The patient's wound-healing status iscertainly an integral part of each initial evaluation in acute care. However,a descriptive history of how the repairprogressed in a patient with well-healed scar will alert the clinician tocertain potential problems. Reports ofprolonged swelling, excessive skinsloughing, dramatic color or temperature changes, progressive pain, andparesthesias alert us to the presenceof associated complications. Theextent of wound infection or dehiscence may predict the amount of scarformed in the tissue. The durationand type of immobilization affects themobility and stability of the scar.Underlying disease processes and pre-injury medications can influence thetiming of repair.
Normal Wound-Healing Phases
All forms of trauma, to any tissue, anywhere in the body, signal the reparative sequence to begin. The sequenceof events is highly organized and predictable. One process is stimulated tobegin, and its completion in turn signals another cellular response untilthe wound is bridged by scar. Theultimate goal in collagen researchmay be the discovery of healing without scar formation. Until then, to prevent scar formation is to preventhealing.The response to injury, either surgically or traumatically induced, isimmediate. The wound then passesthrough three phases toward finalrepair:
the inflammatory phase,
phase, and 3) theremodeling phase. The inflammatoryphase prepares the area for healing,the
phase rebuilds thestructure, and the remodeling phaseprovides the final form.Timetables for the beginning and endof each phase must be understood asgeneral guides. Different tissues healat different rates, and even onewound can show various areas healing rapidly or slowly.
healing complete?This question is important in determining return to work, the timing offurther surgical intervention, and permanent impairment ratings. Knowledge regarding injury time framescombined with objective appraisal ofthe scar give us our best basis onwhich to make these decisions.
Inflammation is a normal and necessary prerequisite to healing. Changesin vascular flow are responsible forthe clinical symptoms we use todetect an inflammatory response. Themajority of the specialized cellsinvolved in this phase of the wound-healing process come from ourblood. Obviously, any blood vesselsthat traversed the wound were cut atthe time of injury. These cut vesselspoured whole blood into the wound,which then coagulated, sealing off theinjured vessels and lymphatic channels, thus temporarily closing thewound.In addition to this direct blood vesselinjury, noninjured vessels dilate inresponse to chemicals released frominjured tissues. Most cells in injuredtissue release histamine. Histaminecauses brief vasodilation in neighboring noninjured vessels. This combination of whole blood exudate andserous transudate creates a reddened,hot, swollen, painful environment.Bradykinins, derived from plasma inthe area of the injury, contribute tomore prolonged vascular permeability. Prostaglandins, produced by allcells in the body, are released withany breach of cell membrane integrity. Certain prostaglandins furthercontribute to long-term vascular vasodilation. The fibrin plugs that clottedin the wound also form in the lymphatic vessels. Lymphatic
sblocked to seal off the wound andprevent the spread of infection. Thesechannels do not reopen until later inthe healing process.
The mast cells also release hyaluronicacid and other proteoglycans into thewound milieu, which bind with thewatery wound fluid to create a gel.
This gel then does not
Theinflammatory edema fills all spaces inthe wound and surrounds all damaged or repaired structures, bindingthem all together as one unit, or onewound (Figure 1A). This type ofedema causes loss of dermal fat, thusthinning normal skin in the area.
This thinning of normal skin ishypothesized to be the cause of theclinical condition of fingertip "pencilpointing" that occurs followingchronic edema conditions.That some swelling in a wound isinevitable and needed is a fact. Yet abalance is needed. If there is noinflammation, healing does not begin.If too little inflammation occurs, healing is slow. If too much inflammationoccurs, excessive scar is produced.This inflammatory fluid, derived fromthe blood, is high in fibrinogen.
Fibrinogen coagulates in the woundand in the surrounding tissues thatare now
filled.The coagulatedgel will later mature into a dense,binding scar (Fig. 1B). Excessiveswelling, therefore, must not be permitted. Primary wound care ensuresthat all blood vessels have beenrepaired, cauterized, or clotted.Hematomas, the result of ongoingbleeding in the wound, create extraexudate, a powerful stimulus to scarformation.
Secondary wound careaddresses the contribution made byinduced vasodilation, which continuesin relation to the severity of thewound. This serous transudate can bediminished by the classic "RICE" regimen of rest, ice, compression, andelevation. Pharmacological use of steroids and aspirin affects the transuda-tive edema.
Their action aids ininhibiting prostaglandin release. Allwounds, and even controlled surgicalprocedures, require edema care.Ward showed that the use of a tourniquet in hand surgery significantlyincreased hand edema, as comparedwith controls, as long as one monthpostoperatively.
Excessive inflammatory fluid alsoaffects joint positioning. Eyring andMurray performed joint distentionstudies by infusing saline in normalhands.
They found that each jointresponds to swelling by assuming aPhysical Therapy/Volume 69, Number 12/December 1989