GENERAL SURGERY FOR DENTAL STUDENTS

GENERAL SURGERY FOR DENTAL STUDENTS
BY Dr. AHMAD K. SHAHWAN PH.D. GENERAL SURGERY

Approach to the Surgical Patient:
The management of surgical disorders requires not only the application of technical skills and training in the basic sciences to the problems of diagnosis and treatment but also a sympathy and indeed love for the patient. The surgeon must be a doctor, an applied scientist, an engineer, an artist. Because life or death often depends upon the validity of surgical decisions, the surgeon's judgment must be matched by courage in action and by a high degree of technical proficiency

History- physical Examination - Investigations- Pre-operative preparation - operation - post-operative treatment- management of complications.

The History : At their first contact, the surgeon must gain the patient's confidence and convey the assurance that help is available and will be provided. The surgeon must demonstrate concern for the patient as a person who needs help and not just as a "case" to be processed. This is not always easy to do, and there are no rules of conduct except to be gentle and considerate.

The History I- The chief complaint :i.e. what the problem that bring the patient to the doctor& its duration . II- The present history: in full detail: 1-when the complaint start exactly ? (day , hour). 2-how it starts? (slowly ,abruptly ) 3-its course ? (increasing , the same or decreasing ). 4- any associated symptoms? (pain vomiting ,fever ,drowsiness ,change in vision ,………..) . 5- the provoking factors: what increase the complaint? 6- the releasing factors;what decrease the complaint ? 7- relieved by medication or not ? 8- constant or intermittent ,its duration & for how long ?

The History The site : The onset :gradual ,sudden or explosive
e.g. The pain: The site : The onset :gradual ,sudden or explosive The character: burning ,colicky, vague ,heaviness,….. The severity: mild ,moderate or sever . constant or intermittent . relieved by medication or not & what medication ? Factors increase it :movement ,eating, standing ,…. Factors decrease it :movement ,eating, standing ,… Radiation to other site ? Associated symptoms: vomiting ,fever …..

The History E.g.: vomiting :
What did the patient vomit? Food ,fluid ,…… How much? How often? What did the color of the vomitus ? yellow ,green, brown,…. Was vomiting projectile? The taste of the vomitus ?acidic , bitter ,…..

The History III- The past history;
Any same complain before ? How it started & how ended? Any other complain before? Related to the complaint or not related ? Any other diseases? hypertension. ,diabetes mellitus , cardiac problem,… IV –The drug history :aspirin ,anticoagulant ,contraceptive pills ,chemotherapy . V- The surgical history :any operation before, type of anesthesia ,any complication?

The History VI- Nutritional history :dehydration . Loss of electrolyte ,protein deficiency. VII- Menstrual history :regularity ,duration , amount,.. VIII-Family history: known disease in the family ,same disease in the family ,hereditary diseases? . IX- Environmental history. X- Habbit history :smoking, alcohol ,drug abuse . XI- Hypersensitivity history .

The physical examination:
All patients are sensitive and somewhat embarrassed at being examined . The examining room and table should be comfortable ,worm, closed, and drapes should be used if the patient is required to strip for the examination. A female nurse should be present if the patient is female. Most patients will relax if they are allowed to talk a bit during the examination, which is another reason for taking the past history while the examination is being done.

The physical examination:
Inspection :any scar, pulsation, swelling, redness, discharge, asymmetry, hair distribution, ulcers, wound ,…. Palpation :(superficial palpation for masses, tenderness,….&deep palpation for deep masses ) Percation :to differentiate between air & solid surfaces. Auscultation :by use stethoscope to hear normal & abnormal sounds.

E.g. if we find a lump (mass), we should know:
The site . The size . The shape . The edge (cut or rounded). Tenderness . Pulsation . Flactuality . Consistency . Mobility . The surface. Reducibility . Regional draining lymph node .

E.g. if we find an ulcer we should know:
The site . The size . The shape . The edge . The base (what you can feel) . The floor (what you can see) . The color . The secretion . The vascularity . Regional draining lymph node .

Investigations I- Simple blood investigations:
C.B.C. (complete blood count) which reveals hemoglobin, white blood cells, red blood cells, platelets count, Blood group & Rh-factor. Blood sugar (fasting or random or post brandial) . The kidney function tests (Blood urea ,serum creatinine) . Electrolyte: Na+ ,K+, Ca++,….. The liver function test (ALT, AST ,Serum bilirubin ,Serum protein & albumin ) . P.T. & P.T.T.

Investigations II- urine exam (general & culture).
III- Stool exam (general & culture). IV- ultrasonography. V- X-ray: 1- simple X-ray (without dye) e.g. chest X-ray ,abdominal X-ray ,K.U.B. ,skull X-ray ,panorama X-ray, …. 2- X-ray with dye :e.g. barium meal ,barium enema, I.V.P…… 3- C.T. ( computerized tomography ) scan . 4- M.R.I. (magnetic resonance imaging) . VI- E.C.G . (electro cardio graphy )

Investigations Special Examinations:
such as cystoscopy, gastroscopy, esophagoscopy, colonoscopy, angiography, and bronchoscopy are often required in the diagnosis of certain surgical disorders. The surgeon must be familiar with the indications and limitations of these procedures and be prepared to consult with colleagues in medicine and other surgical specialties as required.

Pre-operative preparation
According to the type of operation, we should do: All the required investigations Prepare blood . Shaving the operation site. The patient take a bath. Examined by the anesthetist. Prepare I.C.U. if the patient need. Give him premedications like diazepam a night before the operation. Fasting 8 hours before the operation . The patient should enter the operation room in the optimum condition

--operation - --post-operative treatment- --management of complications. (according to the type of the operation.)

Postoperative Care: The recovery from surgery can be divided into three phases: (1) an immediate, or post-anesthetic phase; (2) an intermediate phase, ( the hospitalization period); (3) a convalescent phase. During the first two phases, care is principally directed at maintenance of homeostasis, treatment of pain, and prevention and early detection of complications. The convalescent phase is a transition period from the time of hospital discharge to full recovery. The trend toward earlier postoperative discharge after major surgery make the 3rd phase more important.

1-The Immediate Postoperative Period
The major causes of early complications and death following major surgery are acute pulmonary, cardiovascular, and fluid derangements. The post-anesthesia care unit (PACU) is staffed by specially trained personnel and provided with equipment for early detection and treatment of these problems. All patients should be monitored in this specialized unit initially following major procedures .

1-The Immediate Postoperative Period
The patient can be discharged from the recovery room when cardiovascular, pulmonary, and neurologic function have returned to baseline, which usually occurs 1–3 hours following operation. Patients who require continuing ventilatory or circulatory support or who have other conditions that require frequent monitoring are transferred to an intensive care unit (I.C.U.) . In this setting, nursing personnel specially trained in the management of respiratory and cardiovascular emergencies are available. Monitoring equipment is available to enable early detection of cardio-respiratory derangements.

Postoperative Orders in The Immediate Postoperative Period
The nursing team must be advised of the nature of the operation and the patient's condition. Postoperative orders should cover the following: 1- Monitoring the following: A- Vital Signs : Blood pressure, pulse, and respiration should be recorded frequently until stable and then regularly until the patient is discharged from the recovery room. The frequency of vital sign measurements thereafter depends upon the nature of the operation and the course in the PACU. Continuous electrocardiographic monitoring is indicated for most patients in the PACU. Any major changes in vital signs should be communicated to the anesthesiologist and surgeon immediately.

B-Central Venous Pressure
Central venous pressure should be recorded periodically in the early postoperative period if the operation has entailed large blood losses or fluid shifts, and invasive monitoring is available. A Swan-Ganz catheter for measurement of pulmonary artery wedge pressure is indicated under these conditions if the patient has borderline cardiac or respiratory function.

C- Fluid Balance The anesthetic record includes all fluid administered as well as blood loss and urine output during the operation. This record should be continued in the postoperative period and should also include fluid losses from drains and stomas. This aids in assessing hydration and helps to guide intravenous fluid replacement. A bladder catheter can be placed for frequent measurement of urine output. In the absence of a bladder catheter, the surgeon should be notified if the patient is unable to void within 6–8 hours after operation.

D- Other Types of Monitoring
Depending on the nature of the operation and the patient's pre-existing conditions, other types of monitoring may be necessary. Examples include measurement of intracranial pressure and level of consciousness following cranial surgery and monitoring of distal pulses following vascular surgery or in patients with casts.

2- Respiratory Care In the early postoperative period, the patient may remain mechanically ventilated or treated with supplemental oxygen by mask or nasal prongs. These orders should be specified. For intubated patients, tracheal suctioning or other forms of respiratory therapy must be specified as required. Patients who are not intubated should do deep breathing exercises frequently to prevent atelectasis.

3- Position in Bed and Mobilization
The postoperative orders should describe any required special positioning of the patient. Unless doing so is contraindicated, the patient should be turned from side to side every 30 minutes until conscious and then hourly for the first 8–12 hours to minimize atelectasis. Early ambulation is encouraged to reduce venous stasis; the upright position helps to increase diaphragmatic function. Venous stasis may also be minimized by intermittent compression of the calf by pneumatic stockings.

4- Diet Patients at risk for emesis and pulmonary aspiration should have nothing by mouth until some gastrointestinal function has returned (usually within 4 days). Most patients can tolerate liquids by mouth shortly after return to full consciousness. 5- Administration of Fluid and Electrolytes Orders for postoperative intravenous fluids should be based on maintenance needs and the replacement of gastrointestinal losses from drains, fistulas, or stomas.

6- Drainage Tubes Drain care should be included in the postoperative orders. Details such as type and pressure of suction, irrigation fluid and frequency, and skin exit site care should be specified. The surgeon should examine drains frequently, since the character or quantity of drain output may herald the development of postoperative complications such as bleeding or fistulas. 7- Medications Orders should be written for antibiotics, analgesics, gastric acid suppression, deep vein thrombosis prophylaxis, and sedatives. If appropriate, preoperative medications should be reinstituted. Careful attention should be paid to replacement of corticosteroids in patients at risk, since postoperative adrenal insufficiency may be life-threatening. Other medications such as antipyretics, laxatives, and stool softeners should be used selectively as indicated.

8- Laboratory Examinations and Imaging
The use of postoperative laboratory and radiographic examinations should be to detect specific abnormalities in high-risk groups. The routine use of daily chest radiographs, blood counts, electrolytes, and renal or liver function panels is not useful.

The Intermediate Postoperative Period
The intermediate phase starts with complete recovery from anesthesia and lasts for the rest of the hospital stay. During this time, the patient recovers most basic functions and becomes self-sufficient and able to continue convalescence at home.

1- Care of the Wound : Within hours after a wound is closed, the wound space fills with an inflammatory exudate. Epidermal cells at the edges of the wound begin to divide and migrate across the wound surface. By 48 hours after closure, deeper structures are completely sealed off from the external environment. Sterile dressings applied in the operating room provide protection during this period. Dressings over closed wounds should be removed on the third or fourth postoperative day. If the wound is dry, dressings need not be reapplied; this simplifies periodic inspection. Dressings should be removed earlier if they are wet, because soaked dressings increase bacterial contamination of the wound.

1- Care of the Wound: Dressings should also be removed if the patient has manifestations of infection (such as fever or increasing wound pain). The wound should then be inspected and the adjacent area gently compressed. Any drainage from the wound should be examined by culture and Gram-stained smear. Removal of the dressing and handling of the wound during the first 24 hours should be done with aseptic technique. Medical personnel should wash their hands before and after caring for any surgical wound. Gloves should always be used when there is contact with open wounds or fresh wounds.

1- Care of the Wound : Generally, skin sutures or skin staples may be removed by the fifth postoperative day and replaced by tapes. Sutures should be left in longer (eg, for 2 weeks) in incisions that 1- cross creases (eg, groin, popliteal area); 2-for incisions closed under tension; 3-for some incisions in the extremities (eg, the hand); 4-with incisions of any kind in debilitated patients. Sutures should be removed if suture tracts show signs of infection. If the incision is healing normally, the patient may be allowed to shower or bathe by the seventh postoperative day.

1- Care of the Wound : Fibroblasts proliferate in the wound space quickly, and by the end of the first postoperative week, new collagen is abundant in the wound. On palpation of the wound, connective tissue can be felt as a prominence (the healing ridge) and is evidence that healing is normal. Tensile strength is minimal for the first 5 days. It increases rapidly between the fifth and twentieth postoperative days and more slowly thereafter. Wounds continue to gain tensile strength slowly for about 2 years. In otherwise healthy patients, the wound should be subjected to only minor stress for 6–8 weeks. When wound healing is expected to be slower than normal (e.g., in elderly or debilitated patients or those taking corticosteroids), activity should be delayed even further

1- Care of the Wound : When a wound has been contaminated with bacteria during surgery, it is often best to leave the skin and subcutaneous tissues open and either to perform delayed primary closure or allow secondary closure to occur. The wound is loosely packed with fine-mesh gauze in the operating room and is left undisturbed for 4–5 days; the packing is then removed. If at this time the wound contains only serous fluid or a small amount of exudate, the skin edges can be approximated with tapes. If drainage is considerable or infection is present, the wound should be allowed to close by secondary intention. In this case, the wound should be packed with moist-to-dry dressings, which are changed once or twice daily. The patient can usually learn how to care for the wound and should be discharged as soon as his or her general condition permits. Most patients do not require visiting nurses to assist with wound care at home.

1- Care of the Wound : Wound healing is faster if the state of nutrition is normal and there are no specific nutritional deficits. For example, vitamin C deficiency interferes with collagen synthesis and vitamin A deficiency decreases the rate of epithelialization. Deficiencies of copper, magnesium, and other trace metals decrease the rate of scar formation. Supplemental vitamins and minerals should be given postoperatively when deficiencies are suspected, but wound healing cannot be accelerated beyond the normal rate by nutritional supplements. Wound problems should be anticipated in patients taking corticosteroids, which inhibit the inflammatory response, fibroblast proliferation, and protein synthesis in the wound. Maturation of the scar and gain of tensile strength occur more slowly. Extra precautions include using non-absorbable suture materials for fascial closure, delaying removal of skin stitches, and avoiding stress in the wound for 3–6 months.

2-Management of Drains :
Drains are used either to prevent or to treat an unwanted accumulation of fluid such as pus, blood, or serum. Drains are also used to evacuate air from the pleural cavity so that the lungs can reexpand. When used prophylactically, drains are usually placed in a sterile location. Strict precautions must be taken to prevent bacteria from entering the body through the drainage tract in these situations. The external portion of the drain must be handled with aseptic technique, and the drain must be removed as soon as it is no longer useful. When drains have been placed in an infected area, there is a smaller risk of retrograde infection of the peritoneal cavity, since the infected area is usually walled off. Drains should usually be brought out through a separate incision, because drains through the operative wound increase the risk of wound infection.

Closed drains connected to suction devices are preferable to open drains (such as Penrose) that predispose to wound contamination. The quantity and quality of drainage should be recorded, and contamination minimized. When drains are no longer needed, they may be withdrawn entirely at one time if there has been little or no drainage or may be progressively withdrawn over a period of a few days.

Sump drains (such as Davol drains) have an airflow system that keeps the lumen of the drain open when fluid is not passing through it, and they must be attached to a suction device. Sump drains are especially useful when the amount of drainage is large or when drainage is likely to plug other kinds of drains. Some sump drains have an extra lumen through which saline solution can be infused to aid in keeping the tube clear. After infection has been controlled and the discharge is no longer purulent, the large-bore catheter is progressively replaced with smaller catheters, and the cavity eventually closes.

3-Postoperative Pulmonary Care
The changes in pulmonary function observed following anesthesia and surgery are principally the result of decreased vital capacity, functional residual capacity (FRC), and pulmonary edema. These changes are accentuated in patients who are : obese, who smoke heavily, or who have preexisting lung disease. Elderly patients are particularly vulnerable because they have decreased compliance, increased closing volume, increased residual volume, and increased dead space, all of which enhance the risk of postoperative atelectasis.

3-Postoperative Pulmonary Care
Pain is thought to be one of the main causes of shallow breathing postoperatively. Complete abolition of pain, however, does not completely restore pulmonary function . The principal means of minimizing atelectasis is deep inspiration. Early mobilization, encouragement to take deep breaths (especially when standing), and good coaching by the nursing staff suffice for most patients.

4-Postoperative Fluid & Electrolyte Management
Postoperative fluid replacement should be based on the following considerations: (1) maintenance requirements, (2) extra needs resulting from systemic factors (e.g., fever, burns), (3) losses from drains, and (4) requirements resulting from tissue edema and ileus (third space losses). Daily maintenance requirements for sensible and insensible loss in the adult are about 1500–2500 mL depending on the patient's age, gender, weight, and body surface area. A rough estimate can be obtained by multiplying the patient's weight in kilograms times 30 (e.g., 1800 mL/24 h in a 60-kg patient). Maintenance requirements are increased by fever, hyperventilation, and conditions that increase the catabolic rate.

For patients requiring intravenous fluid replacement for a short period (most postoperative patients), it is not necessary to measure serum electrolytes at any time during the postoperative period, but measurement is indicated in more complicated patients (those with extra fluid losses, sepsis, preexisting electrolyte abnormalities, or other factors). Assessment of the status of fluid balance requires accurate records of fluid intake and output and is aided by weighing the patient daily. As a rule, 2000–2500 mL of 5% dextrose &/or normal saline & / or lactated Ringer's solution is given daily. Potassium should usually not be added during the first 24 hours after surgery, because increased amounts of potassium enter the circulation during this time as a result of operative trauma and increased aldosterone activity.

50 ---- 154 43 31 130 109 28 4 Iso=300 Osmolarity/l 5% glucose 0.9%
Solution Glucose (g/l) Na (meq/l) Cl Hco3 K 5% glucose 50 ---- 0.9% saline 154 dextrose 4.3 % with saline 0.18 % 43 31 Ringer’s lactate solution 130 109 28 4 5% dextrose in 0.9%saline Osmolarity/l Iso=300 Hyper=600

In most patients, fluid loss through a nasogastric tube is less than 500 mL/d and can be replaced by increasing the infusion used for maintenance by a similar amount. About 20 meq of potassium should be added to every liter of fluid used to replace these losses. However, with the exception of urine, body fluids are isosmolar and if large volumes of gastric or intestinal juice are replaced with normal saline solution, electrolyte imbalance will eventually result. Whenever external losses from any site amount to 1500 mL/d or more, electrolyte concentrations in the fluid should be measured periodically, and the amount of replacement fluids should be adjusted to equal the amount lost.

5-Postoperative Care of the Gastrointestinal Tract
In the immediate postoperative period, the stomach may be decompressed with a nasogastric tube. Nasogastric intubation was once used in almost all patients undergoing laparotomy to avoid gastric distention and vomiting, The nasogastric tube should be connected to low intermittent suction and irrigated frequently to ensure patency. The tube should be left in place for 2–3 days or until there is evidence that normal peristalsis has returned (e.g., return of appetite, audible peristalsis, or passage of flatus).

5-Postoperative Care of the Gastrointestinal Tract
Once the nasogastric tube has been withdrawn, fasting is usually continued for another 24 hours, and the patient is then started on a liquid diet. Opioids may interfere with gastric motility and should be stopped in patients who have evidence of gastro-paresis beyond the first postoperative week. After most operations in areas other than the peritoneal cavity, the patient may be allowed to resume a regular diet as soon as the effects of anesthesia have completely worn off.

6-Postoperative Pain Severe pain is a common sequela of intrathoracic, intra-abdominal, and major bone or joint procedures. About 60% of such patients perceive their pain to be severe, 25% moderate, and 15% mild. In contrast, following superficial operations on the head and neck, limbs, or abdominal wall, less than 15% of patients characterize their pain as severe. The factors responsible for these differences include duration of surgery, degree of operative trauma, type of incision, and magnitude of intraoperative retraction. Gentle handling of tissues, expedient operations, and good muscle relaxation help lessen the severity of postoperative pain.

6-Postoperative Pain While factors related to the nature of the operation influence postoperative pain, it is also true that the same operation produces different amounts of pain in different patients. This varies according to individual physical, emotional, and cultural characteristics. Much of the emotional aspect of pain can be traced to anxiety. Feelings such as helplessness, fear, and uncertainty contribute to anxiety and may heighten the patient's perception of pain.

7-Physician-Patient Communication
Close attention to the patient's needs, frequent reassurance, and genuine concern help minimize postoperative pain. Spending a few minutes with the patient every day in frank discussions of progress and any complications does more to relieve pain than many physicians realize.

8-Parenteral Opioids Opioids are the mainstay of therapy for postoperative pain. Their analgesic effect is via two mechanisms: (1) a direct effect on opioid receptors and (2) stimulation of a descending brain stem system that contributes to pain inhibition. Morphine ,pethidine & tramal are the most widely used opioid for treatment of postoperative pain. Morphine may be administered intravenously, either intermittently or continuously

Nonopioid Parenteral Analgesics
They are non-steroidal anti-inflammatory drugs (NSAID) with potent analgesic and moderate anti-inflammatory activities. It is available in injectable form suitable for postoperative use . E.g. aspirin (acetyl salicylic acid ),diclofen sodium ,piroxicam,….

Oral Analgesics Within several days following most surgical procedures, the severity of pain decreases to a point where oral analgesics suffice. Aspirin should be avoided as an analgesic postoperatively, since it interferes with platelet function, prolongs bleeding time, and interferes with the effects of anticoagulants. For most patients, a combination of acetaminophen with codeine (e.g., Tylenol) or with propoxyphene (analgan) suffices. As with all opioids, tolerance develops with long-term use. Continuous Epidural Analgesia Intercostal Block

Postoperative Complications:
Postoperative complications may result from 1- the primary disease, 2- the operation, or 3-unrelated factors. Occasionally, one complication results from another previous one (eg, myocardial infarction following massive postoperative bleeding). The clinical signs of disease are often blurred in the postoperative period. Early detection of postoperative complications requires repeated evaluation of the patient by the operating surgeon and other team members .

Prevention of complications starts in the preoperative period with evaluation of the patient's disease and risk factors. Improving the health of the patient before surgery is one goal of the preoperative evaluation. For example, cessation of smoking for 6 weeks before surgery decreases the incidence of postoperative pulmonary complications from 50% to 10%. Correction of gross obesity decreases intra-abdominal pressure and the risk of wound and respiratory complications and improves ventilation postoperatively. The surgeon should explain the operation and the expected postoperative course to the patient and family. The preoperative hospital stay, if one is necessary, should be as short as possible both to reduce costs and to minimize exposure to antibiotic-resistant microorganisms. Adequate training in respiratory exercises planned for the postoperative period substantially decreases the incidence of postoperative pulmonary complications.

Early mobilization, proper respiratory care, and careful attention to fluid and electrolyte needs are important. On the evening after surgery the patient should be encouraged to sit up, cough, breathe deeply, and walk, if possible. The upright position permits expansion of basilar lung segments, and walking increases the circulation of the lower extremities and lessens the danger of venous thromboembolism. In severely ill patients, continuous monitoring of systemic blood pressure and cardiac performance enables identification and correction of mild derangements before they become severe.

I- Wound Complications
2- Seroma : A seroma is a fluid collection in the wound other than pus or blood. Seromas often follow operations that involve elevation of skin flaps and transection of numerous lymphatic channels (eg, mastectomy, operations in the groin). Seromas delay healing and increase the risk of wound infection. Those located under skin flaps can usually be evacuated by needle aspiration. Compression dressings should then be applied to seal lymphatic leaks and prevent reaccumulation. Small seromas that recur may be treated by repeated evacuation. Seromas of the groin, which are common after vascular operations, are best left to resorb without aspiration, since the risks of introducing a needle (infection, disruption of vascular structures, etc) are greater than the risk associated with the seroma itself. If seromas persist—or if they start leaking through the wound—the wound should be explored in the operating room and the lymphatics ligated.

1- Hematoma : Wound hematoma, a collection of blood and clot in the wound, is one of the most common wound complications and is almost always caused by imperfect hemostasis. Patients receiving aspirin or low-dose heparin have a slightly higher risk of developing this complication. The risk is much higher in patients who have been given systemically effective doses of anticoagulants and those with preexisting coagulopathies. Vigorous coughing or marked arterial hypertension immediately after surgery may contribute to the formation of a wound hematoma. Hematomas produce elevation and discoloration of the wound edges, discomfort, and swelling. Blood sometimes leaks through skin sutures. Neck hematomas following operations on the thyroid, parathyroid, or carotid artery are particularly dangerous, because they may expand rapidly and compromise the airway. Small hematomas may resorb, but they increase the incidence of wound infection. Treatment in most cases consists of evacuation of the clot under sterile conditions, ligation of bleeding vessels, and reclosure of the wound.

3- Wound Dehiscence: Wound dehiscence is partial or total disruption of any or all layers of the operative wound. Rupture of all layers of the abdominal wall and extrusion of abdominal viscera is evisceration. Wound dehiscence occurs in 1–3% of abdominal surgical procedures. Systemic and local factors contribute to the development of this complication. 3-1-- Systemic Risk Factors : Dehiscence is rare in patients under age 30 but affects about 5% of patients over age 60 having laparotomy. It is more common in patients with diabetes mellitus, uremia, immunosuppression, jaundice, sepsis, hypoalbuminemia, and cancer; in obese patients; and in those receiving corticosteroids.

E.g. Adequacy of Closure:
3-2- Local Risk Factors: The three most important local factors predisposing to wound dehiscence are inadequate closure, increased intra-abdominal pressure, and deficient wound healing. Dehiscence often results from a combination of these factors rather than from a single one. The type of incision (transverse, midline, etc) does not influence the incidence of dehiscence. E.g. Adequacy of Closure: This is the single most important factor. The fascial layers give strength to a closure, and when fascia disrupts, the wound separates. Accurate approximation of anatomic layers is essential for adequate wound closure. Most wounds that dehisce do so because the sutures tear through the fascia. Prevention of this problem includes performing a neat incision, avoiding devitalization of the fascial edges by careful handling of tissues during the operation, placing and tying sutures correctly, and selecting the proper suture material. Sutures must be placed 2–3 cm from the wound edge and about 1 cm apart. Dehiscence is often the result of using too few stitches and placing them too close to the edge of the fascia. Ostomies and drains should be brought out through separate incisions to reduce the rate of wound infection and disruption.

II- Respiratory Complications
Respiratory complications are the most common single cause of morbidity after major surgical procedures and the second most common cause of postoperative deaths in patients older than 60 years. Patients undergoing chest and upper abdominal operations are particularly prone to pulmonary complications. The incidence is lower after pelvic surgery and even lower after extremity or head and neck procedures. Pulmonary complications are more common after emergency operations. Special hazards are posed by preexisting chronic obstructive pulmonary disease (chronic bronchitis, emphysema, asthma, pulmonary fibrosis). Elderly patients are at much higher risk because they have decreased compliance, increased residual volumes, and increased dead space, all of which predispose to atelectasis.

II- Respiratory Complications
1- Atelectasis Atelectasis, the most common pulmonary complication, affects 25% of patients who have abdominal surgery. It is more common in patients who are elderly or overweight and in those who smoke or have symptoms of respiratory disease. It appears most frequently in the first 48 hours after operation and is responsible for over 90% of febrile episodes during that period. In most cases, the course is self-limited and recovery uneventful.

Atelectasis is usually manifested by fever (pathogenesis unknown), tachypnea, and tachycardia. Physical examination may show elevation of the diaphragm and decreased breath sounds. Postoperative atelectasis can be largely prevented by early mobilization, frequent changes in position, encouragement to cough, and physiotherapy. Preoperative teaching of respiratory exercises and postoperative execution of these exercises prevents atelectasis in patients without preexisting lung disease. Treatment consists of clearing the airway by chest percussion, coughing, or nasotracheal suction. Bronchodilators and mucolytic agents given by nebulizer may help in patients with severe chronic obstructive pulmonary disease. Atelectasis from obstruction of a major airway may require intrabronchial suction through an endoscope, a procedure that can usually be performed at the bedside with mild sedation

2- Pulmonary Aspiration
Aspiration of oropharyngeal and gastric contents is normally prevented by the gastroesophageal and pharyngoesophageal sphincters. Insertion of nasogastric and endotracheal tubes and depression of the central nervous system by drugs interfere with these defenses and predispose to aspiration. Other factors, such as gastroesophageal reflux, food in the stomach, or position of the patient, may play a role. Trauma victims are particularly likely to aspirate regurgitated gastric contents when consciousness is depressed. Patients with intestinal obstruction and pregnant women—who have increased intra-abdominal pressure and decreased gastric motility—are also at high risk of aspiration. Two-thirds of cases of aspiration follow thoracic or abdominal surgery, and of these, one-half result in pneumonia. The death rate for grossly evident aspiration and subsequent pneumonia is about 50%.

The magnitude of pulmonary injury produced by aspiration of fluid, usually from gastric contents, is determined by the volume aspirated, its pH, and the frequency of the event. If the aspirate has a pH of 2.5 or less, it causes immediate chemical pneumonitis, which results in local edema and inflammation, changes that increase the risk of secondary infection. Aspiration of solid matter can produce airway obstruction. Obstruction of distal bronchi, though well tolerated initially, can lead to atelectasis and pulmonary abscess formation. The basal segments are affected most often. Tachypnea, fever, and hypoxia are usually present within hours; less frequently, cyanosis, wheezing, and apnea may appear. In patients with massive aspiration, hypovolemia caused by excessive fluid and colloid loss into the injured lung may lead to hypotension and shock.

Aspiration can be prevented by preoperative fasting, proper positioning of the patient, and careful intubation. A single dose of cimetidine before induction of anesthesia may be of value in situations where the risk of aspiration is high. Treatment of aspiration involves reestablishing patency of the airway and preventing further damage to the lung. Endotracheal suction should be performed immediately, as this procedure confirms the diagnosis and stimulates coughing, which helps to clear the airway. Bronchoscopy may be required to remove solid matter. Fluid resuscitation should be undertaken concomitantly. Antibiotics are used initially when the aspirate is heavily contaminated; they are used later to treat pneumonia.

3- Postoperative Pneumonia
Pneumonia is the most common pulmonary complication among patients who die after surgery. It is directly responsible for death in more than half of these patients. Patients who’s requiring prolonged ventilatory support are at highest risk for developing postoperative pneumonia. Atelectasis, aspiration, and copious secretions are important predisposing factors. The clinical manifestations of postoperative pneumonia are fever, tachypnea, increased secretions, and physical changes suggestive of pulmonary consolidation. A chest x-ray usually shows localized parenchymal consolidation.

3- Postoperative Pneumonia
Maintaining the airway clear of secretions is of paramount concern in the prevention of postoperative pneumonia. Respiratory exercises, deep breathing, and coughing help prevent atelectasis, which is a precursor of pneumonia. Treatment consists of measures to aid the clearing of secretions and administration of antibiotics. Sputum obtained directly from the trachea, usually by endotracheal suctioning, is required for specific identification of the infecting organism.

III-Fat Embolism Fat embolism is relatively common but only rarely causes symptoms. Fat particles can be found in the pulmonary vascular bed in 90% of patients who have had fractures of long bones or joint replacements. Fat embolism can also be caused by exogenous sources of fat, such as blood transfusions, intravenous fat emulsion, or bone marrow transplantation. Fat embolism symptoms consist of neurologic dysfunction, respiratory insufficiency, and petechiae of the axillae, chest, and proximal arms. Fat embolism characteristically begins 12–72 hours after injury but may be delayed for several days. The diagnosis is clinical. The finding of fat droplets in sputum and urine is common after trauma.

IV- Cardiac Complications
Cardiac complications following surgery may be life-threatening. Their incidence is reduced by appropriate preoperative preparation. Dysrhythmias, unstable angina, heart failure, or severe hypertension should be corrected before surgery whenever possible. Valvular disease—especially aortic stenosis—limits the ability of the heart to respond to increased demand during operation or in the immediate postoperative period. When aortic stenosis is recognized preoperatively , the incidence of major perioperative complications is small. Thus, patients with preexisting heart disease should be evaluated by a cardiologist preoperatively.

IV- Cardiac Complications
General anesthesia depresses the myocardium, and some anesthetic agents predispose to dysrhythmias. Monitoring of cardiac activity and blood pressure during the operation detects dysrhythmias and hypotension early. In patients with a high cardiac risk, regional anesthesia may be safer than general anesthesia for procedures below the umbilicus. Non-cardiac complications may affect the development of cardiac complications by increasing cardiac demands in patients with a limited reserve. E.g. Postoperative sepsis and hypoxemia. Fluid overload can produce acute left ventricular failure. Patients with coronary artery disease, dysrhythmias, or low cardiac output should be monitored postoperatively in an intensive care unit.

V- Complications of Intravenous Therapy & Hemodynamic Monitoring
1- Air Embolism Air embolism may occur during or after insertion of a venous catheter or as a result of accidental introduction of air into the line. Intravenous air lodges in the right atrium, preventing adequate filling of the right heart. This is manifested by hypotension, jugular venous distention, and tachycardia. This complication can be avoided by placing the patient in the Trendelenburg position when a central venous line is inserted. Emergency treatment consists of aspiration of the air with a syringe. If this is unsuccessful, the patient should be positioned right side up and head down, which will help dislodge the air from the right atrium and return circulatory dynamics to normal.

V- Complications of Intravenous Therapy & Hemodynamic Monitoring
2- Phlebitis A needle or a catheter inserted into a vein and left in place will in time cause inflammation at the entry site. When this process involves the vein, it is called phlebitis. Factors determining the degree of inflammation are the nature of the cannula, the solution infused, bacterial infection, and venous thrombosis. Phlebitis is one of the most common causes of fever after the third postoperative day. The symptomatic triad of induration, edema, and tenderness is characteristic. Prevention of phlebitis is best accomplished by observance of aseptic techniques during insertion of venous catheters, frequent change of tubing (ie, every 48–72 hours),

VI-Postoperative Fever
Fever occurs in about 40% of patients after major surgery. In most patients the temperature elevation resolves without specific treatment. However, postoperative fever may herald a serious infection, and it is therefore important to evaluate the patient clinically. Normal body tempreture is 36.7—37.3’c Fever within 48 hours after surgery is usually caused by 1- atelectasis: Re-expansion of the lung causes body temperature to return to normal. 2- reactions to drugs ,anesthesia ,blood transfusion , absorption of haematoma ,

fever appears in the third postoperative day, atelectasis is a less likely explanation. The differential diagnosis of fever at this time includes catheter-related phlebitis, pneumonia, and urinary tract infection. A directed history and physical examination complemented by focused laboratory and radiologic studies usually determine the cause. Patients without infection are rarely febrile after the fifth postoperative day. Fever in the fifth postoperative day suggests wound infection or, less often, anastomotic breakdown and intra-abdominal abscesses.

Fever after the 7th postoperative day (in the 2nd week ) suggests deep venous thrombosis in the calf muscles .

Special Medical Problems in Surgical Patients
Diabetes Mellitus : Diabetic patients undergo more surgical procedures than do non-diabetics, and management of the diabetic patient before, during, and after surgery is an important responsibility of the surgeon. Fortunately, because close control of fluids, electrolytes, glucose, and insulin is now possible in the operating room, control of blood glucose levels during the peri-operative period is usually relatively simple. Marked hyperglycemia should be avoided during surgery; the greater danger, however, is from severe unrecognized hypoglycemia.

Diabetes Mellitus : Preoperative Workup : Blood glucose concentrations may be elevated in diabetic patients during the preoperative period. Physical trauma, if present, combined with the emotional and physiologic stress of the illness may cause epinephrine and cortisol levels to rise, in each case resulting in increased blood glucose levels.

Diabetes Mellitus : The preoperative workup of patients with diabetes mellitus includes A thorough physical examination, with special care to discover occult infections; An ECG to rule out myocardial infarction; A chest x-ray to identify hidden pneumonia or pulmonary edema. A complete urinalysis can rule out urinary tract infection and proteinuria, the earliest signs of diabetic renal disease. Serum potassium levels are measured to check for hypokalemia or hyperkalemia . Serum creatinine levels are used to assess renal function. The serum glucose concentration should ideally be between 100 and 200 mg/dL,

Preoperative & Intraoperative Management of Diabetic Patients
Type 2 (Non-Insulin-Dependent) Diabetes Mellitus Approximately 85% of diabetics over age 50 years have only a moderately decreased ability to produce and secrete insulin, and when at home they can usually be controlled by diet or by oral hypoglycemic drugs. If the serum glucose level is below 200 mg/dL on the morning of surgery, oral hypoglycemic drugs should be withheld; and 5% glucose solution should be administered intravenously at a rate of about 100 mL/h. This means that over a 10-hour period, only 50 g of glucose would be given; by contrast, during an average day, a diabetic on a normal diet would consume four to five times as much carbohydrate (ie, 200–250 g).

Type 1 (Insulin-Dependent) Diabetes Mellitus
If the operation is lengthy, blood glucose levels should be measured every 3–4 hours during surgery to ensure adequate glucose control. The goal is to maintain glucose levels between 100 and 200 mg/dL, Type 1 (Insulin-Dependent) Diabetes Mellitus Type 1 patients require insulin during surgery. It can be administered by any of the following methods: (1) subcutaneous administration of short-acting insulin; (2) constant infusion of a mixture of glucose and insulin; or (3) separate infusions of glucose and insulin. blood glucose levels should be monitored at least every 2 hours during the procedure to avoid hypoglycemia below 60 mg/dL and hyperglycemia above 200 mg/dL. Blood glucose levels can be measured rapidly during surgery with a portable electronic glucose analyzer.

Postoperative Care Hypoglycemia, the most common postoperative complication, most often follows the use of long-acting insulin given subcutaneously before surgery. Although hypoglycemia may also occur if the intravenous insulin infusion is excessive in relation to that of the glucose, an infusion of 1.5 units or less of insulin per hour, when given with 5% glucose, rarely results in hypoglycemia. Blood glucose levels should be measured every 2–4 hours and the patient monitored for signs and symptoms of hypoglycemia (eg, anxiety, tremulousness, profuse sweating without fever). When hypoglycemia is detected, the amount of glucose infused should be promptly increased and the insulin decreased.

Postoperative Care In the intermediate phase ;we do blood sugar every 6 hours & give soluble insulin subcutaneously according to the following table : Less than 200 mg/dl Nothing 5 units 10 units 15 units Above 350 20 units

This is continue till the patient can drink &/0r eat then the patient return to his old medical treatment & do blood sugar twice daily to be sure that its level below 180 mg/dl. A marked increase in glucose and insulin requirements postoperatively suggests the presence of occult infection (eg, wound infection, cellulitis at the intravenous site, urinary tract infection, or unrecognized aspiration pneumonia). Adjustments in the rate of glucose or insulin administration must be based on blood glucose levels.

Hypertension Patients with uncomplicated and controlled hypertension usually tolerate surgery well. The patient advised to took his medication till the day of surgery & at the morning of surgery & continue after the surgery if possible or replace it with parentral drugs. The patient should stop aspirin a week before surgery & an internist should consulted before the operation.

Respiratory Disease Acute Upper Respiratory Tract Infections : Both anesthesia and surgery provide opportunities for the spread of infection because respiratory defense mechanisms are compromised and instrumentation of the airway may be required. Therefore, the presence of a cold, pharyngitis, or tonsillitis is a relative contraindication to elective surgery, since viral infections decrease defense mechanisms against bacterial infections. If surgery is necessary, the appropriate antibiotic should be administered and manipulation of the infected area avoided when possible. Acute Lower Respiratory Tract Infections (Tracheitis, Bronchitis, Pneumonia) : These infections are absolute contraindications to elective surgery. For emergency surgery, therapy includes humidification of inhaled gases, removal of lung secretions, and continued administration of bronchodilators and antibiotics.

Bronchial Asthma : patients with bronchial asthma who are undergoing surgery are at increased risk of pulmonary complications. Preoperative management includes adjustment of bronchodilator medication, cessation of smoking, and treatment of infection. Intraoperative bronchoconstriction from mechanical stimulation of the airway must be prevented so that appropriate anesthetics can be given in adequate concentrations. Since intraoperative use of bronchodilators may be necessary, adverse interactions between anesthetic agents and bronchodilators must be avoided. Many patients with bronchial asthma have been treated with corticosteroids and require corticosteroid therapy in the perioperative period

aneamia Surgical patients with anemia should undergo a thorough workup to identify and treat the underlying cause before elective procedures are undertaken. A detailed history should be obtained to identify any symptoms of blood loss from the genitourinary and gastrointestinal tracts. A history of renal, hepatic, hematologic, or endocrinologic disorders and a medication history should be elicited. A history suggestive of hemolytic episodes or a family history of anemia may offer clues to the diagnosis. Signs of pallor, jaundice, lymphadenopathy, and organomegaly should be sought on physical examination. A complete laboratory evaluation including CBC, reticulocyte count, peripheral smear, and stool test for occult blood should be done. Correctable causes of anemia, like deficiencies of iron, folate, and vitamin B12 , should be treated. Preoperative red blood cell (RBC) transfusions are not routinely recommended, and the decision to transfuse should be based on the need to improve tissue oxygenation.

pregnancy The Pregnancy may alter or mask the signs and symptoms of the particular presentation or course of disease, so that diagnosis is made more difficult. Furthermore, the fetus and changes in maternal physiology and anatomy must be considered in the use of diagnostic tests, medical therapy, and the planning of surgical procedures. Any major operation represents a risk not only to the mother but to the fetus as well. An increase in both preterm delivery and growth restriction in infants that resulted from pregnancies that involved a surgical procedure. Although there is no evidence that congenital anomalies are induced in the developing fetus by anesthesia, semielective procedures should be deferred until the second trimester of pregnancy, exercising the greatest precautions to prevent hypoxia and hypotension. Emergent surgical procedures should proceed as necessary; however, changes in maternal physiology—particularly in cardiac output and maternal blood volume—as well as of the size of the gravid uterus must be considered.

Normal values : Blood urea 25-40mg/dl Serum creatinine 0.7-1.2 mg/dl
Fasting blood sugar mg/dl Post brandial B.S. mg/dl Random B.S. mg/dl Serum sodium meq /l Serum potassium 3.5 – 4.5 meq /l Serum calcium 9 -11 mg/dl WBC cell/dl RBC 4 -10 *10^6 cell/dl Heamoglobin 12-16 gm /dl

Fluid & Electrolyte Management
Fluid intake (input ) is derived from two sources: (1) exogenous; and (2) endogenous. Exogenous water: is either drunk or ingested in solid food. The quantities vary within wide limits, but average 2—3 litres per 24 hours, of which nearly half is contained in solid food. The water requirements of infants and children are relatively greater than those of adults because of: (1) the larger surface area per unit of body weight; (2) the greater metabolic activity due to growth; (3) the comparatively poor concentrating ability of the immature kidney. Endogenous water: is released during the oxidation of ingested food; the amount is normally less than 500 ml / 24 hours. However, during starvation, this amount is supplemented by water released from the breakdown of body tissues.

Fluid output Water is lost from the body by four routes.
1 • By the lungs. About 400 ml of water is lost in expired air each 24 hours. In a dry atmosphere, and when the respiratory rate is increased, the loss is correspondingly greater . 2•By the skin. When the body becomes overheated, there is visible perspiration, but throughout life invisible perspiration is always occurring. The cutaneous fluid loss varies with the atmospheric temperature and humidity, muscular activity and body temperature. In a temperate climate the average loss is between 600 and 1000 ml / 24 hours. 3• Faeces. Between 60 and 150 ml of water are lost by this route daily. In diarrhoea this amount is greatly multiplied. 4• Urine. The output of urine is under the control of multiple influences, such as blood volume, hormonal and nervous influences, among which the antidiuretic hormone acts by stimulating the reabsorption of water from the renal tubules. The normal urinary output is approximately 1500 ml / 24 hours, and provided that the kidneys are healthy, the specific gravity of the urine bears a direct relationship to the volume. A minimum urinary output of approximately 400 ml / 24 hours is required to excrete the end products of protein metabolism.

Water depletion : Pure water depletion is usually due to diminished intake. This may be due to lack of availability, difficulty or inability to swallow because of painful conditions of the mouth and pharynx, or obstruction in the oesophagus. Pure water depletion may also follow the increased loss from the lungs after tracheostomy. This loss may be as much as 500 ml in excess of the normal insensible loss. After tracheostomy, humidification of the inspired air is an important preventive measure. Clinical features : The main symptoms are weakness and intense thirst. The urinary output is diminished and its specific gravity increased. Treatment by drinking water &/or give 5%glucose water solution.

Water intoxication This can occur when excessive amounts of water, low sodium or hypotonic solutions are taken or given by any route. The commonest cause on surgical wards is the over-prescribing of intravenous 5% glucose solutions to postoperative patients. Similarly, water intoxication can occur if the body retains water in excess to plasma solutes. This can be seen in the syndrome of inappropriate antidiuretic hormone (SIADH) secretion which is most commonly associated with lung conditions such as lobar pneumonia, empyema and oat-cell carcinoma of bronchus, as well as head injury.

Clinical features: Treatment :
These include drowsiness, weakness, sometimes convulsions and coma. Nausea and vomiting of clear fluid are common, and, with the exception of the SIADH, usually the patient passes a considerable amount of dilute urine. Laboratory investigations may show a falling haematocrit, serum sodium and other electrolyte concentrations. Treatment : The intake of water having been stopped, the best course is water restriction. If the patient fails to improve, transfer to an intensive care unit will be necessary for more invasive monitoring and controlled manipulation of fluids and electrolytes. The administration of diuretics or hypertonic saline should not be undertaken lightly as rapid changes in serum sodium concentration may result in neuronal demyelination and a fatal outcome.

Haemorrhage The types of haemorrhage : 1- Arterial haemorrhage :
Arterial haemorrhage is recognised as bright red blood, spurting as a jet which rises and falls in time with the pulse. 2- Venous haemorrhage : Venous haemorrhage is a darker red, a steady and copious flow. The colour darkens still further from excessive oxygen desaturation when blood loss is severe. Blood loss is particularly rapid when large veins are opened, e.g. common femoral or jugular. Venous bleeding can be under increased pressure as in asphyxia, or from ruptured varicose veins. Pulmonary artery haemorrhage is dark red (venous blood) , whereas bleeding from the pulmonary veins is bright red (oxygenated).

3- Capillary haemorrhage :
It is a bright red, often rapid, ooze. If continuing for many hours, blood loss can become serious, as in haemophilia. 4- Primary haemorrhage : It occurs at the time of injury or operation. 5- Reactionary haemorrhage : It may follow primary haemorrhage within 24 hours (usually 4—6 hours) and is mainly due to rolling (‘slipping’) of a ligature, dislodgement of a clot or cessation of reflex vasospasm. The precipitating circumstances are: The rise in blood pressure and the refilling of the venous system on recovery from shock; Restlessness, coughing and vomiting which raise the venous pressure (e.g. reactionary venous haemorrhage within a few hours of thyroidectomy).

6- Secondary haemorrhage :
Secondary haemorrhage occurs after 7—14 days, and is due to infection and sloughing of part of the wall of an artery. Predisposing factors are pressure of a drainage tube, a fragment of bone, a ligature in an infected area or cancer. It is also a complication of arterial surgery and amputations. It is heralded by ‘warning’ haemorrhages, which are bright red stains on the dressing, followed by a sudden severe haemorrhage which may be fatal. In advanced cancer, the erosion of a main vessel (e.g. carotid or uterine) by a locally ulcerating growth becomes the way of merciful termination to the patient’s suffering. Secondary haemorrhage is prone to occur with anorectal wounds, for example after haemorrhoidectomy.

7- External haemorrhage :
External haemorrhage is visible, revealed haemorrhage. 8- Internal haemorrhage : Internal haemorrhage is invisible, concealed haemorrhage. Internal bleeding may be concealed as in ruptured spleen or liver, fractured femur, ruptured ectopic gestation or in cerebral haemorrhage. Concealed haemorrhage may become revealed as in haematemesis or melaena from a bleeding peptic ulcer, as in haematuria from a ruptured kidney, or via the vagina in accidental uterine haemorrhage of pregnancy.

Measuring blood loss : Measurement of acute blood loss:
Assessment and management of blood loss must be related to the pre-existing circulating blood volume, which can be derived from the patient’s weight: • infant 80—85 ml/kg; • adult 65—75 ml/kg. Measuring blood loss : 1- Blood clot : The size of a clenched fist is roughly equal to 500 ml. 2- Swelling in closed fractures : Moderate swelling in closed fracture of the tibia equals 500—1500 ml blood loss. Moderate swelling in a fractured shaft of femur equals 500—2000 ml blood loss.

3- Swab weighing : In the operating theatre, blood loss can be measured by weighing the swabs after use and subtracting the dry weight. The resulting total obtained (1 g = 1 ml) is added to the volume of blood collected in the suction or drainage bottles. Blood, plasma and water are also lost from the vascular system because of evaporation from open wounds, sweating and expired water via the lungs. 4- Haemoglobin level : This is estimated in g/100 ml (g/dl), normal values being 12—16 g/100 ml (12—16 g/dl). There is no immediate change in haemorrhage, but after some hours the level falls by influx of interstitial fluid into the vascular compartment in order to restore the blood volume. 5- Measurement of central venous pressure .

The treatment of haemorrhage
1- Pressure and packing The first-aid treatment of haemorrhage from a wound is a pressure dressing made from anything handy which is soft and clean. The dressing or pack should be bound on tightly. Other examples of pressure used to control haemorrhage include digital pressure, for example the use of forefinger and thumb for epistaxis. Packing by means of rolls of wide gauze is an important standby in operative surgery. If several rolls are used, the ends must be tied together to ensure complete removal later. N.B. If on removal of pressure or packing, bleeding appears to have ceased completely, one should not assume that all is well, especially when dealing with deep wounds involving large veins. Continued close observation is required and rapid operative action may be called for .

2- Position and rest Elevation of limbs (e.g. in ruptured varicose veins) employs gravity to reduce bleeding. Elevation also causes helpful vasoconstriction. A bed elevator is often used to raise the foot of the bed, and thus increasing venous return to the heart also augmenting cardiac output. Gravity is also used in certain operations, as in thyroidectomy when the patient is tilted feet downwards (reverse Trendelenburg position) or as in stripping of varicose veins when a head-down tilt is used (Trendelenburg position ). 3- operative techniques Artery forceps (haemostats) and clips are mechanical means of controlling bleeding by pressure. The clamped vessel can be ligated or it can be coagulated with diathermy. Suturing may be employed. The vessel can be underrun or transfixed by needle and suture, and then ligated, while if the continuity of a main vessel is to be restored ;very thin thread is used on atraumatic needle.

4- Other topical applications for oozing include gauze or sponge, which is absorbed by the body. ‘Oxycel’ or gelatin sponge provides a network upon which fibrin and platelets can be deposited. Gauze soaked in adrenalin (1:1000) can be applied. Bone wax is used for oozing bone. The whole or part of a bleeding viscus may have to be excised (e.g. splenectomy ) . A ruptured kidney is treated conservatively if possible .

Natural blood volume and red cell recovery :
The recovery of blood volume begins immediately by the withdrawal of fluid from the tissues into the circulation. There is haemodilution. Plasma proteins are replaced by the liver. Red cell recovery takes some 5—6 weeks. The iron content will be less than normal if stores are depleted or absorption is impaired, for example after gastrectomy.

Transfusion of blood and blood products
The indications for transfusion in surgical practice are as follows : 1• Following traumatic incidents where there has been severe blood loss, or haemorrhage from pathological lesions, for example from the gastrointestinal tract. 2• During major operative procedures where a certain amount of blood loss is inevitable, for example above knee amputation or cardiovascular surgery. 3• Following severe burns where, despite initial fluid and protein replacement, there may be associated haemolysis. 4• Postoperatively in a patient who has become severely anaemic. 5• Preoperatively, usually in the form of packed cells given slowly in cases of chronic anaemia where surgery is indicated urgently, i.e. where there is inadequate time for effective iron or other replacement therapy, or where the anaemia is unresponsive to therapy, for example aplastic anaemia.

Preparation of blood products for transfusion
It is important that blood donors should be fit and with no evidence of infection, in particular hepatitis and human immunodeficiency virus (HIV) infection{ acquired immuno-deficiency syndrome (AIDS)}, which are transmitted in donor blood. Blood is collected into a sterile commercially prepared plastic bag with needle and plastic tube attached in a complete, closed sterile unit. With the donor lying on a couch, a sphygmomanometer cuff is applied to the upper arm and inflated to a pressure of 70 mmHg . After introducing 0.5 ml of local anaesthetic, a big needle is introduced into the median cubital vein and 410 ml of blood allowed to run into the bag containing 75 ml of anticoagulant solution (CPD — citrate potassium dextrose). During collection, the blood is constantly mixed with the anticoagulant to prevent clotting, and at the end of the procedure the tube is clamped and the needle removed. Specimens for use in blood grouping and cross-matching procedures may be obtained by clamping off small sections of the plastic tubing containing the donor blood.

Blood storage : All blood for transfusion must be stored in special blood bank refrigerators controlled at 4’C ± 2’C. Blood allowed to stand at higher temperatures for more than 2 hours is in danger of transmitting infection. CPD blood has a shelf-life of 3 weeks (CPDA of 5 weeks). The red blood cells : or erythrocytes, suffer a temporary reduction (24—72 hours) in their ability to release oxygen to the tissues of the recipient, so if a patient requires an urgent and massive transfusion it is wise to give 1 or 2 units of blood which are less than 7 days old. White blood cells : White blood cells are rapidly destroyed in stored blood. Platelets: At 4 ‘C the survival of platelets is considerably reduced, and few are functionally useful after 24 hours. Platelets which are separated show good survival even after 72 hours. Clotting factors : Like platelets, clotting factors VIII and V are labile and their levels fall quickly

Blood fractions : Packed red cells :
Whole blood may be divided into various fractions. This is not only more economical of blood donors, but certain fractions are more appropriate than whole blood transfusion for certain clinical conditions. Fractionation procedures are relatively safe and simple, using sealed sterile plastic bag units. Packed red cells : Packed red cells are especially advisable in patients with chronic anaemia, in the elderly, in small children and in patients in whom introduction of large volumes of fluid may cause cardiac failure. Packed red cells are suitable for most forms of transfusion therapy, including major surgery. Good packing can be obtained by letting the blood sediment and removing the plasma, or by centrifugation of whole blood at 2000—2300g for 15—20 minutes.

Platelet-rich plasma :
Platelet-rich plasma is suitable for transfusions to patients with thrombocytopenia who are either bleeding or require surgery. It is prepared by centrifugation of freshly donated blood at 150—200 g for 15—20 minutes. Platelet concentrate : Platelet concentrate for transfusion to patients with thrombocytopenia is prepared by centrifugation of platelet rich plasma at 1200—1500 g for 15—20 minutes. Plasma : This is removed after centrifugation of whole blood at 2000—2300 g for 15—20 minutes and it may be further processed or fractionated in various ways. Human albumin 4.5 % : Repeated fractionation of plasma by organic liquids followed by heat treatment results in this plasma fraction, which is rich in protein but free from the danger of transmission of serum hepatitis. This may be stored for several months in liquid form at 4’C and is suitable for replacement of protein, for example following severe burns.

Fresh frozen plasma: Plasma removed from fresh blood obtained within 4 hours is rapidly frozen by immersing in a solid carbon dioxide and ethyl alcohol mixture. This is stored at - 40’C and is a good source of all the coagulation factors. It is the treatment of choice when considering surgery in patients with abnormal coagulation due to severe liver failure. It may also be given in any of the congenital clotting factor deficiency diseases in their milder forms, especially Christmas disease (Factor IX deficiency) or haemophilia (Factor VIII deficiency). Cryoprecipitate: When fresh frozen plasma is allowed to thaw at 4’C a white glutinous precipitate remains and, if the supernatant plasma is removed, this cryoprecipitate is a very rich source of Factor VIII. It is stored at - 40’C and is immediately available for treatment of patients with haemophilia (Factor VIII deficiency). The advantage of cryoprecipitate treatment in haemophilia is the simplicity of administering large quantities of Factor VIII in relatively small volumes by intravenous injection. It is also a rich source of fibrinogen, of value in hypofibrinogenaemic states.

Blood grouping and cross-matching
There are two groups of antigens on the cell surface of human red cells : 1- antigens of the ABO blood groups 2- antigens of the rhesus (Rh) blood groups. Antigens of the ABO blood groups : These are strongly antigenic found on the RBC cell membrane and are associated with naturally occurring antibodies in the serum. Individuals show four different ABO cell groups : A , B , AB & O Antigen Antibody A Anti B B Anti A AB Nothing O Anti A & anti B

Blood group Rh positive Blood group Rh negative
Antigens of the rhesus blood groups : The antigen of major importance in this group is Rh(D), which is strongly antigenic . Antibodies to the D antigen are not naturally present , but their formation may be stimulated by the transfusion of Rh-positive red cells to Rh.negative patient . Such acquired antibodies are capable, during pregnancy, of crossing the placenta and, if present in a Rh-negative mother, may cause severe haemolytic anaemia and even death (hydrops fetalis) in a Rh-positive fetus in utero. Blood group Rh positive Blood group Rh negative A+,B+ AB+, O+ A-,B-, AB- O-

Blood group Give to : Take from : A + A+,AB+ A+,A-,O+,O- A- A+,A-,AB+,AB- A-,O- B+ B+,AB+ B+,B-,O+,O- B- B+,B-,AB+,AB- B- ,O- AB+ A+,A-,B+,B-,AB+,AB-,O+,O-(all blood groups) AB- AB+, AB- A-,B-,AB-,O- O+ A+,B+,AB+,O+ O+,O- O- All blood groups

Incompatibility : If antibodies present in the recipient’s serum are incompatible with the donor’s cells, a transfusion reaction will result. This is the result of agglutination and haemolysis of the donated cells leading in severe cases to acute renal tubular necrosis and renal failure. For this reason, therefore, it is essential that all transfusion should be preceded by: 1• ABO and rhesus grouping of the recipient’s and donor’s cells so that only ABO and Rh(D) compatible blood is given; 2•direct matching of the recipient’s serum with the donor’s cells to confirm ABO compatibility and to test for rhesus and any other blood group antibody present in the serum of the recipient. Blood grouping and cross-matching require full laboratory procedures and take 1 hour. In emergencies it may be necessary to reduce this time. In such emergencies, it may be advisable to restore the patient’s blood volume by saline, gelatin (e.g. Haemaccel), dextran or human albumin 4.5 % until blood has been made available. Alternatively, donor blood, group 0-negative, which is compatible with the majority of individuals, should be given and this should always be available in acute emergency situations.

Giving blood : Blood transfusion is commenced by: 1 • selection and preparation of the site; 2 • careful checking of the donor blood: this should bear a compatibility label stating the patient’s name, hospital reference number, ward and blood group; 3 • insertion of the needle or cannula — the latter may be valuable if intravenous therapy is required for any length of time; 4 • giving detailed written instructions as to the rate of flow, for example 40 drops/m allows one 540 ml unit of blood to be transfused in 4 hours. In acute emergencies, it may be necessary to increase the rate of flow and it is possible to give 1—2 units in 30 minutes using a pressure cuff around a plastic bag of blood. Warming blood : the blood must be warmed before reaching the patient by passing it through a carefully temperature-regulated blood warming unit, thus reducing the risk of cardiac arrest from large volumes of cold blood direct from the refrigerator. Filtering blood : A filter with an absolute filtration rating of 40 micron will filter off platelet aggregates and leucocytes membranes in stored blood.

Auto-transfusion This is an old, well-tried method of immediately restoring a patient’s blood volume, by transfusion with his or her own blood. In an emergency, for example, in a case of ruptured ectopic gestation, the blood is collected from the peritoneal cavity and put into a sterile container suitable for connecting to transfusion tubing. The classical method of filtration of this blood to prevent the transfusion of any small clots is to place a piece of sterile gauze within the container. Nowadays, special autotransfusion apparatus is being marketed. For major elective procedures, the patient may ‘donate’ his or her own blood, withdrawal and storage taking place up to 3 weeks before it is required. Natural blood volume and most of the red cell recovery will have taken place in that time.

Complications of blood transfusion :
1-Congestive cardiac failure This is especially liable to occur in the elderly or where there is cardiovascular insufficiency, and may result from too rapid infusion of large volumes of blood. It is advisable in the individual with chronic anaemia to give packed red cells and, at the same time, give diuretic drugs. The transfusion should be given slowly, i.e. I unit over 4—6 hours and, if necessary, on two separate occasions.

2- Transfusion reactions :
These may be the result of the following problems: 2-1 • Incompatibility. This should be avoided if the correct procedures of grouping and cross-matching have been adopted but, in fact, it is nearly always due to human error in the collection, labelling or checking of the specimens and donor bags. The patient develops a rigor, temperature and pain in the loins, and may become extremely alarmed. The transfusion should be stopped immediately, and a fresh specimen of venous blood and urine from the patient sent together with the residue of all the used units of donor blood to the laboratory for checking. A close watch should be kept on the patient’s pulse, blood pressure and urinary output. Frusemide 80—120 mg i.v. should be given to provoke a diuresis, and repeated if the urine output falls below 30 ml/hour. Dialysis may be necessary. 2-2 • Simple pyrexial reactions in which the patient develops pyrexia, rigor and some increase in pulse rate. These are the result of ‘pyrogens’ in the donor apparatus and are largely avoided by the use of plastic disposable giving sets.

2-3 • Allergic reactions in which the patient develops mild tachycardia and an urticarial rash; This is the result of allergic reaction to plasma products in the donor blood. The reaction is treated by stopping the transfusion and giving an antihistamine drug (chlorpheniramine 10 mg or diphenhydrazine 25 mg). 2-4 • Sensitisation to leucocytes and platelets. This is not uncommon in those patients who have received many transfusions in the past, for example for thalassaemia, refractory anaemia or aplastic anaemia. The individual develops antibodies to donated white cells or platelets, which cause reactions with each transfusion. They may be minimised by giving packed red cells from which plasma is removed . Aspirin, antihistamines or steroids may also be given to the recipient if necessary. 2-5 • Immunological sensitisation. Only the same ABO and Rh(D) groups are considered for blood transfusion. Immune antibodies may be stimulated by transfusion, and may give rise to difficulties with compatibility tests or to haemolytic transfusion reactions.

3-Infections There are four main reasons for blood transfusion causing infection in the recipient. 3-1 • Serum hepatitis virus may be transmitted from the donor and is usually a severe hepatitis arising approximately 3 months after the transfusion. It should be avoided by adequate good screening of the blood donor and by testing for the presence of the hepatitis associated antigen in the blood prior to transfusion. 3-2 • HIV infection can be transmitted by blood and blood products. All donors must be screened . Haemophiliacs are at special risk because of their more frequent requirements for blood products. 3-3 • Bacterial infection may result faulty storage. This arises most commonly from the donor blood being left in a warm room for some hours before the transfusion is commenced. This allows proliferation of any bacteria, and transfusion of such infected blood may result in severe septicaemia in the recipient and rapid death. 3-4 • Malaria can be transmitted by blood transfusion in areas where the disease is endemic. Whenever possible, donors should be screened and the disease eradicated (by treatment of the donors who are positive) before blood is obtained or given. If the need for transfused blood is so urgent that precautions are impossible before transfusion, then the patient should be given prophylactic antimalarial drugs.

4- Thrombo phlebitis 5- Air embolism 6- Coagulation failure Coagulation failure is due to: 6-1 • Dilution of clotting factors/platelets due to large volumes of stored blood being used to replace losses as stored blood is low in platelets, Factor VIII and Factor V; 6-2 • Disseminated intravascular coagulation (DIC) following an incompatible blood transfusion, particularly ABO incompatibility. The further haemorrhage may be treated by replacement of the deficient factors (usually fibrinogen, Factors VIII, V and II, and platelets), with fresh frozen plasma, cryoprecipitate and platelet concentrates. Paradoxically, heparin may be used sometimes for the treatment of DIC.

E.g. of haemorrhagic diseases : 1- Haemophilia :
Haemophilia (haemophilia A) is a haemorrhagic diathesis caused by the congenital deficiency in the blood of Factor VIII [ antihaemophilic globulin (AHG) ]. It is a sex-linked characteristic, transmitted by the asymptomatic female carriers, and manifest only in males. The levels of Factor VIII in the blood of severe haemophiliacs may be less than 1 % of the average normal level. In the case of spontaneous haemorrhage (e.g. into joints) treatment should aim at raising the level to at least 20 %. Should surgery be anticipated in the haemophiliac, the level should be raised to %. 2- Christmas disease : Christmas disease (haemophilia B) is a congenital disease resulting from the deficiency of Factor IX (Christmas factor). Clinically, the manifestations of the disease are similar to haemophilia. Factor IX is replaced by the transfusion of fresh frozen plasma,

3- Von Willebrand’s disease:
is a type of haemorrhagic disease, with low plasma levels of both Factor VIII complement and Factor VIII related antigen, and platelet abnormalities.

Blood substitutes — albumin, dextran, (colloid solution)
One of the most urgent requirements in a patient suffering from acute blood loss is the re-establishment of a normal blood volume. This may be achieved satisfactorily with a number of plasma substitutes. 1- Human albumin 4.5 % was used whilst cross-matching is being performed. Two to three units (1.2 litres) are given intravenously over 30 minutes. It is valuable in patients with burns where there has been severe loss of protein. There is no risk of transmitting hepatitis. 2- Dextrans are polysaccharide polymers of varying molecular weight producing an osmotic pressure similar to that of plasma. They have the disadvantage of inducing rouleaux of the red cells and this interferes with blood-grouping and cross-matching procedures, hence the need for a blood sample beforehand. Dextrans interfere with platelet function and may be associated with abnormal bleeding, and for this reason it is recommended that the total volume of dextran should not exceed 1000 ml.

Parenteral fluid therapy (crystelloid solution )
1• dextrose 5 % is an isotonic solution that supplies calories without electrolytes. It is useful in the postoperative period when sodium excretion is reduced. It is also valuable when the salt requirements of a patient needing much fluid have been satisfied on a particular day. Prolonged administration of 5 % dextrose solution alone is liable to result in hyponatraemia, and may cause thrombosis of the vein used; 2• isotonic (0.9 % ) saline solution is required to replace the normal sodium requirement (500 ml isotonic saline/day) and additional volume is required when a large amount of sodium has been lost by vomiting, or by gastric, duodenal or intestinal aspiration, or excessive sweating. 3• dextrose 4.3 % with saline 0.18 % (one-fifth isotonic saline) — this solution is isotonic. Usually it is referred to as dextrose—saline. It must not be confused with 5% dextrose in saline, which is hypertonic; 4• Ringer’s lactate solution contains sodium, potassium and chloride in almost the same concentrations as they are in the plasma. It also contains some calcium and some lactate. This solution can be used in hypovolaemic shock while awaiting blood. It is also suitable for replacing lost intestinal secretions.

50 ---- 150 43 31 130 109 28 4 + Ca +lactate Iso=300 5% glucose 0.9%
Solution Glucose (g/l) Na (meq/l) Cl Hco3 K 5% glucose 50 ---- 0.9% saline 150 dextrose 4.3 % with saline 0.18 % 43 31 Ringer’s lactate solution 130 109 28 4 + Ca +lactate 5% dextrose in 0.9%saline Osmolarity meq/l Iso=300 Hyper=600

Shock Types of shock : 1- Vasovagal shock : 2- Psychogenic shock :
Shock is a life-threatening situation. It is due to poor tissue perfusion with impaired cellular metabolism, manifested in turn by serious pathophysiological abnormalities. Types of shock : 1- Vasovagal shock : Vasovagal shock is brought about by pooling of blood in larger vascular reservoirs (limb muscles), and by dilatation of the splanchnic arteriolar bed, causing reduced venous return to the heart, low cardiac output and reflex bradycardia due to over stimulation of vagus N. Consequently, the reduced cerebral perfusion causes cerebral hypoxia and unconsciousness, but this leads to reflex vasoconstriction & then increases the venous return and cardiac output as to restore cerebral perfusion and consciousness. It must be remembered that if the patient is maintained in an upright or a sitting position (e.g. in a dental chair) permanent cerebral damage will occur. 2- Psychogenic shock : Psychogenic shock immediately follows a sudden fright (e.g. bad news) or accompanies severe pain (e.g. a blow to the testes) ,also due to over stimulation of vagus N.

3- Neurogenic shock : 4- Hypovolaemic shock :
Neurogenic shock is caused by traumatic or pharmacological blockade of the sympathetic nervous system, producing dilatation of resistance arterioles and capacitance veins leading to relative hypovolaemia and hypotension. There is a low blood pressure, a normal or decreased cardiac output, a normal pulse rate and a warm dry skin. This may be corrected by putting the patient in the Trendelenburg position, the rapid administration of fluids and or a vasopressor drug. 4- Hypovolaemic shock : Hypovolaemic shock is due to loss of intravascular volume by haemorrhage, dehydration, vomiting and diarrhoea (e.g. cholera, acute enterocolitis). Until 10—15 % blood volume is lost, the blood pressure is maintained by tachycardia and vasoconstriction. Fluid moves into the intravascular space from the interstitial space . In addition, the venous capacitance vessels constrict, pushing blood into the arterial system and therefore compensating for the volume deficit.

E.g. of Hypovolaemic shock : 4-1- Traumatic shock:
Traumatic shock is due primarily to hypovolaemia from bleeding externally (open wounds), from bleeding internally (torn vessels in the mediastinal or peritoneal cavities, ruptured organs such as liver and spleen or fractured bones) or by fluid loss into contused tissue or into distended bowel. Traumatic contusion to the heart itself may cause pump failure and shock, while damage to the nervous system or to the respiratory system results in hypoxia. 4-2-Burns shock : Burns shock occurs as a result of rapid plasma loss from the damaged tissues, causing hypovolaemia. When 25 % or more of the body surface area is burnt, a generalised capillary leakage may result in gross hypovolaemia in the first 24 hours. Endotoxaemia due to infection makes matters worse and large volumes of fluids are required for resuscitation.

5- Cardiogenic shock : Cardiogenic shock occurs when more than 50 % of the wall of the left ventricle is damaged by infarction. Fluid overload, particularly when using colloids, can lead to over-distension of the left ventricle, with pump failure. The resultant high filling pressures exerted by the right ventricle make fluid leak out of the pulmonary capillaries, thereby causing pulmonary oedema and hypoxia. If an arrhythmia occurs this will reduce the pumping efficiency of the heart, while hypovolaemia from excess sweating, vomiting and diarrhoea will further diminish cardiac output. Acute massive pulmonary embolism from a thrombus originating in a deep vein or an air embolus (more than 50 ml), if obstructing more than 50 % of the pulmonary vasculature, will cause acute right ventricular failure. This greatly reduces venous return to the left ventricle, and cardiac output falls catastrophically causing sudden death or severe shock.

6- Septic (endotoxic) shock :
6-1- Hyperdynamic (warm) septic shock: This occurs in serious Gram-negative infections , for example from strangulated intestine, peritonitis, leaking oesophageal or intestinal anastomoses, or suppurative biliary conditions. At first, the patient has abnormal or increased cardiac output with tachycardia and a warm, dry skin, but the blood is shunted past the tissue cells, which become damaged by anaerobic metabolism (lactic acidosis). The capillary membranes start to leak and endotoxin is absorbed into the bloodstream, leading to a generalised systemic inflammatory state. The immediate and ready treatment of the cause, including the drainage of pus, is vital to the recovery of the patient at this stage (in strangulated hernia ‘the danger is in the delay, not in the operation’ ). 6-2- Hypovolaemic hypodynamic (cold) septic shock : This follows if severe sepsis or endotoxaemia is allowed to persist. Generalised capillary leakage and other fluid losses lead to severe hypovolaemia with reduced cardiac output, tachycardia and vasoconstriction. The systemic infection induces cardiac depression, pulmonary hypertension, pulmonary oedema and hypoxia which, in turn, reduce cardiac output still further. The patient becomes cold, clammy, drowsy and tachypnoeic, but still can be converted to hyperdynamic (warm) shock by the administration of several litres of plasma or other colloidal solution.

7- Anaphylactic shock : Penicillin administration is amongst the common causes of anaphylaxis. Other causes include anaesthetics, dextrans, serum injections, stings and the consumption of shellfish. The antigen combines with immunoglobin E (IgE) on the mast cells and basophils, releasing large amounts of histamine and SRS-A (slow-release substance-anaphylaxis). These compounds cause bronchospasm, laryngeal oedema and respiratory distress with hypoxia, massive vasodilatation, hypotension and shock. The mortality is around 10 %.

Clinical monitoring 1• pulse;
In summary, patient monitoring in shock should include: 1• pulse; 2• blood pressure (recording systolic and diastolic pressure, the pulse pressure, using an intra-arterial line if necessary); 3• heart rate and rhythm (cardioscope); 4• respiratory rate and depth; 5• CVP; 6• PCWP (pulmonary capillary wedge pressure ) in severe shock when the diagnosis is in doubt; 7• urine output; 8• serial blood gases and serum electrolyte measurements.

Treatment of shock The management of all types of shock should be vigorous and quick . The objectives are to increase the cardiac output and to improve tissue perfusion, especially in the coronary, cerebral, renal and mesenteric vascular beds. The plan of action should be based on: (1) Treat the primary problem —arrest of haemorrhage, draining pus, etc. (2) Improving ventricular filling by giving adequate fluid replacement, for example human albumin solution or fresh frozen plasma, in sepsis and burns; (3) Improving myocardial contractility with inotropic agents — dopamine, dobutamine, adrenaline infusions; (4) Correcting acid—base disturbances, using molar sodium bicarbonate when the pH of arterial blood is less than 7.2, and electrolyte abnormalities, especially potassium and calcium levels.

(5) In endotoxic shock, once the haemodynamic status has been improved, full doses of the appropriate antibiotics are given to treat the causal infection. Usually we use tripple antibiotics (amoxicillin for gram positive infection , gentamycin for gram negative infection & metroniadazole for anaerobic infection ). Diabetic patients in endotoxic shock are in a precarious position. Careful monitoring and control of their nutrition and insulin requirements are necessary under the instruction of a clinician with a special interest in diabetes.

(6) Vasodilators(hydralazine, phentolamine, glyceryl trinitrate infusions and chlorpromazine boluses) may be given provided the blood volume has been corrected and cardiac depression treated such that the systolic blood pressure is 90 mmHg or more. The indication is persistent vasoconstriction with oliguria, high CVP or PCWP and pulmonary oedema. Such therapy will improve cardiac output and tissue perfusion, and reduce the work done by the heart. It must be emphasised that vasodilators can only be used with extreme caution and full haemodynamic monitoring, because the sudden production of vasodilation in a hypovolaemic or dehydrated patient can be followed by a catastrophic fall in arterial blood pressure. These drugs should be given only in small intravenous doses or infusions and only until the extremities become warm and pink, and the veins are dilated and well filled.

Sterilisation Sterilisation by steam :
Instruments can be sterilised by steam under pressure using autoclaves. Vegetative bacteria, including tuberculosis, and viruses such as hepatitis B, hepatitis C and human immunodeficiency virus (HIV) and heat-resistant spores, including Clostridium tetani and Clostridium perfringens, are killed. The combination of pressure, temperature and time with the moist heat is important: • 134’C (30 lb/in.2) for a hold time of 3 minutes; • 121’C (15 lb/in.2) for a hold time of 15 minutes; • prepacked materials and instruments are processed through a porous load autoclave which incorporates a pre-vacuum cycle necessary to extract air. If this is not achieved then the dried saturated steam cannot penetrate efficiently. Unwrapped instruments can be sterilised in a small autoclave within the theatre , which is convenient when instruments are dropped.

Sterilisation by ethylene oxide gas :
Monitoring : All autoclaves must be regularly maintained according to the manufacturer’s instructions, and a record should be kept of the cycle time, the pre-vacuum phase, the pressure and temperature. In addition, the steam penetration test (Bowie—Dick test) and chemical indicators, for example Brownes tubes or impregnated tapes, are used to ensure that such errors as poor packing do not interfere with the efficiency of the process. Biological indicators are not appropriate. Sterilisation by ethylene oxide gas : Ethylene oxide is a highly penetrative non-corrosive gas which has a broad-spectrum cidal action. It is utilised for heat-sensitive materials including electrical equipment. It is not recommended for ventilator ,respiratory equipment or soiled instruments because organic debris, including serum, has a marked adverse effect.

Sterilisation by hot air :
This is inefficient compared with moist steam sterilisation, but it has the advantage in the ability to treat solid non-aqueous liquids grease/ointments and to process closed (airtight) containers. Lack of corrosion may be important, particularly with instruments with fine cutting edges such as ophthalmic instruments. It cannot be used for substances such as rubber, plastics and intravenous fluids which are denatured. Sterilisation by low-temperature steam and formaldehyde : This uses a combination of dried saturated steam and formaldehyde, with the main advantage being that sterilisation is achieved at a low temperature (73’C) and the method is therefore suitable for heat-sensitive materials and equipment with integral plastic components. It is not recommended for sealed, oily items or those with retained air. Some plastics and fabrics absorb formaldehyde, releasing this in a delayed manner which may cause hypersensitivity to the users.

Sterilisation by irradiation :
This technique employs gamma rays or accelerated electrons. It is an industrial process and is particularly appropriate to the sterilisation of large batches of similar products, such as syringes, catheters and intravenous cannulas. The delivery of an irradiation dose in excess of 25 kGy is accepted as providing adequate sterility assurance.

Disinfection Cleaning of items is essential before disinfection is undertaken and the efficiency also depends on: 1. the nature of microorganisms; 2. the load of microorganisms; 3. the duration of exposure to the agent; 4. the temperature.

Disinfection with low-temperature steam :
Typical conditions include exposure to dry saturated steam at a temperature of 73’C for a period of 20 minutes at a pressure below atmospheric. This is a useful process for dealing with dirty returns from the operating theatre or clinics which may be contaminated with protein from bodily secretions and microorganisms. Following this method of disinfection the instruments must be cleaned. Disinfection with boiling water : This utilises soft water at 100’C at normal pressure for 5minutes. Instruments must be thoroughly cleaned before being utilised.

Disinfection with formaldehyde :
Formaldehyde gas is a broad-spectrum antimicrobial agent. This process utilises a cabinet which is airtight and circulates gaseous formaldehyde up to 50’C. Disinfection with glutaraldehyde : A 2 per cent solution of glutataldehyde is effective against most bacterial viruses, including hepatitis B and C and HIV, and is particularly useful for the decontamination of flexible endoscopes. • Thorough cleansing is essential. • The degree of decontamination is proportional to the time of immersion. • It is a toxic substance and causes irritant, allergic reactions to the staff, particularly skin reactions, which limits its use.

Safeguards during sterilisation must include: 1 • thorough cleaning;
Safeguards for equipment during sterilisation : Safeguards during sterilisation must include: 1 • thorough cleaning; 2 • appropriate packing for the sterilisation of disinfection process in order to avoid reduced penetration of the active agent. This is particularly important in the packing in the autoclave; 3 • arrangements of articles so that all surfaces are directly exposed to the agent. This includes opening or unlocking jointed instruments and disassembling instruments; 4 • the use of chemical indicators routinely; 5 • the interval monitoring of sterilisation process with chemical, thermal and, sometimes, biological indicators; 6 • the utilisation of flash sterilisation, where a temperature of 147’C is used at a pressure of 40 lb/in.2, is now rare and should only be considered in an emergency situation; 7 • a careful maintenance plan for all sterilisation processes.

Conclusion : Antibiotics, both prophylactic and therapeutic, have not reduced the essential role of asepsis and sterile precautions. Protocols with regard to instrument sterilisation, equipment maintenance, air filtration and ventilation, and staff behavior are essential. Regular staff education is imperative.

Tumours : A tumour is a new growth of tissue (a mass) which can refer to an inflammatory swelling such as inflammatory tumour or to a neoplastic growth. A neoplastic tumour is an uncontrolled proliferation of a clone of cells without useful function. Causation : Cancer is a disease of genes. The cell is the basic unit of organisation and control. The genetic code is contained within the deoxyribonucleic acid (DNA) molecule present within the cell nucleus. Genes make proteins which govern the function and structure of a cell. There are around genes (human genome) representing approximately 10 % of the DNA; each cell expresses 5— genes. Since all genes are present in each cell nucleus, any gene may be expressed if the gene promoter is switched on, as occurs in neoplasia. Cancer is caused by disease of genes which control production of daughter cells from stem cells, cell proliferation, terminal differentiation and programmed cell death (apoptosis)= from the Greek — shedding of autumn leaves. There are three important classes of genes involved in cancer:

1- tumour suppressor genes, which control the cell cycle by slowing down the cycle or triggering apoptosis (TP53, P16, APC, RB1); 2- oncogenes, which promote cell proliferation by increasing signalling activity from the cell surface to the transcription apparatus on gene promoters (KRAS, ERBB2, C-MYC); 3- growth factors and their receptors which are switched on by oncogenes or switched off by tumour suppressor genes (EGF, TGFa, IGF, FGF). A benign tumour grows by expansion without invasion of the extra-cellular matrix. A malignant tumour (cancer) grows by invasion into the extracellular matrix; most solid tumours also invade the basement membrane of endothelium and metastasise. The unit of cancer is the altered malignant cell which proliferates (clone). Different clones usually arise with different characteristics, such as the ability to metastasise via blood vessels or lymphatics. Cancer is a disease of genes which may be inherited or acquired . Inherited cancers are caused by a specific DNA mutation of a tumour suppresser gene inherited in all cells.

In cells of the organ affected, the (second) homologous gene is lost, initiating a sequence of genetic mutations culminating in cancer. Chemical carcinogens probably account for the majority of sporadic (acquired) cancers. Natives of Kashmir are prone to cancer of the skin of the thighs and lower abdomen. This is due to their habit of keeping warm by squatting and hugging earthenware pots containing glowing charcoal [the pot being termed a fangri ], with the result that the adjacent skin is irritated by heat and fumes. ‘Chimney-sweep’s’ cancer’ , ‘countryman’s lip’, and ‘tar workers’ cancer’ are other examples of carcinoma due to chemical carcinogens. DNA strand breaks are induced by ultraviolet and ionising radiation which, if not repaired, lead to cancer. Cellular instability from ageing of stem cell-lines (many common cancers) or chronic inflammation leads to increased cell proliferation and reduced apoptosis. This results in malignant transformation. Squamous cell carcinoma occasionally occurs in a chronic ulcer or in a scar ‘Marjolin’s ulcer’). A fibrosarcoma also may arise in a scar. At least 20 % of cancers world-wide are caused by oncogenic viruses.

Environmental cofactors are also important
Environmental cofactors are also important. Helicobacter pylori is linked to the development of gastric cancer by an unknown mechanism. A diet high in calories and rich in saturated fats (from red meat) is implicated in many cancers including those of the colorectum and pancreas. In viral carcinogenesis there are specific cofactors for different cancers: malaria (Burkitt’s lymphoma), immunosuppression (post-transport lymphomatous proliferative disease — PTLPD), human immunodeficiency virus (Kaposi’s sarcoma ), smoking (cervical cancer) and aflatoxins (liver cancer).

Definitions : • Hypertrophy :is an increase in the size of an organ without an increase in cell numbers. • Hyperplasia : is an increase in the size of an organ due to an increase in cell numbers. • Metaplasia : The epithelium from which the tumour grows has already changed its characteristics: bladder transitional epithelium to squamous epithelium, gallbladder columnar to squamous epithelium, bronchial columnar to squamous epithelium, gastric columnar epithelial pattern to intestinal epithelial pattern and oesophageal squamous to columnar epithelium (Barrett’s oesophagus). • Dysplasia :This represents the earliest changes of neoplastic transformation than can be detected at the microstructural level (e.g. by light microscopy). In fact, genetic mutations are detectable at an earlier stage. Alterations in intracellular organisation, the individual size and shape of the nucleus, cellular size and shape and intercellular three-dimensional organisation indicate dysplasia. These changes may be classified as mild, moderate or severe dysplasia. Any grade of dysplasia may revert to normal due to elimination of the neoplastic clone, but is least likely with severe dysplasia.

Carcinoma in situ : Severe dysplasia may progress to carcinoma in situ: the cellular, nuclear and three-dimensional architecture resemble cancer but without invasion into the extracellular matrix. • Genotype : This is the molecular structure of any cell. A malignant genotype will have losses and mutations of tumour suppresser genes and the presence of oncogenes. • Phenotype : This is the appearance of a cell at a microstructural level (microscopic phenotype) and its functional state (biological phenotype). A changed genotype will always precede a particular phenotype: for a time the cell may appear to be normal even though it has already acquired a malignant genotype. • Differentiation : Depending on the degree to which the cells and organisation (morphology) of tumours resemble the parent tissue they are divided into well-differentiated, moderately differentiated and poorly differentiated forms.

Anaplasia : Tumours are usually composed of cells which resemble those of the tissue from which they arise. Complete loss of differentiation (anaplasia) is associated with an aggressive cancer. • Teratomas : arise from embryonic stem cells containing representative cells from all three embryonic layers: ectoderm, endoderm, mesoderrn . Teratomatous dermoids contain hair and teeth, muscle and gland tissue. An unusual type is the sacrococcygeal teratoma ,which can be considered as foetus in foeto (an ‘included’ foetus). • Blastomas : develop from ‘unipotent’ cells, and arise from any one of the three embryonic layers (e.g. neuroblastoma).

• Dermoid cysts : ‘Dermoid’ is a loose term given to cysts lined by squamous epithelium occurring in various parts of the body. Sebaceous cysts are lined by superficial squamous cells and should more accurately be called ‘epidermoid’. ---Teratomatous dermoids (see above) are found in the ovary, testis retroperitoneum, superior mediastinurn and the presacral area. Malignant change (carcinomatous or sarcomatous) can occur. — Sequestration dermoids are not new growths, but are formed by the inclusion of epithelial ‘nests’ beneath the surface at places where lines of developing skin meet and join: midline, external angular process, branchial cysts . — Implantation dermoids may follow puncture wounds, commonly of the fingers, when living epithelial cells are implanted beneath the surface.

Benign tumour : A benign tumour is usually encapsulated, and does not disseminate or recur after complete removal. Symptoms and effects, which can be harmful, are due to its size, position, and pressure. Certain adenomas secrete a hormone which may affect bodily functions. Benign tumours are often multiple. Malignant tumour : The characteristics of malignancy are: — invasion of surrounding tissues; — pleomorphism (variable shapes) of cells and nuclei; — rapid growth; — the tendency to spread to other parts of the body (metastasis) by the lymphatics, the bloodstream, along nerve sheaths and across body cavities; — general weight loss (cachexia in advanced disease). At an early stage, evidence of invasion is the most important sign of malignancy. Many cells of a malignant tumour have an abnormal number of chromosomes which is not a multiple of the usual haploid number (= ‘aneuploidy’).

It has been suggested that the division of tumours into these two major groups imposes a concept which is too rigid . A third group of intermediate tumors exists which includes some carcinoid tumours, adenoma of the bronchus, ‘mixed’ salivary tumours and basal-cell carcinoma. These intermediate types invade locally, but are much less inclined to lymphatic or especially vascular dissemination.

Malignant tumours Carcinomas arise from cells which are ectodermal or endodermal in origin, and they are classified squamous, basal-celled or glandular (adenocarcinomas). Sarcomas occur in connection with structures of mesoblastic origin, hence fibrosarcoma, osteosarcoma. Germ cell tumours arise from germ cells (teratoma, seminoma, thecoma). Ovarian cancer is an adenocarcinoma: it does not arise from oocytes. Carcinoma Squamous cancer arises from surfaces covered by squamous epithelium, particularly as a result of ultraviolet or ionising radiation and chronic irritation. Chronic irritation of transitional cells (e.g. by a stone in the renal pelvis) or columnar cells (e.g. the gall bladder) will cause a change in these cells to a squamous type (squamous metaplasia), which may lead on to carcinoma. The regional lymph nodes are likely to be invaded, and may also be infected from the sepsis attendant upon the primary growth. Blood-borne metastases occur, but uncommonly from skin squamous cell carcinoma.

Methods of spread : 2- Lymphatics : by invasion and by embolism.
1- Direct spread (local extension) : Invasion takes place readily along connective tissue planes, but no structures are resistant. Veins are invaded commonly. Arteries are rarely invaded. Muscle is less susceptible to invasion or metastatic deposits than other tissues. Fascia also limits direct extension, 2- Lymphatics : by invasion and by embolism. • Invasion. The malignant cells grow along the lymphatic vessels from the primary growth (permeation). This may even occur in a retrograde direction. The cancer cells stimulate perilymphatic fibrosis, but this does not stop the advance of the disease. In some instances, groups of cells may so overcome the surrounding fibrosis that they give rise to intermediate deposits between the primary growth and the lymph nodes. • Embolism. Cancer cells which invade a lymphatic vessel can break away and are carried by the lymph circulation to a regional node, so that nodes comparatively distant from the tumour may be involved in the early stages. 3- Blood stream : Cancer cells may be detected in the venous blood draining an organ involved in carcinoma. A carcinoma of the kidney may invade the renal vein and grow inside the lumen into the vena cava. Malignant emboli may be arrested in the lungs, liver and bone marrow (secondary deposits — metastases). Thyroid, breast and bronchial cancers also commonly disseminate via the blood stream.

4- Implantation : Implantation of carcinoma has been observed in situations where skin or mucous membrane is in close contact with a primary growth. Examples of this is carcinoma of the lower lip affecting the upper lip . Recurrence after operation is occasionally due to implantation of malignant cells in the wound. Examples of this is nodules of carcinoma in the scar of the incision after mastectomy for a carcinoma of the breast. When a cavity is involved, free-floating cells from a carcinoma may spread like snowflakes all over its serous surface. For the abdomen, transcoelomic spread is specially notable when cells from a colloid carcinoma of the stomach gravitate on to an active ovary and give rise to malignant ovarian tumours (Krukenberg’s tumour ) intracavitary dissemination can also take place within the pleura and cerebrospinal spaces. 5- Nerve sheaths ; Adenocarcinomas, especially pancreas, may disseminate along nerve sheaths.

Grading and staging : Grading and staging are used to assess the degree of malignancy of the tumour as an indication of the prognosis, and may be used as a guide to determine the type and the extent of the treatment which is required. Advanced staging and grading may indicate the need for adjuvant methods of treatment, e.g. by chemotherapy or irradiation. Grading : Grading predicts the aggressiveness of a malignant neoplasm by characterising its microscopic appearance taking into account the degree of differentiation, nuclear and cellular appearance, architectural integrity and the proportion of active mitoses. • Grade 1: well differentiated; • Grade 2: moderately well differentiated; • Grade 3: poorly differentiated. Staging : (i) TNM classification. This has been adopted by the International Union against Cancer (UICC) and has been extended to many sites of cancer. This is a detailed clinical staging which is arrived at simply by the clinician ascertaining the following points. What is the extent of the primary Tumour? Are any lymph Nodes affected? Are there any Metastases? The information so obtained is scored, e.g. ii carcinoma of the breast, as follows:

Tumour Nodes Metastasis
T1 2 cm or less. N0 No nodes M0 No metastasis No skin fixation T2 More than 2 cm, N1 Axillary nodes M1 Metastases are but less than 5 cm. movable (a) not present including Skin tethered or significant, involvement of skin dimpled. No (b) significant beyond breast, and pectoral fixation contralateral nodes T3 More than 5 cm, N2 Axillary but less than 10 cm. nodes fixed Skin infiltrated or ulcerated. Pectoral fixation T4More than 10 cm. N3 Supraclavicular Skin involved but nodes. Oedema not beyond breast, of arm Chest-wall fixation

(i) Thus, for example, one patient may have an early carcinoma which is T1N0M0, while in another late case the extent of the disease may be T2N2M1. (ii) Manchester staging. This is a method of staging clinical spread of carcinoma of the breast . (iii) Dukes’ staging. This is a method of classifying the spread of carcinoma of the rectum and colon .

Benign tumours Adenoma
Adenomas arise in secretory glands, and resemble the structure from which they arise. They are encapsulated, and sometimes they secrete hormones which profoundly influence metabolism, as in the case of the thyroid, parathyroid and pancreas. Occasionaliy an adenoma contains a large proportion of fibrous tissue, e.g. the hard fibroadenoma in the breast, while in other situations, notably the pancreas and thyroid gland, cystic degeneration is common. Those arising from superficial glands of mucous membrane are liable to pedunculation, as in the case of a rectal ‘polyp,.

Papilloma A papilloma consists of a central axis of connective tissue, blood vessels and lymphatics; the surface is covered by epithelium, either squamous, transitional, cuboidal or columnar, according to the site of the tumour. The surface may be merely roughened, or composed of innumerable delicate villous processes, as in the case of those occurring in the kidney, bladder and rectum. In these situations, papillomas resemble malignant tumours, as secondary growths arise by implantation and, sooner or later, the tumour becomes frankly malignant . Other common sites for papillomas are the skin, the colon, the tongue and lip, vocal cords and the walls of cysts (particularly those the breast and ovary).

Fibroma A true fibroma (containing only fibrous connective tissue) is rare. Most fibromas are combined with other mesoderm tissues such as muscle (fibromyoma), fat (fibrolipoma) ,a nerve sheaths (neurofibroma). Multiple tumours are not uncommon as, for example, in neurofibrornatosis (von -Recklinghausen’s disease, Fibromas are either hard or soft, depending on the proportion of fibrous to the other cellular tissue. Soft fibromas a common in the subcutaneous tissue of the face, and appear soft, brown swellings. Desmoid ;This unusual type of flbroma occurs in the abdominal wall . An intraperitoneal form is associated with familial adenomato polyposis . Keloid :This overgrowth of fibrous tissue commonly occurs in scars, especially black people.

Lipoma : A lipoma is a slowly growing tumour composed of fat cells adult type. Lipomas may be encapsulated or diffuse. It occur anywhere in the body where fat is found and earn the titles of the ‘universal tumour’. The head and neck area, abdominal wall and thighs are particularly favoured sites. Encapsulated lipomas are among the commonest of tumours. The characteristic features are the presence of a definite edge and lobulation. A sense of fluctuation may be obtained. As would be expected, a lipoma deeply situated is liable to be mistaken for other swellings. Most lipomas are painless, but some give rise to an aching sensation which may radiate. Multiple lipomas are not uncommon. The tumours remain small or moderate in size, and are sometimes painful, in which case the condition is probably one of neurolipomatosis. Dercum ‘s disease characterised by tender deposits of fat, especially on the trunk. Should the lipoma contain an excessive amount of fibrous tissue, it is termed a fibrolipoma. In other cases, considerable vascularity is present, often with telangiectasis of the overlying skin, in which case the tumour is a naevo-lipoma. Large lipomas of the thigh , the shoulder and the retroperitoneum occasionally undergo sarcomatous changes. Myxomatous degeneration, saponification and calcification sometimes occur in lipomas of long duration.

Clinically, circumscribed lipomas are classified according to their Situation.
• Subcutaneous lipoma : Commonly found on the shoulders or the back, although no part of the body is immune. A lipoma may be present over the site of a spina bifida. Subcutaneous lipomas occasionally become pedunculated. • Sub- fascial lipoma : Occurring under the palmar or plantar fascia, they are liable to be mistaken for tuberculous tenosynovitis, as the tough, overlying fascia masks the definite edge and lobulation of the tumour. Difficulty is encountered in complete removal as pressure encourages the tumour to ramify. Subfascial lipomas also occur in the areolar layer under the epicranial aponeurosis and, if of long duration, they erode the underlying bone, so that a depression is palpable on pushing the tumour to one side. • Sub-synovial lipoma : From the fatty padding around joints, especially the knee. In the knee, they are mistaken from Baker’s cysts but are easily distinguished as, in distinction to a cyst or bursa, their consistency is constant whether the joint is in extension or flexion.

• Intermuscular lipoma : Mainly in the thigh or around the shoulder
• Intermuscular lipoma : Mainly in the thigh or around the shoulder. Owing to transmitted pressure, the tumour becomes firmer when the adjacent muscles are contracted. Weakness or aching results, owing to mechanical interference with muscular action. The condition is often difficult to distinguish from a fibrosarcoma. • Peri-osteal lipoma : occasionally occur under the periosteum of a bone. • Subserous lipoma : is sometimes found beneath the pleura, where they constitute one variety of innocent thoracic tumour. • Submucous lipoma : occur under the mucous membrane of the respiratory or alimentary tracts. Rarely a submucous Iipoma in the larynx causes respiratory obstruction. A submucous lipoma can occur in the tongue. One situated in the intestine is likely to cause an intussusception, which may be the first indication of its presence. • Central nervous system Lipomas : may occur anywhere within the extradural spaces, the spinal cord and brain; they usually arise from the pia mater, within the central subarachnoid spaces; a lipoma of the corpus callosum may be accompanied by calcification . • Intraglandular Lipomas : have been found occasionally in the pancreas, under the renal capsule and in the breast . • Retropenitoneal lipoma :. Large lipomas are seen not infrequently in the retroperitoneal tissues. Some of them turn out to be liposarcomas.

Treatment of lipoma : If a lipoma is causing trouble on account of its site, size, appearance or the presence of pain, removal is indicated. During operation, any finger-like projections of the tumour into the surrounding tissue should also be removed. Although the tumour is relatively avascular, care is needed to obtain complete haemostasis in the resulting cavity otherwise a haematoma is common, which may be followed by infection and delay in wound healing; drainage is often necessary. Diffuse lipoma occasionally occurs in the subcutaneous tissue of the neck, from which it spreads on to the preauricular region of the face. The tumour is not obviously encapsulated, and gives rise to no trouble, beyond being unsightly.

Neuroma : True neuromas are rare tumours, and occur in connection with the sympathetic system. They comprise the following types: • Ganglioneuroma : which consist of ganglion cells and nerve fibres. It arises in connection with the sympathetic ganglia, and therefore is found in the retroperitoneal tissue, or in the neck or thorax. • Neuroblastoma ; which is less differentiated than the ganglioneuroma, the cells being of an embryonic type. The tumour somewhat resembles a round-celled sarcoma, and disseminates by the bloodstream. It occurs in infants and young children. It may occasionally undergo spontaneous remission. • Myelinic neuroma : is very rare, being composed only of nerve fibres, as the ganglion cells are absent. They arise in connection with the spinal cord or pia mater. Neurilemmoma (syn. Schwannoma) These lobulated and encapsulated tumours arise from the neurilemmal cells. They are soft and whitish in appearance. They displace the nerve from which they arise and can be removed .

Neurofibroma Neurofibroma arise from the connective tissue of the nerve sheath. The following varieties are described. A single neurofibroma is usually found in the subcutaneous tissue = The ‘painful subcutaneous nodule’ forms a smooth firm swelling which may be moved in a lateral direction, but is otherwise fixed by the nerve from which it arises. Paraesthesia or pain is likely to occur from the pressure of the tumour on the nerve fibres which are spread over its surface. Cystic degeneration or sarcomatous changes occur occasionally. Neurofibromas may also grow from the sheath of a peripheral nerve or a cranial nerve, e.g. the acoustic tumour . As the nerve fibres are ‘part and parcel’ of the tumour they are difficult to remove without removal of the nerve itself. In major nerves recurrence is a problem, as is malignant (sarcomatous) change.

Plexiform neurofibromatosis :
Generalised neurofibromatosis = (syn. von Rechlinghausen’s disease of nerves) : In this inherited (autosomal-dominant) disease, any cranial, spinal or peripheral nerve may be diffusely or modularly thickened . The overgrowth occurs in connection with the endoneurium. Associated pigmentation (cafe au lait) of the skin is common, and sarcomatous changes may occur. Plexiform neurofibromatosis : This rare condition usually occurs in connection with branches of the fifth cranial nerve , although it may occur in the extremities . The affected nerves become enormously thickened as a result of myxofibromatous degeneration of the endoneurium. False neuroma : Arises from the connective tissue of the nerve sheath after injury to a nerve (lacerations or amputation). These swellings consist of fibrous tissue and coiled nerve fibres.

Haemangiomas : They are represented in various forms, capillary, cavernous and plexiform being common. Glomangioma (syn. glomus tumour) : These tumours arise from a cutaneous glomus composed of a tortuous arteriole which communicates directly with a venule, the vessels being surrounded with a network of small nerves. These specialised organs regulate the temperature of the skin, and are found in the limbs, especially the nail beds. The tumour is compressible. The associated pain is out of all proportion to the size of the tumour, which may be only a few millimetres in diameter. The pain is burning in nature and radiates peripherally, and is more often noticeable when the limb is exposed to sudden changes in temperature. Cutaneous glomus tumours grow very slowly, and do not become malignant. They should be excised.

Hamartoma : The term hamartoma is roughly translated from the Greek as a ‘fault’, and its original meaning was ‘missing the mark in spear throwing’. It is a developmental malformation consisting of overgrowth of tissue or tissues proper to the part. The possible range therefore is very wide and the lesions are often multiple. Common lesions that are hamartomas are benign pigmented moles, and the majority of angiomas and neurofibromas. On rare occasions a malignant change occurs in a hamartoma, but for practical purposes the lesion is benign .

Wounds Wounds and their management are fundamental to the practice of surgery. Any elective surgical intervention will result in a wound in order to gain access to and deal with the underlying pathology. In the surgery of trauma the wound is the primary pathology.In both situations the surgeon’s task is to minimise the adverse effects of the wound, remove or repair damaged structures and harness the processes of wound healing to restore function.

Wound Healing PHASES OF WOUND HEALING ;
The wound healing process follows a predictable pattern that can be divided into : 1- hemostasis and inflammation, 2- proliferation 3- maturation 4- remodeling. This sequence of events is fluid and overlapping. All wounds need to progress through this series of cellular and biochemical events that characterizes the phases of healing to successfully re-establish tissue integrity.

1- Hemostasis and Inflammation ;
Hemostasis precedes and initiates inflammation with the ensuing release of chemotactic factors from the wound site. Wounding disrupts tissue integrity, Leading to division of blood vessels and direct exposure of extracellular matrix to platelets. Exposure of subendothelial collagen to platelets results in platelet aggregation, degranulation, and activation of the coagulation cascade resulting In a fibrin clot. Platelet granules release a number of wound-active substances such as platelet-derived growth factor (PDGF), platelet-activating factor (PAF), fibronectin, and serotonin. In addition to achieving hemostasis, the fibrin clot serves as scaffolding for the migration into the wound of inflammatory cells such as polymorphonuclear leukocytes (PMNs,neutrophils) and monocytes.

Cellular infiltration after injury follows a characteristic, predetermined sequence.PMNs are the first infiltrating cells to enter the wound site, peaking at 24-48h. Increased vascular permeability, local prostaglandin release, and the Presence of chemotactic substances such as complement factors, interleukin-1 (IL-1), tumor necrosis factor-? (TNF-?), platelet factor 4, or bacterial products all stimulate neutrophil migration. The second population of inflammatory cells that invades the wound consists of macrophages. Derived from circulating monocytes, macrophages achieve significant numbers in the wound by 48–96 h post-injury and remain present until wound healing is complete

Macrophages,like neutrophils ,participate in wound d´ebridement via phagocytosis and contribute to microbial stasis via oxygen radical and nitric oxide synthesis. The macrophage’s most pivotal function is activation and recruitment of other cells via mediators such as cytokines and growth factors. By releasing such mediators as TGF?, vascular endothelial growth factor (VEGF), insulin-like growth factor (IGF), epithelial growth factor (EGF), and lactate, macrophages regulate cell proliferation, matrix synthesis, and angiogenesis. Macrophages also play a significant role in regulating angiogenesis and matrix deposition and remodeling. T-lymphocytes comprise an other population of inflammatory / immune cells that routinely invades the wound. Less numerous than macrophages, T- Lymphocyte numbers peak at about 1 week post-injury and bridge the transition From the inflammatory to the proliferative phase of healing.

2- Proliferation : The proliferative phase roughly spans days 4 through 12. During this phase, Tissue continuity is re-established. Fibroblasts and endothelial cells are the last Cell populations to infiltrate the healing wound, and the strongest chemotactic factor for fibroblasts is platelet-derived growth factor (PDGF), On entering the wound environment, recruited fibroblasts first need to proliferate, and then become activated, to carry out their primary function of matrix synthesis and remodeling. This activation is mediated mainly by the cytokines and growth factors released from wound macrophages. Endothelial cells also proliferate extensively during this phase of healing. These cells participate in the formation of new capillaries (angiogenesis). Endothelial cells migrate from intact venules close to the wound. Their migration, replication, and new capillary tubule formation are under the influence of such cytokines and growth factors as TNF-a, TGF-?, and VEGF.

Matrix Synthesis : Biochemistry of Collagen :
Collagen is the most abundant protein in the body. Type I collagen is the major component of extracellular matrix in skin. Type III, which also normally is present in skin, becomes more prominent and important during the repair process. Biochemically, each chain of collagen is composed of a glycine residue in every third position. These changes in the triplet is made up of proline or lysine during the translation process. The polypeptide chain that is translated from mRNA is called protocollagen. Release of protocollagen into the endoplasmic reticulum results in the hydroxylation of proline to hydroxyproline and of lysine to hydroxylysine by specific hydroxylases. Prolyl hydroxylase requires oxygen and iron as cofactors, ?-ketoglutarate as co-substrate, and ascorbic acid (vitaminC) as an electron donor.

In the endoplasmic reticulum, The protocollagen chain assumes an
In the endoplasmic reticulum, The protocollagen chain assumes an ?- helical configuration after its glycosy-lated by the linking of galactose and glucose at specific hydroxy-lysine residues. Three ?-helical chains entwine to form a right-handed superhelical structure Called procollagen . Although initially joined by weak , ionic bonds, the procollagen molecule becomes much stronger by the covalent cross – linking of lysine residues. Extracellularly, the procollagen strands by further polymerization and cross- linking. The resulting collagen monomer is further polymerized and cross-linked by the formation of intra and intermolecular covalent bonds.

Proteoglycan Synthesis :
lycosaminoglycans comprise a large portion of the “ground substance” that makes up granulation tissue. Rarely found free, they couple with proteins to form proteoglycans. The polysaccharide chain is made up of repeating disacaride units , composed of glucuronic or iduronic acid and ahexosamine, which usually sulfated. The disaccharide composition of proteoglycans varies from out 10 units in the case of heparin sulfate to as much as 2000 units in the case of hyaluronic acid. The major glycosaminoglycans present in wounds are dermatan and chonoitin sulfate. Fibroblasts synthesize these compounds, increasing their concentration greatly during the first 3 weeks of healing. The interaction between collagen and proteoglycans is being actively studied. As scar collagen is de-posited , the proteoglycans are incorporated into the collagen scaffolding. However, with scar maturation and collagen remodeling ,the content of proteoglycans gradually diminishes.

3- Maturation and 4- Remodeling :
The maturation and remodeling of the scar begins during the fibroplastic phase, and is characterized by a reorganization of previously synthesized collagen. Collagen is broken down by matrix metallo-proteinases (MMPs). The net wound collagen content is the result of a balance between collagenolysis and collagen synthesis. This will shift toward collagen synthesis and eventually establishment of extracellular matrix composed of a relatively a cellular collagen-rich scar.

Wound strength and mechanical integrity in the fresh wound are determined by both the quantity and quality of the newly deposited collagen. The deposition of matrix at the wound site follows a characteristic pattern: fibronectin And collagen type III constitute the early matrix scaffolding; glycosaminoglycans and proteoglycans represent the next significant matrix components; and collagen type I is the final matrix. By several weeks post-injury the amount of collagen in the wound reaches aplateau, but the tensile strength continues to increase for several more months. Fibril formation and fibril cross-linking result in decreased collagen solubility, increased strength, and increased resistance to enzymatic degradation of the collagen matrix. Scar remodeling continues for many(6–12)months post-injury, gradually result in a mature, avascular, and acellular scar. The mechanical strength of the scar never achieves that of the uninjured tissue.

Epithelialization Although tissue integrity and strength are being re-established, the external barrier must also be restored. This process, beginning within 1 day of the injury, is characterized primarily by proliferation and migration of epithelial cells adjacent to the wound. Marginal basal cells at the edge of the wound lose their firm attachment to the underlying dermis, enlarge, and begin to migrate across the surface of the provisional matrix. Fixed basal cells in a zone near the cut edge undergo a series of rapid mitotic divisions, and these cells appear to migrate by moving over one another in a leapfrog fashion until the defect is covered. Once the defect is bridged, the migrating epithelial cells lose the flattened appearance, become more columnar in shape, and increase their mitotic activity. Layering of the epithelium is re-established, and the surface layer eventually keratinizes.

Re-epithelialization is complete in less than 48 h in the case of approximated Incised wounds, but may take substantially longer in the case of larger wounds in which there is a significant epidermal / dermal defect. If only the epithelium and superficial dermis are damaged, such as occurs in split-thickness skin graft (STSG) donor sites or in superficial second – degree burns ,then repair consists primarily of re-epithelialization with minimal or no fibroplasia and granulation tissue formation. The stimuli for re-epithelialization remain incompletely defined; however, it appears that the process is mediated by a combination of a loss of contact inhibition; exposure to constituents of the extracellular matrix, particularly fibronectin; and cytokines produced by immune mononuclear cells. In particular EGF, TGF-? ,basic fibroblast growth factor (bFGF), PDGF,

Wound Contraction : All wounds undergo some degree of contraction. For wounds that donot have surgically approximated edges, the area of the wound will be decreased by this action (healing by secondary intention) .The myofibroblast has been postulated as being the major cell responsible for contraction, and it differs from the normal fibroblast in that it possesses a cytoskeletal structure. Typically this cell contains smooth muscle actin in thick bundles called stress fibers, giving myofibroblasts contractile capability. The smooth muscle actin is un-detectable until day 6, and then is increasingly expressed for the next 15 days of wound healing. After 4 weeks this expression fades and the cells are believed to undergo apoptosis. the undifferentiated fibroblasts may also contribute to wound contraction.

CLASSIFICATION OF WOUNDS ;
Wounds are classified as either acute or chronic. Acute wounds heal in a predictable manner and timeframe. The process occurs with few, ifany, complications, and the end result is a well-healed wound. Surgical wounds can heal in several ways. An incised wound that is clean and sutured closed is said to heal by primary intention .Often, because of bacterial contamination or tissue loss, a wound will be left open to heal by granulation tissue formation and contraction; this constitutes healing by secondary intention. Delayed primary closure, or healing by tertiary intention, represents a combination of the first two, consisting of the placement of sutures, allowing the wound to stay open for a few days, and the subsequent closure of the sutures. .

Classification of wound
A wound can be caused by almost any injurious agent and can involve almost any tissue or structure. The most useful classification of wounds from a practical point of view is that of Rank and Wakefield into tidy and untidy wounds. 1- Tidy wounds Tidy wounds are inflicted by sharp instruments and contain no devitalised tissue ; such wounds can be closed primarily with the expectation of quiet primary healing. Examples are surgical incisions, cuts from glass and knife wounds. Skin wounds will usually be single and clean cut. Tendons, arteries and nerves will commonly be injured in tidy wounds, but repair of these structures is usually possible . Fractures are uncommon in tidy wounds.

2- Untidy wounds Untidy wounds result from crushing, tearing, avulsion, vascular injury or burns, and contain devitalised tissue . Skin wounds will often be multiple and irregular. Tendons, arteries and nerves may be exposed, and might be injured in continuity, but will usually not be divided. Fractures are common and may be multi-fragmentary. Such wounds must not be closed primarily; if they are closed wound healing is unlikely to occur without complications. At best there may be wound dehiscence, infection and delayed healing, at worst gas gangrene and death may result. The correct management of untidy wounds is wound excision, by this is meant excision of all devitalised tissue to create a tidy wound. Once the untidy wound has been converted to a tidy wound by the process of wound excision it can be safely closed (or allowed to heal by second intention).

Sutures Suture materials are divided to :
1-absorbable & non-absorbable sutures: 1-1- absorbable sutures : A- Plain catgut sutures : which are made from the sub mucosa of the cat intestine ,& usually absorbed in 1-2 weeks . B- Chromic catgut: It is a plain catgut but covered with chrome. It is absorbed in 3-4 weeks

C- Vicryl sutures :which are made of polyglactinic acid & absorbed in 2-3 months.
D- Dexon sutures which absorbed in7-9 months. 1-2- non-absorbable sutures : A- Silk :made of silky material that not absorbed. B- Nylon sutures C- Stainless steel sutures D- Cotton tape sutures

Sutures 2- According to the type of needle: 2-1- cutting needle .
2-2- round needle . 2-3- taper cut needle. All these are curved needles & also there are strait needles differ in its length & thickness 2-4- no needle sutures :which are used for ligation . The suture thread length about 75 cm & its thickness measured by numbers (from thick to thin) ,e.g. 2 , 1 , 0 , 2/0 , 3/0 , 4/0 up to 10/0 which is very thin suture used for eye operations .

Sarcomas : Sarcomas differ from carcinomas, not only in their derivation, but in their earlier age incidence, as they are most common during the first and second decades. Sarcomas often grow rapidly and dissemination occurs early via the bloodstream (e.g. ‘cannon-ball’ secondary deposits in the lung from an osteogenic sarcoma). The macroscopic appearance of a sarcoma varies considerably. As the word implies, most tumours appear as a fleshy mass, but their consistency depends on the relative proportion of fibrous and vascular tissue. Haemorrhage commonly occurs owing to the very thin walls of the veins, which in some places are represented merely by venous spaces. Sarcomatous cells may reproduce tissue similar to that from which the tumour originated, e.g. osteosarcoma or chondrosarcoma. Sometimes a sarcoma develops in preexisting benign tumours, such as fibroma or a uterine fibroid.

Fibrosarcoma : Treatment of sarcoma :
Fibrosarcoma is composed of spindle cells of varying lengths (the rounder they are the more malignant they are), and occurs in muscle sheaths, scars and as a fibrous epulis. A fibrosarcoma of a muscle sheath presents as an elastic or firm and slowly growing swelling. Dilated veins over the tumour suggest malignancy, and if not obvious they may be demonstrated by infrared photography. On palpation the tumour often feels warm and pulsation may even be detected. Fibrosarcomas not uncommonly arise in scar tissue, sometimes many years after the scar developed. Sir James Paget described this as a ‘recurrent fibroid’. Treatment of sarcoma : The spread of a fibrosarcoma is hastened by incomplete removal. The moral is that wide excision with surrounding healthy tissues should be practised in all cases. This may mean amputation in the case of a limb. If untreated or if wide local excision is unsuccessful, a fibrosarcoma eventually fungates through the skin. Metastases are widely scattered and, unfortunately, radiotherapy has but little effect on either the primary growth or the secondary deposits. Sarcomas are often susceptible to anticancer drugs, but fibrosarcomas are more resistant than other types. Sarcoma of bone is sensitive to radiotherapy, which is used in some cases as an alternative to amputation .

Lymphomas : Lymphomas arise in lymph nodes, tonsils, Peyer’s patches or lymph nodules in the intestines. Lymph nodes of the neck or mediastinum are most commonly affected . They have a bad prognosis. Endothelioma; mesothelioma : The endothelial linings of blood vessels, lymphatic spaces and serous membranes occasionally give rise to neoplasms. They can be malignant. They arise from the pleura and rarely from the pericardium or peritoneum. Asbestos inhalation may provoke their development. ‘Blue’ asbestos fibres especially have been shown to be a cause. The original cells are flattened, but they become spheroidal or cuboidal when neop]astic changes occur. The ‘endothelioma’ (meningioma) of the dura mater is thought to arise from the arachnoid membrane, which is not an endothelial structure .

Benign to malignant transformation :
Certain benign neoplasms are prone to undergo malignant changes, and it is important, for both treatment and prognosis, to realise when this occurs. Some or all of the following changes may be recognised: • increase in size: comparatively rapid enlargement is always suspicious, e.g. a neurofibroma which is becoming sarcomatous; • increased vascularity: dilated cutaneous veins, ulceration and bleeding in the case of a superficial growth (e.g. melanoma); • fixity: due to invasion of surrounding structures; • involvement of adjacent structures: e.g. facial palsy suggests malignant change in an otherwise longstanding parotid pleomorphic adenoma; • dissemination: discovery of secondary deposits.

Cysts : The word cyst is derived from the Greek word meaning ‘bladder’. The pathological term ‘cyst’ means a swelling consisting of a collection of fluid in a sac which is lined by epithelium or endothelium. True cysts : True cysts are lined by epithelium or endothelium. If infection supervenes, the true lining may be destroyed and replaced by granulation tissue. The fluid is usually serous or mucoid and varies from brown-staining by altered blood to almost colourless. In epidermoid, dermoid and branchial cysts the contents are like porridge or toothpaste, as a result of the shedding of desquamated cells. Cholesterol crystals are often found in the fluid of branchial cysts.

False cysts (pseudocysts) :
Walled-off collections of fluid not lined by epithelium are not regarded as true cysts. A pseudocyst of the pancreas is an encysted collection of pancreatic enzymerich fluid lined by granulation tissue or fibrous tissue. Pancreatic pseudocysts are often in the retroperitoneum deep to but bulging into the lesser sac; they may occur anywhere in the abdominal cavity and even track into the mediastinum and pleural cavities. In tuberculous peritonitis, fluid may be walled off in cystic form by adherent coils of intestine. Fluid may collect in the centre of a tumour (cystic degeneration), due to haemorrhage or necrosis. This can also happen in the brain as a result of ischaemia, and an ‘apoplectic cyst’ is formed. In acute pancreatitis fluid collections loculated by viscera and fibrin are called ‘acute fluid collections’; these often occur in the lesser sac but are neither cysts nor pseudocysts as they are not lined by either epithelium, granulation tissue or fibrous tissue.

A classification of cysts
Congenital Sequestration dermoids Tubuloembryonic (tubulodermoid) Cyst of embryonic remnants Acquired Retention Distention Exudation Cystic tumours Implantation dermoids Trauma Degeneration Parasitic Hydatid, trichniasis, cysticercosis .

Congenital cysts The sequestration dermoid is due to dermal cells being buried along the lines of closure of embryonic clefts and sinuses by skin fusion. The cyst therefore is lined by epidermis and contains paste-like desquamated material. The usual sites are: • the midline of the body — especially in the neck; • above the outer canthus (external angular dermoid, ; • in the anterior triangle of the neck (branchial cyst. Tubuloembryonic (tubulodermoid) cysts occur in the track of an ectodermal tube used in development, e.g. a thyroglossal cyst from the thyroglossal duct or a postanal dermoid from the postanal gut. In the brain, ependymal cysts arise from the sequestration of cells of the enfolding neurectoderm. Cysts of embryonic remnants. These arise from embryonic tubules and ducts which normally disappear or are only present as remnants. They should not be confused with teratomatous cysts, e.g. dermoid. There are many examples in the urogenital system, e.g. in the male from remnants of the paramesonephric duct (Müllerian) — the hydatid of Morgagni, or from the mesonephric body and duct (Wolffian) . Cysts of the urachus and the vitellointestinal duct are other examples of cysts of embryonic remnants

Acquired cysts Retention cysts are due to the accumulated secretion of a gland behind an obstruction of a duct. Examples are seen in the pancreas, the parotid, the breast, the epididymis and Bartholin’s gland. A sebaceous cyst starts with the obstruction of a sebaceous gland, but this is followed by the down-growth and the accumulation of desquamated epidermal cells, thus turning it into an epidermoid cyst. In the epididymis, if the retention cyst contains sperms, it is known as a ‘spermatocele’. Distension cysts occur in the thyroid from dilatation of the acini, or in the ovary from a follicle. Lymphatic cysts and cystic hygromas are distension cysts. Exudation cysts occur when fluid exudes into an anatomical space already lined by endothelium, e.g. hydrocele, a bursa, or when a collection of exudate becomes encrusted. Cystic tumours. Examples are cystic teratomas (dermoid cyst of the ovary) and cystadenomas (pseudomucinous and serous cystadenoma of the ovary). Ganglia. See Chapter 29. Implantation dermoids arise from squamous epithelium which has been driven beneath the skin by a penetrating wound. They are classically found in the fingers of women who sew assiduously and metal workers (Fig ).

Trauma A haematoma may resolve into a cyst. This sometimes happens to haematomas of muscle masses in the loin and anterolateral aspects of the thigh or the skin. They are located between muscle, facial or subcutaneous planes and contain straw- or brown-coloured fluid containing cholesterol crystals. They become lined by endothelium and calcium salts may be laid down. Aspiration is only of temporary value, and a cure depends upon complete excision of the lining. Within the cranium, a haematogenous cyst can cause the same problems as any expanding, space-occupying lesion. Degeneration cysts These have already been discussed under false cysts. Parasitic cysts These are encrusted forms in the life cycle of various worms: • Hydatid cyst of Taenia echinococcus. This is described later according to the organ involved, e.g. liver, Chapter 52; lung, Chapter 47. • Trichiniasis. Cysts of Trichina spiralis, affecting muscle. • Cysticercosis. Cysts of Taenia solium. A disease of the pig, humans being rarely affected. Eosinophilia is present. The cysts occur in any organ. They calcify and may cause clinical effects according to their situation, especially in the brain. Only those cysts which are actually causing symptoms should be excised.

Clinical features The swelling usually has a smooth, spherical appearance. Fluctuation depends upon the pressure of fluid within: a tense cyst feels like a solid tumour, although careful palpation between two fingers may elicit a characteristic elasticity. In addition, a solid tumour is most hard at the centre; a cyst is least hard at the centre. If fluctuation is present, a cyst may be confused with a cold abscess or a lipoma. A cold abscess usually has a peculiar rim of thickening surrounding the soft centre. A lipoma may well test clinical acumen. Transillumination,while brilliantly clear in cysts containing serous fluid, does not really distinguish between a lipoma and a dermoid or branchial cyst. There is even an old axiom that ‘when in doubt, hedge on fat’. According to circumstances, ultrasonography, computerised tomography (CT) or magnetic resonance imaging (MRI), a test aspiration or excision reveals the true nature of the swelling. Cysts may be painful, especially when infection or haemorrhage causes a sudden increase in intracystic tension. Sometimes they change in size for no apparent reason. Occasionally, they diminish owing to rupture through a facial plane. Effects are according to site and size. As with benign tumours, a cyst may compress ducts and blood vessels, e.g. the main bile duct may be obstructed by a choledochal cyst, a renal cyst or a hydatid cyst. The pelvic veins may be obstructed by an ovarian cyst, the patient presenting for treatment of her varicose veins. The sheer size of an ovarian cyst (Fig ) may so increase intra-abdominal tension as to bring the patient to hospital with symptoms of a hiatus hernia.

Complications Infection The cyst becomes tense and painful, and adherent to surrounding tissues. An abscess may form and discharge on the surface and result in an ulcer or a sinus (viz. Cock’s peculiar tumour, Chapter 13). Healing will not occur until the whole lining of the cyst or the embryonic track is excised. Haemorrhage Sudden haemorrhage, as may occur in a thyroid cyst, causes a painful increase in size. In this particular case, breathing may be difficult because of pressure on the trachea. Torsion Torsion may occur in cysts which are attached to neighboring structures by a vascular pedicle. Ovarian dermoids are sometimes brought to notice in this way as acute abdominal emergencies. The cyst (or cysts — they may be bilateral) turns to a purple or black colour as the venous and then the arterial supply is cut off. Calcification Calcification follows haemorrhage, or infection, and may be the result of reaction to a parasite, e.g. hydatid cyst. Cachexia ovarica Enormous cysts are rarely seen nowadays (Fig ).

Ulcers An ulcer is a discontinuity of an epithelial surface. There is usually progressive destruction of surface tissue, cell by cell, as distinct from death of macroscopic portions, e.g. gangrene or necrosis. Ulcers are classified as nonspecific, specific (e.g. tuberculous or syphilitic) or malignant. Nonspecific ulcers are due to infection of wounds, or physical or chemical agents. Local irritation, as in the case of a dental ulcer, or interference with the circulation, e.g. varicose veins, are predisposing causes. Trophic ulcers [trophe (Greek) = nutrition] are due to an impairment of the nutrition of the tissues, which depends upon an adequate blood supply and a properly functioning nerve supply. Ischaemia and anaesthesia therefore will cause these ulcers. Thus, in the arm, chronic vasospasm and syringomyelia will cause ulceration of the tips of the fingers (respectively painful and painless). In the leg, painful ischaemic ulcers occur around the ankle or on the dorsum of the foot. Neuropathic ulcers due to anaesthesia (diabetic neuritis, spina bifida, tabes dorsalis, leprosy or a peripheral nerve injury) are often called perforating ulcers (Fig ). Starting in a corn or bunion, they penetrate the foot, and the suppuration may involve the bones and joints and spread along fascial planes upwards, even involving the calf. The life history of an ulcer consists of three phases.

Extension During the stage of extension the floor is covered with exudate and sloughs, while the base is indurated. The discharge is purulent and even blood stained. Transition The transition stage prepares for healing. The floor becomes cleaner, the sloughs separate, induration of the base diminishes and the discharge becomes more serous. Small, reddish areas of granulation tissue appear on the floor and these link up until the whole surface is covered. Repair The stage of repair consists of the transformation of granulation to fibrous tissue, which gradually contracts to form a scar. The epithelium gradually extends from the now shelving edge to cover the floor (at a rate of 1 mm per day). This healing edge consists of three zones — an outer of epithelium, which appears white, a middle one, bluish in colour (where granulation tissue is covered by a few layers of epithelium), and an inner reddish zone of granulation tissue covered by a single layer of epithelial cells. The red colour of granulation tissue is due to the high density of new capillaries (neo-angiogenesis).

Clinical examination of an ulcer
This should be conducted in a systematic manner. The following are, with brief examples, the points which should be noted. Site, e.g. 95 per cent of rodent ulcers occur on the upper part of the face. Carcinoma typically affects the lower lip, while a primary chancre of syphilis is usually on the upper lip. • Size, particularly in relation to the length of history, e.g. a carcinoma extends more rapidly than a rodent ulcer, but more slowly than an inflammatory ulcer. • Shape, e.g. a rodent ulcer is usually circular. A gummatous ulcer is typically circular, or serpiginous due to the fusion of multiple circles. An ulcer with a square area or straight edge is suggestive of ‘dermatitis artefacta’ (Fig ). • Edge (Fig ). A healing, nonspecific ulcer has a shelving edge. It is pearly, rolled or rampant if a rodent ulcer, and raised and everted if an epithelioma, undermined and often bluish if tuberculous, vertically punched out if syphilitic. • Floor. The floor is that which is seen by an observer, e.g. watery or apple-jelly granulations in a tuberculous ulcer, a wash-leather slough in a gummatous ulcer. • Base. The base is what can be palpated. It may be indurated as in a carcinoma or attached to deep structures, e.g. a varicose ulcer to the tibia. • Discharge. A purulent discharge indicates active infection. A blue—green coloration suggests infection with Pseudomonas pyocyaneus. A watery discharge is typical of tuberculosis. It is bloodstained in the extension phase of a nonspecific ulcer. Bacteriological examination may reveal colonisation by coagulase-positive staphylococci. Spirochetes are found in a primary chancre (Chapter 8).

Lymph nodes are not enlarged in the case of a rodent ulcer, unless due to secondary infection. In the case of carcinoma, they may be enlarged, hard and even fixed. The inguinal nodes draining a syphilitic chancre of the penis are firm and ‘shotty’, but contrarily the submandibular nodes draining a chancre of the lip are greatly enlarged. • Pain. Nonspecific ulcers in the extension and transition stages are painful (except for the anaesthetic trophic type). Tuberculous ulcers vary, that of the tongue being very painful. Syphilitic ulcers are usually painless, but an anal chancre (of a homosexual) may be painful (cf. anal fissure, Chapter 61). • General examination. Evidence of debility, cardiac failure, all types of anaemia, including sickle-cell anaemia, or diabetes must be sought. • Pathological examinations, e.g. biopsy, will confirm carcinoma. The serological and Mantoux tests may be of value for syphilis and tuberculosis, respectively. • Marjolin’s ulcer. See Chapter 13

local (topical) treatment of nonspecific ulcers
Any underlying cause is treated, e.g. varicose veins (Chapter 16), diabetes, arterial disease. Many lotions and nonadhesive applications are used to aid the separation of sloughs, hasten granulation and stimulate epithelialisation. The basic requirements of an ideal dressing are that should: •maintain a high humidity between the wound and the dressing; •remove excess exudate and toxic compounds; •permit gaseous exchange of oxygen, carbon dioxide and water vapour; •provide thermal insulation to the wound surface and be impermeable to microorganisms; •be free from particles and toxic wound contaminants •allow easy removal with no trauma at dressing change; •be safe to use and be acceptable to the patient; •be cost-effective.

Antiseptics and topical antibiotics
Antiseptics can do more harm than good when used inappropriately. They can interfere with the normal healing process, are toxic to fibroblasts and may permit more virulent organisms to dominate. The routine use of antiseptic and hypochlorite solutions should be avoided. If a wound needs cleaning, this can be achieved safely and more economically with normal saline warmed to body temperature prior to use. If a topical antiseptic is necessary, aqueous chlorhexidine 1 in 5000 solution is effective against a wide range of Gram-positive and -negative organisms and some fungi, but not spores. Povidone iodine has a broad spectrum of activity but its antibacterial effect is reduced by contact with pus or exudate. It should not be used on patients who are sensitive to iodine. Topical antibiotics are not recommended routinely as resistance and sensitisation following application may arise. Flamazine is a hydrophilic cream containing silver sulphadiazine 1% which is a broad-spectrum antibacterial agent and very effective against Pseudomonas, useful for the prevention of Gram-negative sepsis in patients with severe burns.

Wound dressings Hydrocolloid dressings such as Granuflex or Comfeel consist of a thin polyurethane foam sheet bonded on to a semipermeable polyurethane film, which is impermeable to exudate and microorganisms. When the dressing comes into contact with wound exudate it interacts to form a gel which expands into the wound. The moist conditions produced under the dressing promote angiogenesis and wound healing without causing maceration. They can be used in the treatment of leg ulcers, pressure sores, minor burns and many types of granulating wound. A hydrocolloid dressing can be applied to small wounds containing dry slough or necrosis: the dressing prevents the loss of water vapour from the surface of the skin, and this effectively rehydrates the dead tissue which is then removed by autolysis. Hydrogel (Intrasite gel) is a pale yellow/colourless transparent aqueous gel. When it comes into contact with a wound, the dressing absorbs excess exudate and produces a moist environment at the surface of the wound without causing tissue maceration. It may be applied to many different wounds including leg ulcers, pressure sores, surgical wounds and granulating tissue. It is particularly useful in the treatment of dry, sloughy or necrotic wounds, promoting rapid débridement by facilitating rehydration and autolysis of dead tissue. It reduces the feeling of pain and can be used as a carrier of other medicines, e.g. metronidazole, for the control of odour caused by infection with sensitive organisms. (It is useful in fungating tumours where the aim is not to heal the wound but to manage the distressing symptoms caused by it.) Intrasite should be secured with a secondary dressing such as an absorbent pad or Tegaderm depending on the wound.

Alginates (Kaltostat) consist of an absorbent fibrous fleece composed of the mixed sodium and calcium salts of alginic acid. In the presence of exudate or other body fluids containing sodium ions, the fibres absorb liquid and swell, calcium ions present in the fibre are partially replaced by sodium, causing the dressing to take on a gel-like appearance which promotes healing. The fibres are held in place with a secondary dressing such as an absorbent pad or Tegaderm depending on the amount of exudate. Alginate dressings can be used for the management of bleeding wounds including cuts and lacerations and also for a wide range of exuding lesions including leg ulcers, pressure sores and most other granulating wounds. Most suitable for heavy to moderately exudating wounds. In the presence of low exudate the Kaltostat must be moistened with saline before application to avoid adherence. The alginates are biodegradable so it is not necessary to remove every fibre if it will damage the healing tissue. Lyofoam is a low-adherent conformable polyurethane foam sheet. The side of the dressing that is to be placed in contact with the skin has been heat treated to render it hydrophilic, whilst the outer surface remains hydrophobic. The dressing is freely permeable to gases and water vapour but resists the penetration of aqueous solutions and exudate. The dressing absorbs blood and any other tissue fluids but the aqueous component is lost by evaporation through the back of the dressing. Strike-through occurs laterally and not at the top of the dressing. The dressing maintains a moist warm environment at the surface of the wound, which is conducive to granulation and epithelialisation. Foam sheet dressings may be used on a variety of exudating wounds including leg ulcers, pressure sores, sutured wounds, burns and donor sites.

Tegaderm consists of a thin polyurethane membrane coated with a layer of an acrylic adhesive. The dressing allows for a moist environment at the surface of the wound by reducing water vapour loss from the exposed tissue. It is permeable to both water vapour and oxygen and impermeable to microorganisms, providing an effective barrier to external contamination. Scab formation is prevented and epidermal regeneration takes place at an enhanced rate, compared with that which occurs in wounds treated with traditional dry dressings. Tegaderm may be used in the treatment of minor burns, pressure areas, donor sites, postoperative wounds and a variety of minor injuries. It is also effectively used as a protective cover to prevent skin breakdown due to friction or continuous exposure to moisture. Alleyvncavity wound dressing is a highly comfortable absorbent dressing consisting of a soft, polymeric outer membrane with a three-dimensional honeycomb-like structure containing a mass of hydrophilic polyurethane chips. The outer membrane is perforated to allow exudate to be drawn into the interior of the dressing where it is absorbed and retained by the ‘chips’. This type of dressing is used for heavily exudating, full-thickness sloughy wounds, usually combined with Intrasite gel; it can be used alone with clean, deep, ex~ daring wounds. Most of the above dressings are also available with added properties which improve their basic function, such as Kaltocarb. This is Kaltostat with a layer of activated charcoal cloth attached. This is effective as a primary dressing in the management of infected malodorous wounds. As the wound heals if granulation tissue continues to grow past the epidermal layer, the dressing used to stimulate granulation should be discontinued and a Lyofoam dressing should be applied. If after 1 week there is no improvement Tetra-cortil ointment containing hydrocortisone and oxytetracycline applied sparingly to the wound may be effective. This should be covered with a Lyofoam dressing and should be used for no longer than 5 days. Silver nitrate may be used with heavy overgranulating tissue but it is not recommended, usually because of its toxicity and the risk of sensitivity and staining.

Oriental sore (syn. Delhi boil, Baghdad sore, etc.)
This disease is due to infection by a protozoal parasite, Leishmania tro pica, and is a common condition in Eastern countries which is occasionally imported to Western zones. An indurated papule appears on an exposed surface, usually the face. If untreated, this breaks down to form an indolent ulcer, which eventually leaves an ugly, pigmented scar. The condition readily responds to intravenous injections of antimony tartrate, but very small lesions can be treated by carbon dioxide snow, and also curettage. Bazin’s disease (syn. erythema induratum) is due to localised areas of fat necrosis and particularly affects adolescent girls. Symmetrical purplish nodules appear, especially on the calves, and gradually break down to form indolent ulcers, which leave in their wake pigmented scars. Tuberculosis may be a cause in many instances, the ulcers responding to antituberculous drugs (Fig ) (Chapter 8).

Sinuses and fistulas A sinus (Latin a hollow; a bay or gulf) is a blind track (usually lined with granulation tissue) leading from an epithelial surface into the surrounding tissues. Pathological sinuses must be distinguished from normal anatomical sinuses (e.g. the frontal and nasal sinuses). A fistula (Latin = a pipe or tube) is an abnormal communication between the lumen or surface of one organ and the lumen or surface of another, or between vessels. Most fistulas connect epitheliallined surfaces (Fig ). Sinuses and fistulas may be congenitalor acquired. Forms which have a congenital origin include preauricular sinuses (Chapter 37), branchial fistulas (Chapter 43), tracheo-oesophageal fistulas (Chapter 50) and arteriovenous fistulas (Chapter 15). The acquired forms often follow inadequate drainage of an abscess. Thus, a perianal abscess may burst on the surface and lead to a sinus (erroneously termed a blind external ‘fistula’). In other cases, the abscess opens both into the anal canal and on to the surface of the perineal stem resulting in a true fistula-in-ano (Chapter 61). Acquired arteriovenous fistulas are caused by trauma or operation (for renal dialysis). Persistence of a sinus or fistula The reason for this will be found among the following: • a foreign body or necrotic tissue is present, e.g. a suture, hairs, a sequestrum, a faecolith or even a worm (see below); • inefficient or nondependent drainage: long, narrow, tortuous track predisposes to inefficient drainage; • unrelieved obstruction of the lumen of a viscus or tube distal to the fistula; • high pressure, such as occurs in fistula-in-ano due to the normal contractions of the sphincter which force faecal material through the fistula; • the walls have become lined with epithelium or endothelium (arteriovenous fistula); • dense fibrosis prevents contraction and healing; • type of infection, e.g. tuberculosis or actinomycosis; • the presence of malignant disease • ischaemia; • drugs, e.g. steroids, cytotoxics; • malnutrition; • interference, e.g. artefacta; • irradiation, e.g. rectovaginal fistula after treatment for a carcinoma of the cervix; • Crohn’s disease; •high-output fistula, e.g. duodenocutaneous fistula.

Treatment . The remedy depends upon e removal or specific treatment of the cause (see appropriate pages). Guinea worm (syn. dragon worm, Dracunculusmedinensis) (Fig ) This is a cause of a persisting sinus on the lower leg. The larval form enters through the wall of the stomach or duodenum in drinking water contaminated by a tiny cyclops crustacean which has consumed the larvae. Settling in the abdominal connective tissue, the male and female mate, the pregnancy lasting about a year, and the female wanders in the subcutaneous tissues to select for egg laying a part of the anatomy likely to be submerged in water (containing the cyclops), usually the lower leg. Cellulitis, abscesses, ulcers and sinuses follow, through which the embryos are discharged, hopefully to be eaten by the cyclops. Baid travelled the interior of India and in 500 cases discerned a syndrome of the infestation, presenting with conjunctivitis (allergic) in 11 per cent, fibrous contracture of joints in 19 per cent, periostitis with osteomyelitis in 21 per cent and acute arthritis in 65per cent.

Wound Healing : In human regeneration is limited to epithelium and the liver; most tissues heal by repair resulting in scarring. Wound healing is the summation of a number of processes which follow injury including coagulation, inflammation, matrix synthesis and deposition, angiogenesis, fibroplasia, epithelialisation, contraction, remodelling and scar maturation . Where wound edges are apposed healing proceeds rapidly to closure; this is known as healing by first intention or primary healing . Where the wound edges are apart, such as when there has been tissue loss, the same biological processes occur, but rapid closure is not possible. Angiogenesis and fibroblast proliferation result in the formation of granulation tissue. This contracts to reduce wound area and allows epithelialisation across its surface to achieve wound closure. This is known as healing by second intention . This process is slower, the contraction involved may cause contracture and functional restriction ,and the resultant healed surface is a thin layer of epithelium on scar tissue that may not prove durable in the long term. In general, healing by second intention will give a worse aesthetic outcome. It is because of the poor functional and aesthetic results of healing by second intention that surgical endeavour is usually directed towards achieving primary wound healing.

Wound excision The most important step in the management of any untidy wound is wound excision. This process is sometimes called ‘wound toilet’ or ‘debridement’. The former implies washing and the latter laying open or fasciotomy, all of which may be important in wound management but do not describe excision of devitalised tissue which is the most important process. For this reason the term ‘wound excision’ is preferred. In order to excise a wound adequate anaesthesia — local, regional or general must be provided. Where possible a bloodless field also aids identification of structures. For superficial wounds the use of local anaesthetic with 1 in adrenaline gives good haemostasis of skin edges. In the limbs a pneumatic tourniquet is used. It is helpful to use a skin marking pen to plan the skin excision and any wound extensions. Excision should proceed in a systematic fashion dealing with each tissue layer in turn, usually starting superficial and moving deep.

Longitudinal structures such as blood vessels, nerves and tendons are identified and exposed, but left in continuity. With experience the surgeon learns to recognise dead tissues. Devitalised dermis is pink rather than white; devitalised fat is pink rather than yellow; devitalised muscle is a dark colour, has lost its usual sheen and turgor, and does not twitch when picked up with forceps. Bone fragments with no soft-tissue attachment or non-vital soft tissue attachments are also discarded. This approach to radical wound excision is sometimes called a ‘pseudotumour’ approach, because the entire wound is excised with an appropriate margin back to healthy tissue . At the end of wound excision the wound should resemble an anatomical dissection. Normal bleeding should be observed from each layer. Occasionally in very extensive wounds this radical approach must be modified. Where radical wound excision would threaten the viability or function of the limb it is reasonable to excise what is definitely nonviable, carry out fasciotomy as appropriate and dress the wound, with a view to returning 48 hours later for a second look, and thereafter further serial wound excisions until a tidy wound is achieved.

Wound closure : Wound closure can be achieved by number of differing techniques. Most tidy wounds that do not involve loss of tissue can be closed directly. Where there is tissue loss a technique to import appropriate tissue is needed. Reconstructive plastic surgical techniques can range from simple skin grafts to complex composite free tissue transfers . This list used to be described as a ‘reconstructive ladder’; unfortunately this implies that the correct approach is to use the simplest technique and only when it fails move to a more complex technique. This approach is not appropriate in modern surgical practice. The available techniques should be regarded as a ‘toolbox’ from which to select the technique that provides most rapid healing, earliest return to function and superior aesthetic outcome.

Scars The most superficial wounds such as superficial burns and abrasions will heal by epithelialisation alone without scar formation. In these circumstances adnexal structures are preserved and the epithelium regenerates from these structures. This may leave alterations in keratinisation, texture or pigmentation of the healed area, but not scarring as such. A scar is the inevitable consequence of wound repair. The final phase of wound repair is the process of remodelling and scar maturation . The fibroblasts, capillaries, glycosaminoglycans, and immature collagen of granulation tissue and the newly healed wound are replaced by relatively acellular, avascular scar tissue composed of mature collagen with scattered fibroblasts. This biological process is manifested by a change in appearance of the scar from a red, raised, firm, contracting, perhaps itchy nodule to a pale, flat, softer, static, symptomless plaque of mature scar. The rate at which any given scar passes through this process can vary widely depending on the age of the individual, the site of the wound, the time the wound took to heal, the direction of the scar and the tension across it . In general, scars in younger patients with wounds on the trunk that heal slowly, perhaps with infection or dehiscence, and scars that have a lot of tension across them will take much longer to mature than scars in older people, in thin-skinned areas, that heal rapidly by first intention and that have minimal tension across them . It is important to be aware of this variation in the natural history of scar maturation in order to counsel patients regarding the likely progress and outcome of their scar, advise those having elective surgery what the consequences in terms of scarring will be, and to recognise the various types of adverse scarring which can occur. One of the most frequent types of adverse scar, a hypertrophic scar, is one that remains red, raised, itchy and tender for longer than might generally be expected.

Adverse scar There are many types of adverse scar (Table 3.3), many of which can be avoided or prevented by correct incision planning and adequate wound management. Some types, however, cannot be prevented and are unpredictable in their occurrence. The appearance of some scars can be improved by surgical or other means, but scars can never be removed totally. The types of adverse scar will be discussed and suggestions for avoidance or management made. Wrong direction Incisions that pass along ideal lines are more likely to leave acceptable scars. There are many types of ‘lines of election’ for incisions, most of which pass along skin wrinkles or along relaxed skin tension lines (that is a line along which maximal skin tension passes when the part is in a relaxed position). These lines have minimal tension across the wound edges. A scar which crosses these lines will have a greater tendency to stretch or become hypertrophic, and even if not hypertrophic will usually appear more conspicuous than one which follows a relaxed skin tension line. Other ideal positions for scars are at junctions between anatomical areas such as the nose and the cheek, the cheek and the ear or the junction between a hairy and hairless area

Poor alignment of features
Where a scar crosses the junction between distinct anatomical features, such as the vermillion of the lip, it is essential that these features are accurately realigned. Such misalignments result in conspicuous adverse scars. Stretched scar Scars from excisional wounds on the trunk and limbs often stretch. It has been shown that the width of a scar depends on the tension across the wound at the time of wound closure. In general, steps to avoid excessive tension across the wound will be rewarded with narrower scars. Where tension cannot be avoided there is evidence that prolonged wound support with buried nonabsorbable or long-term absorbable sutures can minimise scar stretching. Contracted scar The process of wound contraction continues in the remodeling phase of scar maturation such that a scar will always be shorter than the incision from which it results. Where a linear scar crosses a flexor surface this shortening may result in a scar contracture which may prevent full extension of that part. This will occur on the flexor surface of a finger if a straight-line incision is used. Curved or zigzag incisions will avoid this problem. Where scarring is extensive such as burn scars then scar contractures may be inevitable. Linear scar contractures can be corrected by realignment of the scar; there are various techniques to do this including Z-plasty and multiple Y—Vplasty. More extensive contractures will require release and introduction of additional skin by means of grafts or flaps.

Pigment alteration The new epidermis of a scar will often not have the same degree of pigmentation as surrounding unscarred areas. Most scars are hypopigmented, but hyperpigmentation can also occur. The only ways to deal with this problem are cosmetic camouflage or tattooing. - Contour deformity Where wound edges are not anatomically aligned in the vertical plane or where a bevelled cut is not repaired accurately there is a risk of contour irregularity in the healed scar. This can usually be avoided by accurate wound repair, if necessary excising bevelled edges to restore even vertical edges for repair. A variation of this problem occurs when a curved laceration heals, in that the scar shortens and that portion of skin within the concavity of the curved scar tends to become raised. This problem is known as trapdooring or mushrooming. It will often improve with time, but scar revision is sometimes indicated to correct it.

Tattooing In traumatic wounds it is possible for particles of grit, dirt or soot to become implanted in the wound as it heals. Thisresults in tattooed scars where the particles of foreign material show through as blue or black discoloration of the scar. Adequate primary wound management can avoid this. Abrasions with ingrained dirt should be scrubbed with a stiff brush; more deeply tattooed wounds should be excised. Late correction of tattooed scars can be very difficult. Stitch marks If skin sutures are left in place for more than 7 days then scars from the stitch marks will usually result. This problem can be avoided by using subcuticular sutures wherever possible, removing skin sutures before 7 days and, where prolonged wound support is needed, supplementing skin sutures with subcuticular sutures allowing early removal of the skin sutures. Adverse scars due to prominent stitch marks can rarely be improved by scar revision.

Hypertrophic scars In some circumstances scars remain in the remodelling phase for longer than is usual. These hypertrophic scars are more cellular and more vascular than mature scars, there is increased collagen production and collagen breakdown, but the balance is such that excess collagen is produced. Clinically these scars are red, raised, itchy and tender (Fig. 3.14). Such scars will eventually mature to become pale and flat, and it is this spontaneous resolution which distinguishes hypertrophic scars from keloid scars. Hypertrophic scars typically occur in wounds where healing was delayed, perhaps where complications such as infection or dehiscence occurred. They are more common in children and where skin tension is high such as the tip of the shoulder or any scar that runs across relaxed skin tension lines. The risk of developing a hypertrophic scar can be minimised by ensuring quiet primary healing. Where hypertrophy does occur patience is usually rewarded by improvement with time. Massage of the scar with moisturising cream or the application of pressure to the remodelling scar can accelerate the natural process of maturation. Patients with hypertrophic bum scars are supplied with custom made Lycra pressure garments that promote acceleration of scar maturation. Revision of hypertrophic scars is appropriate where they cross skin tension lines or where a specific wound healing complication occurred. In the absence of these factors scar revision should be avoided as it will usually be met with recurrence.

Keloid scars In some situations there is an extreme overgrowth of scar tissue that grows beyond the limits of the original wound and shows no tendency to resolve. Keloid scars are biologically identical to hypertrophic scars that fn turn are an extension of normal scar behaviour. Whilst it is usually possible to make the distinction between these scar types, they are best regarded as a spectrum of scar behaviour (Table 3.4). Keloid scars are more frequent in Afro-Caribbean and oriental racial groups (Fig. 3.15).They often occur in wounds that healed perfectlywithout complications. They are more common in certain sites such as the central chest, the back and shoulders and the ear-lobes. Many keloid scars are untreatable and surgical treatment as a single modality will usually be met with recurrence. Some keloid scars will improve with the application of pressure. Intralesional injections of steroids such as triamcinolone can be helpful. The best cure rates are achieved with a combination of surgery and postoperative interstitial radiotherapy.

GENERAL SURGERY FOR DENTAL STUDENTS

Similar presentations

Presentation on theme: "GENERAL SURGERY FOR DENTAL STUDENTS"— Presentation transcript:

Similar presentations

About project

Feedback

Log in

Auth with social network:

GENERAL SURGERY FOR DENTAL STUDENTS

Similar presentations

Presentation on theme: "GENERAL SURGERY FOR DENTAL STUDENTS"— Presentation transcript:

Similar presentations

About project

Feedback