suction irrigation system inserted.
Intermittent or constant irrigation of affected bone
with antibiotics .
Protection on limb or surgical site with casts or
braces .
Negative pressure to draw wound together.
64

Collaborative------
Hyperbaric oxygen therapy with 100% oxygen
as adjunct therapy:
 Stimulate circulation and healing.
Orthopedic prosthetic devices, if source of
infection must be removed.
Muscle flaps, skin grafting provide wound
coverage over dead space (cavity) in bone.
65

Collaborative------
Bone grafts may help restore blood flow
Amputation may be indicated if
Extensive bone destruction.
Necessary to preserve person’s life / improve
quality of life
66

Collaborative------
 Long-term and mostly rare complications.
Septicemia.
Septic arthritis.
Pathologic fractures.
Amyloidosis
67

Musculoskeletal trauma
FRACTURE :-
It is a break in the continuity of bone.
Is defined according to its type and extent.
Fractures occur when the bone is subjected to stress
greater than it can absorb.
It is a structural breech in the normal continuity of
bone
68

MECHANISM OF INJURY
1- Tubular bone: -
 Direct violence to the bone
 Indirectly due to twisting or angulation.
2. Cancellous /spongy bone: -
 may be fractured by compression
e.g. Clash fracture of vertebral body or by
traction
e.g. Transverse fracture of the patella
69

BONE HEALING PROCESS
 Inflammation.
 Bone Production.
 Bone Remodeling
70

Bone healing process---
 PROGRESSES THROUGH:
 The phase of hematoma
Cellular proliferation
Callus formation and remodeling
 Generally takes longer than soft tissue healing
 In general, a long bone takes 6-12 weeks to heal in
an adult and 3-6 weeks in children.
71

INFLAMMATION.
Lasts a few days.
Causes blood clotting in fractured area.
Clotting creates a stability and
Framework for new bone production
72

BONE PRODUCTION.
Blood clotted areas are replaced with “soft callus”
(fibrous tissue and cartilage).
Then replaced with “hard callus” (hard bone)
73

BONE REMODELING
Lasts a few months.
Bone continues to form, grow stronger, become
compact, and return to original form.
Growing stronger results from little exercise
(like standing and walking)
74

Once bone is healed pretty well, physical therapy
will help to regain strength.
 If bone is healing slowly the Nurse may:-
 Longer immobilization
 Bone stimulation
 Surgery
 Bone growth proteins
75

Maintaining & restoring function
• To promote bone and soft tissue healing
 Swelling= is controlled by elevating the injured
extremity and applying ice as prescribed
 Neurovascular status =(circulation,
movement, sensation) is monitored.
Patient participation in activities of daily living
(ADLs) is encouraged.
76

FACTORS ENHANCE FRACTURE HEALING
Immobilization of fracture fragments
Maximum bone fragment contact
Sufficient blood supply
Proper nutrition
77

FACTORS ENHANCE----
Exercise: weight bearing for long bones
Hormones: growth hormone, thyroid, calcitonin,
vitamin D, anabolic steroids
Electric potential across fracture
78

Factors affecting fracture healing
 LOCAL FACTORS: -
 Degree of soft tissue injury
Pattern and site of fracture
Presence of Infection
Adequacy of reduction
 Adequacy of immobilization
79

FACTORSAFFECTING FRACTURE------
 SYSTEMIC FACTORS:
Like debilitating diseases
immunosuppressive drugs
Impaired healing.
80

Classification
 Fractures may be classified in several ways.
the most important clinical classification is:
 Closed vs
 open (compound) fracture
81

common types of Fractures
Some broken bone
Types.
 Comminuted Fracture.
 Spiral Fracture.
 Compound Fracture.
 Greenstick Fracture.
 Transverse Fracture.
 Simple Fracture.
 Oblique Fracture
82

Types of Fractures-----
COMPLETE FRACTURE
 Involves a break across the entire cross-section of the
bone and is frequently displaced .
 INCOMPLETE FRACTURE
 The break occurs through only part of the cross-
section of the bone.
(e.g. greenstick fracture)
83

Types of Fractures-----
COMMINUTED FRACTURE.
 produces several bone fragments
CLOSED FRACTURE
 It is simple fracture that does not cause a break in
the skin.
OPEN FRACTURE.
 The skin / mucous membrane wound extends to the
fractured bone.

Specific Types of Fractures
A fracture in which one
side of a bone is broken
and the other side is bent
85

Oblique
A fracture occurring at
an angle across the
bone(less stable than a
transverse fracture)
87

Comminuted fracture
 A fracture in which bone
has splintered into several
fragments
88

Spiral fracture
A fracture that twists
around the shaft of the
bone

Open Displaced
Through the skin.
Not aligned.
Can have displaced fx
that do not come through
the skin
90

TRANSVERSE/NON-DISPLACED
A fracture that is straight
across the bone.

AVULSION/POTTS FX
A fracture in which a
fragment of bone has
been pulled away by a
ligament or tendon and
its attachment
92

COLLES FX
Broken wrist. When a
patient sustains a Colles'
fracture, there is
displacement of the bone
such that the wrist joint
rests behind its normal
anatomic position.
A Colles' fracture is most
commonly found after
falling on to an
outstretched hand.
93

STRESS
FRACTURE
 Overload caused by muscle contraction, altered
stress, change in ground reaction, rhythmic
repetition.
 Obvious reaction in the bone.
 A fracture that results from repeated loading without
bone and muscle recovery.

Specific Types of Fx----
COMPRESSION: -
 A fracture in which bone has been compressed(seen
in vertebral fractures)
DEPRESSED:
 A fracture in which fragments are driven inward
(seen frequently in fractures of skull and facial
bones)
EPIPHYSEAL: a fracture through the epiphysis
95

Specific Types of Fx----
PATHOLOGIC FRACTURE :-
 a fracture that occurs through an area of diseased
bone
e.g: Osteoporosis, bone cyst, Paget’s disease,
bony metastasis, tumour
96

CAUSES
Direct blows.
Crushing/devastating forces .
sudden twisting motions.
Extreme muscle contractions
97

Clinical Manifestations of FXs
Pain
 Loss of function
Deformity
 Shortening of the extremity
98

CLINICALMANIFESTATIONS----
Local swelling.
Discoloration
Crepitus/grating sound
N.B :Not all of these clinical manifestations are present
in every fracture
• Testing for crepitus can produce further tissue
damage and should be avoided
99

DIAGNOSTIC STUDIES
 Clinical: - History of trauma
 Pain, swelling
 Inability to use the injured body part
 Tenderness
 Swelling and bruising
 Deformity, abnormal movement are (sure signs of
fracture)
100

DIAGNOSTIC STUDIES
 Complete blood count (CBC):
 Hematocrit (Hct) increased (hemo-
concentration) or decreased (signifying
hemorrhage at the fracture site or at distant
organs in multiple trauma)
 Increased white blood cell (WBC) count is a
normal stress response after trauma.
101

DIAGNOSTIC STUDIES
Urine creatinine (Cr) clearance:-
 Muscle trauma increases load of Cr for renal
clearance.
Coagulation profile: -
 Alterations may occur because of blood
loss, multiple transfusions, or liver injury.
102

X-RAY:INVESTIGATION
 A suspected fractured bone should be x-rayed.
 X-ray should be taken in at least two planes
(AP and lateral)
 Should always include the joints proximal and
distal to the fracture.
103

X-RAY:INVESTIGATION---
 Look in the X-ray for:
 Presence of fracture
 The part of bone fractured
 The pattern of the fracture which can be transverse,
comminuted, oblique, spiral, segmental.
104

X-RAY:INVESTIGATION---
 Look in the X-ray for:
Presence and type of displacement which can be
lateral
shift, angulation, rotation, overlap, distraction
Quality of bone: check for: Osteoporosis
Pathological fracture, etc
105

Management of a patient with fracture
 GENERALTREATMENT:
Evaluation of associated life threatening injuries
Always assess the status of distal circulation and
neurological function.
Administer anti pain
 Splint all fractures before sending the patient for x-
ray or referring.
106

Local treatment of the fracture:-
 -REDUCTION
 Bringing the fractured bone to normal or near to
normal anatomic position.
This is needed only for displaced fractures
Age and function of the patient are important in
considering the goals of reduction
 Reduction may be done in various ways:
Using gravity E.g. Humeral shaft fracture
107

REDUCTION-------
 Closed reduction by:
 Manipulation e.g. Colle’s fracture
 Traction e.g. Femoral shaft fracture
Open (Operative) reduction:
Used when other methods are not possible,
have failed or a perfect anatomic reduction is
needed. e.g. displaced intra articular fractures.
108

Local treatment of the fracture-----
IMMOBILIZATION:
 The purpose of immobilization is to:
To prevent re displacement of a reduced fracture
 To decrease movement at the site of fracture
To prevent further soft tissue injury
 To Relieve pain
109

METHODS OFIMMOBILIZATION------
 Plaster of Paris (POP) cast:
Is the safest and cheapest method
Immobilization includes two adjacent joints
Joints should be immobilized in a functional position
Complications include joint stiffness&compartment
syndrome.
110

METHODS OFIMMOBILIZATION
 TRACTION:
 Using gravity: e.g. U-slab for humeral shaft fracture
 Skin traction: A method of applying traction using
bandage, usually used in children
Temporarily in adults. The maximum weight that can
be applied is 2kg.
 Skeletal traction: Traction applied via a pin inserted
into the bone distal to the fracture. e.g. Tibial pin
traction for femoral fracture
111

EXTERNAL FIXATION
 method of fixing the fracture by metal pins passed
through the bone above and below the fracture and
connected to a metal frame.
It is mostly used in compound fractures as it
combines good access for wound care with
immobilization
112

INTERNALFIXATION
Internal fixation is a method of operative fixation
of fractures by plates,nails, screws, pins and wires
The rigid fixation allows patients to get out of bed
early
 It’s employed when operative reduction has been
done for any of the reasons mentioned before.
113

INTERNALFIXATION
It’s also indicated in poly traumatized patients whose
confinement in bed
 if not treated on time it results in high morbidity and
mortality.
Infection is the main complication and may result in
chronic osteomyelitis
 It also needs expertise and orthopedic surgical
facilities.
114

REHABILITATION
Preserving muscle
Preserving joint function both during and after
treatment is an essential component of fracture
treatment for a good result.
115

Open (compound) fracture
 A fracture in which the fracture hematoma
communicates with skin or mucous membrane.
Infection is the most feared complication of
compound fractures and
It may cause delayed healing, non union, sepsis
or even death.
 It is a surgical emergency
116

Principles of management
 Early wound debridement
 thorough irrigation with saline
 Antibiotics: Broad spectrum e.g. Penicillin +
Aminoglycoside should be given IV at least for 48 hrs.
 Tetanus prophylaxis
 Rigid immobilization with access to the wound e.g.
external fixation
 Delayed wound closure!
117

Nursing management of Fx
 Relief of pain
Assess type and location of patient’s pain
 Handle the affected extremity gently
 supporting it with hands or pillow.
 Apply Buck’s traction as prescribed,Use
trochanter roll.
118

Nursing management of Fx----
To use pain relief measures before pain is
“unbearable”
 Evaluate patient’s response to medications
and other pain-reduction techniques.
 Consult with physician if relief of pain is not
obtained.
 Position for comfort and function.
 Assist with frequent changes in position
119

Providing wound healing
Monitor vital signs
Perform aseptic dressing changes.
Assess wound appearance and character of
drainage.
 Assess report of pain.
 Administer prophylactic antibiotic if prescribed,
and observe for side effects
120

Complications of Fractures
 SOFT TISSUE INJURIES
Arteries, Nerves and Viscera may be injured
 Compartment syndrome
Is a dangerously increased pressure within the
enclosed fascial compartments of extremities,
especially forearm and leg.
The high compartmental pressure causes Ischemia
and necrosis of soft tissues in the compartment.
121

Complications of Fractures-----
 It may be aggravated by application of tight bandages or
circular POP casts on a freshly injured limb.
 Severe pain, especially with passive flexion of fingers is
the earliest indicator.
 Paresthesia, Paralysis, Pallor or Pulselessness,pain
 Early diagnosis and complete splitting of a tight bandage
or circular POP cast may resolve the situation.
 Fasciotomy is done if the above measures have failed.
122

 INFECTION:
Usually complicates open fractures
Chronic osteomyelitis may be the result.
Adequate debridement is the most critical
factor in preventing infection
123

 Bone healing abnormalities:
 Delayed Union
 Failure of a fracture to heal in the expected time period.
 Non union
 Total failure of the fracture to heal with formation of a
false joint between the fractured ends (pseudoarthrosis)
124

 Malunion:
Healing occurs with deformity
 Avascular necrosis:
Necrosis of part of the fractured bone occurs
due to disruption of its vascular supply.
e.g. Femoral head.
125

 Joint complications:
Joint stiffness
 Secondary Hemarthrosis
 Osteoarthritis
126

 Systemic complications:
Usually follow poly-trauma and major long
bone fracture.
 Includes ARDS and fat embolism syndrome
127

OSTEOPOROSIS
Is reduced bone mineral density (BMD).
A disease of bones that leads to an increased risk of
fracture .
Bone micro architecture deteriorates.
The amount and variety of proteins in bone are
altered.
128

osteoporosis----
The disease may be classified as primary type 1,
primary type 2, or secondary.
Osteoporosis common in women after menopause, is
referred to as primary type 1 / postmenopausal
osteoporosis.
Primary type 2 osteo-porosis /senile osteoporousis
occurs after age 75.
129

osteoporosis----
It is seen in both females and males at a ratio of 2:1.
Secondary osteoporosis may arise at any age and
affect men and women equally.
It results from chronic predisposing medical problems
/ disease/prolonged use of medications such as
glucocorticoids, when the disease is called steroid-or
gluco-corticoid induced osteoporosissis.
130

OSTEOPOROSIS MGT
 Lifestyle change includes :
Diet.
Exercise.
prevention of falls.
The utility of calcium and vitamin D
131

DISLOCATION
Total disruption of joint with no remaining contact
between the articular surface .
A sublaxation is partial joint disruption with partial
remaining but abnormal contact of articular surface
132

TYPES OF DISLOCATION
Traumatic dislocation .
Pathological/ spontaneous dislocation.
Recurrent dislocation.
Congenital dislocation .
133

TRAUMATIC DISLOCATION
Caused by trauma
A force strong enough to disrupt the joint
capsule .
Supporting ligamentous structures dislocates a
previously normal joint due to trauma .
134

dislocation-------
 PATHOLOGICAL/SPONTANEOUS DISLOCATION
Occurs when pathological condition in the joint
causes abnormality in the structural integrity of
the joint
e.g. septic hip dislocation
135

dislocation-----
 RECURRENT DISLOCATION
Which repeatedly occurs after trivial/minor
injuries .
It is due to weakening of the supportive joint
structure .
136

Dislocation----
CONGENITAL DISLOCATION
Which present congenitally since birth
e.g congenital hip dislocation
137

DIAGNOSIS
The limb assumes an abnormally fixed position with
loss of normal range of movement in the affected
joint.
Associated soft tissue injuries should be looked for:
e.g. Popliteal artery in knee dislocation
.Sciatic nerve in posterior hip dislocation
 X-ray in various planes and views confirms
diagnosis
138

Management of dislocation
Early reduction of the dislocation
Immobilizing the joint
 Allow time for rest the supporting structures of the
joint to heal.
Rehabilitation of the joint
139

Amputation
 It is removal or excision of part or whole of the
limb.
INDICATIONS
 Dead limb ( gangrene) :-
 Due to trauma, embolism ,major arterial injury and
diabetic gangrene,crushing injuries ,burns,
malignant tumors (in young pts )
Peripheral vascular diseases account more(elder pt)
140

indications
 Deadly limb :-
Due to life threatening infection e.g.Gas gangrene
Gas gangrene is a bacterial infection that produces
gas within tissues.
Life threatening malignancies which can’t be
controlled by other local measures.
141

indications ----
 Dead loss :-
Sever soft tissue injury .
Nerve tissue is associated.
Commonly occurs in compound fracture
142

Level of amputation
 Depends on :
Age
Nature and extent of pathology , e.g neoplasm,
trauma
Vascularity of the tissue(circulation in the part)
 Functional usefulness(requirements of prosthesis)
143

Level of amputation ---
Presence of infection
Status of the joints ( preserving knee and
elbow joints are desired.)
Access to the various types of prostheses
144

Syme’s (modified ankle disarticulation amputation )
for extreme foot trauma.
Below knee amputation is preferred to above knee
amputation,because of the importance of the knee
joint and the energy requirements for walking .
145

Generally the most distal point level that will heal
& still provide a functional stump is selected.
In the upper limb ,attempt should be made to
conserve every possible inch.
In the lower limb important factor is conserving
the knee joint.
Amputation performed in the face of infection , be
left open for a later closure.
146

Complications of amputation
Edema
Hematoma
2dry and reactionary hemorrhage
Infection
Ischemic skin necrosis
Flexion contracture ,chronic pain –psychogenic ,
neuromas
147

CHRONIC PAIN –PSYCHOGENIC
 PHANTOM LIMB PAIN:
Occurs 2-3 months after amputation
More frequently occurs above knee amputation
Pt describes pain/unusual sensation in amputated
part.
The sensation creates a feeling that the extremity is
present,crushed,cramped/twisted in an abnormal
position
148

SOFT TISSUE INJURIES
SPRAIN:- An injury to joint, ligament, muscle or
tendon in the region of joint.
 Ligaments are tissues that connect bones at a joint.
 Cause :-Forcing limb beyond normal range of
motion / movement .
 Falling, twisting, or getting hit
Common site: ankle, wrist, knee
149

TYPES OF SPRAIN injury
 There are three types :-
Grade 1 sprains:- are slight damage to ligaments
Grade 2 sprain:- stretching and damage to the
fibers of the ligament.
Grade 2 is partial tearing of the ligament. Laxity or
looseness, of the joint.
150

TYPES OF SPRAIN-----
 Grade 3 sprains:-
Are complete tearing of the joint may occur.
Complete tearing of the ligament, gross
instability may occur.
151

Soft tissue injuries
 SIGN AND SYMPTOMS :-
 Swelling , bruising , instability
Pain /Tenderness
Dislocation , functional loss.
152

First aid for sprain
If the victim’s ankle or knee is affected, do not allow
him to walk.
Loosen or remove the victim’s shoes.
Apply the pillow or blanket splint and elevate the
victim’s leg, because swelling may produce greater
disability than the original injury itself.
153

First aid for sprain-----
In mild sprains, Elevate the affected part.
Apply cold wet pad or place small bag of ice on the
affected area over a thin towel to protect the victim’s
skin.
If swelling and pain persist, Seek medical help.
154

TREATMENT OF A SPRAIN
 Grade 1 and Grade 2 sprain use=- “R.I.C.E.”
R Rest.
I Ice application .
C compression.
E Elevation of the part
155

TREATMENT OF A SPRAIN-----
 Treating a Grade 3 sprain:-
 May result in permanent instability.
Surgery is rarely needed.
A short leg cast or cast-brace may be needed.
156

Treated with surgery
 There are 2 common methods :-
Arthroscopy:-a surgeon will go in and look to
visualize loose fragments or pieces of bone or
cartilage damaged .
Reconstruction:- a surgical team will repair joint,
the torn ligament with stitches or use ligaments
from the foot to repair the damaged ligament.

REHABILITATION OF A SPRAIN
 Phase 1 :- Resting and protecting the ankle while
reducing swelling.
 Phase 2:- works on restoring the motion flexibility
and strength of the ankle.
 Phase 3:- includes returning to activity that does not
twist or turn the ankle while doing maintenance
exercises.
The length of your recovery depends on the severity
of the sprain and rehabilitation could take weeks to
months
158

Health education on sprain
 Rest your ankle by not walking on it.
 Ice your ankle for 20-30 minutes 3-4 times daily .
 Combine with wrapping to decrease pain & dysfunction.
 Compression dressings, or bandages to support and
immobilize the injured ankle.
 Elevate your ankle above the heart for 48 hours.
 When treating a Grade 2 sprain use “R.I.C.E.” but allow
for more time to heal.
159

PREVENTION OF A SPRAIN
Maintain flexibility.
 Good strength of muscle.
Pay attention to walking and warm up before you
exercise.
 Pay attention to your body’s balance .
 Wear good shoes, choose running surfaces.
Slow down when you feel pain or fatigue.
160

Soft tissue injuries-----
 STRAIN:-
Injuries to muscle resulting from over stretching
and the affected muscle some times partially torn.
 COMMON SITE: -
On muscle of back due to poor lifting technique
161

Soft tissue injuries-----
 PREVENTION :-
 place feet close to the object to lift.
 squat – keep back straight as possible.
 Lift slowly, pushing up with strong thigh & leg muscles
bearing the weight.
 Do not jerk
 To lower a heavy object reverses the above procedure.
162

First aid for strain
Bed rest on hard board under mattress for firm
support is recommended for a person with a
strained back.
Application of warm moist compress and rest.
Administer Analgesics if it is available.
Seek medical help if necessary.
163

RHEUMATOID ARTHRITIS (RA)
A chronic multi systemic inflammatory disorder of
the lining of the joints.
It also affect organs like skin, eyes, lungs, heart,
blood, or nerves
 The body tissue is mistakenly attacked by its own
immune system
RA is a chronic disorder, may be occasional
symptom-free periods,
164

RA---
 Usually involving peripheral joints
 Its involvement is symmetrical distribution
 It causes subsequent changes in joint integrity is the
hallmark of the disease.
 the disease can worsen over time and may never go away.
 Early, aggressive treatment is key to slowing or stopping
its progression.
165

Epidemiology of RA
Statistics about 1% of the worlds population is
afflicted
Women almost 3 times more often than men.
F: M 3: 1
It is 4 times more common among smokers than
non-smokers.
Some Native American groups have a higher
prevalence rate.
166

Epidemiology of RA----
Genetics or family history play a big role.
Onset is uncommon under the age of 15.
No age is immune/age difference diminishes
in older age group.
Most commonly diagnosed between the ages of 40
and 50 years and prevalence increases with age.
Normally no later than 80 years of age.
167

ETIOLOGY
RA remains unknown. But two factors
1.Genetic factors =high with monozygotic twins 4x
and 1st degree relatives.
2. Environmental
Infectious agents eg. rubella ,mycoplasma,CMV,
bacteria
168

Clinical symptoms
 RA comes with pain, warmth, and swelling.
 The inflammation is symmetrical
 Occurs on both sides of the body( wrists, knees/ hands).
 Moring joint stiffness lasts 1hrs/after periods of inactivity.
 Ongoing fatigue & low-grade fever.
169

CLINICAL FEATURES---
Acute onset in 10% of pts
Symptoms typically develop gradually over years, but
can come on rapidly for some people.
Articular /joint manifestation: pain ,swelling
,tenderness, agrravated by movement
Generalized joint stiffness .
Bilateral symmetrical small joint involvement is
typical for RA
170

Commonly affected joints
Wrist joints : synovitis of wrist is very common in
RA
Meta-carpophalangial joints (mcp)
Proximal interphalagial (PIP) joints
Elbow joints =leads to flexion contracture
Knee joint involved synovial hypertrophy, chronic
effusion
Forefoot, ankles, subtalar joints
171

Deformity and loss of function the joints.
172

Clinical symptom-----
 Affected areas of the body other than the joints
Rheumatoid nodules : firm lumps under the skin &
internal organs
Sjogren's syndrome: inflammation and damage of
the glands of the eyes and mouth.
 Pleuritis: inflammation of the lung lining
173

Symptoms ------
Pericarditis: inflammation of lining surrounding the
heart
Anemia: reduction of red blood cells
Felty syndrome: reduction of white blood cells,
associated with enlarged spleen
Vasculitis: blood vessel inflammation, which can
impair blood supply to tissues
174

Juvenile RheumatoidArthritis (JRA)
JRA: is the most common type of arthritis in kids.
 It causes joint inflammation, stiffness, and damage.
 it can also affect a child's growth.
JRA is also known as juvenile idiopathic arthritis.
"Idiopathic" means no known cause
175

RAand Pregnancy
 Surprisingly, rheumatoid arthritis improves in up to
80% of women during pregnancy.
 It will likely flare up after delivery.
 How and why this happens is still unclear.
 Changes in your medication may be necessary before
you become pregnant and during pregnancy.
177

Diagnosing RA: Evaluating Symptoms
 Diagnosing RA in its early stages is challenging.
 Proper history taking
Morning joint stiffness
Swelling/fluid around several joints at the same time
Swelling in the wrist, hand, or finger joints
Same joints affected on both sides of your body
Firm lumps under the skin(rheumatoid nodules)
178

Investigation Testing
Hematological =CBC,ESR
Rheumatoid factors =IgG (autoantibodys)
X Rays of hands and feet.
Magnetic Resonance Imaging (MRI).
Ultrasounds.
179

Revised criteria for Diagnosis
1) Morning stiffness lasting more than 1 hour most mornings for
at least 6 weeks.
2) Arthritis and soft-tissue swelling of more than 3 joints .
3) Arthritis of hand joints, present for at least 6 wks.(MCP, PIP)
4) Symmetrical arthritis.
5) Rheumatoid nodules
6) Radiological changes suggestive of joint erosion.
7) Serum rheumatoid factors
180

Criteria for diagnosis------
INTERPRETATION:
 Four of seven criteria are required to classify pt
Patient with two more criteria ,the clinical diagnosis
of RA is not excluded.
Goals of therapy.
Short term =controlling pain and reducing
inflammation with out causing undesired side effect.
Long Term= preservations of joint function and the
ability to maintain life-style.
181

Treatment
1) First line treatment: NSAIDs
 Used to control symptoms and signs
 These agents are rapidly effective .
 Aspirin,Ibuprofen,diclofenac, indomethacin
Dose:
 Aspirin 900mg po Tid
 Ibuprofen 400mg po bid
 Diclofenac 50 mg Po bid/Tid
182

Treatment ----
 Second line treatment
 Low dose oral corticosteroids
 Systemic administration in severe cases
 Dose : 5-10mg daily then taper the dose
 Local steroid injection to joint space

Is Surgery an Option for RA?
 After significant joint damage has occurred
 When pain or disability becomes unbearable surgery is
done to improve: function & relieve pain.
 Joint replacement is the most frequently performed
surgery for RA patients.
 With the knee and hip joints most often replaced. Other
types of surgery, such as arthroscopy (inserting a tube-like
instrument into the joint to see and repair abnormal
tissues) and tendon reconstruction.
184

SUPPORTIVE THERAPIES
Weight Loss
Occupational Therapy.
Physiotherapy.
Moist heat, relaxation remedies, acupuncture
185

Supportive therapy---
 Regular exercise helps:
 Maintain joint function,
 Reduce stiffness
Relieve fatigue
It helps relieve aching joints by strengthening
the muscles that support them.
186

SUPPORTIVE THERAPY-----
Exercise reduces risk of diabetes and heart disease.
Stop Smoking
Use Assistive devices to reduce joint stress
It will take 20-30% of the weight off the joint &
improve stability.
187

Supportive therapies-----
 Balanced in nutrients:
 Free of high saturated fats
 Tomatoes, citrus fruits, white potatoes, peppers,
coffee, and dairy -- worsen RA symptoms.
 Fish oil, seed oil
188

Prognosis
Disability=daily living activities are impaired.
After 5 years of disease, approximately 33% of
sufferers can no longer work.
After 10 years of disease, approximately 50% of
sufferers have substantial functional disability.
Some people have mild or short-term symptoms,
but in most cases, the disease is progressive for
life
189

GOUTY ARTHRITIS
 A group of disorders of purine metabolism.
 Characterized by elevated serum urate concentration
(hyperuricemia) .
 It is urate deposits in articular/extra-articular tissues
 Only 10% of patients with hyper-uricemia develop
gout.
 Some factors predisposes patients to develop urate
deposition and articular inflammation.
 Uric acid nephrolithiasis is a common problem. 190

URATE, HYPERURICEMIA& GOUT
Urate: End product of purine metabolism.
Hyperuricemia: serum urate with greater urate
solubility (> 6.8 mg/dl)/ concentration.
Gout: deposition of uric acid crystals in
tissues.
191

Value
 Hyperuricemia : serum uric acid >7mg%
(males) and >6mg% (females)
192

cause
 Hyperuricemia caused by:
 Serum uric acid over production.
 Serum uric acid under excretion.
No, Gout with out uric acid crystal deposition
193

Gout signs and symptoms
Pain in joint followed by warmth, swelling, reddish
discoloration, and marked tenderness
Kidney stones
Blockage of the kidney filtering tubules with uric
acid crystals
The small joint at the base of the big toe is the most
common site for an attack.
Leading to kidney failure.
194

signs and symptoms----
 Affected joints are ankles, knees, wrists, fingers&elbows.
 In some people, the acute pain is so intense that even a bed
sheet touching the toe causes severe pain.
 These painful attacks usually subside in hours to days, with
/without medication.
 In rare instances, an attack can last for weeks. Most people
with gout will experience repeated bouts over the years.
195

GOUT:AChronic Disease of 4 stages
Asymptomatic hyperuricemia
Acute flare/ burn of crystallization
Intervals between flares
Advanced Gout & complications
196

ACUTE GOUTY FLARES
Abrupt onset of severe joint inflammation, often
nocturnal, Warmth, swelling, erythema & pain,
Possibly fever.
Untreated? Resolves in 3-10 days.
90% 1st attacks are monoarticular.
50% are podagra/ painful condition of big toe due
to gout(meta-tarso-phallangeal joint)
197

SITES OF ACUTE FLARES
 90% of gout patients
eventually have podagra : 1st
metatarsal phalanges joint
198

Sites
 Can occur in other joints,
bursa & tendons
 Bursae (a small fluid-filled
sac lined by synovial
membrane)

INTERVALS with/out FLARES
Asymptomatic
If untreated, may advance
Intervals may shorten
Crystals accumulations in joints increases
Body urate stores increase
200

FLARE INTERVALS
Silent tissue deposition
& Hidden Damage

ADVANCED GOUT
Chronic Arthritis
X-ray Changes
Tophi Develop
Acute Flares continue
202

ADVANCED GOUT
 Chronic Arthritis
 Polyarticular acute
flares with upper
extremities more
involved

TOPHI
 Solid urate deposits in
tissues.

TOPHI
 Irregular & destructive

TOPHI RISK FACTORS
Long duration of hyperuricemia
Higher serum urate
Long periods of active, untreated gout
206

GOUT RISK FACTORS.
Male
Postmenopausal female.
Older.
Hypertension.
Pharmaceuticals:
Diuretics, ASA, cyclosporine

GOUT RISK FACTORS------
Transplant.
Alcohol intake.
 Highest with beer
 Not increased with wine
High BMI (obesity)
Diet high in meat & seafood
208

GOUT RISK FACTORS------
 Diabetes mellitus
 Hypertension
 Hyperlipidemia
 Atherosclerosis
 Hypothyroidism
 Abnormal kidney function
209

Who'sAffected by Gout?
The prevalence in U.S. affects 8.3 million (4%)
Americans.
Gout is more common in men than in women and
more prevalent in African-American men than white
men.
The chances of having gout rises with age, with a peak
age of 75.
In women, gout attacks usually occur after
menopause.
Among the U.S. population, about 21% have elevated
blood urate.
210

AFFECTED ----
Prevalence of hyperuricemia
2.3 – 41.4% in various populations.
Corresponds with serum creatinine /BUN levels, body
weight, height, age, blood pressure, and alcohol
intake.
Body bulk (by body weight, surface area, or body
mass index).
211

What Gout Looks Like: The Big Toe
The joint at the base of the big toe is the most
common site of an acute gout attack.
These attacks can recur unless gout is treated.
Seek help even if the pain from gout is gone.
Over time, they can harm joints, tendons, and other
tissues
212

 What Gout Looks Like: The Fingers?
Pple may experience gout with deposits of uric acid
crystals in their finger joints.
To ease the pain during a gout attack, rest the joint that
hurts.
 What Gout Looks Like: The Elbow?
Gout can also attack joints such as the elbows and
knees. Notice the protrusion on the elbow.
213

RA vs Gout
Both have polyarticular.
Both have symmetric arthritis.
Tophi can be mistaken for RA nodules
214

criteria for acute gout Dx
 The presence of characteristic urate crystals in the
joint fluid.
 The presence of 6 of the following 13 clinical,
laboratory, and radiographic phenomena:-
1.More than one attack of acute arthritis
2. Maximum inflammation developed within 1 day
3. Monoarthritis attack
216

Criteria-----
4. Redness observed over joints .
5. First metatarso-phalangeal joint painful or swollen.
6. Unilateral, first metatarso-phalangeal joint attack
7. Unilateral tarsal joint attack .
8. Tophus (proven or suspected)
9. Hyperuricemia
217

Criteria----
10.Asymmetric swelling within a joint on x ray/exam .
11. Subcortical cysts without erosions on x ray.
12. Monosodium urate monohydrate microcrystals in
joint fluid during attack .
13. Joint fluid culture negative for organisms during
attack.
218

Classification
Urate overproduction
(10%–20%)
Idiopathic.
Uric acid under
excretion(80%–90%)
Idiopathic
 Myeloproliferative/ Lymphopr
oliferative diseases
/ Hemolyticanemias/ Polycyth
emia vera/Other malignancies
 Uric acid under-excretion
 Renal insufficiency
 Polycystic kidney disease
 Drugs(Diuretics,Salicylates
( Pyrazinamide, Ethambutol)
219

Outcomes in Gout
 Clinical outcomes.
60% of untreated gout have attacks within 1 yr, 78%
have recurrence in 2 yrs, 7% have no attacks in 10 yrs.
Chronic tophaceous gout develops after 10 -20 yrs of
untreated gout.
Hyperuricemia control superior to self medication
alone.
220

Economic outcomes
 Direct burden annually is 27.4 million USD.
(men only)
 Patients with acute gout miss 3-5 days of work
annually.
 Adherence to allopurinol
221

Diagnosing Gouty Arthritis
History of repeated attacks of painful arthritis,
especially at the base of the toes ,ankles, knees.
The most reliable test is detecting uric acid crystals
in the joint fluid obtained by joint aspiration.
This common office procedure is performed with
topical local anesthesia.
Using sterile technique, fluid is withdrawn aspirated
from the inflamed joint with a syringe and needle.
222

 Diagnosing Gout: Joint Fluid Analysis
Joint fluid analysis for uric acid crystals and
infection.
Blood test to measure the amount of uric acid in
your blood.
223

Diagnosis---
 Clinical :
 In men , initial attack monoarticular,
Other joints involved are – instep/knees/wrists/
olecranon bursa. Often begins at night. Usually
abrupt , severely painful.
 Later attacks – polyarticular , associated with
systemic signs., most often initial presenting
complaint in women. (hands/tarsal joints/knees
224

Diagnosis -----
Laboratory:- GOLD STANDARD
 WBC ct – 2000-100 000/ml .
 Serum Uric acid level – important in
monitoring treatment (42% - normal levels) not
reliable .
 24 hr uric acid collection –useful in young pts
with gout.
 Synovial fluid analysis
225

Diagnosis -----
 Radiologic
X RAY
CT
MRI
US
Bone scan
226

SERUM URATE LEVELS
Not reliable
May be normal with flares
May be high with joint Sx from other causes
227

Treatment of acute gout
1.Colchicine :effective in 85% of the patient
dose: 0.6mg po every hr until pain relief
intravenous injection in unconscious pt
2.NSAID:
A. Indomethacine :25-50mg po tid
B. Ibuprofen: 800mg po tid
C. Diclofenac 25-50mg po tid
228

Treatment of acute gout----
3. Corticosteroid :
A. Oral prednisole 30-50 mg /day as initial dose
and tapered over 5-7days.
B. Intraarticular injection of steriods if problem
with other routes
229

Treatment of acute gout----
A. Allopurinol: alters serum uric concentration
300mg po single dose initially and can be increased to
800mg.it is reduced if there is renal failure for
toxicity.
A. Probenicide: alters serum uric concentration
200mg po bid.
230

ENDING ACUTE FLARES
Control inflammation & pain & resolve the flare.
No a cure.
Crystals remain in joints.
Don’t try to lower serum urate during a flare
231

Acute Flare Medics Choices
NSAIDS
Colchicine
Corticosteroids

MED Considerations
 Colchicine :
Not as effective “late” in flare.
 Drug interaction: Statins, Macrolides,
Cyclosporine.
 It is Contraindicated in dialysis pts
Cautious use in : renal or liver dysfunction; active
infection, age > 70
233

MED Considerations------
 Corticosteroids :-
 Worse glycemic control.
 May need to use moderate-high doses
234

 How Are Gout Attacks Prevented?
Maintaining adequate fluid intake
The fluid decreases the risk of kidney stone
formation
Alcohol has diuretic effects contributing to
dehydration & precipitate acute gout attacks.
235

How are Gout attacks Prevented?
Alcohol also affects uric acid metabolism and cause
hyper-uricemia.
It causes gout by slowing down the excretion of uric
acid from the kidneys
It is also causing dehydration, w/c precipitates the
crystals in joints.
236

PREVENT DISEASE PROGRESSION
Colchicine : 0.5-1.0 mg/day
Low-dose NSAIDS
 Both drugs decrease freq & severity of flares .
 Prevent flares with start of urate-lowering RX best
with 6 months of concomitant RX
 Won’t stop destructive aspects of gout.
237

PREVENT DISEASE-----
 Lower urate to < 6 mg/dl :
Depletes total body urate
 pool deposited crystals
 RX is lifelong & continuous
238

More Prevention Techniques
Dietary changes can help reduce uric acid levels.
Purine-rich foods should be avoided.
Avoid foods rich in purines include shellfish and organ
meats (liver, brains, kidneys).
Weight reduction is helpful in lowering the risk of
recurrent attacks of gout.
239

Overview of back pain
It affects most people at least once over their
lifetime.
It can be a cause for lost wages & productivity
Most people will become better in 6 weeks with
appropriate treatment
240

LOW BACK PAIN
DEFINITION :Pain that occurs in an area with
boundaries between the lowest rib and the crease of
the buttocks
242

Chronic Low Back Pain
Duration greater than 3 months
 Pain that persists longer than the expected
time period for healing
243

Anatomy
 The back is composed of
vertebrae, muscles, ligaments,
intervertebral disc,& nerves.
 There are 7 cervical, 12 thoracic,
5 lumbar & 5 coccygeal
vertebrae
 Spinal cord has cervical lordosis,
Thoracic kyphosis,
& lumbar lordosis
244

Assessment of Low Back Pain
Exacerbation of pain
Limitation of spinal motion
Lower back disability
Muscle spasm: has localized tenderness
 Increase in muscle tone
245

Causes of back pain
Pain sensitive structures are the supporting bone,
articulations, meninges, nerves, muscles, & aponeuroses
Vertebral body being short
Nerve injury (dorsal roots )
 sprain or strain of the back muscles & ligaments
246

Spinal causes
 Osteoporosis
 Osteomylitis
 Herniated Disc
 Spondylolisthesis
 Spondylolysis
 Facet hypertrophy
 Ischemia of the spinal
cord
247

Causes ----
Osteoporosis
Vertebral osteomyelitis
Vertebral metastases
Vertebral metastases:
 Thoracic spine is most commonly affected
Herniated Disc
248

DIAGNOSIS
History taking
p/E:
 Palpation: Gentle & systemic palpation of the
back, coccyx, sacrum, levator ani, coccygeus, &
associated ligament done
Plain X-rays of spine
Pain on percussion occurs with metastases
249

Treatment of Back Pain
Walking is best exercise
Physical therapy for core stabilization
Spinal manipulation & manual therapy
Analgesics (acetaminophen, NSAID’S,
antidepressants
Application of heat or ice
Acupuncture
Corticosteroid injections
250

Treatment of Chronic Back Pain
Treat the cause (osteomyelitis surgery with antibiotics)
Vertebral metastasis will respond to high doses of
dexamethasone.
Definitive treatment with radiation & surgery
Osteoporosis treated with Biphosphonate, Robaxifene
Muscle spasms may respond to muscle relaxants
251

Back Exercises
 Ankle pump
 Heel slides
 Abdominal contraction
 Wall squats
 Heel raises
 Straight leg raises
 Knee to chest stretch
 Hamstring stretch
 Exercises with swiss ball
252

Epidural steroid injection
 Epidural space identified w
loss of resistance tech or
fluoroscopy
 60-80 mg of triamcilone with
0.25% bupivacaine injected
253

WHO Pain Ladder
Step 1 Mild (pain rating 1-3):Non opioid + analgesics
e.g. NSAID+ muscle.relax.
Step 2 Moderate (pain rating 4-6): Opioid (hydrocortisone
mg, Codeine 30 mg) + analgesics muscle Relaxant.
Step 3 Severe ( pain rating 7-10):Pure opioids + co-
analgesics- e.g. Morphine , NSAID + above.
254

CONCLUSIONS
Gout is chronic disease with 4 stages.
Uncontrolled gout can lead to severe disease.
Separate RX for flares & preventing advancement.
Many meds for flares.
Treating the disease requires lowering urate.
Get a 24-hr urine for urate excretion
255

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