Nursing 200 Foundations > Quiz 9 > Flashcards
Quiz 9 Flashcards
T1 to T2
Thoracic vertebrae, one to twelve
T&A
Tonsillectomy and adenoidectomy
t/o
Telephone order
TAH
Total abdominal hysterectomy
TB
Tuberculosis
TBI
Traumatic brain injury
TCDB
Turn, cough and deep breath
TEE
Transesophageal echocardiogram
TF
Tube feeding
TIA
Transient ischemic attack
tid
Three times a day
TKO
To keep open
TPA
Tissue plasminogen activator
TPN
Total parenteral nutrition
TPR
Temperature, pulse and respiration
TSH
Thyroid stimulating hormone
TURP
Transurethral resection, prostate
U/A
Urinalysis
UAP
Unlicensed assistive personnel
UE
Upper extermity
U/O
Urinary output
URI
Upper respiratory infection
UTI
Urinary tract infection
Approximated
Closed. Most wounds heal with primary intention, which means closing the wound right away.1 Wounds that fit neatly together are referred to as “well approximated.” This is when the edges of a wound fit neatly together, such as a surgical incision, and can close easily.
Debridement
Removal of necrotic material. The procedure is essential for wounds that aren’t getting better. Usually, these wounds are trapped in the first stage of healing. When bad tissue is removed, the wound can restart the healing process.
Wound debridement can: help healthy tissue grow, minimize scarring, reduce complications of infections
Debridement isn’t required for all wounds.
Typically, it’s used for old wounds that aren’t healing properly. It’s also used for chronic wounds that are infected and getting worse.
Debridement is also necessary if you’re at risk for developing problems from wound infections.
Type of debridement: biological, enzymatic autolytic, mechanical
Dehiscence
Partial or total rupturing of a sutured wound/approximated wound edges, due to a failure of proper wound healing. This scenario typically occurs 5 to 8 days following surgery when healing is still in the early stages. The causes of dehiscence are similar to the causes of poor wound healing and include ischemia, infection, increased abdominal pressure, diabetes, malnutrition, smoking, and obesity.[1] Superficial dehiscence is when the wound edges begin to separate and by increased bleeding or drainage at the site. The clinician should investigate the wound for worrisome signs, including infection or necrosis.[2] Prompt identification is important for preventing worsening dehiscence, infection, and other complications. Evisceration is a complication of complete wound dehiscence, where intraabdominal organs herniate through the open wound.
Issues of Concern
Proper wound healing occurs in three general phases, allowing the damage to heal and new tissue to replace the damaged tissue. The three phases include inflammation, proliferation, and maturation.[3][4][5] The repaired wound can be expected to obtain 80% of the original tensile strength over two years, but will not achieve the same level of pre-injury strength. Poor wound healing can occur due to the disruption of any of the three phases of healing. Common risk factors for abnormal healing include the presence of necrotic tissue, infection, ischemia, smoking, diabetes, malnutrition, glucocorticoid use, and radiation exposure.
When dehiscence is identified, it is crucial to determine the extent of wound failure. Superficial dehiscence can be managed with abdominal binders to reduce strain on the wound and prevent further dehiscence. The existing wound failure may be allowed to heal by secondary intention or can close secondarily. Deep dehiscence of the underlying fascia is a surgical emergency and must be closed in the operating room, as this can lead to evisceration. If the wound shows signs of evisceration, the wound can be covered with a sterile saline dressing until the herniating organs can be reduced back into the abdomen.
Clinical Significance
Poor Perfusion/Ischemia - Healing wounds have an increased demand for oxygen and other factors to promote proper repair. Wounds with poor perfusion or ischemia do not receive sufficient blood flow to meet demand and are unable to heal correctly. Patient comorbidities, including vascular disease or venous insufficiency, increases patient risk for wound failure and dehiscence. Careful suturing can reduce local ischemia to the wound, preventing local wound failure.
Infection - Infected wounds are unable to heal appropriately and become ‘stuck’ in the inflammation phase. Without proper resolution of wound inflammation, proliferation, and maturation of the wound are unable to occur.
Smoking - Tobacco smoking has a vasoconstrictive effect leading to decreased wound perfusion. Nicotine also impairs proper macrophage migration and fibroblast activation, impeding the wound healing process.
Diabetes - Microvascular disease caused by diabetes can impair blood flow, leading to poor wound perfusion. Hyperglycemia also increases the risk of wound infection, decreasing healing.
Malnutrition/Hypoalbuminemia - Protein status is essential for fibroblast proliferation, collagen synthesis, and angiogenesis. Without adequate protein stores, proper wound healing becomes slowed. Limited carbohydrate reserves can lead to protein catabolism and wound breakdown. Deficiencies of vitamin C and zinc also lead to impaired wound healing. Optimizing a patient’s nutrition before surgery can decrease the risk of wound failure.
Radiation - Surgery should be avoided in patients receiving radiation whenever possible. Radiation leads to microvascular obliteration, leading to a gradual decrease in tissue perfusion towards the epicenter of the radiated target area, compromising wound repair. Radiation can also lead to altered cellular replication and increased fibrosis, inhibiting proper wound healing.
Epithelial tissue
Epithelial tissues are widespread throughout the body. They form the covering of all body surfaces, line body cavities and hollow organs, and are the major tissue in glands. They perform a variety of functions that include protection, secretion, absorption, excretion, filtration, diffusion, and sensory reception.
The cells in epithelial tissue are tightly packed together with very little intercellular matrix. Because the tissues form coverings and linings, the cells have one free surface that is not in contact with other cells. Opposite the free surface, the cells are attached to underlying connective tissue by a non-cellular basement membrane. This membrane is a mixture of carbohydrates and proteins secreted by the epithelial and connective tissue cells.
Epithelial cells may be squamous, cuboidal, or columnar in shape and may be arranged in single or multiple layers.
Simple cuboidal epithelium is found in glandular tissue and in the kidney tubules. Simple columnar epithelium lines the stomach and intestines. Pseudostratified columnar epithelium lines portions of the respiratory tract and some of the tubes of the male reproductive tract. Transitional epithelium can be distended or stretched. Glandular epithelium is specialized to produce and secrete substances.
Eschar
A wound covering of dried plasma proteins and dead cells that occurs if the wound does not close by epithelialization
Eschar is a type of necrotic tissue that can develop on severe wounds. It is typically dry, black, firm, and usually adhered to the wound bed and edges. Eschar can occur on full thickness injuries, which are wounds that extend below the epidermis and dermis. Examples include third degree burns, or stage three and four pressure injuries. Additionally, eschar can be present on some skin rashes associated with infections, such as ecthyma gangrenosum, scrub typhus, rickettsialpox, and anthrax.
Eschar differs from a scab, which is formed when platelets and fibrinogen form a fibrin mesh, trap red blood cells on surface wounds, and form a clot that dries into a scab. Instead, eschar is formed when slough, or other dead tissue debris, from a full thickness wound dries out and hardens.
Should eschar be removed?
-Because eschar and other types of necrotic tissue impede healing, it is broadly recommended that it be removed. The process of tissue death causes growth factors to be inactivated and slows the formation of granulation tissue in the wound bed. When dead tissue dries out and becomes hardened eschar, it causes wound contraction to be physically obstructed and stunts epithelialization.
-Research supports that debriding eschar early in the healing process can decrease healing time. In certain wounds, such as circumferential burns, constriction caused by the presence of eschar can also cause compartment syndrome, which is an increase in pressure within a muscle compartment that can ultimately cause muscle and nerve damage. A notable exception to early debridement could be a stable eschar (i.e., an eschar that is dry, adherent, and intact) that is present on a heel or ischemic limb. Due to inherent decreased blood flow to these areas, some experts argue that the benefit of leaving the eschar in place to reduce the risk of infection outweighs the benefits of debriding.
-Because of the firm, dry nature of eschar, sharp debridement with a scalpel may be difficult. Other debridement techniques that can be used include surgical, enzymatic or chemical, mechanical, and biological methods. During surgical debridement, the individual is usually placed under anesthesia to remove dead tissue. Enzymatic, or chemical debridement, occurs when a topical enzyme is used on the eschar to break down the necrotic tissue over time. Mechanical debridement can be performed with dressing types designed to soften and remove the eschar, such as wet-to-dry dressings. Other mechanical options include whirlpool baths or pulse lavage. Biological debridement uses sterile maggots to eat away at the dead tissue, while not harming live tissue.
Excoriation
Area of loss superficial layer of the skin. Overview
Peeling, damaged skin on the lips can happen with dermatillomania.
Lip damage from picking or biting can be a sign of dermatillomania.
What is dermatillomania?
Dermatillomania is a mental health condition where a person compulsively picks or scratches their skin, causing injuries or scarring. Also known as excoriation disorder or skin-picking disorder, this condition falls under the category of obsessive-compulsive disorders (OCDs). When it leads to significant scarring and injuries, this condition can severely affect a person’s mental health, well-being and quality of life.
-Obsessive-compulsive disorder (OCD) is a specific condition that also lends its name to a category of mental health conditions. While dermatillomania falls under the overall category of obsessive-compulsive disorders, it still has some key differences from the specific condition of OCD.
-Obsessions. OCD involves obsessions, which are thoughts or urges that a person can’t control and doesn’t want. Those kinds of obsessions don’t happen with dermatillomania.
Feeling of reward. When people with dermatillomania pick at their own skin, they often feel relief or other positive emotions. That doesn’t happen with OCD.
Damage. OCD rarely involves any kind of self-damage or self-injury. With dermatillomania, that kind of self-injury is extremely common.
Exudate
Material that has escaped from BVs during the inflammatory process and is deposited in the tissue or on the tissue surface.
Exudate consists of fluid and leukocytes that move to the site of injury from the circulatory system in response to local inflammation. This inflammatory response leads to blood vessel dilatation and increased permeability, resulting in increased production of exudate. The nature and quantity of exudate depend on the nature and severity of the tissue damage. The exact amount of wound exudate and moisture to promote moist wound healing is unknown. This moisture balance is essential to promote healing and is oftentimes a major challenge to the wound care provider
Wound exudate is not simply an inert liquid. It can help provide valuable clinical information to wound care specialists and podiatrists regarding etiology, the progression of a wound, and the presence of infection. The biochemical properties of wound exudate are altered depending on the wound micro environment. Therefore, its composition can help wound care specialists determine whether a wound is acute or chronic.
Generally speaking, a healthy wound has a small amount of exudate visible on its surface. Wound exudate can be classified into the following types depending on the morphological appearance:
Serous: it appears thin, watery, and straw-colored. It is normal.
Fibrinous: it is thin, watery, and cloudy in appearance. It contains fibrin which is a normal finding
Bloody: it is thin, watery, and bright red
Serosanguineous: it is thin, watery inconsistency, and pale pink to bright red in appearance
Purulent: it contains inflammatory cells and debris resulting from an infection2
The causative factor of the wound influences the volume of wound exudate. Patients with venous and infectious etiology have excessive exudate production. The presence of systemic conditions like congestive heart failure can also increase the amount of wound exudate.
Evisceration
Protrusion of the internal viscera through an incision.
Evisceration is a rare but severe surgical complication where the surgical incision opens (dehiscence) and the abdominal organs then protrude or come out of the incision (evisceration). Evisceration is an emergency and should be treated as such.
Evisceration can range from less severe, with the organs visible and slightly extending outside of the incision to very severe. For instance, intestines may spill out of an abdominal incision.
Treating Evisceration
About 20% to 45% of cases of dehiscence become evisceration. The risk of death is much higher once an evisceration develops.
Evisceration is always a medical emergency. If you see tissue or organs protruding from a surgical wound, call 911 or go to the nearest hospital emergency room.
It’s important to keep the wound moist.10 To care for it on your way to seek medical attention or while waiting for EMS, cover the opening and organs with a moist, sterile bandage or sheet.
Wound evisceration is treated with emergency surgery.
Granulation tissue
The initial translucent, fragile tissue that forms during the proliferative phase of wound healing. Granulation tissue is an important component in the wound healing process. Wounds can heal by primary intention (wound edges approximate easily) and secondary intention (wounds edges do not approximate). Granulation tissue matrix will fill wounds that heal by second intention. This tissue type is also present in chronic wounds that have many different causes. This article will discuss the mechanism of wound healing and repair, the role that granulation tissue plays in that process, the pathophysiology resulting in chronic wounds and persistent granulation tissue, and the clinical significance of granulation tissue.
Granulation tissue is a type of new connective tissue, and microscopic blood vessels have three main functions.
Immune: Protects the wound surface from microbial invasion and further injury.
Proliferative: Fills the wound from its base with new tissue and vasculature.
Temporary plug: Replaces necrotic tissue until replacement by scar tissue.[1][2]
https://www.ncbi.nlm.nih.gov/books/NBK554402/#:~:text=Granulation%20tissue%20is%20an%20important,that%20heal%20by%20second%20intention.
Hematoma
A localized collection of blood underneath the skin that may appear as reddish-blue swelling
A hematoma is a bad bruise. It happens when an injury causes blood to collect and pool under the skin. The pooling blood gives the skin a spongy, rubbery, lumpy feel.
A hematoma usually is not a cause for concern. It is not the same thing as a blood clot in a vein, and it does not cause blood clots.
Hemostasis
Cessation of bleeding.
Definition. Hemostasis is the mechanism that leads to cessation of bleeding from a blood vessel. It is a process that involves multiple interlinked steps. This cascade culminates into the formation of a “plug” that closes up the damaged site of the blood vessel controlling the bleeding. It begins with trauma to the lining of the blood vessel.
Stages. The mechanism of hemostasis can divide into four stages. 1) Constriction of the blood vessel. 2) Formation of a temporary “platelet plug.” 3) Activation of the coagulation cascade. 4) Formation of “fibrin plug” or the final clot.
Purpose. Hemostasis facilitates a series of enzymatic activations that lead to the formation of a clot with platelets and fibrin polymer. This clot seals the injured area, controls and prevents further bleeding while the tissue regeneration process takes place. Once the injury starts to heal, the plug slowly remodels, and it dissolves with the restoration of normal tissue at the site of the damage.
Primary hemostasis (platelet clotting)
Primary hemostasis is when your body forms a temporary plug to seal an injury. To accomplish that, platelets that circulate in your blood stick to the damaged tissue and activate. That activation means they can “recruit” more platelets to form a platelet “plug” to stop blood loss from the damaged area. That clot works much like a cork or bottle stopper, keeping blood in and debris or germs out. Primary hemostasis may also involve constriction (narrowing) of the damaged blood vessel, which can happen because of substances that activated platelets release.
Secondary hemostasis (coagulation cascade)
The platelet plug is the first step to stop bleeding, but it isn’t stable enough to stay in place without help. The next step, which stabilizes the plug, is secondary hemostasis. This step, sometimes called coagulation, involves molecules in your blood called “coagulation factors.” Those factors activate in sequence, the “coagulation cascade,” which amplifies clotting effects as the sequence continues. Ultimately, the coagulation cascade forms a substance called fibrin. During this step, the platelet plug acts like bricks and the fibrin acts like mortar. Together, they form a solid, stable clot.
Fibrin clot remodeling
The last stage of hemostasis is when your body remodels the existing clot into a fibrin clot. Your body does that because blood clots are a temporary patch, not a permanent solution. That removal involves a process called fibrinolysis. During fibrinolysis, your body remodels the clot into the same kind of tissue that was there before the injury.
Ischemia
Ischemic ulcers (wounds) can occur when there is poor blood flow in your legs. Ischemic means reduced blood flow to an area of the body. Poor blood flow causes cells to die and damages tissue. Most ischemic ulcers occur on the feet and legs. These types of wounds can be slow to heal.
Causes
Narrowed arteries (atherosclerosis) are the most common cause of ischemic ulcers.
Narrowed arteries prevent a healthy supply of blood from flowing to the legs. This means that the tissues in your legs do not get enough nutrients and oxygen.
The lack of nutrients causes cells to die, damaging the tissue.
Damaged tissue that does not get enough blood flow also tends to heal more slowly.
Conditions in which the skin becomes inflamed and fluid builds up in the legs can also cause ischemic ulcers.
People with poor blood flow often also have nerve damage or foot ulcers from diabetes. Nerve damage makes it harder to feel an area in the shoe that rubs and causes a sore. Once a sore forms, poor blood flow makes it harder for the sore to heal.
Symptoms
Symptoms of ischemic ulcers include:
Wounds may appear on legs, ankles, toes, and between toes.
Dark red, yellow, gray, or black sores.
Raised edges around the wound (looks punched out).
No bleeding.
Deep wound through which tendons may show through.
Wound may or may not be painful.
Skin on the leg appears shiny, tight, dry, and hairless.
Dangling the leg down off the side of a bed or chair causes the leg to turn red.
When you raise the leg, it turns pale and cool to touch.
Aching pain in the foot or leg, often at night. Pain may go away when the leg is dangled down.
Keloid
Hypertrophic scar. Keloids are benign, dermal growths related to previous skin trauma or inflammation. Lesions may develop as early as 1 to 3 months or as late as one year after injury. Spontaneous lesions have been reported. However, it is more likely that the injury was not recalled due to its insignificance or that the keloid development was delayed by months or even years. Keloids may develop anywhere, but the most commonly affected locations include deltoid, pre-sternal chest, upper back, and ear. Unusual locations for these growths include eyelids, genitalia, palms, and soles. Keloids present as firm, rubbery nodules and frequently project above the underlying skin. They may have a narrow base, resulting in pedunculated lesions, or develop into a more a broad-based plaque. As stated above, an important differential diagnosis includes hypertrophic scar which will not project above underlying skin further than 4 millimeters and, as a rule, will never extend beyond the initial area of injury. In contrast, keloids always extend beyond the area of original trauma. Color ranges from erythematous, flesh-colored, or hyperpigmented and may change with the evolution of the lesion. Although these lesions are benign, they are frequently symptomatic. In one study, 86% of patients complained of pruritus while 46% experienced pain. Other reported symptoms include tenderness and burning. Finally, keloids may have significant cosmetic implications for affected patients as they can grow to be large and disfiguring.[1][9]
Maceration
Tissue softened by prolonged wetting or soaking. Excessive exposure to moisture can cause maceration, a serious problem for your skin.
Skin maceration happens when your skin is broken down by moisture on a cellular level. Once this damage occurs, your skin is much more vulnerable to other types of problems and complications.
Moisture-associated skin damage (MASD) is an umbrella term for four types of skin problems caused by prolonged exposure to moisture:
Incontinence-associated dermatitis (IAD)
Intertriginous dermatitis (ITD)
Periwound skin damage
Peristomal MASD
MASD often happens to people who sweat excessively or come into contact with urine or feces for a long time due to incontinence. It can also happen to people who have larger wounds that expel fluid, or exudate, when the wound isn’t kept clean and dry.
Cases of skin maceration are becoming more common in the world of healthcare, mainly due to an increase in the aging population. People who suffer from moisture-related skin damage can experience the following symptoms:
Pain
Tenderness in the area
A burning sensation
Extremely itchy skin, also known as pruritus
People who suffer from skin maceration are also prone to developing other complications around the area. Bacterial or fungal infections can develop in macerated skin because these microbes flourish in a dark, damp environment.
Incontinence is strongly associated with skin maceration. Because incontinence can cause an environment full of moisture, the skin can become macerated if it’s left for an extended period of time.
When the skin is macerated, its protective barriers are broken down. This leaves the door open for bacterial and other infections to take hold.
Urine and feces are not only irritants for the skin, but feces especially can contain bacteria that worsen cases of skin maceration. Incontinence-related maceration can develop in as little as four days.
It usually shows up in the skin folds, inner thighs, and buttock areas.
Pressure ulcer/pressure injury
Pressure injuries, also termed bedsores, decubitus ulcers, or pressure ulcers, are localized skin and soft tissue injuries that form as a result of prolonged pressure and shear, usually exerted over bony prominences.[1][2] These ulcers are present 70% of the time at the sacrum, ischial tuberosity, and greater trochanter. However, they can also occur in the occiput, scapula, elbow, heel, lateral malleolus, shoulder, and ear.[3] Besides bony prominences, they can also occur due to medical or other devices, such as cell phones.[4] Pressure injuries vary in severity and characteristics.
Etiology
The development of pressure injuries is complex and multifactorial. External and internal factors co-occur to form these ulcers. Externally, prolonged pressure, friction, shear force, and moisture can lead to tissue deformation and ischemia. Internal factors such as malnutrition, anemia, and endothelial dysfunction can speed up the process of tissue damage.[6][7]
Decreased mobility, skin moisture, poor nutritional status, and loss of sensory perception stand out as the most common risk factors. However, researchers have also identified older age, cognitive impairment, and comorbid conditions affecting tissue healing.[1]
Prolonged pressure on tissues can cause capillary bed occlusion, reducing oxygen levels in the area. Over time, the ischemic tissue begins to accumulate toxic metabolites. Subsequently, tissue ulceration and necrosis occur. Immobility of only two hours in a bedridden patient or patient undergoing surgery is sufficient to form the foundation of a decubitus ulcer.[7]
The dysfunction of nervous regulatory mechanisms responsible for regulating local blood flow is also somewhat culpable in forming these ulcers.[8]
Patients with the following conditions exhibit a predisposition to decubitus ulcers:
Neurologic disease
Cardiovascular disease
Prolonged anesthesia
Dehydration
Malnutrition
Hypotension
Surgical patients
Epidemiology
Pressure ulcers are a significant healthcare problem worldwide, which affects several thousands of people each year.[7] Up to 3 million adults are affected annually in the United States alone.[3] Pressure injury management is a significant source of economic burden. In 2019, Padula and Delarmente estimated that hospital-acquired pressure injury (HAPI) costs could exceed $26.8 billion.[9] Their study simulated an incidence of 8.3 HAPI per 100 acutely ill patients. This number is consistent with previous studies, which showed that 7.9% of at-risk patients had HAPI.[10]
Sacral decubitus ulcers usually occur in elderly patients. Patients who are incontinent, paralyzed, or debilitated are more prone to getting them. Patients with normal sensory status, mobility, and mental status are less likely to form these ulcers because their regular physiologic feedback system leads to frequent physical positional shifts. As stated above, older patients are more prone to sacral decubitus ulcers, and two-thirds of ulcers occur in patients older than 70 years. Some data show that 83% of hospitalized patients developed ulcers within 5 days of hospitalization.[7]
Pathophysiology
Decubitus ulcer formation is multifactorial, but these ulcers result in a common pathway to ischemia and necrosis. Tissues can sustain an abnormal amount of external pressure, but constant pressure exerted over a prolonged period is the main culprit. External pressure must exceed the arterial capillary pressure of 32 mm Hg to impede blood flow. The pressure must be greater than the venous capillary closing pressure of 8 to 12 mm Hg to impair venous blood return. Sustaining pressure above these values leads to tissue ischemia and necrosis.[11] This significant pressure can result from compression by a firm mattress, hospital bed railings, or any hard surface in contact with the patient.
In addition, the EPUAP emphasized the link between the pathophysiology of COVID-19 and the development of pressure ulcers. The panel attributed the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha, abundant in COVID-19 patients, as a contributor to the onset and maintenance of inflammation following cell death and the formation of a pressure ulcer.[11] Friction caused by skin rubbing against surfaces like clothing or bedding can also lead to the development of ulcers by contributing to breaks in the superficial layers of the skin. Moisture can cause ulcers and worsen existing ulcers via tissue breakdown and maceration.
Primary intention healing
Occurs where the tissue surfaces have been approximated, and there is minimal or no tissue loss.
The tissues approximated by surgical sutures or tapes with minimal loss of tissue are said to heal by primary union or by first intention. Such wounds heal with a clean, neat and thin scar [17]. Primary closure of wounds other than head and neck can be safely done up to a maximum of 19 h after the wound. Wounds of the face and scalp can be primarily closed whenever they are seen, as long as infection is not already present [18]. Within 24 h, neutrophils appear at the margins of incision moving toward the fibrin clot. The epidermal continuity is re-established in 24–48 h. By day 3, neutrophils largely disappear and are replaced by macrophages. By day 5, incisional space is filled with granulation tissue, neovascularisation is maximal. During 2nd week, there is continuous accumulation and proliferation of fibroblasts. By end of 1st month, scar comprises of a cellular connective tissue devoid of inflammatory infiltrate, covered by an intact epidermis.
Reactive hyperemia
Red flush of skin that occurs when pressure is relieved from an area. You remove the dental floss you wrapped around a finger.
Secondary intention healing
When there is more extensive loss of cells, or surface wounds that create large defects, the reparative process is more complicated. Granulation tissue grows in from the margins to complete the repair. These wounds heal with an ugly scar [17]. This is referred to as healing by secondary intention. It differs from primary healing in several respects, i.e. in secondary healing:
Inflammatory reaction is more intense.
Much larger amounts of granulation tissue are formed.
Wound contraction is much more.
Shearing force
Shear is a horizontal force that causes the bony prominence to move across the tissue as the skin is held in place, and results from patient movement, nurse movement of the patient, and bed movement. There are seven basic requirements a support surface must meet in order to prevent pressure and shear: The surface must (1) conform to bony prominences without resistance, (2) not have significant memory, (3) allow patient immersion, (4) not bottom out, (5) relieve shear caused by patient movement, (6) prevent skin maceration, and (7) provide patient comfort. Six types of support surfaces are listed along with a summary of each surface’s theoretical ability to deal with the forces described in this article. Understanding the physical forces that contribute to pressure ulcers, and each support surface’s theoretical ability to relieve these forces, should make it easier to choose an appropriate support surface for each patient.
Tertiary intention
Tertiary healing (third intention) is delayed primary wound healing after 4–6 days. This occurs when the process of secondary intention is intentionally interrupted and the wound is mechanically closed. This usually occurs after granulation tissue has formed.
Vasodilation
the widening of blood vessels as a result of the relaxation of the blood vessel’s muscular walls. Vasodilation is a mechanism to enhance blood flow to areas of the body that are lacking oxygen and/or nutrients.
In humans, an increase in internal core temperature elicits large increases in skin blood flow and sweating. The increase in skin blood flow serves to transfer heat via convection from the body core to the skin surface while sweating results in evaporative cooling of the skin. Cutaneous vasodilation and sudomotor activity are controlled by a sympathetic cholinergic active vasodilator system that is hypothesized to operate through a co-transmission mechanism
