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Case Study: Non healing wounds

Brooke Munson
5/27/2016
An estimated 6.5 million patients are affected by chronic wounds in the United States and this
number is increasing due to an aging population, rise in diabetes, and obesity. It is claimed that 25 billion
is spent on non-healing wounds annually. In 2009 over 1000 outpatient wound centers were operating in
the United States, however wounds are also taken care of in hospitals, long term facilities, doctors
offices, and nursing homes (Sen et al., 2009).
The normal wound healing process is well organized and systematic. The process has
three overlapping phases that include coagulation/inflammation, proliferative phase, and remodeling
phase. In the coagulation/ inflammation phase, the blood-clotting cascade is initiated and platelets gather
at the wound site. The platelets then release growth hormones that attract inflammatory cells (white blood
cells: leukocytes, neutrophils, and macrophages). These cells fight and kill the bacteria and other invaders
that are present in the wound site. To resolve the inflammatory phase, the inflammatory cells undergo
apoptosis (Demidova-Rice, Hamblin, & Herman, 2012). The proliferative phase follows and overlaps the
inflammatory phase. It is also known as the reconstruction phase and is the process of re-epithelialization
(forming of new skin cells). Bright red granulation tissue fills the wound and degrades the present bloot
clot. Fibroblasts and endothelial cells, the most prominent cell types, present during the reformation,
support capillary growth (angiogenesis) and collagen formation (Guo & DiPietro, 2010). Capillaries bring
oxygen, nutrients and carry away waste products. Fibroblasts and the continual degradation and formation
of new tissue cause the edges of the wound to gradually pull together in this phase. Maturation is the last
stage, occurring after the wound is closed, and it can take up to two years to complete. The dermis tensile
strength is increased, functional fibroblasts are added (non-functional are degraded), and the number of
capillaries are decreased.
Guo & DiPietro (2010) explain how factors affecting wounds are put into the categories of either
local or systemic factors. They also review several factors that fit into these categories. Local factors

directly influence the wound itself and the biggest local factors are oxygenation and infection. Oxygen is
not only important for cells energy production, but it also prevents wounds from infection, induces
angiogenesis, increases keratinocyte differentiation, migration, and re-epithelialization, enhances
fibroblast proliferation and collagen synthesis, and promotes wound contraction (Guo & DiPietro, 2010).
Superoxide production is also dependent on the presence of oxygen, which is produced by leukocytes to
kill pathogens. The early stages of a wound are hypoxic, which triggers the wound healing process, but if
a wound stays in a hypoxic state (as in a chronic wound) then a wound will not heal. Several systemic
conditions, including advancing age and diabetes, can decrease vascular flow, which sets the stage for
poor oxygenation (Guo & DiPietro, 2010).
Infection is another local factor. If the wound is not effectively decontaminated, the presence of
bacteria and endotoxins will lead to a prolonged inflammatory phase. If this continues, the wound will
move into chronic state. One concern that occurs is an increase in metalloproteases, which degrade the
extracellular matrix. There is also a decrease in protease inhibitors. This causes the degrading of needed
growth factors. Another concern is the development of bacteria microenvironments.
Several systemic factors affect wound healing such as age, stress, diabetes, obesity, alcohol and
tobacco usage, and nutrition. Studies have shown that there is a delay in the components of the
inflammatory phase in the older population; however the quality of healing is not affected. Exercise has
been shown to help stimulate the delayed process. The decreased sex hormones in the elderly also impairs
healing, but studies suggest that treatment with estrogen may improve age-related impairment.
Physiological stress also affects wound healing by the release of stress hormones that in turn
decrease certain chemoattractants that are necessary for the initiation of the inflammatory phase.
Stressed individuals are more likely to have unhealthy habits, which include poor sleep patterns,
inadequate nutrition, less exercise, and a greater propensity for abuse of alcohol, cigarettes, and other
drugs (Guo & DiPietro, 2010). All these may have an effect on wound healing.
Diabetes is another concern since diabetics are known to have impaired healing and can develop
diabetic foot ulcers, which proceed 84% of all diabetic lower leg amputations (Guo & DiPietro, 2010).

When a person has diabetes, there is decreased blood flow to the wound site that causes hypoxia, which
amplifies the early inflammatory response. This prolongs the healing process and increases (along with
hyperglycemia) oxidative species without sufficient anti-oxidants. In diabetic mice, hyperglycemia caused
formation of advanced glycation end-products (a type of oxidative species) and their interaction with their
receptors were associated with impaired healing. It can alter the cells structure and function (Uribarri et
al, 2013). An increased number of proteases are found in diabetic foot ulcers, which as explained earlier
promotes cell destruction. Several dysregulated cellular functions are involved in diabetic wounds, such
as defective T-cell immunity, defects in leukocyte chemotaxis, phagocytosis, and bactericidal capacity,
and dysfunctions of fibroblasts and epidermal cells. These defects are responsible for inadequate bacterial
clearance and delayed or impaired repair in individuals with diabetes. Neuropathy is also suspected to
impair wound healing due to a decrease in neuropeptides, which have several relevant wound healing
processes. (Guo & DiPietro, 2010).
Medications that interfere with clot formation obviously have an effect on wound healing, but
other drugs like glucocorticoid steroids, non-steroidal anti-inflammatory drugs, and chemotherapeutic
drugs do as well. Glucocorticoid steroids affect wound repair via global anti-inflammatory effects and
suppression of several different cellular wound responses. No data suggests that short term non-steroidal
anti-inflammatories have an effect on wound healing, but long-term usage may reduce proliferation. Long
term use results in decreased numbers of fibroblasts, weakened strength, reduced wound contraction,
delayed epithelialization, and impaired angiogenesis. Most chemotherapeutic drugs inhibit cellular
metabolism, rapid cell division, and angiogenesis, which are all needed for proper wound repair (Guo &
DiPietro, 2010).
Several factors affect wound healing in obese patients. Local wound conditions that obese
patients experience are decreased vascularity in adipose tissue, skin folds harbor microorganisms, friction
caused by skin on skin, increased tissue pressure, increased incidence of hematoma and seroma
formation, and venous hypertension. Obesity associated diseases also contribute to wound healing
impairment. Research is finding that adipose tissue is very bioactive. Adipose tissue houses both

adipocytes as well as macrophages, both are known to produce bioactive molecules and hormone-like
substances that may impact the wound healing process, though research/evidence is lacking (Guo &
DiPietro, 2010).
Smoking and alcohol both have major negative impacts on wound healing. Acute ethanol
exposure can lead to impaired wound healing by impairing the early inflammatory response, inhibiting
wound closure, angiogenesis, and collagen production, and altering the protease balance at the wound
site. Smoking cessation has been shown to lead to improved repair and reduces wound infection (Guo &
DiPietro, 2010).
Nutrition is very important in the wound healing process. Fat and carbohydrates are the main
sources of energy in wound healing. Since cellular energy production relies heavily on glucose,
carbohydrates are necessary. Glucose provides the energy for angiogenesis and deposition of new tissue.
Also the proper amount of glucose prevents depletion of protein in the body.
Protein is essential in wound healing and a deficiency can impair capillary formation, fibroblast
proliferation, proteoglycan synthesis, collagen synthesis, and wound remodeling. A deficiency in protein
can also weaken the immune system, which can increase susceptibility to infection. Two important amino
acids in wound healing are arginine and glutamine. Both have major roles in the proliferation phase; and
a deficiency in either is associated with poor wound healing (Guo & DiPietro, 2010).
Omega-3s also may impact wound healing. Though their effects are not conclusive, they affect
pro-inflammatory cytokine production, cell metabolism, gene expression, angiogenesis in wound sites,
and improve systemic immune function. Fats also help meet the high energy demands that patients with
wounds have (Guo & DiPietro, 2010).
Vitamin C and A both have anti-inflammatory and antioxidant effects and play their own
role in the proliferation phase. Vitamin C deficiencies result in impaired healing. And have been linked
to decreased collagen synthesis and fibroblast proliferation, decreased angiogenesis, and increased
capillary fragility (Guo & DiPietro, 2010). Vitamin A is also associated with fibroblast proliferation and
collagen synthesis, but also impacts modulation of cellular differentiation and proliferation, hyaluronate

synthesis, and decreased extracellular matrix degradation. Vitamin E stabilizes cellular membranes. (Guo
& DiPietro, 2010).
There are several micronutrients that are co-factors for different reactions in wound healing.
These nutrients are magnesium, copper, zinc, and iron. A deficiency in any of these can lead to chronic
wounds since reactions may fail to happen.
In conclusion, normal wound healing consists of coagulation/inflammation, proliferation, and
maturation. There are local and systemic factors that cause chronic wounds and many of the factors
overlap one another. In individuals with non-healing wounds, many factors and potential disease states
play into their medical state.

Introduction of the Subject


Name: LD
Age: 57
Gender: Male
Race: Caucasian
Married
Patient History
Medical history: Insulin dependent DM, HTN, hyperlipidemia, obesity, MRSA, CAD, peripheral artery
disease. CKD stage 2. Right BKA 2014.
Anthropometric data:

Ht: 187.9 cm,

Wt: 144.2 kg,

Amputation: right lower leg with foot

Amputation %: 5.9%

Estimated amputee IBW: 82 kg

IBW %: 176%

BMI: 40.8

Dx: Osteomyelitis, chronic non healing wound of left ankle.


Medications: Atorvastatin, carvedilol, docusate sodium, insulin aspart, iron polysaccharide, Kefir liquid,
neurontin, polyethylene.
Lab values: Glucose: 176, ALT: 74, albumin: 3.4 (no CRP), monocyte: 0.8, eosinophil 0.8.
Diet intake assessment: Meal intakes 0-100%, Average food selection 2322 kcal/d and 112g protein/day.
Without supplements patient met 83% kcal and 96% protein needs, which meets nutritional goal of
consuming >75% of assessed needs.
Assessed needs: 2460-2870 kcal/d ( 30-35 kcal/kg) & 102.5-123g protein/d (1.25-1.5g/kg). Weight used:
82 kg (adjusted for amputation).
Nutrition Diagnosis and PES Statement
Increased nutrient needs related to medical condition as evidenced by chronic wounds on the first, second,
and thirds toes of left foot.
Interventions
Primary nutrition intervention would be consuming adequate calories and supplementing as necessary.
Education on the need for extra calories may also be beneficial to the patient. A secondary intervention
would possibly be blood glucose control education since diabetes can impair healing and lead to diabetic
foot ulcers.
Proposed outcomes to monitor and evaluate.
While the patient is in the hospital intakes should be monitored to ensure that the patient is receiving
adequate calories for the healing process. Glucose should be monitored in diabetics. The wound would be
further monitored and evaluated by the doctor.
Conclusion

In conclusion there are many factors that contribute to chronic wounds. LD was a 57 year old male who
suffered from osteomyelitis and a non-healing wound. The primary nutrition intervention was increasing
calories and protein consumed, which for this patient was done orally.
Bibliography
Guo, S., & DiPietro, L. (2010, March). Factors Affecting Wound Healing. Journal of Dental Research,
89(3), 219-229. doi: 10.1177/0022034509359125
Demidova-Rice, T. N., Hamblin, M. R., & Herman, I. M. (2012, July). Acute and Impaired Wound
Healing: Pathophysiology and Current Methods for Drug Delivery, Part 1: Normal and Chronic Wounds:
Biology, Causes, and Approaches to Care.HHS Public Acess, 25(7), 304-314. doi:
10.1097/01.ASW.0000416006.55218.d0
Sen, C. K., Gordillo, G. M., Roy, S., Kirsner, R., Lambert, L., Hunt, T. K., & Gottrup, F. (2009,
December). Human Skin Wounds: A Major and Snowballing Threat to Public Health and Economy. HHS
Public Access, 17(6), 763-771. doi:10.1111/j.1524-475X.2009.00543.x
Uribarri, J., Woodruff, S., Goodman, S., Cai, W., Chen, X., Pyzik, R., & Young, A. (2012, June).
Advanced Glycation End Products in Foods and a Practical Guide to Their Reduction in the Diet. Journal
American Diet Association, 110(6), 911-916. doi:10.1016/j.jada.2010.03.018

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