Complications of fractures

1. Complications of fractures

2. Classification •Complications of fractures tend to be classified according to whether they are local or systemic and when they occur – IMMEDIATE EARLY LATE

3. IMMEDIATE HYPOVOLAEMIC SHOCK Commonest cause of death following fractures Cause- external/internal haemorrhage Treatment Iv crystalloids-ringer lactate,followed by colloids and blood

4. Early complications •Early complications occur at the time of the fracture (immediate) or soon after. •They are again classified into- local Systemic •Early local complications tend to affect mainly the soft tissues

5. Local Early complications •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 { volkmanns ischemia}

6. •Wound Infection, more common for open fractures •Tetanus •Gas gangrene •Injury to joints

7. Vascular injury

8. Blood vessels lie close proximity to bones ,hence liable to injured Popliteal is commonly injured one Consequences- exercise ischemia-ischemic contracture-gangrene Signs-5ps-pain,absent pulse,pallor,parasthesia,paralysis

9. Visceral injuries Commonly seen in pelvic and rib fractures

10. Nerve and skin tissue damages

11. Radial nerve is commonly injured Consequences- lead to neurapraxia,axonotmesis or neurotmesis Axillary n- dislocatn of shoulder-deltoid paralysis Radial n-#shaft of humerus -wrist drop Median n- supracondylar # of humerus -pointing index Ulnar n-#medial epicondyle humerus -claw hand Sciatic n- posterior dislocation of hip-foot drop

12. Haemarthrosis Bleeding in the joint because of fracture

13. Compartment syndrome •Fractures of the limbs can cause severe ischaemia , even without damage to a major blood vessel •. Bleeding or oedema in an osteofascial compartment increases pressure within the compartment, reducing capillary flow and causing muscle ischaemia •A vicious circle develops of further oedema and pressure build-up, leading swiftly to muscle and nerve necrosis. Limp amputation may be required if untreated

14. •Compartment syndromes can also result from ; Crush injuries caused by falling debris or from a patient’s unconscious compression of their own limb Swelling of a limb inside an over tight cast

15. •Compartment syndrome can occur in any compartment, e.g. the hand, forearm, upper arm, abdomen, buttock, thigh, and leg. •40% occur following fracture of the shaft of the tibia (with an incidence of 1-10%) and about 14% following fracture of a forearm bone. •Risk is highest in those under 35 years

16. •Compartmental syndrome may lead to the Volkmann's ischaemia

17. Presentation:- Signs of ischaemia (5 P's: Pain,Paraesthesia , Pallor, Paralysis,Pulselessness ) Signs of raised intracompartmental pressure: 1.Swollen arm or leg 2.Tender muscle - calf or forearm pain on passive extension of digits 3.Pain out of proportion to injury 4.Redness, mottling and blisters Watch for signs of renal failure{ low-output uraemia with acidosis)

18. management Remove/relieve external pressures ( fasciotomy ) Prompt decompression of threatened compartments by open fasciotomy Debride any muscle necrosis Treat hypovolaemic shock and oliguria urgently Renal dialysis may be necessary

19. • Complications Acute renal failure secondary to rhabdomyolysis DIC Volkmann's contracture (where infarcted muscle is replaced by inelastic fibrous tissue)

20. Gas gangrene • Clostidium welchii ( perfringens ) •Clinical presentation Subcutaneous crepitations Myonecrosis •Treatment Debridement pencillin

21. tetanus Causative agent Clostidium tetani TRISMUS DYSPHAGIA RISUS SARDONICUS OPIS THOTONUS Treatment Bed rest and sedation Immunoglobulin Respiratory support pencillin

22. Systemic early complications •Fat embolism •Shock •ARDS • Thromboembolism (pulmonary or venous) •Exacerbation of underlying diseases such as diabetes or CAD Pneumonia Aspectic traumatic fever Septicemia Crush syndrome

23. Fat embolism •This is a relatively uncommon disorder that occurs in the first few days following trauma with a mortality rate of 10-20% •Fat drops are thought to be released mechanically from bone marrow following fracture, coalesce and form emboli in the pulmonary capillary beds and brain, with a secondary inflammatory cascade and platelet aggregation •An alternative theory suggests that free fatty acids are released as chylomicrons following hormonal changes due to trauma or sepsis

24. •Risk factors Closed fractures Multiple fractures Pulmonary contusion Long bone/pelvis/rib fractures

25. •Presentation •Sudden onset dyspnoea •Hypoxia •Fever •Confusion, coma, convulsions •Transient red-brown petechial rash affecting upper body,especially axilla Diagnosis Retinal artery emboli-striate hges & exudates Sputum & urine-fat globules X-ray chest –snow storm appearance

26. Treatment :- Respiratory support Heparinisation Intravenous low molecular weight dextran ( lomodex 20) and corticosteroids Iv 5% dextrose solution with 5% alcohol –helps in emulsification of fat globules

27. Deep vein thrombosis Common complication associated with lower limb injuries and with spinal injuries •D.V.T. proximal to the knee is a common cause of life threatening complication of pulmonary embolism Causes Immobilization following trauma Fracture of leg Symptoms Leg swelling Calf tenderness

28. Consequences:- pulmonary embolism Tachypnoea Dyspnoea 4-5 days after trauma • Treatment:- Elevation of the limb Anti coagulating therapy Respiratory support and heparin therapy{ respiratory embolism} Early internal fixation of fractures Active mobilization of the extremity

29. Aseptic traumatic fever •Aseptic traumatic fever: This is supposed to be due to absorption of fibrin ferment taking place. •It may, however, be due to some irritation, as of a badly fitting splint, and disappears on removal of it

30. Septicaemia •Because of trauma a large amount of bacteria can enter in the blood stream and may cause septicemia Symptom s Rash Fever and vomiting Cold extremitis Rapid breathing Stomach pain and joint pain drowsy

31. Management Initial Resuscitation - ABC 1.Secure airway 2. Support breathing 3.Restore circulation Fluid therapy Inotropic Support Antimicrobial therapy Respiratory Support

32. Crush syndrome •Crushing injury to skeletal muscles because of the fracture Cause - crushing of muscles- myohb enters to circulation- ppt in renal tubules-a/c renal failure • Complications shock Renal failure • Management To avert disaster, a limb crushed severely and for several hours should be amputated

33. Late complications •Late complications are those which occur after a substantial time has passed and are as a result of defective healing process or because of the treatment itself. •They are again classified in to 2 groups Imperfect union of the fracture others

34. Other late complications • Avascular necrosis •Shortening •Joint stiffness • Sudeck’s dystrophy • Osteomyelitis •Volkmann’s Ischaemic contracture • Myositis ossificans •Osteoarthritis

35. Imperfect union of the fracture •They are again classified into four sub groups: Delayed union Non union Mal-union Cross-union

36. Delayed union •When a fracture takes more than the usual time to unite, it is said to have gone in delayed union •Causes: Inadequate blood supply infection Incorrect splintage 1.Insufficient splintage 2.excessive traction

37. •Signs: The fractured site is usually tender The bone may appear to move in one piece, if however, it is subjected to stress , pain is immediately felt and the bone may angulate ; The fracture is not consolidated X-ray: the fractured site is still clearly visible, but the bone ends are not sclerosed

38. •Treatment Conservative: 1.Plaster should be sufficiently extensive and must fit accurately 2.Replace traction by plaster splintage 3.Use of functional bracing Operative: Bone grafting with or without IF

39. Non-union •When the process of fracture healing comes to a stand before its completion, the fracture is said to have gone in non –union. •It is not before six months that a fracture can be so labelled .  Nonunion is one endpoint of delayed union

40. Causes : The injury 1.Soft tissue loss 2. Bone loss 3.Intact fellow bone 4.Soft tissue inter position The bone 1.Poor blood supply 2. Poor haematoma 3. Infection 4. Pathological lesion

41. Presentation Pain at fracture site Nonuse of extremity Tenderness and swelling Joint stiffness (prolonged >3 months) Movement around the fracture site ( pseudarthrosis ) Investigations Absence of callus ( remodelled bone) or lack of progressive change in the callus suggests delayed union. Closed medullary cavities suggest nonunion. Radiologically , bone can look inactive, suggesting the area is avascular (known as atrophic nonunion) or there can be excessive bone formation on either side of the gap (known as hypertrophic nonunion).

42. Treatment Conservative: 1.Occasionally symptom less, needing no treatment 2.Functional bracing may be sufficient to induce union 3.Electrical stimulation promotes osteogenesis Operative 1.Very rigid internal fixation with hypertrophic non-union 2.Fixation with bone graft is needed in case of atrophic non union

43. Mal-union  occurs when the bone fragments join in an unsatisfactory position, usually due to insufficient reduction. Causes primary 1.The fracture was never reduced and has united in a deformed position. 2.Shortening is, of course, one type of deformity. Secondary 1.The fracture was reduced but the reduction was not held 2.Redisplacementmay occur during the first week, and a check x-ray at 1 week is adviseable

44. . •Signs: The deformity is usually obvious There may be painful limitation of joint movements At elbow, valgus deformity may present with delayed ulnar  nerve palsy

45. Treatment Conservative 1.If shortening is the main feature a raised shoe is usually sufficient 2.In child usually no treatment is required because it is expected to correct by remodelling Operative 1. Osteotomy 2.Excision of protruding bone 3. Osteoclasis 4.Redoing the fracture surgical

46. Avascular necrosis •Blood supply of some bones is such that the vascularity of a part of it is seriously jeopardized following fracture, resulting in necrosis of the part.

47. Consequences:- Avascular necrosis causes deformation of the bone. This leads, a few years later, to secondary osteoarthritis and causes painful limitation of joint movement. Diagnosis:- X-ray changes:-- 1.Sclerosis of the necrotic area 2.Deformity of the bone 3. Osteoarthritis Bone scan:- changes can be seen before X-ray changes: 1.Visible as cold area on the bone

48. •Treatment:- Avascular necrosis can be prevented by early, energetic reduction of susceptible fractures and dislocations. Treatment options: 1.Delay weight bearing till revascularization to prevent collapse 2. Revascularization 3.Excision of the avascular segment 4.Total joint replacement

49. Shortening •It is a common complications of fractures and results from:- 1.Mal union of the long bones 2.Crushing: Actual bone loss 3.Growth defects: growth plate or epiphyseal injuries

50. Treatment:- Shortening of upper limbs goes unnoticed For lower limb treatment depends upon the amount of shortening: 1.Shortening less than 2 cm: compensated by shoe raise 2.Shortening more than 2 cm: limb length equalization procedures

51. Joint stiffness •It is a common complications of fracture treatment. •Shoulder, elbow and knee joints are particularly prone to stiffness following immobilization

52. Causes Intra- articular or Para- articular adhesions secondary to immobilizations Contracture ofthe musclesaround a joint because of prolonged immobilizations Tethering of muscles at fracture site Myositis ossificans •Consequences:- Hampers the normal physical activity Results in late osteoarthritis

53. Treatment:- Heat therapy and exercise Manipulation of the joint under anesthesia Surgical interventions 1.To excise an extra articular bone block 2.To lengthen contracted muscles 3.Joint replacement, if there is pain due to secondary arthritis

54. Algodystrophy / Sudeck's dystrophy •Also known as Reflex Sympathetic Dystrophy. •Involves a disturbance in the sympathetic nervous system. •Consequences:- pain Hyperaesthesia Tenderness Swelling

55. Skin become red, shiny and warm in early stages Progressive atrophy of the skin, muscles and nails in later stages Joint deformity and stiffness ensues X-ray shows characteristic spotty rarefraction

56. Treatment:- Occupational therapy and physiotherapy constitutes the principle modality of treatment. Use of β-blocker. In resistant cases, sympathetic blocks have been shown to aid in recovery

57. Osteomyelitis • Osteomyelitis is an infection of a bone. •Many different types of bacteria can cause osteomyelitis . •However, infection with a bacterium called Staph. aureus  is the most common cause. Infection with a fungus is a rare cause

58. Treatment:- •After operative treatment of fracture bacteria may spread to the bone and may cause osteomyelitis . antibiotics Surgery: 1.in case of abscess formation 2.The infection presses on other important structures 3.The infection has become 'chronic' (persistent) and some bone has been destroyed. 4. Hyperbaric oxygen

59. Volkmann’s ischaemic contracture •This a sequel to Volkmann's ischaemia . •The ischaemic muscles are replaced by fibrous tissue •If the peripheral nerves are also affected, sensory or motor paralysis may happen Clinical features:- Marked atrophy Flexion deformity Nails shows atrophic changes Skin becomes dry and scaly

60. Treatment:- Mild deformity can be corrected by passive stretching using a turn-buckle splint (Volkmann's splint) For moderate deformities, a soft tissue sliding operation, where the flexor muscles are released from their origin, is performed For a severe deformity, bone shortening operations may be required

61. Myositis ossificans • Myositis ossificans is where calcifications and bony masses develop within muscle and can occur as a complication of fractures. •It may also happens because of the ossification of the hematoma around a joint after a compound fractures

62. Clinical features:- Pain Tenderness , Focal swelling, and Joint/muscle contractions •Treatment:- Massage following injury is strictly prohibited. In early stages rest is advised NSAIDS may help to reduce pain

63. In late stages Occupational and Physiotherapy is prescribed to regain movements Ultra sound In some cases surgical excision of myositic mass is done

64. osteoarthritis •Osteoarthritis is liable to follow malunion and traumatic injuries to the joints. •Joint surfaces become incongruent •Direction of stress transmission is abnormal •Increase wear and tear at the joint

65. Treatment:- Osteoarthritis cannot be cured, but it can be treated The goal of every treatment for arthritis is to:- 1.reduce pain and stiffness, 2.allow for greater movement, and 3.slow the progression of the disease Anti-Inflammatory Medications

66. Cortisone Injections Occupational and physiotherapy Weight Loss Activity Modification Diet: obesity is a risk factor for developing osteoarthritis

67. Iatrogenic complications Casts Pressure ulcers Thermal burns during plaster hardening Thrombophlebitis

68. Traction Traction prevents patients mobilising , causing additional muscle wasting and weakness. Other complications include: Pressure ulcers Pneumonia/urinary tract infections Permanent footdrop contractures Peroneal nerve palsy Pin tract infection Thromboembolism

69. External fixation Problems include: Pin tract infection Pin loosening or breakage Interference with movement of the joint Neurovascular damage due to pin placement Misalignment due to poor placement of the fixator

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