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BUKOVINIAN STATE Medical university




on the methodical conference of department

of patients’ care and higher

nurse education

“ ” ________ 200_ protocol N __

Chief of department, associate professor I.A. Plesh




the wounds.

complications of the wounds.


nursing in surgery

for 3nd year students

of medical faculty №4,

specialty "nurse business''

Methodical instruction was prepared by:

Assistant Riabyi S.I.

Assoc. professor O.Y. Khomko

Chernivtsi - 2010

^ 1. Topic: the wounds. complications of the wounds.

(The main notions about wound, classification, characteristic of different kinds of wounds. Clinical signs of wounds. Phases of wound healing. Types of wound healing. Nurse’s tactics in case of bites wounds. Complications of wounds, requirements, prevention. Active and passive immunity against tetanus. Symptoms of purulent complications. Participation of nurse in conservative and surgical treatment of wounds. Nurse’s care of wound).

^ 2. Duration of the class: 4 academic hour.

3. Study aim:

3.1. The student should know:

  • Wounds: definition, classification.

  • Frame of a wound and a course of a wound process in a clean wound.

  • The characteristic of separate types of wounds and a first aid at them.

  • Conditions of occurrence of an infection in a wound, elimination of these conditions.

  • Frame of a clean wound.

  • The initial surgical treatment of a wound.

  • Kinds of initial seams.

  • Treatments of a clean wound in the postoperative period.

  • Contaminated wounds.

  • Course of a wound process in a purulent wound.

  • The surgical treatment of a purulent wound, kinds of secondary seams.

  • Treatments of a purulent wound according a phase of a wound process.

  • Kinds of a drainage of a purulent wound.

  • Concepts about a traumatism.

  • Clinical symptoms of the closed damage of soft tissues, skull, a thorax, organs of abdominal cavity.

  • Prophylaxis of development of a traumatic shock, a pheumothorax, an internal bleeding.

  • Features of first-aid treatment and transportation of patients at these damages.

^ 3.2. The student should be able:

    • To apply occlusive bandage at penetrating damage of a thorax

    • To diagnose phases of a wound process;

    • To determine a kind of wound's healing;

    • To take a material for cytologic and microbiological researches;

    • To render the first medical aid at wound;

    • To apply and remove sutures.

    • To carry out a dressing of a purulent wound with application of modern antiseptics;

    • To impose an immovable bandage.

    • To allocate the basic clinical attributes of damage of a forward abdominal wall, hollow and parenchymatous organs of abdominal cavity;

    • To make the circuit of diagnostic search;

    • To estimate results of laboiratory - instrumental methods of diagnostics;

    • To prove main principles of treatment of separate damages of a stomach (an abdominal wall, hollow and parenchymatous organs).

^ 3.3. The student should master practical skills:

    • applying bandage;

    • dressing of clear wound;

    • dressing of purulent wound;

    • taking a material for cytologic and microbiological researches;

    • first medical aid at wound;

    • applying and removing sutures.

·4. Advice for students:

Types of wounds

According to aetiology, the types of wounds are:

1. Incised wounds.

2. Chopped wounds.

3. Lacerated wounds.

4. Contused wounds.

5. Bruise wounds.

6. Flesh wounds with defect of skin.

7. Puncture wounds

8. Bites wounds.

9. Ischemic or necrotic wounds.

10. Gunshot wounds.

Rapid healing of the wound, particularly rapid skin cover, is the ideal objective - the first intention of the surgeon. This is brought about by joining together the edges of the wound by sutures, clips, or by adhesive materials, film or tape.

Alternative methods of closure used to achieve protection against infection by skin cover include delayed primary suture, secondary suture, and skin grafting.

Most wounds may be treated by wound excision and primary suture of the skin (with drainage if needed), within 6 hours of injury. Each layer is tackled in turn and devitalised tissue is carefully trimmed away. The object of wound excision is to convert the injury from a jagged lacerated wound into one which approximates to the incised wound. However, a certain amount of damaged but recoverable tissue remains in the wounds, and for this reason it is usually unwise to attempt complicated repairs of deep structures such as tendons and nerves in these wounds. As soon as the skin wound is soundly healed, probably in 4 to 6 weeks' time, a formal secondary repair of any divided tendons and nerves can be carried out.

^ The phases of wound healing

The lour basic processes which take place in wound healing are:

1. Phase of traumatic inflammation. Immediately after disruption of tissue integrity either by accidental trauma or by surgeon's knife, inflammation starts. After a transient: vasoconstriction, all local small vessels dilate. As dilatation occurs, capillaries become abnormally permeable to proteins and plasma leaks into the site of injury. The blood vessels undergo transient vasoconstriction followed by vasodilatation. Platelets become adherent and with clotting factors form a haemostatic plug to stop bleeding from the small vessels. Histamine is considered to be the primary mediator of inflammatory vascular responses. This is liberated by platelets, mast cells and granulocytes. Histamine produces local vasodilatation and increases permeability of small vessels. With increase of permeability, proteins and plasma leak out of the vessels. However the action of histamine is short lasting and local sources are depleted rapidly. Soon the kinins. a series of biologically active peptides and the prostaglandins, principally PEG and PEG, take over the job of implicating local inflammatory vascular responses from histamine. Kallikrein, an enzyme found in plasma and in granulocytes, releases bradykinin and kallidin. In the presence of kinins, the local ceils produce a variety of prostaglandins. These prostaglandins seem to be the final mediators of acute inflammation and may play a chemolactic role for white cells and fibroblasts. Aspirin and indomethaein are potent inhibitors of prostaglandin biosynthesis and the antiinflammatory action of these drugs actually results from their effects on prostaglandin metabolism.

In the early stages of inflammation, actively motile white cells migrate into the wound and start engulfing and removing cellular debris and injured tissue fragments. At first, polymorphonuclear leucocytes dominate. This stage has also chemical mediators. Leukotaxine, a peptide formed in damaged tissues by the enzymatic destruction of albumin, is thought to be the chemotactic agent - attracting leucocytes into the wound.

As the transient phase of white cell migration ends, the granulocytes with shorter life die and release acid hydrolases into the local environment. Previously the proportion of granulocytes and monocytes in the wound area were in the same ratio as they are in the blood. As the granulocytes die, the proportion of monocytes increases significantly and these monocytes continue their scavenging activity for weeks. Monocytes become the dominant cell type by the 5th day. They are phagocytic and ingest cellular debris. It has been found out experimentally that wound healing may proceed normally in the absence of granulocytes and lymphocytes, but monocytes must be present to create normal fibroblasts production. Depression of monocytes will delay wound healing.

Clinically, inflammation is presented by redness, tenderness, heat, swelling and loss of function.

2. Phase of demolition (pyogenic for secondary wound healing).

The dead tissue cells liberate their autolytic enzymes. Similarly disintegrating polymorphs liberate proteolytic enzymes. The mononuclear cells along with large phagocytic macrophages infiltrate and ingest particulate matters. They either digest or remove them. Fusion of these macrophages results in the formation of foreign body giant cells.

3. Granulation tissue formation. The granulation tissue is mainly formed by proliferation and migration of the .surrounding connective tissue elements. It is in fact composed of in the first instance by capillary loops and fibroblasts with a variable number of inflammatory cells. So initially it is a highly vascular tissue, which gradually turns into an avascular scar tissue. The two stages are considered in this process: a) stage of vascularisation and b) stage of devascularisation.

Stage of vascularisation. As mentioned above the wound clot is invaded by macrophages, which with their phagocytic activities remove the particulate matters and move towards the centre of the wound. This process is followed by capillary loops and fibroblasts. The ingrowth of 204 capillary loops and fibroblasts which help to form living granulation tissue is known as organization. Solid buds of endothelial cells grow out of the existing damaged blood vessels at the surface of the wound. These undergo canalization and by anastomosis with their neighbours form a series of vascular arcades. Under the electron microscope, gaps are seen between the endothelial cells and the basement membrane is poorly formed. These newly formed capillary loops leak protein and thus the tissue fluid which is formed is a very suitable medium for fibroblastic growth.

Gradually these capillary loops differentiate, a few acquire muscle coat and become arterioles, whereas others enlarge to form thin walled venules. A few disappear or persist as pan of the capillary bed. The source of smooth muscle fibres to form arterioles is either cell migration or differentiation of existing primitive mesenchymal cells. Direct arteriovenous shunts are also formed.

The fibroblasts, which accompany the capillary loop, gradually become larger to become elongated fibrocytes. During this process of fibrogenesis, pH becomes alkaline. From these fibroblasts ultimately collagen is formed. Collagen is an extracellular secretion from specialised fibroblasts and the basic molecules which fibroblasts synthesise are frequently called tropocollagen. This tropocollagen condenses in the mucopolysaccharide extracellular space to form fibrils. These fibrils are grouped together to form the reticulin fibres. These fibrils when condensed together form the collagen fibres. This collagen is not inert and it undergoes constant turnover under the influence of tissue collagenase. More thicker collagen fibres are laid down haphazardly.

There are several types of collagen which differ in the aminoacid sequence of the constituent chains, though hydroxyproline, proline and glycin dominate. Type I collagen is found in the tendon, ligament, skin and bone. Type II collagen is found in cartilage, mainly in articular and 205 costal cartilages. Type III collagen is found in foetal dermis and later on is replaced by type I collagen at birth. Type III collagen appears to be an important component of tissues with unusual degree of elasticity such as aorta, oesophagus and uterus. The aminoacids found in collagen are hydroxyproline and hydroxylysine. Other fibrous tissues such as elaslin do not contain significant amount of hydroxyproline.

Fibroblasts are also thought to be responsible for the production of mucopolysaccharide ground substance.

Stage of devascularisation. In this stage fibroplasia proceeds and some vessels undergo atrophy, whereas others show endarteritis obliterans, that means their lumens become obliterated due to ultimate proliferation. So the granulation tissue looks pale at this stage, which is known as devascularisation.

At the beginning of this stage, nerve fibres and lymphatics form. With the ingrowth of nerve fibres, the arterioles exhibits rhythmic contraction. The new lymphatics develop from existing lymphatics in the same way as do the capillary loops. Mast cells also make their appearance and their granules are derived from the ground substance. At later stage these mast cells disappear and hyalinisation occurs. There is also formation of scar tissue. This process is known as cicatrization. Collagen turn over and remodelling in the scar never stops. In fact the turn over of collagen in scar tissue is faster than in other tissues. The phenomenon of scar remodelling is the basic function of injured tissues.

4. Epithelisation. While dead material is being removed from deeper areas, important events occur at the edges of epithelial wounds. In skin wounds, the epidermis immediately adjacent to the wound edge begins thickening within 24 hours after injury.

Epithelisation of the wound mainly occurs by proliferation and migration of the marginal basal cells lying close to the wound margin. There is no regeneration of hair follicles, sebaceous and sweat glands in the new epidermis. 206

In case of the wounds with skin loss, healing of the skin layer is of importance not only in its own right but because the healing of deeper structures, such as the tendons and bones, can only take place satisfactorily in the presence of an intact skin cover. Furthermore, the longer any exposed surface remains raw the greater will be the deformity and disability. In all wounds with skin loss therefore, the skin loss should be repaired as soon as is practicable and as follows:

1. Clean incised wounds with skin loss - primary grafting.

2. Lacerated wounds with skin loss - wound excision and primary grafting.


Bites of animals such as the horse, cat, and dog require the usual treatment of wounds. Where there is the slightest suspicion that the animal is suffering from rabies, the bite should be freely excised. If possible, the responsible animal should be kept under observation, or, if it has been killed, Negri bodies should be sought in the brain.

Human Bites. Because the wound becomes contaminated with so many types of bacteria a human bite can prove very dangerous to life or limb. Although not strictly a bite, a common type of injury of this kind is an incised, wound over the knuckles resulting from a clenched fist of one combatant striking the front teeth of his opponent. The joint is usually penetrated, but the track closes when the fingers are extended. In such a case the wound must be excised.

^ Gunshot wounds

Mechanism. The amount of damage caused by bullets is dependent on the kinetic energy (KB) released by the bullet as it traverses tissue. The energy can be calculated from the formula KE = 0.5mv2 where m is the mass and v the velocity of the bullet.

The low velocity bullet from a pistol, travelling below 1,500 feet per second, produces injury by its direct effect on tissue by laceration and crushing, within the narrow confines of the bullet track. The high velocity bullet has a much greater lethal potential. Tissue necrosis occurs several centimeters on either side of the bullet track due to the associated shock-wave and a phenomenon known as cavitation. The penetrating high velocity bullet releases energy which is absorbed by adjacent tissue particles, imparting to them an acceleration which flings them forwards and outwards producing the temporary cavity (Fig.1).

Fig.1. Gunshot wound. Cavitational destructive effect

due to the energy oj the high velocity missile

Tissue necrosis occurs especially in muscle at some distance from the bullet track and forms a perfect culture medium for pathogenic organisms sucked in from the entrance and exit wounds by the negative pressure in the cavity.

The amount of damage caused by a high velocity bullet is also dependent on the density and structure of the target organ. Comparatively, little damage occurs in the through and through wound of a lung, whereas the passage of such a bullet through or sometimes close to the liver may completely shatter that organ. All bullet injuries should undergo the operation of wound debridement, which literally means to debridle or unleash. The entrance and exit wounds, frequently of only small diameter, do not indicate the considerable damage that may have occurred to the deeper structures within. The higher the velocity of the bullet, the greater the area of damage around the bullet track, and the greater the accompanying tissue necrosis and oedema.

^ Factors of the wound healing

The various factors which influence wound healing can be divided into two groups - general factors and local factors.

General factors:

1. Age. Wound healing is fast in the young, but it is normal in old age unless associated with debilitating diseases or ischaemia or diabetes etc.

2. Nutrition :

a) Protein deficiency. As mentioned above, protein depletion causes impairment of granulation tissue and collagen formation. It should be noted that it is not always due to inadequate intake, but may be due to excessive loss e.g. nephrotic syndrome, cirrhosis, chronic inflammatory conditions, etc.

b) Vitamin A is required for proper epithelialisation, which may be hampered due to its deficiency.

c) Zinc, Calcium, Copper and Manganese deficiency. Zinc is an essential component of many enzymes which are involved in protein synthesis. There is some failure of granulation tissue formation in case of zinc deficiency. Others are essential minerals which are also required for proper wound healing. They may be depleted in intestinal fistulas.

3. Hormones:

a) Corticosteroids. The effects of this hormone on granulation tissue formation and wound contraction have been discussed above.

b)Desoxycorlicosterone acetate and anabolic steroids like testosterone are also concerned with increase in the speed of wound ealing.

The following conditions delay or hamper the quality of wound healing. These are :

4. Anaemia.

5. Uraemia.

6. Jaundice.

7. Diabetes. 8. Blood dyscrasias.

9. Malignant disease.

10. Cytotoxic drugs.

Local factors:

1. Position of skin wound. As mentioned above when the skin wounds are parallel to the lines of Langer. they heal faster. These lines of Lunger are due to arrangements of collagen bundles in the dermis. The wounds right angle to these lines lend to gape and the healing is delayed.

2. Blood supply. Wounds with poor blood supply heal slowly. That is why wounds in the pretibial region take much more time to heal than those in the face, which are well vascularised. Wounds of the leg in patients with varicose veins are slow to heal. Similarly wounds in the ischaemic limbs also heal slowly.

3. Tension. If the wound is in tension, its healing will be jeopardized. Haematoma and infection increase tension.

4. Infection. Once infection occurs in a wound, healing is always delayed. It may be considered as the most important factor that delays healing. Due to infection, fibroblasts face tough time to persist as they have to compete with inflammatory cells and bacteria for oxygen and nutrients. So proper granulation tissue formation and collagen formation become affected. This has been often the cause of "burst wound" which requires secondary sutures.

5. Movement. Movement itself delays wound healing. So rest is very essential for wound healing. The delicate capillary loops of the granulation tissue and the delicate epithelium are damaged due to movement. Frequent change of dressing also has the same adverse effect and should be avoided. Movement also causes entry of infection.

6. Exposure to ionizing radiation. Previous X-irradiation may affect vascularity of the part. It also causes delay in the formation of granulation tissue. But most important is that it inhibits wound contraction.

7. Foreign bodies. These include tissue reaction and inflammation. If sutures ave kept for longer period, it may cause aseptic abscess.

8. Adhesions to bony surfaces cause delay in wound healing probably by preventing proper wound contraction. This is particularly seen in wounds over the tibia.

9. Necrosis. This obviously retards healing.

10. Lymph drainage. Impairment of lymph drainage, which causes oedema of the part, jeopardises the process of wound healing. Elevation of such limb often facilitates wound healing.

11. Ultraviolet light is well known clinically to increase the rate of healing. This has been confirmed experimentally.

12. Faulty technique of wound closure is obviously responsible for delay in wound healing in many cases.

^ 5. Study questions:

  1. Definition of concept of a wound;

  2. Classification of wounds;

  3. Principles of wound's healing, features of each phase of a wound process;

  4. Definition of concept of an primary surgical treatment of a wound, initial and secondary seams;

  5. A technique of realization of an primary surgical treatment of a contaminated wound;

  6. Indications to performance of an primary surgical treatment and applying of a different kind of seams.

  7. Definition of concept " a primary surgical treatment of wounds ", " initial and secondary seams ";

  8. The basic characteristics of the general condition of the patient, ways of their definition;

  9. Conditions which assist development of a pyesis of a wound;

  10. Principles of antibacterial therapy;

  11. Principles of a surgical treatment of contaminated wounds (their advanced processing);

  12. Methods of a stimulation of processes of regeneration;

  13. Local and general treatment of contaminated wounds.

^ 6. The literature:

6.1. Basic :

  1. Textbook of basic nursing / Caroline Bunker Rosdahl. – J. B.Lippincott Company. Philadelphia. - 6th ed. –1995.– 1518 p.

  2. Fundamentals of nursing /Taylor Mary Carol, Mary Carol, Lillis Carol– J. B.Lippincott Company. Philadelphia. - 1989.– 1356 p.

6.2. Аdditional:

  1. Gostishev V.K. "Guidance to practical employments on general surgery". M., "Medicine" - 1987.

  2. P. of Brown. Operating block. Operating brigade. – Kharkov, 1997. – with. 1-32.

Methodical instruction was prepared by

Assistant Riabyi S.I.

A review is positive, associate professor Chomko O.J.

Materials of control of base level of preparation of students: tests.

Multiple Choices.

Choose the correct answer/statement:

  1. Secondary infection of wounds is probably at infringement corrected asepsises:

    1. At the moment of granting the first medical service;

    2. During a dressing;

    3. During operation;

    4. During reception of a wound;

    5. All answers true.

  2. The penetrating wound of abdomen refers wound with damage:

    1. Skin;

    2. A subskin fat;

    3. Muscles;

    4. Parietal peritoneum;

    5. Visceral peritoneum.

  3. What wound is healed faster others:

    1. Incized;

    2. Chopped;

    3. Bite;

    4. Contused;

    5. Gunshot.

  4. For freshen wounds typically all without:

    1. Pain;

    2. Bleeding;

    3. Defect of tissues;

    4. Sensations of twitching in a wound;

    5. Hiatus

Real-life situations to be solved:

  1. The patient for the fourth day after appendectomy had throbbing pain in the region of a postoperative wound, the body temperature increased, the leukocytosis is observed.
    What complication has arisen at the patient?

  2. After the transferred traffic accident to the patient of 63 years old in conditions of a dressing room of admitting room have not washed out a cavity of a wound a solution of oxidizers, did not drain a wound, and on have indistinctly sewed up.

Whether doctors have correctly arrived? What possible complications it is necessary to wait in the postoperative period?

Answers to the Self-Assessment:





Postoperative wound infection.

Incorrectly. Development of anaerobic surgical infection.


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