Med-Surg Exam 1 Ch 11 review

Infection

Increased risk of infection when wound contains necrotic tissue or blood supply is decreased, patients immune function is decreased (from immunosuppressive drugs such as corticosteroids), undernutrition, multiple stressors, and hyperglycemia in diabetes.

Stage I (Nonblanchable Erythema)

Intact skin with nonblanchable redness of localized area usually over a bony prominence. Darkly pigmented skin may not have viable blanching. Its color may differ from the surrounding area. The area may be painful, firm, soft, warmer, or cooler as compared to adjacent tissue.

Contractions

Normal part of healing Complications occur when excessive contraction results in deformity. Shortening of muscle or scar tissue, especially over joints, results from excessive fibrous formation.

Evisceration

Occurs when wound edges separate to the extent that intestines protrude through wound.

Fibrinous

Occurs with increasing vascular permeability and fibrinogen leakage into interstitial spaces. Excessive amounts of fibrin that coats tissue surfaces may cause them to adhere. (report to DR)

Dehiscence

Separation and disruption of previously joined wound edges. Usually occurs when a primary healing site burst open. May be caused by: infection causing inflammation granulation tissue not strong enough to withstand forces Obesity because of less blood supply and cause slow wound healing. Pocket of fluid (seroma, hematoma) developing between tissue layers and preventing the edges of the wound from coming together.

Types of inflammatory exudate

Serous fluid Serosanguineous fluid Fibrinous fluid Hemorrhagic fluid Purulent fluid (pus) Catarhal fluid

Tertiary intention

(Delayed primary) healing occurs with delayed suturing of wound in which two layers of granulation tissue are sutured together. Occurs when a contaminated wound is left open and sutured closed after the infection is controlled. Also occurs when primary wound becomes infected, is open, is allowed to granulate and then sutured. Usually results in larger scar than primary and secondary.

Neutrophils

1st leukocytes to arrive when there is an infection(1st responder), usually between 6 and 12hrs. They phagocytize (engulf) bacteria/foreign material. Have short lifespan, between 24 and 48Hrs. In time they accumulate with bacteria and other debris and form PUS. Bone marrow create and release mature neutrophils called segs when there is an infection, this is what causes an elevated WBC. When the demand is too much, immature neutrophils (bands) are released. The finding of increased bands in the blood is referred to and a SHIFT TO THE LEFT, which is commonly found in patients with acute bacterial infection.

WBC

A test that measures how many white blood cells are in the blood. WBC are also called LEUKOCYTES. They help fight infection. There are 5 main types: Neutrophils (Segs and Bands), Lymphocytes (T cells, B cells, Natural killer cells), Monocytes, Eosinophils, and Basophils.

Fistula formation

Abnormal passage between organs or a hollow organ and skin (abdominal perianal fistula)

Types of Inflammation

Acute: Healing occurs in 2 to 3 weeks and usually leaves no residual damage. Neutrophils are the predominant cell type at the site of inflammation. Subacute: Has the features of the acute process but last longer. Ex: infective endocarditis is a smoldering infection with acute inflammation, but it persists for weeks or months. Chronic: Last for weeks, months, or even years. The injuriois agent persists or repeatedly injures tissue. The predominant cell types present at the site of inflammation are lymphocytes and macrophages. EX: rheumatoid arthritis and osteomyelitis. The prolongation and chroinicity of any inflammation may be the result of an alteration in the immune response (autoimmune disease) and can lead to physical deterioration.

Complications of wound healing

Adhesions Contractions Dehiscence Evisceration Excess granulation tissue (proud flesh) Fistula formation Infection Hemorrhage Hypertrophic scars Keloid formation

Risk for pressure ulcers

Advanced age Anemia Contractures (a condition of shortening and hardening of muscles, tendons, or other tissue, often leading to deformity and rigidity of joints.) Diabetes Elevated body temp Friction (rubbing of surfaces together) Immobility impaired circulation Incontinence Low diastolic blood pressure(<60) Mental deterioration Neurologic disorders Obesity Pain Prolonged surgery Vascular disease

Monocytes

Are the 2nd type of phagocytic cells (eat/engulf). Usually arrive at site within 3-7 days after onset of inflammation. When entering the tissue space from the bloodstream, they transform into macrophages and assist in phagocytosis (eating) the inflammatory debris. MAIN ROLE: is cleaning before healing can occur. They have a long lifespan.; can multiply and stay in damaged tissue for weeks. They are important for the healing process. When particles are too large for a single macrophage, they fuse together to form a multinucleated giant cell that is then encapsulated by collagen, leading to the formation of a granuloma. Example is TB of the lungs.

Lymphocytes

Arrive later at the site of injury. Primary role is related to humoral and cell-mediated immunity. Some will enter your bloodstream, but most will move through your lymphatic system. (The lymphatic system is the group of tissues and organs, like the spleen, tonsils, and lymph nodes, that protect your body from infection). About 25 percent of the new lymphocytes remain in the bone marrow and become B cells. The other 75 percent travel to your thymus and become T cells There are different kinds of B cells and T cells. These include: EFFECTOR CELLS: that are activated by antigens to fight an active infection. MEMORY CELLS: that have been in your body long enough to recognize and "remember" past infections and go into action quickly if you become re-infected with an antigen. B lymphocytes and T lymphocytes work together to fight infection. B lymphocytes recognize antigens and become plasma cells that produce antibodies to fight them. There are three types of T lymphocytes, and each plays its own role. These include: cytotoxic T cells (killer T cells) helper T cells regulatory T cells Cytotoxic T cells, often called killer T cells, destroy cells in your body that have been infected with an antigen, cancer cells, and foreign cells like transplanted organs. Helper T cells direct the immune response of B cells and other T cells. Regulatory T cells suppress your immune system to keep its response in check. In addition to preventing autoimmune disease, they also prevent other white blood cells from fighting real or perceived antigens. Perceived antigens include substances like allergens and normal flora bacteria in the gastrointestinal tract. Allergens are things that cause an allergic reaction, which could include pollen, molds, or pet dander.

Adhesions

Bands of scar tissue that forms on or around organs. Adhesions may occur in the abdominal cavity or between the lungs and the pleura. Adhesions in abdomen may cause an intestinal obstruction

Nursing implementation for inflammation

Best management is to prevent infection, trauma, surgery, and contact with potentially harmful agents (this is not always possible. EX: mosquito bite. Adequate nutrition Early recognition signs Acute care: Observation of vital signs. A person whom is immunosuppressed (taking corticosteroids or chemo) may mask the signs. The early signs for this person may be malaise or just not feeling well. FEVER: Although fever is usually regarded as harmful, an increase in body temp is an important defense mechanism. MODERATE FEVERS (up to 103 F) (39.4 C) usually [produce few problems in most patients. However if the patient is very young or very old, is extremely uncomfortable, or has a significant medical problem (severe cardiopulmonary disease, brain injury), the use of antipyretics should be considered. Fever in the immunosupressed patient should be treated immediately with antibiotics because infection can rapidly progress to septicemia. FEVER (especially greater than 104 F (40 C) can damage body cell, dilirium and seizures can occur. OLDER ADULTS have a blunted febrile response to infection. Note: Antipyretic drugs: asprin, Acetaminophen (Tylenol), NSAIDs (Ibuprofen) Advil. Antiinflammatory drugs: Asprin Corticosteriods (prednisone) NSAIDs: Ibuprofen, pironxicam (feldenel)

Hemorrhage

Bleeding is normal immediately after tissue injury and ceases with clot formation. Hemorrhage occurs as abnormal internal or external blood loss caused by suture failure, clotting abnormalities, dislodged clot, infection, or erosion of blood vessel by foreign object (tubing, drains), or infection process.

WBC w/Diff

Determines the percent of each white blood cell in your body. Neutrophils 40-80%), Lymphocytes (T cell, B cell, Natural killer cells) (20-40%), Monocytes (2-10%), Eosinophils (1-6%), and Basophils (1-2%). It can also detect if there are any immature (Bands) white blood cells in your body.

Pain (dolor)

Cause: Change in pH. Nevre stimulation by chemicals (histamine, prostaglandins). Pressure from fluid exudate.

Swelling (tumor)

Cause: Fluid shift to interstitial spaces. Fluid exudate accumulation.

Redness (rubor)

Cause: Hyperemia from vasodilation

Heat (calor)

Cause: Increased metabolism at inflammatory site

Loss of function

Cause: Swelling and pain

Histamines

Chemicals released by the body as an allergic response Source: Produced/Stored in granules of basophils, mast cells, and platelets. Mechanism of action: causes vasodilation and increased capillary permeability (pass through) When the body gets in contact with an allergen, histamine is released to try and help the body deal with the irritation of the allergy which actually caused the symptoms of allergies (watery eyes etc). With serve allergy, the release of histamine can be deadly.

Purulent (pus)

Consists of WBCs, microorganisms (dead and alive), liquefied dead cells, and other debris.

Excess granulation tissue (proud flesh)

Excess granulation tissue may protrude above surface of healing wound. if the granulation tissue is cauterized or cut off. healing continues in normal manner.

Serosanguineous

Found during the midpoint in healing after surgery or tissue injury. composed of RBCs and serous fluid, which is semi-clear pink and may have red streaks.

Cartarrhal

Found in tissues where cells produce mucus. Mucus production is accelerated by inflammatory response.

Unstageable Full-thickness skin or tissue loss (depth unknown)

Full-thickness tissue loss in which actual depth of ulcer is completely obscured by slough (yellow, tan, gray, green, pr brown) and or eschar (tan, brown or black) in wound bed. Until enough slough and or eschar are removed to expose the base of wound, the true depth cannot be determined; but it will be either a stage III or stage IV. Stable (dry, adherent, intact without erythema, or fluctuance) eschar on heels serves as "the bodys natural cover" and should not be removed.

Stage IV full-thickness tissue loss

Full-thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present. Often includes undermining and tunneling. Depth of a stage III ulcer varies by anatomic location. Can extend into muscle and or supporting structures (fascia, tendon, or joint capsule) making osteomyelitis likely to occur. Exposed bone/muscle is viable or directly palpable.

Stage III full-thickness skin loss

Full-thickness tissue loss. Subcutaneous fat may be viable but bone, tendon, or muscle are not exposed. Slough may be present but does not obscure depth of tissue loss. May include undermining and tunneling. The depth of a stage III ulcer varies by anatomic location.

Keloid formation

Great protrusion of scar tissue that extends beyond wound edges and may form tumor-like masses of scar tissue. Permanent without any tendency to subside. Patients often complain of tenderness, pain, and hyperpparesthesia, especially in early stages. Thought to be a hereditary condition occurring most often in dark-skinned people, particularly African Americans.

Nutritional therapy

High fluid intake is needed to replace fluid loss from perspiration and exudate formation. People whom suffer from wound healing problems are those with malabsorption problems: crohns disease, GI surgery, liver disease. Undernutriton = at risk for poor wound healing. You need diet high in protein, carbohydrates, and vitamins, with moderate fat intake if necessary to promote healing. Vitamin C needed for: capillary synthesis and collagen production by fibroblasts. B-complex vit. are necessary as coenzymes for many metabolic reactions. if vit. B deficiency develops, disruption of protein, fat, and carb metabolism will occur. Vitamin A: aids in the process of epithelialization. increases collagen synthesis and tensile strength of wound healing. If pt unable to eat, enteral feedings are the 1st choice if GI tact is functional. Parenteral nutrition is indicated when enteral feedings are contraindicated or not tolerated.

Mediators for inflammation

Histamine Serotonin Kinins Complement components Prostaglandins and leukotrienes Cytokines

Hypertrophic scars

Inappropriately large, raised red and hard scars. Occur when an overabundance of collagen is produced during healing.

Assessing a person with dark skin

Look for changes in skin color, such as that is darker (purplish, brownish, bluish) than surrounding skin. Use natural or halogen light source to accurately assess the skin color. Fluorescent light casts blue color, which can make skin assessment difficult. Asses the area for the skin temperature using your hand. The area may feel initially warm then cooler. Touch the skin to feel its consistency. Boggy or edematous feel may indicate a stage I ulcer. Ask the patient if he or she has any pain or itchy sensation.

Stage II Partial thickness

Partial-thickness loss of dermis presenting as a shallow open ulcer with a red-pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled or serosanguineous-filled blister. Presents as a shiny or dry shallow ulcer without slough or bruising. (Bruising indicated deep tissue injury).

Pressure ulcer nursing assessment

Past health history: stroke, spinal cord injury, bed-rest, circulatory impairment. poor nutrition, surgery, altered mental status etc. Nutritional-metabolic history Elimination habits: con/incont Activity level Fever Diaphoresis edema discolorations Diagnosis findings: Leukocytosis, positive cultures for microorganisms from ulcer

Types of wound healing

Primary intention Secondary intention Tertiary intention

Suspected deep tissue injury (depth unknown)

Purple or maroon localized area of sicolred intact skin or blood-silled blister due to damage of underlying soft tissue from pressure and or shear. The area may be preceded by tissue that is painful, firm, mushy, boggy, warmer, or cooler as compared to adjacent tissue. Deep tissue injury may be difficult to detect in individuals with dark skin tones. Evolution may include a thin blister over dark wound bed. The wound may further evolve and become covered by thin eschar. Evolution may be rapid, exposing additional layers of tissue even with optimal treatment.

Local manifestations of inflammation

Redness (rubor): Heat (calor) Pain (dolor) Swelling (tumor) Loss of function (funcio laesa)

Hemorrhagic

Results from rupture or necrosis of blood vessel walls. Hematoma, bleeding after surgery or tissue trauma.

Serous

Results in outpouring of fluid. Seen in early stages of inflammation or when injury is mild. Example: skin blisters, pleural effusion

Complement components

Source: Anaphylatoxic agents generated form complement pathway activation. Mechanisms of action: Stimulate histamine release and chemotaxis.

Prostaglandins and leukostrinees

Source: Produced from arachidonic acid. Mechanisms of action: PGs cause vasodilation. LTs stimulate chemotaxis.

kinins

Source: Produced from precursor factor kininogen as a result of activation of hageman factor XII of clotting system. Mechanisms of action: Causes contraction of smooth muscle and dilatation. Result in stimulation of pain.

Serotonin

Source: Stored in platelets, mast cells, enterochromaffin cells of GI tract. Mechanisms of action: Caused validations and increased capillary permeability. Stimulates smooth muscle contraction. Serotonin or 5-hydroxytryptamine (5-HT) is a neurotransmitter and hormone that contributes to the regulation of various physiological functions by its actions in the central nervous system (CNS) and in the respective organ systems. Peripheral 5-HT is predominantly produced by enterochromaffin (EC) cells of the gastrointestinal (GI) tract. These gut-resident cells produce much more 5-HT than all neuronal and other sources combined, establishing EC cells as the main source of this biogenic amine in the human body. Peripheral 5-HT is also a potent immune modulator and affects various immune cells through its receptors and via the recently identified process of serotonylation. Alterations in 5-HT signalling have been described in inflammatory conditions of the gut, such as inflammatory bowel disease. The association between 5-HT and inflammation, however, is not limited to the gut, as changes in 5-HT levels have also been reported in patients with allergic airway inflammation and rheumatoid arthritis. Based on searches for terms such as '5-HT', 'EC cell', 'immune cells' and 'inflammation' in pubmed.gov as well as by utilizing pertinent reviews, the current review aims to provide an update on the role of 5-HT in biological functions with a particular focus on immune activation and inflammation.

Cytokienes

Source: see table 13-3

Pressure Ulcer staging

Stage I Stage II Stage III Stage IV "Unstageable" Suspected deep tissue injury (depth unknown)

Primary intention

Takes place when wound margins are neatly approximated like a surgical procedure or a paper cut. A continuum of processes is associated with primary healing. These processes include 3 phases: Initial: 3 to 5 days. Mirgration of epithelial cells. Clot form serving as meshwork for starting capillary growth. An acute inflammatory reaction occurs. Granulation: 5 to 4 weeks. mirgration of fibroblasts. Secretion of collagen. Abundance of capillary buds. Wound fragile. (Scar tissue) wound pink and vascular. This is where the wound is at risk for dehiscence, and resistant to infection. Maturation phase and scar contraction: 7 days to several months. Remodeling of collagen. Strengthening of scar. The scar may be for painful in the phase.

Basophils

The least common of the granulocytes, representing about 0.5 to 1% of circulating white blood cells. However, they are the largest type of granulocyte. They are responsible for inflammatory reactions during immune response, as well as in the formation of acute and chronic allergic diseases, including anaphylaxis, asthma, atopic dermatitis and hay fever. They can perform phagocytosis (cell eating), produce histamine and serotonin that induce inflammation, and heparin that prevents blood clotting, although there are less than that found in Mast cell granules. It used to be thought that basophils that have migrated from blood into their resident tissues (connective tissue) are known as mast cells, but this is no longer thought to be the case.

Eosophils

They are released into the bloodstream as neutrophils are, eosinophils reside in tissue. They are found in the medulla and the junction between the cortex and medullaa of the thymus, and, in the lower gastrointestinal tract, ovary, uterus, spleen, and lymph nodes, but not in the lung, skin, esophagus, or some other internal organs[vague] under normal conditions. They play a key role in allergic reaction. The presence of eosinophils in these latter organs is associated with disease. For instance, patients with eosinophilic asthma have high levels of eosinophils that lead to inflammation and tissue damage, making it more difficult for patients to breathe. Eosinophils persist in the circulation for 8-12 hours, and can survive in tissue for an additional 8-12 days in the absence of stimulation.Pioneering work in the 1980s elucidated that eosinophils were unique granulocytes, having the capacity to survive for extended periods of time after their maturation as demonstrated by ex-vivo culture experiments.

Secondary intention

Wounds that occur from trauma, ulcerations, and infection have larger amounts of exudate and wide irregular wounds may have edges that cannot be approximated (bring together). Inflammation reaction may be greater than in primary so more debris, cells, and exudate may be present and need to be cleaned. Wound healing is the same as primary and healing and granulation take place from the edges inward and from the bottom of the wound upward until filled. There is more granulation tissue so the scar may be bigger.