AIM : To manage the complications of fractures .

Early complications

Local:

Vascular injury causing haemorrhage, internal or external

Visceral injury causing damage to structures such as brain, lung or bladder

Damage to surrounding tissue, nerves or skin

Haemarthrosis

Compartment syndrome (or Volkmann's ischaemia)

Wound infection, more common for open fractures

Systemic:

Fat embolism

Shock

Thromboembolism (pulmonary or venous)

Exacerbation of underlying diseases such as diabetes or CAD

Pneumonia

Late Complications

Local:

Delayed Union

Non-union

Malunion

Joint stiffness

Contractures

Systemic:

Gangrene, tetanus, septicaemia

Fear of mobilising

Osteoarthritis

Myositis ossificans

Avascular necrosis

Algodystrophy (or Sudeck's atrophy) Osteomyelitis

Growth disturbance or deformity

1. HYPOVOLAEMIC SHOCK

It is commonest cause of death following fractures if major bones such as pelvis and femur. Its frequency is on the increase due to arise in number of patients with multiple injuries the cause of hypovolaemia could be extrenal or internal haemorrhage. External may result from a compound fracture with or without an associated injury to a major vessel to a limb. Internal is difficultto diagnose, usually massive bleading such as chest or abdomen.

Management:

Keep the person comfortable and warm (to avoid hypothermia).

Have the person lie flat with the feet lifted about 12 inches to increase circulation. However, if the person has a head, neck, back, or leg injury, do not change the person's position unless he or she is in immediate danger.

Do not give fluids by mouth.

If person is having an allergic reaction, treat the allergic reaction, if you know how.

If the person must be carried, try to keep him or her flat, with the head down and feet lifted. Stabilize the head and neck before moving a person with a suspected spinal injury.

The goal of hospital treatment is to replace blood and fluids. An intravenous (IV) line will be put into the person's arm to allow blood or blood products to be given.

Medicines such as dopamine, dobutamine, epinephrine, and norepinephrine may be needed to increase blood pressure and the amount of blood pumped out of the heart (cardiac output).

Chest physiotherapy to improve respiratory function

Limb supporting splint .

2. ARDS ACUTE RESPIRATORY DESTRESS SYNDROME

The exact mechanism is not known, but it is supposed to be due release of inflammatory mediators which cause disruption of microvasculature of pulmonary system.

ARDS typically occurs in people who are already critically ill or who have significant injuries. Severe shortness of breath the main symptom of ARDS usually develops within a few hours to a few days after the original disease or trauma.

Many people who develop ARDS don't survive. The risk of death increases with age and severity of illness. Of the people who do survive ARDS, some recover completely while others experience lasting damage to their lungs.

Management :

Supplemental oxygen. For milder symptoms or as a temporary measure, oxygen may be delivered through a mask that fits tightly over your nose and mouth.

Mechanical ventilation. Most people with ARDS will need the help of a machine to breathe. A mechanical ventilator pushes air into your lungs and forces some of the fluid out of the air sacs.

Fluids

Carefully managing the amount of intravenous fluids is crucial. Too much fluid can increase fluid buildup in the lungs. Too little fluid can put a strain on your heart and other organs and lead to shock.

Medication

People with ARDS usually are given medication to:

Prevent and treat infections

Relieve pain and discomfort

Prevent clots in the legs and lungs

Minimize gastric reflux

3. FAT EMBOLISM

This is the most serious complications, the essential feature being occlusion of small vessels by fat globules.

This is a relatively uncommon disorder that occurs in the first few days following trauma with a mortality rate of 10-20%. Various theories: Fat drops from bone marrow following fracture, coalesce and form emboli in pulmonary capillary beds and brain, with an inflammatory cascade and platelet aggregation. Alternative theory suggests that FFAs are released as chylomicrons following hormonal changes due to trauma or sepsis. Also seen following severe burns, CPR, bone marrow transplant and liposuction.

Risk factors

Closed fractures

Multiple fractures

Pulmonary contusion

Long bone/pelvis/rib fractures

Presentation

Sudden onset dyspnoea

Hypoxia

Fever

Confusion, coma, convulsions

Transient red-brown petechial rash affecting upper body, especially axilla

Management

Supportive treatment

Corticosteroid drugs

Surgical stabilisation of fracture

4. DEEP VEIN THROMBOSIS (DVT) AND PULMONARY EMBOLISM

DVT is a common complication associated with lower limb injuries and with spinal injuries.

Clinical features of a DVT

Swelling of the extremity

Tenderness or a feeling of cramping of the calf muscles that is increased with dorsiflexion (Homan's sign)

Inflammation and discoloration/redness of the extremity

Clinical features of a Venous Thromboembolism

Calf pain and/or tenderness

Swelling with pitting edema

Swelling below the knee (distal deep vein thrombosis) or up to the groin (proximal deep vein thrombosis)

Increased skin temperature

Superficial venous dilation

Management :

Anticoagulation is the usual treatment for DVT. Patients are generally initiated on a brief course (i.e., less than a week) of heparin treatment while they start on a 3-6 month course of warfarin (or related vitamin K inhibitors). Once the thrombosis is treated with RBC-thinning agents, the affected area has a fair chance of returning to its normal proportions. However, thinning agents do not lessen the chance of embolism to the pulmonary or coronary arteries.

Thrombolysis

Thrombolysis is generally used for an extensive clot. Although a meta-analysis of randomized controlled trials by the Cochrane Collaboration shows improved outcomes with thrombolysis, there may be an increase in serious bleeding complications.

Compression stockings

Elastic compression stockings should be routinely applied "beginning within 1 month of diagnosis of proximal DVT and continuing for a minimum of 1 year after diagnosis".

5. CRUSH SYNDROME

This syndrome results from massive crushing of the muscles, commonly associated with crush injuries sustained during earthquakes, mining and other such accidents. A similar effect may follow the application of tourniquet for an excessive period.

Causes: crushing of muscles results in entry of myohaemoglobin into circulation , which precipitates in renal tubules , leading to acute renal tubular necrosis.

Symptoms :

Scanty urine

Apathy

Restlessness

Delirium

6. INJURY TO MAJOR BLOOD VESSELS

Blood vessels lie in close proximity to the bones, and hence are liable to injury with different fractures and dislocations. The popliteal artery is the most frequently damaged vessel.

Causes: the artery maybe damaged by the object causing the fracture or by a sharp edge of a bone fragment. The damage to the vessel may vary from just a pressure from outside to a complete rupture

Consequences: obstruction to the blood flow will not always lead to gangrene. where the collateral circulation is good

the following may result:

1. No effect

2. Exercise ischeaemia

3. Ischaemic contracture

4. Gangrene

Management:

Localised pressure at bleeding points

Compression bandage

Limb support and keep in elevation

Early possible active , or assisted movements to distal joints.

7. PROBLEMS WITH BONE HEALING ( DELAYED UNION, MAL UNION , NON UNION )

Delayed union is failure of a fracture to consolidate within the expected time - which varies with site and nature of the fracture and with patient factors such as age. Healing processes are still continuing, but the outcome is uncertain.

Non-union occurs when there are no signs of healing after >3-6 months (depending upon the site of fracture). Non-union is one endpoint of delayed union..

Malunion occurs when the bone fragments join in an unsatisfactory position, usually due to insufficient reduction.

Management :

Non-surgical approaches:

Early weight bearing and casting may be helpful for delayed union and non-union.

Bone stimulation can sometimes be used. This delivers pulsed ultrasonic or electromagnetic waves to stimulate new bone formation. It needs to be used for up to an hour every day, and may take several weeks to be effective.

Medical treatments such as teriparatide have also been used to promote fracture healing, particularly in patients with osteoporosis.

Surgical approaches:

Debridement to establish a healthy infection-free vascularity at the fracture site.

Bone grafting to stimulate new callus formation. Bone may be taken from the patient or may be cadaveric.

Bone graft substitutes/osteobiologics.

Internal fixation to reduce and stabilise the fracture. (Bone grafting provides no stability).

Depending on the type of non-union, any combination of the above.

8. COMPARTMENT SYNDROME

Fractures of the limbs can cause severe ischaemia by damage to a major artery or by increasing the osteofascial compartment pressure by swelling due to bleeding or oedema.

capillary flow muscle ischaemia. more oedema more pressure capillary flow.

Thus rapid pressure build-up, leading to muscle and nerve necrosis.

Compartment syndromes can also result from crush injuries (falling debris or simple

compression if patient unconscious for length of time) or an over-tight cast.

Any compartment, but tibia shaft # & forearm # greatest risk. Esp if age