October 29, 2004
Obesity: Impediment to Postsurgical Wound Healing
To provide physicians and nurses with an overview of the impact of obesity on postoperative wound healing and how preplanning protocols can minimize skin and wound care problems in this patient population.TARGET AUDIENCE
This continuing education activity is intended for physicians and nurses with an interest in reducing skin and wound care problems in their patients who are obese.
After reading the article and taking the test, the participant will be able to:
1. Identify obesity-related changes in body systems and how these impede wound healing.
2. Identify complications of postoperative wound healing in obese patients and the assessments and intervention strategies that can reduce these complications.
3. Identify skin and wound care considerations for obese patients and the role of preplanning protocols in avoiding problems.
ADV SKIN WOUND CARE 2004;17:426-35; QUIZ 442-3.
In 2000,19.8% of adults in the United States were identified as obese, a 61% increase since 1991.1 By the year 2000, a total of 38.8 million American adults met the classification of obesity, according to the Centers for Disease Control and Prevention.1
Obesity and being overweight are different and are determined by body mass index (BMI) scores. BMI is one of the most accurate ways to determine whether an adult is overweight. BMI uses a person's weight and height to gauge total body fat. BMI is calculated by dividing weight by height (squared). Obesity is indicated by a BMI of 30 or more; a BMI between 25 and 29.9 indicates that the person is overweight.2
Providing health care for a population that is obese requires special equipment, skilled balancing of nutritional needs, professional psychological skills, and expert knowledge of the physiologic demands of body systems. Obese persons regularly undergo surgery, experience trauma, and often develop chronic wounds. A major challenge for health care personnel caring for these individuals after surgery is to achieve wound healing without complications, such as seroma, hematoma, infection, and wound separation. Providing wound care for an obese patient requires an understanding of the intrinsic changes in body systems induced by obesity and how these changes impede wound healing.
In obese patients, the workload of the heart is frequently increased by the strain of supplying oxygenated blood to all tissue. Wound healing depends on the circulatory system to provide oxygen and nutrients to tissue. Ischemia, the deficiency of blood to tissue, may lead to tissue necrosis. Ischemia can be caused by vessel constriction or obstruction, external pressure, or the failure of the heart to pump adequately. Adipose tissue is poorly vascularized and known to be less tolerant of ischemia and hypoxia than the epidermis.3
Delivery of oxygen to cells in the body depends on lung ventilation, diffusion of oxygen from the alveoli into capillary blood, perfusion of systemic capillaries with oxygenated blood, and diffusion of oxygen from systemic capillaries into the cells.4 Hyperventilation is the typical respiratory pattern of many obese patients5; the diaphragm is unable to fully descend because of abdominal adipose tissue. Chest expansion is impaired, and the resulting decreases in vital capacity and tidal function compromise tissue oxygenation, adversely affecting wound healing.
Fibroblasts need an oxygen pressure greater than 15 mm Hg for adequate collagen formation. In patients who are not obese, the partial pressure of arterial oxygen (FaO^sub 2^) has been found to be 60 to 90 mm Hg in the wound and near O mm Hg at the wound edges.5 From this, it would be reasonable to assume that the FaO^sun 2^ of a wound in an obese patient would be lower due to avascularlty of adipose tissue.5
Oxygen, like moisture, requires a balancing act to heal wounds, and healthy subjects can usually accomplish that without significant clinical interventions. Collagen synthesis requires oxygen, and when oxygen at the tissue level is deficient, leukocyte and phagocytic activities are impeded.6 The processes of proliferation and migration of cells, which eventually epithelialize a wound from the wound margins inward, are also oxygen-dependent. However, significant hypoxia serves as a stimulating factor for angiogenesis, which initiates the process that builds granulating tissue. Wound healing factors are produced essentially by hypoxic conditions. These factors stimulate the actual cellular repair processes, which are oxygen-dependent.7
All phases of wound healing depend on adequate supplies of protein, carbohydrates, vitamins, and minerals. Proteins are the building blocks of cells. Wounds with exudate can lose protein, lowering albumin levels. Carbohydrates provide a source of cellular energy for the wound healing process. Vitamin C is essential to collagen synthesis. Vitamin A is required for an adequate inflammatory response and has been used to counter the catabolic effect that glucorticosteroids exert on wound healing. Given its role in rapid tissue growth and protein synthesis, zinc is thought to be involved in wound healing as well.8
Appropriate classification is a useful mechanism in understanding and healing wounds (Table 1). The etiology of acute wounds is either traumatic or iatrogenic. Examples of iatrogenic wounds are incisions or grafts. Traumatic wounds include burns, stab or gunshot wounds, or other injuries resulting from trauma. Acute wounds are usually a result of an injury that disrupts blood vessels and initiates clotting, which stimulates the release of growth factors to initiate the wound healing cascade.
Chronic wounds are wounds with delayed healing, such as pressure and vascular ulcers. Chronic wounds may result from pathologic disease processes. Necrotic tissue, bacterial contamination, and local tissue ischemia are common in chronic wounds. An acute wound that does not proceed to heal in an orderly manner, such as a dehisced incision, may become a chronic wound.
The literature is replete with references to the higher incidence of infection among obese patients.5,9-12 Avascularity effectively decreases the ability to combat infection: insufficient oxygen impedes neutrophils from phagocytizing bacteria.5 Perioperative complications were found to be significantly higher in morbidly obese patients undergoing total knee arthroplasty.13 It may be assumed that these complications can be easily translated to other surgeries as well. Reasons for complications in morbidly obese patients can be attributed to technical difficulties in operating on obese patients; operations taking more time, thus increasing the chances of contamination; more trauma; and even necrosis of the abdominal wall because of more forceful retraction during surgery. Suturing into the fat layer or using 2 subcutaneous drains were investigated in the mid1980s, but neither showed an advantage or reduced incidence of wound infections in obese patients.9
Explanations for the frequency of dehisced incisions among morbidly obese patients include increased tension on the fascia! edges at the time of wound closure, thus increasing tissue pressure and reducing microperfusion and the availability of oxygen.12-14 Outcomes from different suturing techniques have been studied in several prospective randomized trials. A continuous monofilament fascial closure technique, as opposed to an interrupted technique, improves wound healing in morbidly obese patients undergoing gastric operations.12'15
Hematoma and seroma formation
Collection of pooled blood or serous fluid is an additional risk for obese patients. The formation of hematomas and seromas creates internal pressure and adds tension on sutured incisions. A review of the literature suggests that obese patients are more prone to hematoma formation, causing healing delays by reducing tissue oxygenation.9 A study on the effect of obesity on flap and donor- site complications in free transverse rectus abdominis myocutaneous (TRAM) flap for breast reconstruction found that overweight patients had a significantly higher incidence of total flap loss, hematoma, seroma, and mastectomy skin flap necrosis.16 In addition, more donor- site infections, donor-site seromas, and hernias were found in obese patients than in normal-weight patients.16 Obese women undergoing cesarean delivery are considered to be difficult surgery cases because of the physical exertion associated with increased efforts at retraction and potential complications. The large pannus predisposes patients to fluid accumulation, creating an environment conducive to seroma formation, infection, and wound edge separation or dehiscence.17
With decreased vascularity in adipose tissue, the obese patient is at high risk for pressure ulcers. The difficulty or inability of obese patients to reposition themselves or to help clinicians do so is a precursor to pressure-related injuries. Turning and repositioning is a basic preventive intervention to reduce and relieve pressure from body tissue. Adipose tissue does not equate to padding. Two or more clinicians are often needed to turn and reposition morbidly obese patients. Unfortunately, this intervention is risky on some hospital bed frames. Obese patients have fears that hospital equ\ipment will not safely accommodate their size, body configuration, or weight.18 As a result, they are frequently afraid to be repositioned.The implementation of bariatric beds resolves a safety/risk issue in addition to calming patient fears. Low-air- loss surfaces for bariatric beds are an option to help reduce pressure.
Moisture and incontinence are other risk factors predisposing patients to pressure ulcers. Skin folds on obese patients harbor microorganisms that thrive in moist areas and contribute to breakdown. Friction caused by skin on skin invites ulceration. Edema caused by excessive fluid resuscitation may be difficult to assess in an obese patient. This condition can exacerbate the problem of pressure caused by skin on skin (Figures 1 to 3).
OBESE PATIENT WITH PRESSURE ULCERS
Skin-on-skin pressure from massive edema caused this full- thickness wound (left), a necrotic pressure ulcer across the posterior waistline of an obese trauma patient. The same patient had a pressure ulcer covered with eschar on the right buttock (middle). The wound has been scored to allow penetration of a wound gel to initiate autolytic debridement. Following surgical debridement, 2 connecting Stage IV pressure ulcers with a deep cavity evolved. The photograph at right depicts improvement after 10 days of treatment with negative pressure wound therapy (V.A.C.; KCI, San Antonio, TX).
Goals for treatment of obese patients include management of wound drainage, prevention or resolution of infections, healing of pressure ulcers, protection of periwound skin, and enhancement of the patient's comfort.18
Obesity can induce venous hypertension.19 Venous hypertension results when incompetent valves in the lower extremities prevent venous return, causing blood to pool and thus increasing the venous pressure. The failure of venous pressure to fall as the blood flows from the superficial veins to the deep veins creates a climate of venous hypertension.20
Obesity that prevents ambulation exacerbates venous hypertension because the calf muscle is not working to keep the veins pumping the blood out of the leg. Extra girth composed of adipose tissue and fluid contributes to venous hypertension (Figure 4).
The cause of leg ulcerations is not as clear in the literature. Three theories are prominent: the fibrin cuff theory, the white blood cell trapping theory, and the trapping theory.19-20 The fibrin cuff theory originally proposed that fibrinogen leaked into dermal tissue; the fibrinogen hardened around capillaries, resulting in a barrier to oxygen and nutrients, causing tissue death and ulceration.21 More recent studies, however, have shown that fibrin cuffs do not disturb transcutaneous oxygen levels and that venous ulcers can heal in the presence of fibrin cuffs.20 The white blood cell trapping theory suggests that leukocytes are trapped due to sluggish blood flow, causing the capillaries to become plugged and resulting in tissue ischemia.21 Falanga and Eaglstein have suggested that leaked macromolecules trap growth factors and matrix material, rendering them unavailable to maintain normal tissue and repair wounded tissue.22
Management of venous ulcers includes compression wrapping to reduce edema and local wound care to heal ulcers. However, the most important issue to address is the underlying disease process and resulting comorbidities.
Stress response -
Pain, anxiety, hypovolemia, and hypothermia trigger the stress response, causing the release of epinephrine, norepinephrine, and other catecholamines. This results in peripheral vasoconstriction, thus decreasing subcutaneous tissue oxygenation.
For example, norepinephrine is increased 3-fold in the early, postoperative hours, peaking with the patient's first expression of pain.23 Adrenocorticotrophic hormones secreted during stress cause a decreased inflammatory response, the second phase of wound healing.21 Deficits in circulatory fluid volume (hypovolemia) and decreases in venous return result in reduced cardiac output and systemic hypotension, further compromising tissue perfusion. Hypothermia is also common immediately postoperatively, causing increased oxygen; demands and raising metabolism.
Pain-relieving narcotics and immobility can cause constipation in any postoperative patient. Straining causes intra-abdominal pressure, which is known to disrupt wounds and cause dehiscence. Using stool softeners can prevent some problems.
PATIENT WITH VENOUS HYPERTENSION
This morbidly obese male patient's abdominal girth contributes to resistance to return of venous blood flow. Treatment of his multiple venous ulcers includes bilateral Unna's boots.
ASSESSMENT AND INTERVENTION
Initial assessment of an obese patient should include an inventory of special equipment needed to eliminate risk of injury to the patient and staff, such as:
* a bed wide enough for the patient to turn independently
* a walker to support the weight for the first few postoperative days, if the patient is undergoing surgery
* an overhead trapeze to help the patient reposition himself or herself
* lifts for moving the patient safely
* a bedside commode.24
It is important to convey to the patient that the clinician is skilled and knowledgeable in the use of special equipment; many obese patients fear injury to themselves or to their caregivers.18
In addition to equipment, assess the need for and obtain any special supplies, such as extra wound care dressings and special- sized gowns. This will ensure that all patient care needs are met in an adequate and prompt manner.
Postoperatively, assess incision sites. Hematoma formation can be caused by inadequate hemostasis. Signs and symptoms include skin discoloration at the incision site and vitals signs consistent with blood loss.5
Assess for nausea if the patient has an abdominal incision- abdominal wounds in obese patients have excess tension due to adipose tissue and edema. Vomiting can add intra-abdominal pressure at the incisional area. The patient may require a nasogastric tube or antiemetics, or he or she may need to be kept NPO until the nausea and vomiting subside.
Assess respiratory function and encourage use of inspiratory spirometers. Slow, deep breaths can help increase oxygen levels.Vigorous coughing can add intrathoracic pressure and more stress on the abdominal incision. Provide pillows to splint incisions when patients do cough.
Binders are helpful with abdominal incisions. Binders should be released slowly and fastened gently. Abruptly ripping away tape over incisions can separate approximated edges and cause stripping damage to the skin. Use the press/lift technique of lifting tape with one hand while gently pressing the fingers of the other hand on the skin and closely following the tape.
Wet, soiled dressings should be removed. They indicate a draining and possibly dehisced wound, and they can be irritating to the skin. Record the condition of the incisional wound, including the presence or absence of edema, induration, color, and drainage. It is important to note the approximation of wound edges, or lack of it, and where separation is occurring.
Closed wound suction devices, such as the Jackson-Pratt drain, should be checked frequently for proper functioning. The bulb is compressed to create negative pressure required to move air and secretions so that seromas or hematomas will not develop.5 Record amounts of drainage emptied from them and the nature of the drainage.
For wounds to heal, a patient must be in a state of positive nitrogen balance. Nitrogen balance is defined as the difference between nitrogen intake and nitrogen excretion. When a patient's nitrogen intake exceeds his or her nitrogen excretion, the resultant"positive"nitrogen balance suggests the availability of protein for repair of nutritional deficits.8 Serum albumin is the major protein synthesized by the liver. It maintains plasma oncotic pressure and delivers metabolites, enzymes, drugs, and hormones in the bloodstream. Albumin facilitates wound healing. During trauma, albumin synthesis decreases and utilization of albumin increases at wound sites.8 Low serum albumin values are an indicator of impaired wound healing. Any obese patient should have a nutritional consult and discharge planning should include a follow-up for nutritional counseling.
Pain assessment and intervention are paramount to successful recovery. One study found that obese patients given epidural morphine were more able to sit, stand, ambulate, and tolerate more vigorous physiotherapy postoperatively than obese patients who received intramuscular morphine. There were fewer pulmonary complications in the patients receiving epidurals, and wound healing was unimpaired.25
Pressure ulcer prevention
The Braden Scale for Predicting Pressure Sore Risk is a cumulative score from 6 subscales to determine risk for development of pressure ulcers.26 A score is assigned to each subscale: sensory, nutrition, mobility, moisture, activity, and friction and shear. Some critics claim that this risk assessment tool leaves out factors, such as circulation, that would make it more beneficial in the critical care setting,27 where most obese postsurgical patients are managed. Some have proposed adaptations or alternative risk assessment tools more customized to intensive care units (ICUs). One study designed the Heel Pressure Ulcer Risk Assessment Tool, a 3- part risk assessment/prevention tool specifically for patients in ICUs.28 Regardless of what the critics say, the important point is that any risk assessment scale is intended to identify risks and prompt interventions to reduce those risks (such as using a moisture barrier in skin folds to prevent friction-induced ulcers).
Turning patients at least every 2 hours-more if indicated by the patient's condition-is a standard inter\vention to prevent pressure ulcers. In the ICU, however, many patients cannot be turned. Instead, positional changes of legs and arms are beneficial. Heels should always be"floated."Heel ulcers are the only pressure ulcers that are preventable, yet the heels consistently : appear in the literature as the second most common site of pressure ulcers.29,30
A team approach, in which goals are mutually established and the patient is a cooperative participant, is considered to be most effective means of managing an obese patient. A frank, nonjudgmental discussion should be conducted about the effects of obesity on the outcomes of wound healing, as well as therapeutic options.
Obese patients present specific challenges to care. If clinicians are knowledgeable about obese patients' risks, they are more able to intervene to eliminate or reduce potential problems. Understanding basic wound care and the assessment process is a precursor to identifying the special physiologic responses in postsurgical patients who are obese.
1. Centers for Disease Control and Prevention. 1991-2001 prevalence of obesity among U.S. adults, by characteristics. Available at http://www.cdc.gov/nccdphp/dnpa/obesity/ trends/ prevjhar.htm; accessed August 3,2004.
2. American Obesity Association. What is obesity? Available at http://www.obesity.org/ subs/fastfacts/obesity_what2.shtml; accessed August 3,2004.
3. Maklebust J, Sieggreen MY. Pressure Ulcers: Guidelines for Prevention and Nursing Management, 2nd ed. Springhouse, PA: Springhouse Corporation; 1996.
4. Brashers VL, Davey SS. Alterations of pulmonary function. In: McCance KL1 Huether SE, editors. Pathophysiology: The Biologic Basis for Disease in Adults and Children, 3rd ed. St. Louis, MO: Mosby; 1998. p 1158-1200. 5. Groszek DM. Promoting wound healing in the obese patient. AORN J 1982;5:1132-8.
6. Jacobson TM. Obesity and the surgical patient: nursing alert. Ostomy Wound Manage 1994;40(2):56-8, 60-3.
7. Van Meter K. Systemic hyperbaric oxygen therapy as an aid in resolution of selected chronic problem wounds. In: Krasner D, Kane D, editors. Chronic Wound Care: A Clinical Source Book for Professionals, 2nd ed. Wayne, PA: Health Management Publications Inc.; 1997. p 260-75.
8. Pinchofsky-Devin G. Nutritional assessment and intervention. In: Krasner D, Kane D, editors. Chronic Wound Care: A Clinical Source Book for Professionals, 2nd ed. Wayne, PA: Health Management Publications Inc.; 1997. p 73-83.
9. Armstrong M. Obesity as an intrinsic factor affecting wound healing. J Wound Care 1998;7:220-1.
10. Johnson RG, Cohn WE, Thurer RL, McCarthy JR, Sirois CA, Weintraub RM. Cutaneous closure after cardiac operations: a controlled, randomized, prospective, comparison of intradermal versus staple closures. Ann Surg 1997;226:606-12.
11. Printen KJ, Paulk SC, Mason EE. Acute postoperative wound complications after gastric .
surgery for morbid obesity. Am Surg 1975;41:483-5
12. Derzie AJ, Silvestri F, Liriano E, Benotti P. Wound closure technique and acute wound complications in gastric surgery for morbid obesity: a prospective randomized trial. J Am Coll Surg 2000:191:238-43.
13. Winiarsky R, Barth P, Lotke P. Total knee arthroplasty in morbidly obese patients. J Bone Joint Surg Am 1998;80:1770-4. '
14. Hopf H, Hunt T, West J, et al. Wound tissue oxygen tension predicts the risk of wound infection in surgical patients. Arch Surg 1997;132:997-1004.
15. lsraelsson LA, Jonsson T. Overweight and healing of midline incisions: the importance of suture technique. Eur J Surg 1997;163:175-80.
16. Chang DW, Wang B, Robb GL, et al. Effect of obesity on flap and donor-site complications in free transverse reclus abdominis myocutaneous flap breast reconstruction. PIaSt Reconstr Surg 2000:105:1640-8.
17. Houston MC, Raynor BD. Postoperatiave morbidity in the morbidly obese parturient woman: supraumblilical and low transverse abdominal approaches. Am J Obstet Gynecol 2000:182:1033-5.
18. Murphy K, Gallagher S. Care of an obese patient with a pressure ulcer. J Wound Ostomy Continence Nurs 2001 ;28:171-6.
19. Davis JM, Crawford PS. Persistent leg ulcers in an obese patient with venous insufficiency and elephantiasis. J Wound Ostomy Continence Nurs 2002:29:55-60.
20. FalangaV. Venous ulceration: assessment, classification and management. In: Krasner D, Kane D, editors. Chronic Wound Care: A Clinical Source Book for Professionals, 2nd ed. Wayne, PA: Health Management Publications Inc.; 1997. p 165-171.
21. Doughty DB, Waldrop J, Ramundo J. Lower-extremity ulcers of vascular etiology. In: Bryant R, editor. Acute and Chronic Wounds: Nursing Management, 2nd ed. St. Louis, MO: Mosby; 2000. p 265-300.
22. Falanga V, Eaglstein WH. The "trap" hypothesis of venous ulceration. Lancet 1993;341:1006-8.
23. West JM, Gimbel ML. Acute surgical and traumatic wound healing In: Bryant R, editor. Acute and Chronic Wounds: Nursing Management, 2nd ed. St. Louis, MO: Mosby; 2000. p 189-96.
24. Gallagher S. Bariatric surgery: An important tool for treatment and weight loss of the obese patient. Xtra-Wise 2001 ;3(1):3. SIZEWise Rentals, Prairie Village, KS.
25. McCaffery M, Pasero C. Pain: Clinical Manual, 2nd ed. St. Louis, MO: Mosby; 1999.
26. Bergstrom N, Braden BJ, Laguzza A, Holman V. The Braden Scale for Predicting Pressure Sore Risk. Nurs Res 1987;36:205-10.
27. Jiricka MK, Ryan P, Carvalho MA, Bukvich J. Pressure ulcer risk factors in an ICU population. Am J Grit Care 1995;4:361 -367.
28. Blaszczyk J, Majewski M, Sato F. Make a difference: standardize your heel care practice. Ostomy Wound Manage 1998;44(5):32-40.
29. Carlson EV, Kemp MG1 Shott S. Predicting the risk of pressure ulcers in critically ill patients. Am J Crit Care 1999;8:262-9.
30. Cuddiggan J, Ayello EA, Sussman C, editors. Pressure Ulcers in American: Prevalence, Incidence, and Implications for the Future. Reston, VA: National Pressure Ulcer Advisory Panel; 2001.
Case REPORT: Complications of Gastric Bypass Surgery
A 54-year-old Hispanic female presented for a second gastric V bypass surgery. At 5-foot, 1-inch and 289 pounds, she was more than twice her ideal weight. Significant history included hypertension, gastroesophageal reflux, nocturnal oxygen desaturation requiring home oxygen, degenerative joint disease, venous hypertension with ulceration, and degenerative joint disease. She denied smoking and drinking and did not have diabetes.
The patient had undergone gastric bypass surgery in 1994 via the Roux-en-Y procedure to reduce her weight after years of battling obesity. Her bypass was effective for 3 to 4 years. Then she began gaining weight again. Because of her decreasing ability to ambulate and failing self-esteem, she initiated another evaluation for a redo gastric bypass in early 2001.
An upper gastrointestinal (Gl) series revealed a gastric fistula. This indicated the breakdown of her staple line, allowing an increased capacity for intake. After psychological evaluation and preoperative assessment, she underwent a second Roux-en-Y, a partial gastrectomy, a small bowel resection, and 2 enteroenterostomies on July 13, 2001. Her laboratory results at the time of admission reported a low albumin level of 2 mg/dL and hemoglobin and hematocrit levels of 11 and 33, respectively.
Postoperatively, the patient was transferred to the intensive care unit (ICU). An epidural catheter provided a route for morphine administration for pain relief. Two abdominal drains were inserted to prevent fluid collection in the abdominal tissue, and a nasogastric tube was utilized to minimize gastric contents to protect the gastric suture line. The patient retained 15 L of resuscitation fluids, adding more weight and workload to her heart, lungs, and kidneys. Patients with edematous tissue risk having complications of incisional breakdown, anastomotic leaks, and a prolonged ileus.1
The following describes the postoperative condition of the patient's lungs, Gl tract nutritional status, and abdominal wound. The events are reported by the intrinsic factors that impede wound healing in the obese patient, rather than chronologically, to better associate the cause and effect of each complication. As the physiologic insults to each organ system accumulated, the outcome for this patient became worrisome.
Postoperatively, the patient was extubated in the recovery room and placed on 100% oxygen via face mask. Obese people are chronically hypoxic because of hypoventilation due to restricted lung capacity.2 This patient was known to require home oxygen therapy at night. On July 15, she became hypotensive (blood pressure 75/34 mm Hg), with shortness of breath, which raised concerns of a myocardial infarction (Ml). The Ml was ruled out, but a chest X-ray demonstrated bibasilar atelectasis.
The patient emergently returned to surgery on July 25 for repair of an incarcerated bowel that threatened the viability of the gut. She was kept heavily sedated on the ventilator to maximize oxygnation with minimal effort and to prevent straining of the suture lines. She developed pleural edema and worsening bibasilar air space on July 28 and remained on the ventilator until August 8. One day later she developed severe tachycardia, tachypnea, and a dramatic drop in her oxygen saturation levels. Pneumonia was confirmed, and she was once again placed on the ventilator. A tracheostomy was performed on August 17 to reduce complications from long-term endotracheal intubation. Chest X-rays continued to identify pneumonia, and attempts to wean her from the ventilator failed. Oxygenation to support wound healing, angiogenesis, and collagen formation remained compromised throughout the first 1 months after the original surgery.
Increased intra-abdominal pressure
The first sign of potential wound dehiscence appeared on July 17 with the leakage of a small amount of serous fluid at the distal end of the incision. Cooper^sup 3^ described serous drain\age from the wound bed that occurs between the 5th and the 12th day postoperatively as a classic sign of pending dehiscence. On the 5th postoperative day (July 18), the patient complained of nausea and experienced several episodes of vomiting, which caused increased intra-abdominal pressure against the gastric and abdominal suture lines. An upper Gl series indicated slow passage of contrast material. A computerized tomography (CT) scan confirmed an ileus, which added back-flow pressure to the suture lines; no bowel dilation or leaks were found.
On July 21, wound dehiscence was declared secondary to an abdominal abscess. The distal sutures were removed from the incision and 30 cm^sup 3^ of purulent drainage was collected. Two days later, the wound, ostomy, and continence nurse was called to assess the wound because greenish-yellow output had become part of the exudate. A small bowel fistula was evident.
On July 23, a repeat CT scan indicated possible incarceration of the bowel within a large ventral hernia, an additional cause of increased bowel pressure. Surgery was performed to relieve it the following day. The bowel was found kinked and twisted, with necrosis and perforation. The incision (30 cm wide and 25 cm long) was left open to heal by secondary intention. The episodes of vomiting, the ileus, and the abscess were paramount issues in affecting the integrity of the abdominal and bowel suture lines.
Stress and pain management
Pain is a Stressor to the healing process. According to Chang et al,4 the body's reaction to stress causes vasoconstriction from the action of epinephrine, leading to decreased blood perfusion to all tissues including the wound. In an obese person, circulation is already compromised because adipose tissue is poorly vascularized.2,5-7 When pain control was inadequate via her epidural catheter, the patient become agitated and hypertensive (190/100 mm Hg) due to vasoconstriction. Minimizing anxiety by anticipating her discomfort and medicating her appropriately were imperative to prevent the stress response. After the epidural was discontinued, she received a patient-controlled analgesia pump. This gave her the ability to manage her own pain, which allayed fears of waiting for pain medication to be delivered. The stress reaction decreased blood flow to the wound sites and negatively affected optimal healing.
seepage of serous drainage appearing between the distal sutures on July 17 was the first sign of a wound complication. In obese patients, seromas and hematomas develop easily in the dead space of the fatty tissue, which is poorly perfused.2'58 Despite placement of Jackson-Pratt drains during the initial and subsequent surgeries, this patient developed a seroma in the subcutaneous fatty tissue. On July 18, the lower sutures were removed so that the seroma could drain.
On July 25, the patient was returned to surgery for exploration of the surgical site. An abscess was located and intubated with a catheter to drain the pocket. The abscess fluid cultured Escherich/ a coil and the health care provider ordered the antibiotics piperacillin (Zosyn) and enoxaparin sodium (Lovenox). A bowel perforation and contamination caused peritonitis. Because of the infection and fistula output, the wound was left open to heal by secondary intention.
Over the next 2 months this patient had a Candida alfacans infection and was treated with amphotericin B. Pseudomonas aeruginosa was found in the sputum and urine. A second abdominal abscess was identified in August and was treated with gentamicin sulfate (Garamycin). A methicillin resistant Staphylococcus aureus was detected at the central line insertion site on August 25 and the patient was placed in isolation.
During October, November, and December, Pseudomonas continued to be present in the urine and sputum. S aureus was still growing in the sputum and blood cultures just before discharge in December. The burden of infection compromised oxygnation and circulation early in the recovery period, causing necrosis of the bowel and fistula formation, failure of initial skin grafts to take, and wound dehiscence.
Protein provides the building blocks for tissue repair.1 On admission, the patient had a low albumin of 2 g/dL (normal 3.5 to 5 g/dL). Albumin reflects the patient's nutritional status about 20 days prior to the blood draw.1 By the second surgery on July 25, her albumin had dropped to 1.2 g/dL, depicting the utilization of proteins required during traumatic events to the body.1 She had been NPO for 2 weeks after surgery and so tube feedings were attempted. Because of the ileus, increased fistula output, and leakage around the gastric tube, feedings were stopped and total parenteral nutrition was begun. A prealbumin level was obtained, which provided a more current nutritional picture.1 It measured a low 11.1 (normal 18 to 45).
Skin grafts cover the wound surface. A gully is seen at 6 o'clock below the fistula. A small fistula is seen in the upper center of the wound.
The site is prepared with Skin Bond Cement, Strip Paste (to fill the ridge), and Soft Flex barrier rings (to fill the gully). The barrier rings were cut to fit and layered until level with the skin.
A Durahesive wafer with a convex insert and urostomy pouch was used to contain the main fistula.
The upper fistula was pouched with Stomahesive flexible wafer and urostomy pouch to prevent undermining of the lower wafer.
The third surgery on August 11 was intended to close the fistula and apply skin grafts to the abdominal wound. Tube feedings were resumed on August 13, but were discontinued because of fistula recurrence. Progress to heal these body insults was interrupted by each surgery because the increased nutritional demands for healing were greater than her body's resources to build tissue. The patient was in a state of carbohydrate and protein malnutrition.
Initiatives for wound management
The patient's immediate postoperative plan of care progressed on schedule. She was out of bed with 2 abdominal binders in place on July 14. She started a gastric I diet. Then the difficulties began. The fecal material found in the exudate halted her oral intake. Temperature elevations caused excessive weakness, leaving her unable to perform daily personal care. Surgery performed on July 25 left a large open abdominal wound to heal by secondary intention.
The wound was managed with gauze impregnated with petrolatum to keep the wound bed moist and protected from the fistula effluent. The enterocutaneous small bowel fistula was located above the bottom rim of the wound at 6 o'clock. A large Malecot catheter was swaddled in moist saline gauze and placed beneath the active fistula to draw the drainage out of the wound. The wound area was much too large to pouch with a wound manager, and so the entire site was packed with moist normal saline Kerlix (Tyco Healthcare/Kendall, Mansfield, MA) and covered with loban (3M Health Care, St. Paul, MN), a larger, thicker transparent film dressing found in the operating room. The periwound skin was protected from this adhesive dressing by applying a hydrocolloid platform around the entire wound margin. This sealed system was connected to low wall suction.
After 3 attempts, skin grafting succeeded in covering the majority of the wound, allowing the use of a pouching system to collect the output (Figures 1 and 4). Skin Bond Cement (Smith & Nephew, Largo, FL) was applied to the skin grafted area of the abdomen and the backs of the wafer pieces. Containment of the output was complicated by the narrow gully between the stoma at 6 o'clock and the lower skin margin. Coloplast Strip Paste (Coloplast Corp., Marietta, GA) was used as a filler along the rim. To enhance the wafer seal, Hollister SoftFlex skin barrier rings (Hollister Incorporated, Libertyville, IL) were used to fill the gap below the fistula and the rim of the lower wound margin until it was at the level of the abdominal skin (Figure 2). A Durahesive wafer (ConvaTec, Skillman, NJ) with a convex insert was used to contain the main fistula (Figure 3).
The mucous fistula above and central of the bowel fistula produced copious amounts of thin, mucus-like output. It was also pouched to prevent undermining of the larger fistula's wafer (Figure 4). After placement of pouches, the wafer margins around the main fistula were extended with Stomahesive wafer strips (ConvaTec, Skillman, NJ) to ensure contact to healthy skin for stability.
Wearing time for the system was unpredictable and ranged from 2 to 7 days. Her husband was instructed in many problemsolving tricks to maintain the seal. He helped maintain the pouching system at the rehabilitation center and at home. He was a wonderful source of encouragement to his wife and his ability to manage the collection system gave her confidence in going to the rehabilitation center.
After 52 days in ICU and 168 days (more that 5 months) in the hospital, this patient was sent to a rehabilitation center. When pouching failures became more frequent after the wound margins became less pronounced, the husband was given a Hollister Drainable Fecal Incontinent Collector (Hollister Incorporated, Libertyville, IL) to serve as the fistula pouch. The large pouch capacity, along with a drain spout that was attached to a bedside drainage bag at nighttime, was an improvement.
Following 3 months of rehabilitation, the patient went home. She was seen in the enterostomal therapy clinic for special supply acquisition. At that time, she was increasing her activities at home, was well dressed, and had been to the hair salon. Her attitude about recovery continued to be optimistic.
Three weeks after her discharge, however, she developed lower back pain and fever and was readmitted to the hospital. Within 8 hours, she was found to have \a spinal abscess that quickly caused lower extremity paralysis. She was placed on a bariatric bed frame and a rotating pressure relief mattress to assist in respiratory toileting. An increasing temperature and respiratory distress sent her to the ICU. She developed sepsis and respiratory failure, and she died of her complication only 10 months after her second elective bypass surgery.
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Joyce A. Wilson, MSN, RN, CWOCN * Wound, Ostomy, Continence Consultant * Department of General Surgery * Wilford Hall Medical Center * Lackland Air Force Base * San Antonio, TX
Jan J. Clark, BSN, RN, CWOCN * Wound, Ostomy, Continence Consultant * Department of General Surgery * Wilford Hall Medical Center * Lackland Air Force Base * San Antonio, TX
The authors have disclosed that they have no significant relationship with or financial interest in any commercial companies that pertain to this educational activity.
Adapted from Wilson JA, Clark JJ. Obesity: impediment to wound healing. Crit Care Nurs Q 2003:26:119-32.
Copyright Springhouse Corporation Oct 2004