G.Surgery Module PDF (3rd Year Dental Students)

3rd YEAR DENTAL STUDENTS GENERAL SURGERY MODULE 1  3rd YEAR DENTAL STUDENTS General Surgery Module Department of General Surgery Faculty of Medicine Menoufia University 2  ‫رسالة...

3rd YEAR DENTAL STUDENTS GENERAL SURGERY MODULE 1  3rd YEAR DENTAL STUDENTS General Surgery Module Department of General Surgery Faculty of Medicine Menoufia University 2  ‫رسالة الكلية‬ ‫تعمل كلية طب األسنان جامعة المنوفيه‬ ‫على اعداد كوادر ماهره في مجال طب األسنان‬ ‫متميزون علميا وعمليا وقادرون علي المنافسة‬ ‫ومواكبة المستجدات العلمية الحديثه‬ ‫وخدمة المجتمع لتلبية احتياجات سوق العمل‬ ‫وإجراء األبحاث العلمية المختلفه‬ ‫وكذلك بناء شراكات محليه وعالميه‬ ‫في مجال طب األسنان وأمراض الفم‬ ‫‪3‬‬ Topics of this book have been collected and written by the staff members of the General Surgery Department at Faculty of Medicine, Menoufia University. Authors are eager to provide the 3rd year students with the essential and up- to-date of different territories of General Surgery. Whether scientific knowledge or the necessary clinical experience within a frame of profession and ethics of medical practice required by the Dentist. 4 Overall aims of the course: It is expected that all students, by the end of the General Surgical module will be able to: 1. Obtain the essential knowledge regarding the necessary surgical disorders and its management 2. Able to perform the necessary clinical examination for patients before any dental maneuver. 3. Demonstrate adequate skills regarding patient interview and education taking in consideration patient's compliance with respect to medical ethics and infection control measures. 5 Contributors Prof. Dr / Ayman Ahmed Omer Professor of General & Vascular Surgery Head of General Surgery Department Prof. Dr/ Mahmoud Abdellatif Bahram Professor of General, GIT & Laparoscopic Surgery Dr/ Naglaa Amer Fathy Lecturer of General Surgery Dr/ Athar Lashin Lecturer of Emergency Medicine Dr/ Mohamed Ettman Lecturer of General Surgery Dr/ Abdel Aziz Ragab Saker Lecturer of General Surgery 6 Index of This Book 1 Care of polytrauma patients 8 2 Shock 16 3 Blood transfusion 20 4 Haemostasis 25 5 1. wounds 30 6 1. Wound healing 35 7 2. Surgical site infection 42 8 3. Cellulitis & Pyogenic abscess 50 9 4. Tetanus 53 105. Oncological principles 55 116. Preoperative care 62 127. Postoperative care 66 7 Post-trauma physiological effect: Defined as “a clinical state following injury to the body leading to profound physio metabolic changes involving multisystem’’. It could be detected in patient with anyone of the following combination of injuries: Two major systems + one major limb injury. One major system + Two major limb injury. One major system + One open grade III skeletal injury. Unstable pelvic fracture with associated visceral injuries. Incidence: ⚫ Worldwide No.1 killer amongst the younger age group (18-44 yrs.). ⚫ Third most common cause of death in all age group. ⚫ Great economic & social loss to country. ⚫ Less than 2% of budgets for health services spend on trauma patients. Peaks of death: 1st peak: within minutes at the site of accident ❖ Severe head injury, Brain stem injury ❖ High spinal cord injury ❖ Heart, Aorta injury and massive blood loss. 2nd peak: The golden hour ❖ Intracranial bleeding, chest injury ❖ Intraabdominal bleeding, Pelvic bleeding ❖ Multiple limb fractures 3rd peak: Within several days or weeks and influenced by early management ❖ Sepsis ❖ Organ failure 8 Life salvage: ⚫ 50% deaths due to trauma occur before the patient reaches hospital. ⚫ 30% occur within 4 hours of reaching the hospital. ⚫ 20% occur within next 3 weeks in the hospital. ⚫ If preventive measures are taken 70% deaths can be prevented meaning 30% deaths are non-salvageable deaths. Aims in management: “To restore the patient to the preinjury status” Having the following priorities: ⚫ Life salvage ⚫ Limb salvage ⚫ Salvage of the total function if possible Philosophy of management: Advanced trauma life support “based on treat lethal injury first the reassess and treat again” The steps in management are: Primary survey Resuscitation Secondary survey Definitive care Team approach: A team consists of Anesthetist, General surgeon, Neurosurgeon, Orthopedic surgeon, and cardiothoracic surgeon. The team must be: a) able to evaluate the patient swiftly. b) Willing to discuss the effect of the management of one problem on other. c) Able to arrive at decisions quickly. d) Efficient regarding performing lifesaving procedures. Prehospital phase: Basic Emergency Medical Technician Skills: 1. Maintenance of airway (endotracheal intubation?). 9  2. Cardiopulmonary resuscitation. 3. Intravenous access and Ringer’s lactate therapy. 4. Reduction and splintage of fractures. 5. Perform primary survey of patient and report to destination center. Triage: It involves sorting patients into three groups by colored labels according to their injury and availability of resources as follow: Black: those who will die anyway whether they receive medical attention or not. Red: those who will survive only if they receive timely medical attention. The first few hours after injury are called golden hour. Yellow: Non-life-threatening injuries and medical attention can be delayed Green: Minor injuries those who will survive anyway whether they receive medical attention or not. Primary survey: ⚫ Airway with cervical spine control. ⚫ Breathing and ventilation ⚫ Circulation –control external bleeding. ⚫ Dysfunction of the central nervous system ⚫ Exposure (undress)/Environment(temperature) Control During the primary survey life threatening conditions are identified and management is instituted simultaneously. Priorities for the care of Adult, Pediatrics & Pregnancy women are all the same. Assess Airway: ⚫ If pt. conscious airway is maintained ⚫ Open if necessary, using jaw-thrust maneuver ⚫ Consider Oro- or naso-pharyngeal airway ⚫ Signs of airway obstruction: LOOK LISTEN FEEL SPEECH?” HOW ARE AGITATION YOU’’ FRACTURE CREPITUS. POOR AIR MOVT. HOARSENESS. TRACHEALDEVIATION. RIB RETRACTION NOISY BREATHING HEMATOMA. DEFORMITY GURGLE. Maxillofacial fractures. FOREIGN MATERIAL. STRIDOR. 10 Definitive airway: Cuffed tube in trachea secured thoroughly with oxygen enriched gas supplementation. Indications for definitive airway: A=Airway-Obstructed airway -Inadequate Gag reflex B=Breathing-Inadequate breathing. -oxygen saturation less than 90%. C=Circulation-systolic BP < 70 mm Hg despite resuscitation. D=Disability-Coma. -GCS less than 8/15. E=Environment-Hypothermia - Core temp 1ml /kg/hr ⚫ No requirement of inotropic support Secondary survey: Does not begin until the primary survey (ABCDEs) is completed, resuscitative effort are well established & the pt is demonstrating normalization of vital sign. Head to Toe evaluation & reassessment of all vital signs. A complete neurological exam is performed including a GCS score. Adjuncts to the secondary survey: include additional x-ray and all other special procedure. RE-EVALUATION DEFINITE CARE Polytrauma in pregnant female: ⚫ priorities are same as for non pregnant pt ⚫ Pt can loss upto 35%of blood before tachycardia and hypotension appears ⚫ Fetus may be in shock while mother appears normal ⚫ 1st resuscitate the female than monitor the fetus Definition of patient’s conditions: Stable: no life threatening injuries, haemodynamically stable Borderline: intially respond to resuscitation but can deteriorate Unstable: remain haemodynamically unstable despite initial resuscitation Extremis: close to death uncontrollable blood loss 14 Damage control strategy: ⚫ Described by USA navy in the 2nd world war as the capacity of ship to absorb damge and maintain integrity ⚫ In Polytrauma pts, it means that surgical tratements intends to control but not to defenitively repair the trauma induced injuries early after trauma ⚫ Used in unstable and extremis pts ⚫ Staged surgery: Stage 1: Minimum surgery is done: achieve haemostasis. Limit the contamination Temporary stabilisation of unstable fractures Stage 2: Physiological restoration in ICU. Stage 3: Return to operation theatre for definitive surgery. 15  Shock Definition: Shock is the state of insufficient blood flow to the tissues of the body. The term “shock” may refer to a psychologic or a physiologic type of shock. Shock can lead to multiple organ failure as well as life-threatening complications. What are the signs and symptoms of shock? Signs and symptoms of shock include the following: Early Rapid, weak, or absent pulse  Irregular heartbeat Rapid, shallow breathing Cool, clammy skin lackluster eyes Chest pain Nausea Anxiety Decrease in urine Thirst and dry mouth Low blood sugar Late ( confusion, loss of consciousness, cardiac arrest) What are the major types of shock? There are four major types of shock, each of which can be caused by a number of different events. 1-Obstructive shock Obstructive shock occurs when blood can’t get where it needs to go. A pulmonary embolism is one condition that may cause an interruption to blood flow. Conditions that can cause a buildup of air or fluid in the chest cavity can also lead to obstructive shock. These include: pneumothorax (collapsed lung) hemothorax (blood collects in the space between the chest wall and lung) 16  cardiac tamponade (blood or fluids fill the space between the sac that surrounds the heart and the heart muscle) 2-Cardiogenic shock Damage to the heart can decrease the blood flow to the body, leading to cardiogenic shock. Common causes of cardiogenic shock include: o damage to your heart muscle o irregular heart rhythm o very slow heart rhythm 3-Distributive Shock Conditions that cause blood vessels to lose their tone can cause distributive shock. When the blood vessels lose their tone, they can become so open and floppy that not enough blood pressure supplies the organs. Distributive shock can result in symptoms including: flushing low blood pressure loss of consciousness There are a number of types of distributive shock, including the following: A-Anaphylactic shock is a complication of a severe allergic reaction known as anaphylaxis. Allergic reactions occur when the body mistakenly treats a harmless substance as harmful. This triggers a dangerous immune response. Anaphylaxis is usually caused by allergic reactions to food, insect venom, medications, or latex. B-Septic shock is another form of distributive shock. Sepsis, also known as blood poisoning, is a condition caused by infections that lead to bacteria entering your bloodstream. Septic shock occurs when bacteria and their toxins cause serious damage to tissues or organs in the body. 17 C-Neurogenic shock is caused by damage to the central nervous system, usually a spinal cord injury. This causes blood vessels to dilate, and the skin may feel warm and flushed. The heart rate slows, and blood pressure drops very low. D-Hypovolemic shock Hypovolemic shock happens when there isn’t enough blood in the blood vessels to carry oxygen to the organs. This can be caused by severe blood loss, for example, from injuries. How is shock diagnosed? First responders and doctors often recognize shock by its external symptoms. They may also check for: low blood pressure weak pulse rapid heartbeat Once they’ve diagnosed shock, their first priority is to provide lifesaving treatment to get blood circulating through the body as quickly as possible. This can be done by giving fluid, drugs, blood products, and supportive care. It won’t resolve unless they can find and treat the cause. Imaging tests: Such tests include: ultrasound X-ray CT scan MRI scan Blood tests: (CBC, cardiac enzymes, CRP, …..) 18 How is shock treated? Doctor’s treatment plan for shock will depend on the cause of the condition. Different types of shock are treated differently. For example, the doctor may use: epinephrine and other drugs to treat anaphylactic shock blood transfusion to replace lost blood and treat hypovolemic shock medications, heart surgery, or other interventions to treat cardiogenic shock antibiotics to treat septic shock 19  Blood Transfusion Blood is precious component for human being. Blood transfusion saved lives of many humans. Collection and storage of blood Blood is collected into a citrate anticoagulant solution that contains dextrose to maintain RBCs viability. Blood is kept at2-6 c during storage. Every blood unit bag contains 400-450 ml of blood plus 70-100 ml of anticoagulant. Indications of Blood transfusion 1. Whole blood transfusion used for patients with class III & IV hemorrhage. 2. Packed red cells: The transfusion of packed red cells is very useful in anaemic patients, in the elderly and in Cardiac patients to improve the oxygenation ability without overloading the circulation. 3. Fresh plasma: It is rich in platelets & coagulation factors and can be obtained from blood after separation of packed RBCs. Indicated in patients with coagulopathy. 4. Fresh frozen plasma (FFB): Plasma removed from fresh blood is rapidly frozen and stored at – 40°C. It is a good source of all the coagulation factors. It’s useful with hemophilia , liver failure &couramin overdose. 5. Platelet concentrates: should be freshly prepared as half-life of platelets is very short. It is used for patient with Thrombocytopenia. 6. Cryoprecipitate: prepared from FFB & is very rich in factor VIII &fibrinogen. It is stored at -40°C. Complications of blood transfusion The majority of these procedures are simple and pass safe, yet some are immediately fatal & others produce chronic serious illness as hepatitis & AIDS. 20 Attention to strict rules of donation & administration of blood greatly reduces the incidence of these complications. I. Complications to the donor 1. Neurogenic shock. 2. Anemia if repeated amounts are taken. 3. Local thrombophlebitis in the veins. II. complications to the recipient 1.Immunological complications of blood Transfusion: Incompatible red cells – acute hemolytic reaction. Incompatible white cells – pyogenic reaction. Incompatible platelets – purpura. Reaction to a protein in the plasma – allergic reaction. a. Acute hemolytic reactions Due to presence of antibodies in the recipient’s blood against antigens in the donor’s red Cells. Clinical Picture - After the transfusion of < 50 ml: fever, chills, constricting pain in the chest, dyspnea & pain in the flanks, tachycardia, hypotension. - In anesthetized pts: there will be sudden tachycardia, hypotension & bleeding Tendency. - A major hemolytic reaction leads to jaundice hemoglobinuria& Acute renal failure (ARF). Treatment - Stop the transfusion immediately. - Repeat typing & matching. - Correct shock by infusion of crystalloid solution (Lactated Ringer) &IV Corticosteroids. - Monitor urine output. - An osmotic diuretic as mannitol may be needed. Keep urine alkaline by IV Bicarbonate to protect against ARF 21  - If ARF develops, it must be treated. b. Pyogenic reaction (The most common complication) Due to presence of recipient Abs against the donor’s WBC’s or bacterial *The patients develop fever, chills, headache and vomiting. *Treatment ; Stop transfusion, Give aspirin or paracetamol IV. C. Allergic reaction Clinical Picture varies from mild itching &urticaria to severe reaction with Laryngeal edema &collapse. Due to: The recipient’s response to allergens in the donor’s *Treatment should include anti-histaminics & Corticosteroids If the reaction is severe, blood Tran fusion should be topped. D. Post transfusion purpura occurs in patients who have been sensitized to a foreign platelet antigen. 2. Congestive heart failure Occurs in: elderly persons if a large volume of blood is administered too rapidly. It is recommended to transfuse packed red cells Rather than whole blood to correct anemia in elderly persons. 3.Transmission of infection Viral hepatitis (B or C): This is now the most feared complication. Whole Blood or blood products can transmit the virus. It is now obligatory to test donor for hepatitis viruses. AIDS infection. Septicemia: Bacteria can survive, but they can’t multiply significantly in Refrigerated blood. However, if the blood Is allowed to warm, bacteria grow & endotoxins released causing septicemic shock. Malaria by RBCs only. Syphilis: spirochetes Can’t survive at blood bank temperature for > 4 days. 22 4.Hyperkalemia With prolonged storage of blood, there is progressive loss of K from erythrocytes into plasma. Transfusion of several units of aged blood may produce cardiac arrhythmias or even arrest due to hyperkalemia. 5.Citrate intoxication: Excess citrate will bind to the recipient’s Calcium leading to hypocalcaemia that augments the effects of hyperkalemia on the myocardium. Prevention: If > 2 units of blood are administered, it is important to administer 10 ml of 10% Ca gluconate for each 2 units of blood. 6.Air embolism 7.Acute lung injury Due To incompatibility Between Donor’s Abs & recipient granulocytes. 8.Complications of massive blood transfusion It is defined as transfusion of 2500 ml of blood at one time or 5000 ml or more Over 24 hrs. a. Hypothermia: A special warming unit should be used to warm blood before transfusion as hypothermia causes acidosis & arrest. b. Hyperkalemia. c. Hypocalcemia. d. Coagulation failure: As stored blood is poor in platelets, factor VIII & factor V. In these situations it is recommended to transfuse one unit Of fresh frozen plasma & platelets for every unit of stored blood. e. Diminished 0 2 carrying capacity of red cells Methods To minimize the need for homologous blood transfusion 1. Autologous blood transfusion: The patient who is going to have a major elective operation, can donate some Units of his own blood Over several days. The blood Is kept in the refrigerator to be given back to him during surgery. 23 2. Preservation of the blood lost during surgery and its reinfusion to the patient: This needs a special apparatus ( cell saver). 24  Haemostasis Natural haemostasis A. Primary haemostasis; Arrest of haemorrhage within the first few minutes is achieved by; 1. Vasoconstriction of the injured vessel. It is more efficient in arteries than veins as arteries contain more muscle fibres. 2. Platelets plug formation. 3. Tamponed of bleeding by surrounding tissue tension. Interstitial haemorrhage tends to be less perfuse than external or internal haemorrhage. B. Secondary haemostasis: Maintenance of haemostasis after the first few minutes requires platelet plug reinforcement by fibrin deposition through activation of coagulation mechanisms that occurs by two ways extrinsic and intrinsic ways. C. Fibrinolysis Once haemostasis occurs, the clot is digested through binding of plasminogen activator to the clot. The product of fibrinolysis are called fibrin degradation products(FDP). Haemostatic disorders I. Hypercoaguable states associated with increased tendency of thrombosis include; *Pregnancy, estrogen use , post operative and malignancy. *Deficiency of natural anticoagulant (protein c, protein s and anti thrombin III). II. Bleeding disorders 1. Congenital disorders a. Haemophilia A and B These are due to deficiency of factors VIII and IX respectively. Haemophilia A is the most common type. It is sex linked inherited d. It varies in presentation from spontaneous bleeding in childhood to bleeding only after 25  trauma or surgery. Patient should receive this factor within 1 hour before surgery and for 10 days after surgery. b. Von Willebrand disease (vWD) It is inherited as autosomal dominant disease. It is caused by deficiency of vW factor that acts as a carrier of factor VIII and enhance platelets adhesion. 2. Acquired disorders a. Hepatic disorders Hepatic patients have high tendency for bleeding due to deficiency of almost all coagulation factors, thrombocytopenia and increased fibrinolysis. Treatment *Vitamin k administration *Before an invasive procedures, fresh frozen plasma and cryoprecipitate are taken. *Desmopressin can raise levels of factor VIII and vWF before an invasive procedures. b. Vitamin k deficiency Causes of deficiency are; * Inadequate diet * mal absorption * obstructive jaundice * oral anticoagulants Function of vitamin k; It is co- factor for synthesis of factors II, VII, IX & X. Treatment includes parenteral injection of vitamin k before elective procedures. In emergency FFP or factor concentrates II, VII, IX and X may be needed. c. Disseminated intravascular coagulation Two processes occurs in DIC : 26  1. Activation of coagulation system in whole circulation leading to consumption of coagulation factors and deficiency of platelets. 2. Increased levels of FDP which worsen coagulopathy. Causes: *Shock, trauma, septicaemia and burns. *ABO incompatible transfusion. *obstetric catastrophes (eclampsia, abruption placenta and retained dead foetus ). *Malignancies ( lung cancer, GIT malignancy and leukaemia ). Treatment *Treatment of underlying cause. *Replacement of deficient coagulation factors and platelets with FFP, cryoprecipitate, platelets & blood transfusion. d. Anticoagulants Bleeding may occur if the dose of anticoagulant is not adjusted properly. Preoperative patients on oral coagulants should replace it with heparin injection before and few days post operative then they can reused oral anticoagulants e. Massive blood transfusion f. Platelets disorders *Thrombocytopenia results from decrease production by bone marrow,( leukemia &cancer infiltration) or increased destruction of platelets (ITP, drug induced or hypersplenism ). *The platelets may be normal in count but mal functioning (drug induced or uremia). Preoperative evaluation of haemostasis History: *positive family history of bleeding tendency suggests hereditary disorders. 27 *History of bleeding tendency in the patient and time of onset if in childhood, it suggests hereditary disorders or if late suggests acquired disorders (liver disease, renal failure or massive blood transfusion). *Character of bleeding Defects in primary haemostasis usually present with superficial bleeding i.e. ecchymosis, epistaxis, bruises and oozing. While defects in secondary haemostasis presents with deep hematomas in muscle, viscera and retroperitoneal. Examination: Complete examination should be performed carefully to detect any petichae, ecchymosis and hematomas. Hepatomegaly and splenomegaly may help to diagnose the certain cause of bleeding tendency. Tests of primary haemostasis 1. Platelets counts If less than 50000_100000/UL , prolonged bleeding occurs with major surgery. If less than 50000/UL, prolonged bleeding Occurs with minor surgery or spontaneous. 2Bone marrow aspirate to detect the cause of thrombocytopenia either in bone marrow synthesis or peripheral destruction of it. 3.Bleeding time is prolonged in platelets and vascular defects. Tests of secondary haemostasis Prothrombin time , partial thromboplastin time and thrombin time all used to detect defects in coagulation system either extrinsic or intrinsic pathways. Excessive operative and post operative bleeding Causes; 1.Inadequate surgical haemostasis. 28 2.haemorrhagic disorders not detected preoperative. 3.Acquired intraoperative coagulopathy DIC from incompatible transfusion or massive blood transfusion. Management 1.Proper surgical haemostasis. 2.FFP and platelets transfusion 3.Correction of hypothermia and acidosis. Surgical haemostasis During surgery bleeding can be controlled by; 1.ligation of bleeding vessels. 2.under running sutures. 3.Electrocautary for vessels about 3mm in diameter or less 4.Clips. 5.laser. 6.Repair of injured large vessels. 29  Wounds & wound healing Wound Definition: A wound is a break in the integrity of the skin or tissues , which may be associated with disruption of the structure and function. Ulcer is disruption or break in the continuity of any lining—may be skin, mucous membrane or others. Ulcer is one of the types of wounds. CLASSIFICATION OF WOUNDS 1. Tidy wounds They are wounds like surgical incisions and wounds caused by sharp objects. It is incised, clean, healthy wound without any tissue loss. 2. Untidy wounds They are due to: – Crushing, Tearing, Vascular injury, Multiple irregular wounds, Burns. Fracture of the underlying bone may be present. Wound dehiscence, infection, delayed healing are common. Classification based on the type of the wound A. Clean incised wound: It is a tidy, clean-cut wound with linear cut edges. Usually due to a sharp object like blade, glass piece or knife. 30 B. Lacerated wound: It has ragged edges with some part of the tissues getting devitalized Proper adequate wound excision, thorough warm saline wash and suturing of the wound layer-by-layer is required. C. Bruise or contusion: It is due to blow or blunt force to the skin that cause broken vessels underneath without breaking the skin, the accumulating trapped blood underneath and tissues causing skin discolouration. It is more on the skin over the bones; lax area like face, eyes; vascular areas; children, old aged, fair skin people. D. Haematoma: It is a localized collection of blood after blunt trauma or after surgery. Collected fluid blood in few minutes to hours gets clotted; later eventually it gets liquefied and shows discoloured fluid. It may be subcutaneous/ intramuscular/subfascial/intra-articular. Large haematoma may get infected to form an abscess; so large haematoma needs drainage under general or regional anaesthesia. Small haematoma usually gets absorbed (like scalp haematoma). 31 E. Abrasion: It is superficial injury (scratch) and is due to shearing of the skin where the surface is rubbed off. The loss of epidermis exposing dermal vessels and nerves leading into profuse painful oozing. F. Puncture wounds and bites: It is usually a stab wound with a pointed object. Here depth of the wound is more than the width. Deeper vital structures or organs may be injured, so should be assessed. 32 G. Penetrating wounds: They are similar like puncture wounds, due to stab. Abdomen and chest are common sites. Liver, bowel, spleen, major vessels and other visceral organs may be involved. H. Traction and avulsion injuries: These are complex injuries with tissues getting displaced from its normal anatomical position and alignment. like in machinery injuries, major injuries or degloving injuries. Ischaemia, bleeding, sepsis, loss of wide tissue area are common problems. I. Crush injury: It is due to major wounds, war wounds, natural disaster like earth quake injuries. It leads into compartment syndrome; muscle ischaemia; loss of tissues; gangrene; sepsis. Muscle will lose its viability which is identified by its colour (dark coloured with loss of shining); loss of contractility; turgid, and will not bleed on cutting. J. Gunshot injuries: These injuries may be superficial or deep. Usually entry wound and exit wound will be present. It causes explosive and destructive injuries along with burn injuries in the deeper planes and organs. It can be high velocity injuries with massive bleeding and major organ injuries. K. Closed blunt injury: It may be due to fall, blunt injury wherein no obvious external injury may be seen but deeper injury occurs. it may be often severe enough to cause major injury like in blunt abdominal injury causing bowel/liver/spleen/ renal injuries. 33 Classification based on thickness of the wound ▪ Superficial wound involving only epidermis and dermal papillae. ▪ Partial thickness wound with skin loss up to deep dermis with only deepest part of the dermis, hair follicle shafts and sweat glands are left behind. ▪ Full thickness wound with loss of entire skin and subcutaneous tissue causing spacing out of the skin edges. ▪ Deep wounds are the one extending deeper, across deep fascia into muscles or deeper structures. ▪ Complicated wounds are one associated with injury to vessels or nerves. ▪ Penetrating wound is one which penetrates into either natural cavities or organs. Classification of surgical wounds a. Clean wound Herniorrhaphy, Excisions, Surgeries of the brain, joints, heart, transplant. Infective rate is less than 2%. b. Clean contaminated wound Appendicectomy, Bowel surgeries, gastrojejunostomy, Gallbladder, biliary and pancreatic surgeries. Infective rate is 10%. C. Contaminated wound Acute abdominal conditions, Open fresh accidental wounds. Infective rate is 15–30%. d. Dirty infected wound Abscess drainage, Pyocele, Empyema gallbladder, Faecal peritonitis. Infective rate is 40–70%. 34  Wound healing Wound healing is complex method to achieve anatomical and functional integrity of disrupted tissue by various components like neutrophils, macrophages, lymphocytes, fibroblasts, collagen; It is an organized staged pathways—haemostasis → inflammation → proliferation → matrix synthesis (collagen and proteoglycan ground substance) → maturation → remodeling → epithelialization → wound contraction (by myofibroblasts). Types of Wound Healing I. Primary Healing (First Intention) It occurs in a clean incised wound or surgical wound. Wound edges are approximated with sutures. There is more epithelial regeneration than fibrosis. Wound heals rapidly with complete closure. Scar will be linear, smooth, and supple. II. Secondary Healing (Second Intention) It occurs in a wound with extensive soft tissue loss like in major trauma, burns and wound with sepsis. It heals slowly with fibrosis. It leads into a wide scar, often hypertrophied and contracted. It may lead into disability. Re-epithelialisation occurs from remaining dermal elements or wound margins 35. III. Healing by Third Intention (Tertiary Wound Healing or Delayed Primary Closure) After wound debridement and control of local infection, wound is closed with sutures or covered using skin graft. Primary contaminated or mixed tissue wounds heal by tertiary intention. 36 Phases of Wound Healing 1-Inflammatory phase (Exudative Phase) It begins immediately after formation and lasts for 72 hours. There is initial arteriolar vasoconstriction, platelet aggregation and thrombus formation (due to endothelial damage and release of adenosine diphosphate (ADP). Later vasodilatation and increased vascular permeability develops. Here haemostasis, coagulation and chemotaxis occur. 2-Proliferative Phase (Collagen/Fibroblastic phase) It begins from 3rd day and lasts for 3–6 weeks. There will be formation of granulation tissue and repair of the wound. Granulation tissue contains fibroblasts, neocapillaries, collagen, fibronectin and hyaluronic acid. It is divided into 3 stages: (1) Initial angiogenesis (growth of new blood vessels) occurs by release of vascular endothelial cell growth factor (VEGF) by keratinocytes. (2) Eventual fibroplasia develops by fibroblast activity with formation of the collagen and ground substance/ glycosaminoglycans. Type III collagen is deposited initially in a random fashion. (3) Later re-epithelialisation of the wound surface occurs by migration of basal layer of the retained epidermis which proliferates, differentiates and stratifies to form wound closure. 3-Remodelling phase (Maturation Phase) It begins at 6 weeks and lasts for 6 months to 1 or 2 years. There is maturation of collagen by cross linking and realignment of collagen fibers along the line of tension, which is responsible for tensile strength of the scar. There is reduced wound vascularity. 37  Fibroblast and myofibroblast activity causes wound contraction. Type III collagen is replaced by type I collagen causing maturation of the collagen. Scar strength is 3% in 1 week; 20% in 3 weeks; 80% in 12 weeks. Final matured scar is acellular and avascular. Factors affecting Wound Healing Age: In younger age group wound healing is faster and better. In elderly healing is delayed due to reduction in collagen synthesis, epithelialization, growth factors and angiogenesis. Nutrition: Adequate vitamin, trace elements, fatty acids and proteins are essential for wound healing. Wound infection: Infection prolongs inflammatory phase, releases toxins and utilizes vital nutrients thereby prevents wound epithelialization Formation of biofilms on the wound surface by microorganisms prevents wound healing. Anaemia: Haemoglobin less than 8g % causes poor oxygenation of tissues preventing healing of the wounds. Hypoxia: Hypoxia prevents fibroblast proliferation and collagen synthesis. it also promotes bacterial invasion into the wound. Causes of hypoxia are—arterial diseases, cardiac failure, respiratory causes, hypotension, smoking, tobacco, infection, diabetes mellitus and radiation. 38 Radiotherapy: Both external radiotherapy or ionizing radiation cause endarteritis, fibrosis and delay in wound healing. Radiation may itself cause local tissue necrosis, sepsis and hypoxia. Systemic and metabolic causes: Diabetes mellitus affects all stages of wound healing. Cardiac, renal, hepatic, respiratory diseases prevent wound healing. Tissue oedema impairs wound healing. HIV and immunosuppression of varying causes, malignancy leads into poor wound healing. Jaundice interferes with wound healing. Obesity causes hypoperfusion, reduced microcirculation, increased wound tension and hence prevents wound healing. Drugs: Steroids interfere with activation of macrophages, fibroblasts and angiogenesis in the early phase of healing (proliferative). Non-steroidal anti-inflammatory drugs (NSAIDs) decrease collagen production. Chemotherapeutic agents used in oncology inhibit cellular proliferation, protein synthesis. Alcohol consumption decreases the phagocyte response and pro- inflammatory cytokine release; diminishes host response and thus increasing the infection rate. Complications of wound healing Wound failure(dehiscence); ulcers, fistula, burst abdomen. Hyperteophic scar; scar is raised above the surface but remains within the confines of the wound. 39 Keloid; Excessive scar which is raised above surface and extends beyond the confines of the original wound. Predisposing factors; dark skin, familial, certain areas. Treatment options; Continuous pressure by silicone gel sheets. Steroids ( topical, intralesional) Surgical excision , high recurrence. Laser, radiotherapy. Contracture; Over joints causing deformity. Surgical site infection. Management of Wounds Wound cleaning Wound cleaning is needed to optimize the healing environment. It is achieved by removing visible devitalized tissues or dressing materials or excess exudates or crusts. Absolute aseptic technique should be used while cleaning the wound. Gentle irrigation of warm saline using a sterile syringe on the wound surface is ideal. Specific Management ABC: in polytrauma patients. If it is an incised wound then primary suturing is done. If it is a lacerated wound then the wound is excised and primary suturing is done. If it is a crushed or devitalised wound there will be oedema and tension in the wound. So after wound debridement or wound excision by excising all devitalised tissue, the oedema is allowed to subside for 2–6 days. Then delayed primary suturing is done. 40  If it is a deep devitalised wound, after wound debridement it is allowed to granulate completely. Later, if the wound is small secondary suturing is done. If the wound is large a split skin graft (Thiersch graft) is used to cover the defect. In a wound with tension, fasciotomy is done so as to prevent the development of compartment syndrome. Vascular or nerve injuries are dealt with accordingly. Internal injuries (intracranial by craniotomy, intrathoracic by intercostal tube drainage, intra-abdominal by laparotomy) has to be dealt with accordingly. Fractured bone is also identified and properly dealt with. Antibiotics, fluid and electrolyte balance, blood transfusion, tetanus toxoid (0.5 ml intramuscular to deltoid muscle), or anti-tetanus globulin (ATG) injection. 41  Surgical Site Infections (SSI) Why this topic? 1. SSI is most common hospital acquired infection in surgical patients. 2. 3rd most common hospital acquired infection. 3. Preventable. 4. Prolong the hospital stay. 5. Expenditure. 6. Over one-third of postoperative deaths. 7. Poor scar, persistent pain and itching, restriction of movement and a significant impact on emotional wellbeing. What is SSI? Infections that occur in the wound created by an invasive surgical procedure are generally referred to as surgical site infections Superficial incisional surgical site infections 42 Criteria for defining SSIs: 1. Infection occurs within 30 days of procedure. 2. Involve skin or subcutaneous tissue: - Signs or symptoms of infection. - Purulent drainage +/-. - Organisms isolated. - Diagnosis by experience. 3. Stitch abscess, episiotomy, circumcision in infant, burn wound. Deep incisional surgical site infections Infection occurs within 30 days of procedure (or one year in the case of implants). Involve deep soft tissues, such as the fascia and muscles and characterized by: - Purulent drainage, signs of infection. - Spontaneously dehisces or opened by surgeon. - An abscess or other evidence of infection. Organ or space Surgical site Infection Infection that involves any part which was opened or manipulated other than the incision by: - Purulent discharge from a drain. - Isolated an organism. - Abscess or other evidence of infection. Time: Early: Infection presents within 30 days of procedure. Intermediate: Occurs between one and three months. Late: Presents more than three months after surgery. Severity: Minor: Wound infection is described as minor when there is discharge without cellulitis or deep tissue destruction. 43  Major: When there is pus discharge with tissue breakdown, Partial or total dehiscence of the deep fascial layers of wound or if systemic illness is present. Pathogenesis of surgical site infection 1. Contamination: - Endogenous infection. - Exogenous infection. - Haematogenous spread. - Staph aureus. - Enterobacte organisms and anaerobes. 2. Proliferation of bacteria. 3. Induce inflammation – signs appear. 4. Self-resolving >> resolve by treatment >> sepsis and death. Classification of Surgical Wounds Category Criteria Infection rate No hollow viscus entered. Primary wound closure. Clean No inflammation. 1%-3% No breaks in aseptic technique. Elective procedure. Hollow viscus entered but controlled. No inflammation. Clean- Primary wound closure. 5%-8% contaminated Minor break in aseptic technique. Mechanical drain used. Bowel preparation preoperatively. Contaminated Uncontrolled spillage from viscus. 20%-25% Inflammation apparent. 44  Open, traumatic wound. Major break in aseptic technique. Untreated, uncontrolled spillage from viscus. Dirty Pus in operative wound. 30%-40% Open suppurative wound. Severe inflammation. Types of Surgery / class of wound Clean Hernia repair breast biopsy. 1.5% Clean- Cholecystectomy planned bowel 2-5% Contaminated resection. Contaminated Non-prepared bowel resection. 5-30% Dirty/infected Perforation, abscess. 5-30% Risk Factors for Development of Surgical Site Infections: - Patient factor. - Local factor. - Microbial factor. Patient factors - Older age - linear trend. - Immunosuppression. - Obesity. - Diabetes mellitus. - Chronic inflammatory process. - Malnutrition. - Peripheral vascular disease. 45  - Smoking. - Anemia. - Radiation. - Steroid use. Local factors - Poor skin preparation. - Contamination of instruments. - Inadequate antibiotic prophylaxis. - Prolonged procedure. - Site and complexity of procedure. - Local tissue necrosis. - Hypoxia. - Hypothermia. Microbial factors - Wound Class. - Prolonged hospitalization (leading to nosocomial organisms). - Resistance. Management of Incisional surgical site infection - Removal of sutures with drainage of pus. - Debridement and open wound care. - delayed primary or secondary suture. - 15% of postoperative wounds are treated with antibiotics -> inappropriate -> resistance. - Wound bed preparation. 46 Guidelines for prevention of Surgical Site Infection - Preoperative phase. - Intra operative phase. - Post-operative phase. Preoperative phase: - Preoperative showering ( chlorhexidine/soap). - Hair removal. - Patient theatre wear. - Staff theatre wear. - Staff leaving the operating area. - Nasal decontamination - mupirocin? - Mechanical bowel preparation. - Hand jewellery, artificial nails and nail polish. - Antibiotic prophylaxis. Operative Antibiotic Prophylaxis - Decreases bacterial counts at surgical site. - Given within 30-120 minutes prior to surgery – Cefazolin. - Re-dose for longer surgery - twice the half-life of drug. Intra-operative phase Hand decontamination. Incise drapes. Use of sterile gowns. Gloves. Antiseptic skin preparation. Maintaining patient homeostasis - temp oxygen glucose. Diathermy. 47  Wound irrigation and intra-cavity lavage. Antiseptic and antimicrobial agents before wound closure. Wound dressings, Closure methods. Postoperative phase Changing dressings. Postoperative cleansing. Use tap water for wound cleansing after 48 hours. No Topical antimicrobial agents - primary intention. Dressings - secondary intention. Debridement. Antibiotic treatment. Practices to prevent SSI are therefore aimed at minimizing the number of microorganisms introduced into the operative site, for example by: Removing microorganisms that normally colonize the skin. Preventing the multiplication of microorganisms. Enhancing the patient's defenses against infection. Preventing access of microorganisms into the incision postoperatively. 48  Cellulitis Spreading infection of subcutaneous and fascial planes. Common in diabetics, immunosuppressed and old age. Commonly due to Streptococcus pyogenes Clinical presentation: Pain and tenderness, red, shiny area with stretched warm skin. TTT: Antibiotics and drainage If there is pus formation Pyogenic Abscess Definition: localized collection of pus in a cavity lined by granulation tissue. It contains pus. Pus contains dead WBC’s, multiplying bacteria, toxins and necrotic material. Predisposing Factors ▪ General condition of the patient: malnutrition, anaemia, age of the patient ▪ Associated diseases: Diabetes, HIV, immunosuppression ▪ Trauma, haematoma, road traffic accidents Mode of Infection Direct Haematogenous Lymphatics Extension from adjacent tissues Bacteria Causing Abscess o Staphylococcus aureus. o Streptococcus pyogenes 49 Clinical Features 1. Fever often with chills and rigors. 2. Localized swelling which is smooth, soft and fluctuant. 3. Signs of pus formation ▪ Fever becomes hectic ▪ Throbbing pain ▪ Pointing ▪ Fluctuation Treatment of an Abscess Abscess should be formed before draining. Exceptions for this rule are: ❖ Parotid abscess ❖ Breast abscess ❖ Preineal ❖ Perinephric ❖ Brain Hilton’s method of draining an abscess. Skin is incised adequately, in the line parallel to langhans lines pyogenic membrane is opened using Sinus forceps parallel to the neuro- vascular bundle as in parotid abscess Pus is sent for culture and sensitivity. 50  Tetanus Definition: It is an infective condition caused by Clostridium tetani organisms leading to reflex muscle spasm, often associated with convulsions. Predisposing Factors for Tetanus Trauma with lacerations, deep wounds, crush devitalized wounds, presence of foreign body, wounds with anaerobic environment in the tissues. Organism: Clostridium tetani is a Gram-positive, anaerobic, non-capsulated, organism with terminal spores C.P.: Trismus, due to spasm of masseter and pterygoids. Risus sardonicus (smiling facies), a bitter smile due to spasm of the facial muscle. Spasm and rigidity of all muscles. Opisthotonus: Posterior muscles are acting more, so backward Bending Neck rigidity Respiratory changes due to laryngeal muscle spasm, infection, aspiration. Tonic clonic convulsions. Symptoms will be aggravated by stimuli like light, noise. Differential diagnosis Strychnine poisoning (here patient is normal in between): Strychnine blocks synopsis Trismus due to dental, oral, tonsillar sepsis, temporomandibular joint dysfunction Meningitis Hydrophobia Convulsive disorders 51  Tetany Drug induced extrapyramidal reaction by metoclopramide, Phenothiazines Prophylaxis against tetanus ✓ In infants—triple antigen (DPT) at 2,4,6,12months, 18 months, and 6 years ✓ To pregnant mother tetanus toxoid injections are given in 4th and 6th months of pregnancy. Cause of death in tetanus ❑ Respiratory failure with aspiration pneumonia and ARDS ❑ Severe carditis—an ominous sign Management of Tetanus Isolation is advised in a dark quiet room Eliminating the Source of the Toxin Clostridium tetani are sensitive to penicillins, metronidazole, Neutralizing the Unbound and Circulating Toxins It is done ideally by Human Tetanus Immunoglobulin (HTIG/ATG)—3000–6000 units. Intra- muscularily Active Immunization Tetanus toxoid should be given as disease will not give immunity against further infection. Symptomatic treatment - IV diazepam 20 mg 6th hourly - IV phenobarbitone 30 mg 6th hourly - IV chorpromazine 25 mg 6th hourly - Endotracheal intubation and ventilator support - Tracheostomy if there is severe respiratory secretions Wound Management Wound debridement, drainage of pus when present and injection of HTIG 500 units into wound area to reduce the effects of toxins local 52  o Hand decontamination. o Incise drapes. o Use of sterile gowns. o Gloves. o Antiseptic skin preparation. o Maintaining patient homeostasis - temp oxygen glucose. o Diathermy. o Wound irrigation and intra-cavity lavage. o Antiseptic and antimicrobial agents before wound closure. o Wound dressings, Closure methods. Postoperative phase o Changing dressings. o Postoperative cleansing. o Use tap water for wound cleansing after 48 hours. o No Topical antimicrobial agents - primary intention. o Dressings - secondary intention. o Debridement. o Antibiotic treatment. Practices to prevent SSI are therefore aimed at minimizing the number of microorganisms introduced into the operative site, for example by: 1. Removing microorganisms that normally colonize the skin. 2. Preventing the multiplication of microorganisms. 3. Enhancing the patient's defenses against infection. 4. Preventing access of microorganisms into the incision postoperatively. 53  Oncological Principles Definitions Metaplasia. Reversible transformation of one type of terminally differentiated cell into another fully differentiated cell type. Dysplasia. Potentially premalignant condition characterized by increased cell growth, atypical morphology, and altered differentiation. Neoplasia. Autonomous abnormal growth of cells which persists after the initiating stimulus has been removed. A neoplasm is a lesion resulting from neoplasia. Metaplasia This represents an adaptive response of a tissue to environmental stress. It is mediated by changes in expression of genes involved in cellular differentiation. It does not progress to malignancy: if the environmental changes persist, dysplasia may result and progress to malignancy. For example: Change from ciliated to squamous cells in the respiratory epithelium of the trachea and bronchi in smokers. Change from squamous to columnar cells in the oesophageal epithelium of patients with gastro-oesophageal reflux disease(Barrett’s) Dysplasia Potentially premalignant condition. May be a response to chronic inflammation or exposure to carcinogens. Early forms may be reversible: severe dysplasia has a high risk of progression to malignancy, for example: Dysplasia arising in colonic epithelium due to chronic ulcerative colitis. Squamous dysplasia in the bronchi of smokers (sputum cytology). Classification of tumours Use this classification to give a differential diagnosis for any neoplasm. Tissue of origin. Organ and tissue type Behavior. Benign or malignant. 54  Primary or secondary. Benign tumours Slow growing, usually encapsulated, do not metastasize, do not recur if completely excised, rarely endanger life. Effects are due to size and site. Histology: well differentiated, low mitotic rate, resemble tissue of origin. Malignant tumors These expand and infiltrate locally, encapsulation is rare, metastasize to other organs via blood, lymphatics or body spaces, endanger life if untreated. Histology: varying degrees of differentiation from tissue of origin, pleomorphic (variable cell shapes), high mitotic rate. Structural Classification Tissue of origin and Tumour type Epithelium Benign: papilloma, adenoma (glandular epithelium) Malignant: carcinoma (adenocarcinoma, squamous cell carcinoma indicate cell types) Connective tissue Benign: fibroma (fibrous tissue), lipoma (fat), chondroma (cartilage), osteoma (bone), leiomyoma (smooth muscle), rhabdomyoma (striated muscle) Malignant: sarcoma, e.g. fibrosarcoma, osteosarcoma, etc. (if well differentiated); spindle cell sarcoma, etc. (if poorly differentiated) Neural tissue These arise from nerve cells, nerve sheaths, and supporting tissues, e.g. astrocytoma, medulloblastoma, neurilemmoma, neuroma, etc. Haemopoietic The leukaemias, Hodgkin’s disease, multiple myeloma, lymphosarcoma, reticulosarcoma Melanocytes Melanoma Mixed origins: fibroadenoma, nephroblastoma, teratoma (all three germ layers), choriocarcinoma 55 Developmental blastomas E.g. neuroblastoma (adrenal medulla), nephroblastoma (kidney), retinoblastoma (eye) Invasion Invasion is the most important single criterion for malignancy and is also responsible for clinical signs and prognosis as well as dictating surgical management. Factors that enable tumours to invade tissues include: Increased cellular motility. Loss of contact inhibition of migration and growth. Secretion of proteolytic enzymes, such as collagenase, which weakens normal connective tissue bonds. Decreased cellular adhesion. Metastasis Metastasis is a consequence of these invasive properties: it is the process by which malignant tumours spread from their site of origin (primary tumour) to form secondary tumours at distant sites. Carcinomatosis denotes extensive metastatic disease. The routes of metastasis are: Haematogenous. Via the bloodstream. Five tumours—breast, bronchus, kidney, thyroid, prostate— classically metastasize via haematogenous spread to bone. Lung, liver, and brain are common sites for secondaries. Lymphatic. To local, regional, and systemic nodes. Transcoelomic. Across pleural, pericardial, and peritoneal cavities. Implantation. During surgery or along biopsy tracks. Carcinogenesis Carcinogenesis is the process that results in malignant neoplasm formation. Usually more than one carcinogen is necessary to produce a tumour, a process which may occur in several steps in multistep hypothesis Initiators produce a permanent change in the cells, but do not themselves cause cancer, e.g. ionizing radiation: this change may be in the form of gene mutation. 56  Promoters stimulate clonal proliferation of initiated cells, e.g. dietary factors and hormones: they are not mutagenic. Latency is the time between exposure to carcinogen and clinical recognition of tumour due to: Time taken for clonal proliferation to produce a significant cell mass. Time taken for exposure to multiple necessary carcinogens. Persistence is when clonal proliferation no longer requires the presence of initiators or promoters and the tumour cells exhibit autonomous growth. Tumour growth Tumour doubling time depends on cell cycle time, growth function, and cell loss fraction. In tumours such as leukaemias, the doubling time remains remarkably constant: the cell mass increases proportionally with time. This is exponential growth. In solid tumours, doubling time slows as size increases. This is referred to as Gompertzian growth. Genetic abnormalities in tumours Two genetic mechanisms of carcinogenesis are proposed: Oncogenes. Enhanced expression of stimulatory dominant genes. Tumour suppressor genes. Inactivation of recessive inhibitory genes. Oncogenes At least 60 oncogenes have been identified. They can be classified according to the function of the gene product (e.g. growth factors, cell signalling agents). The proteins produced (oncoproteins) can be produced in abnormal quantities or be abnormally active forms and cause: Independence from extrinsic growth factors. Production of tumours in immunotolerant animals. Production of proteases to assist in invasion of normal tissues. Reduced cell cohesiveness assisting metastasis. Growth to higher cell densities and abnormal cellular orientation. Examples include BRCA1, p53, k-ras, APC, DCC. 57  Common risk factors for cancer Chemicals Polyaromatic: hydrocarbons Lung cancer (smoking), skin cancers Aromatic amines: Bladder cancer (rubber and dye workers) Alkylating agents: Leukaemia Viruses HIV: Kaposi’s sarcoma, lymphoma Epstein–Barr virus: Burkitt’s lymphoma, nasopharyngeal cancer Human papillomavirus: Squamous papilloma (wart), cervical cancer Hepatitis B virus: Liver cell carcinoma Radiation UV light (UVB>UVA): Malignant melanoma, basal cell carcinoma Ionizing radiation: Particularly breast, bone, thyroid, marrow Biological agents Hormones, e.g. oestrogens Breast and endometrial cancer Mycotoxins, e.g. aflatoxins Liver cell carcinoma Parasites, e.g. schistosoma Bladder cancer Miscellaneous Asbestos: Mesothelioma and lung cancer Nickel: Nasal and lung cancer Grading and staging Key facts The objectives of staging and grading a tumour are: To plan appropriate (treatment) for the individual patient. To give an estimate of the prognosis. To compare similar cases when assessing outcomes or designing clinical trials. Staging and grading methods Staging is the process of assessing the extent of local and systemic spread of a malignant tumour or the identification of features which are risk factors for spread. Grading is the process of assessing the degree of differentiation of a malignant tumour. 58 Staging The commonest system is the internationally agreed TNM classification. It is not appropriate for leukaemia, lymphomas, or myeloma. A four-stage classification (I. II, III, IV) is also often used and is compatible with TNM. Staging may be: Radiological (often performed preoperatively): Radiological staging is used to plan treatment (e.g. neoadjuvant therapy, selection for surgery, planning of surgery). Pathological (performed on surgical specimens): Pathological staging is used to plan adjuvant treatment (chemotherapy or radiotherapy) and for informing prognosis. An example of lung cancer staging is: Stage I (T1N0, T2N0), 85% 5y survival with surgery. Stage II (T1N1, T2N1, T3N0), 60% 5y survival with surgery. Stage IIIa (T3N1 or any N2), 20% 5y survival with surgery. Stage IIIb (any T4, any N3), 70 years with limited physiological reserve in one or more vital organs Extensive surgery for carcinoma Acute abdominal catastrophe with haemodynamic instability (e.g. peritonitis) Acute massive blood loss >8 units Septicaemia Positive blood culture or septic focus Respiratory failure: PaO2 0.4 or mechanical ventilation >48 hours Acute renal failure: urea >20 mmol or creatinine >260 mmol/L 65  Post-operative care POSTOPERATIVE OBSERVATIONS The patient’s vital signs (including pulse, blood pressure and pulse oximetry reading), level of consciousness, pain and hydration status are monitored in the recovery room and supportive treatment is given. The following six simple physiological parameters, which are routinely measured, are used to calculate the score: 1 respiration rate. 2 oxygen saturation. 3 systolic blood pressure. 4 pulse rate. 5 level of consciousness or new-onset confusion, disorientation and/or agitation 6 temperature. Each measured parameter is allocated a score depending on how much it varies from a normal value. Two points are added if the patient needs supplemental oxygen. The score is then aggregated. An aggregate score places patients in different risk categories (low to high risk) that trigger an appropriate clinical response. Depending on the risk categories patients may need level 2 or level 3 care. Patients who are in the high-risk category of clinical deterioration will need urgent assessment by staff with critical care experience and airway skills. Surgery-specific observations, such as Doppler flow for a free fap, regular neurological evaluation and laboratory tests, such as blood gas analysis, should also be performed when necessary. The patient can be discharged from operation room when they fulfill the following criteria: they are fully conscious; respiration and oxygenation are satisfactory; they are normothermic, not in pain and not nauseous; cardiovascular parameters are stable; oxygen, fluids and analgesics have been prescribed; there are no concerns relating to the surgical procedure. 66 POSTOPERATIVE COMPLICATIONS Postoperative complications are an important cause of morbidity, mortality, extended hospital stay and increased costs. Most patients at increased risk of developing postoperative complications can be identified prior to surgery at the preoperative assessment clinic. Early identification of risk allows for targeted, appropriate, anticipatory and supportive medical care, which will reduce both the incidence and severity of such complications when they occur. 67  GENERAL POSTOPERATIVE COMPLICATIONS Bleeding ▪ Postoperative hemorrhage is most common in the immediate postoperative period. It may be caused by an arterial or venous leak, but also by a generalized ooze or a coagulopathy. ▪ All patients must have their vital signs (pulse rate, blood pressure, oximetry, central venous pressure, if available, and urine output) monitored regularly. ▪ Dressings and drains should be inspected regularly in the first 24 hours after surgery. If hemorrhage is suspected, blood samples should be taken for a full blood count, coagulation profile and crossmatch. ▪ The treatment of haemorrhage is both to stop the bleeding and supportive. Supportive treatment includes oxygen and fluid resuscitation. It may require correction of coagulopathy. Deep Vein Thrombosis ▪ Deep vein thrombosis (DVT) is a well-known and, when complicated by pulmonary embolus, potentially fatal complication of surgery ▪ Risk assessment should occur within 24 hours of admission. ▪ Methods of prevention are guided by the risk score and include the use of compression stockings, calf pumps and pharmacological agents, such as low-molecular-weight heparin. ▪ The symptoms and signs of DVT include calf pain, swelling, warmth, redness and engorged veins. However, most will show no physical signs. On palpation the muscle may be tender and there may be a positive Homans’ sign (calf pain on dorsiflexion of the foot). Fever About 40% of patients develop pyrexia after major surgery; however, in most cases no cause is found. The inflammatory response to surgical trauma may manifest itself as fever, and so pyrexia does not necessarily imply sepsis. However, in all patients with a pyrexia, a focus of infection should be sought. The causes of a raised temperature postoperatively include: atelectasis of the lung; superficial and deep wound infection; chest infection, urinary tract infection and thrombophlebitis. wound infection, anastomotic leakage, intracavitary collections and abscesses. 68  The possible causes of pyrexia of a non-infective origin include: DVT Transfusion reactions Wound hematomas Atelectasis Drug reactions Patients with a persistent pyrexia need a thorough review. Relevant investigations include full blood count, urine culture, sputum microscopy and blood cultures. 69