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- Mohammad Ashraf

- Bahaa Najjar

- Mousa Al-Abbadi

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Fractures (cont’d).

Healing of fractures: There are a lot of factors determine the proper

healing of the fracture. For example: Displaced fractures heal for a

longer time than non-displaced fractures, and simple fracture heals

faster than comminuted, and a child will heal faster than an elder.

Other factor is inadequate immobilization: Any fracture must heal faster

with adequate immobilization, and inadequate immobilization will delay

the healing, and may cause complications (like malunion).

Sometimes the fracture doesn’t heal well causing Pseudarthrosis (which

is a bad complication), it’s a joint formed at the fractured place. And

sometimes we have infections (the enemy of healing) especially if there

is an opening in the skin, because everything under the skin is exposed

to infectious agents (like bacteria), and if the patient is

immunocompromised the infection is worse.

If the patient takes steroid drug (in asthma or arthritis) this will make

the healing takes longer, and malnutrition also makes the healing longer

in time, so the injured person should eat well in order to speed up

healing because of the increased needs of materials that we get from

food.

This picture shows the inflammatory

response toward fractures. In the first 1-2

days we see organizing hematoma, (but

sometimes in greenstick fractures in

children we don’t see hematoma except

after 2 days). Then we see soft callus after

1-2 weeks (we can see it by x-ray as non-

calcified callus, so we say it’s soft). Then

repair starts by removing osteoclasts and

woven bone (from soft callus to boney

callus and) starting endochondral

ossification and connecting the 2 separated

bones. Healing usually ends by the third

week in children.

Note : if you see woven bone after healing

, this case maybe cancer .

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Osteonecrosis (AVASCULAR NECOSIS)

Infarction (ischemic necrosis) of bone and marrow. The main reason of it

is vascular compromised.

Associated conditions:

1- Vascular injury: trauma (car accident, bullet) or vasculitis (may cause

by inflammation of blood a vessel complicated by thrombosis so no

blood supply > necrosis).

2- 2- Drugs: steroids. (patients who take steroids are at higher risk to

develop avascular necrosis of the head of the femur which is the

most common bone involved.

3- Systemic diseases: sickle cell disease. (Patients with severe cases of

sickle cell suffer from a lot of pain because they get thrombi (blood

clots) everywhere and they are at higher risk of developing

osteonecrosis.

4- Radiation. (blood supply gets affected by radiation especially in

some patients who have cancer and get cured by radiation).

Mechanism:

Mechanical disruption: by trauma.

Thrombotic occlusion: sickle cell disease.

Extravascular compression: like tumors.

The femoral head is the most bone

involved in osteonecrosis. This picture is a

longitudinal section of the femoral head.

The two red arrows indicate the

separation in the articular cartilage, and

within the bone you can see a lighter area

(triangular and the base is the articular

surface) which is the avascular necrosis

area.

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Osteomyelitis

Inflammation of the bone and marrow due to infection.

Important note: In the future, you -as a doctor- SHOULD NOT miss any

case of osteomyelitis, because it’s an acute emergency case, especially in

children. So, when there is a suspicion of osteomyelitis more diagnosis

should be done.

Osteomyelitis could be part of systemic infection (bacteremia,

septicemia) , but most of the cases are called primary solitary focus

which are localized.

Any organism can case acute osteomyelitis, however, the most common

organism to cause osteomyelitis is Staph. Aureus (gram positive cocci)

which case (80-90%) of all cases. Other organisms are E. Coli,

Pseudomonas and Klebsiella and they’re more common when recurrent

UTI or IV drug abuse are present. Also, sicklers (who have sickle cell

disease), Salmonella patients are at higher risk to develop osteomyelitis,

but still, staph. aureus is the most cause of osteomyelitis.” مهم سؤال

باالمتحان "

Note : salmonella in sicklers patient have higher risk to develop

osteomyelitis , but the most common organism cause osteomyelitis in

sicklers also is staph. Aureus.” ممكن السؤال يكون عىل هاي النقطة"

Clinical case: When you diagnose osteomyelitis in a patient with sickle

cell disease, you should give him antibiotics empirically that cover staph.

aureus and salmonella, and culture from the pus should be sent to the

lab to make sensitivity test to determine the best antibiotic and if there

is any resistance toward the antibiotic you gave empirically so you

change it.

Note maybe important: can the culture result is negative from any

bacteria, this because abuse take of antibiotic.

Mechanisms of developing osteomyelitis:

1- hematogenous spread (by blood) in children, and it’s cause by

previous infection.

2- Extension from contiguous site in adults, especially in diabetic

patients (diabetic foot, infections and deep ulcers that reach the bone).

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3- Direct implantation, after orthopedic surgery.

In neonates: can be caused by H.influanzae and Group B strep.

In adults: long bones are affected in both metaphysis and epiphysis,

however, in children, it’s just epiphysis or metaphysis which is affected.

Phases of osteomyelitis:

1- Acute inflammation of bone marrow (neutrophils included).

2- Spread of inflammation along the marrow spaces.

3- Thrombosis of blood vessels, so certain areas of the blood are without

blood supply.

4- Necrosis of bone.

5- Liquefaction of necrotic tissues. Macrophages and osteoclasts are

trying to repair the dying tissue.

6- Lifting of periosteum causing further necrosis. (pus under the

periosteum which you can see with x-ray).

Consequentially, a necrotic bone appears, and it’s called Sequestrum.

# مهم ممكن سؤال خصوصا عىل

(Sequestrum , involucrum)

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Sequestrum is necrotic bone that is embedded in the infected

granulation tissue. Around this area a reaction occurs by living bone to

fill the spaces making Involucrum, which is the new bone laid down by

periosteum that surrounds the sequestra.

Finally, there is an opening in the involucrum which pus and sequestra

make their way out, and it’s called Cloaca.

In acute phases of osteomyelitis (early phase) we can see pus and neutrophils (under the microscopy), and in the chronic phase (late and more complicated and dangerous) we can see lymphocytes and plasma

cells.

The doctor pointed out again and again to not miss diagnose osteomyelitis, otherwise it will become chronic which is hard to treat.

Osteomyelitis Clinically:

Hematogenous spreading causing fever, malaise, chills and leukocytosis. Also, patients complain of a localized pain which helps us determining the location of infection. Localizing of pain is harder in infants. So, you should have high index of suspicion of osteomyelitis and keep it in your mind when you see these clinical features.

Also, do not rely on x-ray during diagnosis because x-ray picture maybe normal in early phases, if we wait till x-ray changes we will be late to treat, so do not wait till we see x-ray lytic changes and use more fast and sensitive ways like MRI.

After diagnosis we give the patient antibiotic IV empirically assuming that it’s caused by Staph. aureus, then we change the antibiotic if we need to according to lab sensitivity test.

Sometimes we need to do surgical procedure especially big collection of pus

Chronic osteomyelitis:

Acute osteomyelitis should not develop to chronic case with proper diagnosis and treatment, but unfortunately 5-25% of acute cases persists as chronic, and it’s very bad debilitating disease and very hard to cure.

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Causes of chronic osteomyelitis:

1- Delay in diagnosis.

2- Extensive necrosis, especially in immunosuppressed patients.

3- Inadequate therapy (use of antibiotics for short time or not enough concentration or give it orally instead of IV). So, concentration of drug in the place of infection should be high.

4- Weakened host immunity.

Complication of chronic osteomyelitis:

In addition to chronic pain and inability to function, those patients have:

1- Pathologic fractures: Any minimal trauma can case fracture.

2- Secondary amyloidosis: deposition of amyloid. (we’ll study about that in the future).

3- Endocarditis: Shooting bacteria into the heart.

4- Sepsis: Systemic infection.

5- Squamous cell carcinoma of draining sinus (Cloaca).

6- Patients who have chronic osteomyelitis for the last 10-20 years are at higher risk to develop osteosarcoma of the bone which becomes

secondary not primary.

Mycobacterial Osteomyelitis:

Also called Tuberculous osteomyelitis or TB of the bone.

Used to be a disease of developing countries, but now it’s coming back worldwide because of increasing on immunosuppressant’s (due to steroid treatment or anticancer treatment) and due do immigration.

1-3% of patients with pulmonary or extrapulmonary TB can have bone involved, but pulmonary is so much more common than Tuberculous osteomyelitis.

Mechanism of spread: Hematogenous or direct spread.

Diagnosis is not easy, so you should keep it in your mind while diagnosis, but you have clues, for example: if the patient had TB in the lung before or anyone around to him (like a family member) has TB.

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When you take biopsy from the area involved by infection you can see necrotizing granulomatous inflammation (left picture). Then we can see the bacteria by acid fast-stain (ziehl-neelsen stain) (right picture).

Pott disease (TB spondylitis): TB that infects the vertebrae and intervertebral discs (black area in the vertebrae). It may lead to compression fractures, you can see necrotizing granulomatous inflammation, and it’s difficult to treat, and it also may lead to neurologic deficit, scoliosis and kyphosis.