DEEP VEIN THROMBOSIS ,PULMONARY EMBOLISM AND AVASCULAR NECROSIS

DEEP VEIN THROMBOSIS AND PULMONARY EMBOLISM


Introduction

Deep vein thrombosis (DVT) is a crucial complication seen after fractures of spine, pelvis, femur, tibia, etc. Virchow’s triad of venous stasis,  the vascular damage and hypercoagulability has express the pathogenesis.

DEEP VEIN THROMBOSIS
DEEP VEIN THROMBOSIS


Clinical features
The patient complains of mild-to-severe calf pain, swelling, difficulty in standing or walking and cramps within the calf muscles or foot. The clinical signs  are include increased temperature,unilateral leg swelling, enlarged superficial veins, tenderness pitting edema,erythema, palpable cord along the involved veins,  etc. Homan’s sign: When forced ankle dorsiflexion produces calf pain, Homan’s sign is said to be positive and is pathognomonic of DVT.
HOMANS"S SIGN


Investigations
Laboratory investigations particularly BT, CT, prothrombin time, blood group, etc needs to be done.

Treatment
Prophylactic methods consist of early ambulation, foot elevation, elastocrepe bandaging, exercises, etc. Anticoagulant therapy: This consists of aspirin (600650 mg), heparin (low dose), low molecular weight dextran, low dose warfarin (2.5-16 mg/day daily orally), etc.

Complications
Pulmonary thromboembolism is a serious complication of DVT. The patient with pulmonary embolism complains of unexplained dyspnea, pleuritic chest pain, hypoxia, tachypnea, tachycardia, signs of cor pulmonale, etc. Heparin therapy is the treatment of choice. Chronic venous insufficiency is the common longterm complication of DVT.



Embolic facts
Other important predisposing factors for DVT

• Surgery—orthopedic/thoracic/abdominal/GU systems.

• Immobilization due to CCF, MI, stroke, etc.

• Neoplasms

• Oestrogen therapy

• Pregnancy • Obesity

• Age > 40 years

• TAO, Beh├žet’s disease, etc.

• Hypercoagulable states.

• Total hip and knee replacement, etc

INJURY TO BLOOD VESSELS
Blood vessels are injured in the close proximity to the bones, during the fractures and the dislocations.

Causes of Injury
The blood vessels could also be injured in one among the subsequent rays: Reflex vasospasm, compression by the fracture fragments or hematoma, incomplete tear, complete tear, partial tear, internal thrombus, tight encircling bandages, etc.


Effects of Injury
In the initial stages, it's going to range from mild ischemia to gangrene. In the late stages ischemic contractures may develop.

Clinical Features
Apart from the standard features, the patient may show impending signs of vascular disaster recognized by 5Ps: Pain, pulselessness, paresthesia, pallor and paralysis. Cold extremities herald the onset of gangrene.

Investigations
Consists of radiograph of the part, Doppler angiogram studies, etc.

Treatment
This consists of prompt reduction of fractures and dislocations and removal of all tight encircling bandages. Thrombectomy, direct end-to-end repair, injection of xylocaine, papaverine, and sympathectomy to relieve the vasospasms are some of the commonly recommended methods of treatment. Amputation is considered in irreversible loss of blood supply.





Avascular necrosis

Avascular necrosis may be rare, but severe complication of certain fractures. Avascular necrosis occurs when the blood supply to a segment of the bone is affected.

Causes
Extensvie stripping of soft tissue, which damage the periosteal blood supply
In certain bones where the blood supply is unique and undirectional, eg. Talus, scaphoid, neck of femur.
Other causes like steroid therapy, caissons diseases etc which may causes on embolic block of the blood vessels.

Common sites
Common sites of Avascular necrosis are head of the femur in fracture neck of femur and the dislocations of hip, body of the talus in fracture through the neck of talus, proximal pole of scaphoid in fracture through the waist of the scaphoid.

Problems
The loss of blood supply to a major bone segment impairs healing because the avascular segment cannot participate in the reparative process. This defecrive healing makes the bone weak and susceptible to external forces. This results in collapse of the bone and late osteoarthritis changes.

Clinical features
Avascular necrosis of a bone usually asymptomatic in the early stages. In the later stages patient may complaint of pain, limp and slight loss of movements. In very advanced cases, patient will show the features of the osteoarthritis.

Investigations
In the early stages, AVN can be detected by the bone scan and the radiosotope study. In the later stages, of the investigations ,radiograph shows dense changes in the bone, collapse and osteoarthritis features.

avascular necrosis
Plain x-ray showing extensive secondary OA changes


Treatment
Early stages require no treatment. Protective braces could also be given to stop bone collapse. Surgical decompression has a doubtful role. In the stages, total hip replacement is advocated for AVN head of the femur. AVN in scaphoid needs open reduction and bone grafting.

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