on 02-Dec-2021 (Thu)

The healing of fractures is in many ways similar to the healing of soft tissue wounds, except that soft tissue heals with fibrous tissue, and end result of bone healing is mineralised mesenchymal tissue, i.e. bone. A fracture begins to heal soon after it occurs, through a continuous series of stages

This stage lasts up to 7 days. When a bone is fractured, blood leaks out through torn vessels in the bone and forms a haematoma between and around the fracture. The periosteum and local soft tissues are stripped from the fracture ends. This results in ischaemic necrosis of the fracture ends over a variable length, usually only a few millimetres. Deprived of their blood supply, some osteocytes die whereas others are sensitised to respond subsequently by differentiating into daughter cells. These cells later contribute to the healing process.

This stage lasts for about 4-12 weeks. In this stage, the granulation tissue differentiates further and creates osteoblasts. These cells lay down an intercellular matrix which soon becomes impregnated with calcium salts. This results in formulation of the callus, also called woven bone. The callus is the first sign of union visible on X-rays, usually 3 weeks after the fracture (Fig-2.4). The formation of this bridge of woven bone imparts good strength to the fracture. Callus formation is slower in adults than in children, and in cortical bones than in cancellous bones

Formerly called the stage of consolidation. In this stage, the woven bone is replaced by mature bone with a typical lamellar structure. This process of change is multicellular unit based, whereby a pocket of callus is replaced by a pocket of lamellar bone. It is a slow process and takes anything from one to four years.

Formerly called the stage of remodelling. In this stage the bone is gradually strengthened. The shapening of cortices occurs at the endosteal and periosteal surfaces. The major stimulus to this process comes from local bone strains i.e., weight bearing stresses and muscle forces when the person resumes activity. This stage is more conspicuous in children with angulated fractures. It occurs to a very limited extent in fractures in adults.

The healing of fractured cancellous bone follows a different pattern. The bone is of uniform spongy texture and has no medullary cavity so that there is a large area of contact between the trabeculae. Union can occur directly between the bony trabeculae. Subsequent to haematoma and granulation formation, mature osteoblasts lay down woven bone in the intercellular matrix, and the two fragments unite.

Compartment syndrome can be diagnosed early by high index of suspicion. Excessive pain, not relieved with usual doses of analgesics, in a patient with an injury known to cause compartment syndrome must raise an alarm in the mind of the treating doctor. Injuries with a high risk of developing compartment syndrome are as follows: • Supracondylar fracture of the humerus • Forearm bone fractures • Closed tibial fractures • Crush injuries to leg and forearm. Stretch test: This is the earliest sign of impending compartment syndrome. The ischaemic muscles, when stretched, give rise to pain. It is possible to stretch the affected muscles by passively moving the joints in direction opposite to that of the damaged muscle’s action. (e.g., passive extension of fingers produces pain in flexor compartment of the forearm). Other signs include a tense compartment, hypo- aesthesia in the distribution of involved nerves, muscle weakness etc. Compartment syndrome can be confirmed by measuring compartment pressure. A pressure higher than 40 mm of water is indica- tive of compartment syndrome. Pulses may remain palpable till very late in impending compartment syndrome, and should not provide a false sense of security that all is well.

When a fracture takes more than the usual time to unite, it is said to have gone in delayed union. A large percentage of such fractures eventually unite. In some, the union does not progress, and they fail to unite. These are called non-union. Conventionally, it is not before 6 months that a fracture can be declared as non-union. It is often difficult to say whether the fracture is in delayed union, or has gone into non- union. Only progressive evaluation of the X-rays over a period of time can solve this issue. Presence of mobility at the fracture after a reasonable period is surely a sign of non-union. Presence of pain at the fracture site on using the limbs also indicates non-union. Non-union may be painless if pseudo joint forms between the fracture ends (pseudoarthrosis).

LV remodeling devel- ops in response to a series of complex events that occur at the cellular and molecular levels (Table 252-3). These changes include (1) myocyte hypertrophy; (2) alterations in the contractile properties of the myo- cyte; (3) progressive loss of myocytes through necrosis, apoptosis, and autophagic cell death; (4) β-adrenergic desensitization; (5) abnormal myocardial energetics and metabolism; and (6) reorganization of the extracellular matrix with dissolution of the organized structural col- lagen weave surrounding myocytes and subsequent replacement by an interstitial collagen matrix that does not provide structural support to the myocytes. The biologic stimuli for these profound changes include mechanical stretch of the myocyte, circulating neurohormones (e.g., norepinephrine, angiotensin II), inflammatory cytokines (e.g., tumor necrosis factor [TNF]), other peptides and growth factors (e.g., endo- thelin), and reactive oxygen species (e.g., superoxide). The sustained overexpression of these biologically active molecules contributes to the progression of HF by virtue of the deleterious effects they exert on the heart and the circulation. Indeed, this insight forms the clinical rationale for using pharmacologic agents that antagonize these systems (e.g., angiotensin-converting enzyme [ACE] inhibitors, angiotensin receptor-neprilysin inhibitors [ARNIs] and beta blockers) in treating patients with HF