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Nursing care in Plastic Surgery

Jeng-Yee Lin MD PhD Division of Plastic Surgery, Taipei Medical University Hospital nad Taipei Medical University

Wound Healing
Wound healing process: Hemostasis phase Inflammatory phase Proliferation phase Scar Remodeling

Hemostasis (0-3hr)
Vasoconstriction Platelet aggregation PDGF Coagulation cascade reaction

Inflammatory phase (0-3day)


1.Neutrophil infiltration due to cytokine releaseswelling, vasodilatation, and pain 2.Macrophage migration kill bacteria, debris

Proliferation phase (3-21 day)


Granulaton tissueNeoangiogenesis Wound contraction Epithelialization

Remodeling phase (21day~)


Procollagen sysnthesis Collagen/fibril deposition Collagen remodeling/maturation scar maturation Wound strength increased

Reconstructive ladder/ principle


Suture/wound closure Skin graft Local flap Pedicle flap Tissue expander Free flap

Sugical wound dressing

Biological wound dressing: Autograft skin: STSG FTSG; xenograft skin Synthetic wound dressing

Autologous tissue coverage


Skin grafts: FTSG STSG Flaps: local flap, pedicle flap, free flap

Surgical wound dressing


Open wound dressing: used in infected wounds; adequate draining of the exudate; promote mechanical debridement. Closed wound dressing: promote wound healing, autolytic wound debridement, and granulation growth; can not be used in infected wound, or dirty wound

Wound dressing

VAC-negative pressure dressing: promote cell cycle and granulation tissue growth. continue draining of exudate of the wound. avoid its use in malignancy.

Wound dressing
Foam: polyurathane film or porous sponge. Hydrogel: water 70-90%, alternative to wet dressing. Hyrocolloid: Duoderm, Comfeel,Alleyvn, slowly absorbing water. Calcium alginate: promote hemostasis Collagen-base bilayer skin substitute: Biobrane, Integra Silver containing dressing: Ag coated high densisty

1.Synthetic dressing: Hydrocolloid,CMC, 2.Biologic dressing: collagen/matrix base (bovine)

Burn injury mangement


Initial fluid resuscitation: Parkland formula 4 x burn area (%) x body weight (kg) Half in initial 8 hr with crystalloid/ Lactated Ringer soln Half in the following in 16 hr

Fluid resuscitation
1.Crystalloid but not colloid fluid resuscitation in the first 24 hr. 2.Colloid fluid can be infused 24 hr after burn injury. 3.Volume of resuscitation can be more than Parkland formula if inhalation injury is suspected. 4. General guideline: keep 30-50ml/hr urine output after acute stage.

Body surface area


Head and neck: 9% Each upper limb:9% Each lower limb:18% Ant trunk and abdomen: 18% Back and buttock: 18% Perineum:1%

Burn injury type


Scald burn Flame burn Contact burn Chemical burn Electric burn Steven Johnson syndrome /Toxic epidermal necrosis

Burn center admission


Pediatric or elderly burn or with associated

advanced medical disease (DM) > 10% major burn injury >20% burn injury involving joints or perineum

Burn wound management


Wound dressing with sulfa silverdiazine (U burn) cream- leukopenia/reversible Debridement Skin graft

Facial trauma
Facial bone fracture Facial lacerations

Facial laceration
Watch out for lacrimal duct, facial nerve, or salivary gland injury

s/s in faical bone injury


Perioribital numbness (infraorbital nerve) Diplopia Malocclusion Trismus Facial deformity Watch out for associated head injury

Image study
X-ray Waters view: Zygoma /arch view: Nasal bone: most common facial fx CT scan: more sensitive and specific than CT

Upper & lower extremity injury


Open bone fracture Tendon /muscle injury Nerve injury Vascular injury/amputation Compartment syndrome

Compartment syndrome
Etiology : Trauma/bone fracture Crush injury Burn injury Vascular injury Tight cast Drug overdose

s/s of compartment syndrome


Traditional 5 P of acute ischemia are not reliable. Pain out of proportion to the injury and worsens on passive movement should arouse suspicion. Usually tissue pressure > 35 mmHg

Tx of compartment syndrome
Early and prompt fasciotomy prevent further tissue and nerve injury. Fasciotomy is urgently done based on clinical finding not measurement of an absolute value in tissue pressure

Diabetic foot
Etiological risk: 1.Peripheral neuropathy 2 Peripheral vascular disease

Decubitus ulcer
Ischemic tissue due to pressure on tissue greater than the arteriole oncotic pressure. Presure time relationship Grade I-IV

Risk factors
Moisture Friction: Shear force: avoid > 30 degree head up in supine position

Decubitus ulcer
Tx Osteotomy of bony prominence Debridement VAC negative pressure wound closure.

PAOD (Peripheral arterial occlusion disease)

S/S: 5P: pain, paresthesia, pallor, pulselessness, poikilothermia hairless & scaly skin, intermittent claudication Ankle-brachial index (ABI) <1

PAOD

Image study: CT angiography, angiography Intervention: angioplasty. Bypass surgery

Venous ulcer
Venous congestion results in hypoxia of local tissue Perivascular thick fibrin also impede oxygen diffusion Leukocyte migrate more slowly than usual and become activated, damaging the vascualr endothelium. Macromolecule/hemosiderin leaking into the

Tx of venous ulcer
Keep wound moist and clean Compression and debridement Skin graft or bilayer skin substitute. Hyperbaric oxygen therapy may help stasis dermititis healing.

Diabetic ulcer
Neuropathic impairment of musculoskeletal balance Decrease immune system from leukocyte dysfunction and peripheral vascular disease Tx : Keep wound clean and moist, attentive debridement and use of PDGF and TGF-beta growth factor topical agent may improve wound