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Surgery tutorials for medical students

principles of surgery

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Surgery tutorials for medical students

  1. 1. bbinyunus2002@gmail.com Page 1 TUTORIALS COMPILED BY DR BASHIR BIN YUNUS (MBBS, ZARIA) SURGICAL RESIDENT AMINU KANO TEACHING HOSPITAL
  2. 2. bbinyunus2002@gmail.com Page 2 Contents PART ONE Surgical infections……………………………………………………………………………………… Wound and wound healing………………………………………………………………………… Sutures …………………………………………………………………………………………………….. Cutaneous ulcers……………………………………………………………………………………….. Fluid and electrolytes therapy…………………………………………………………………….. Shock …………………………………………………………………………………………………………. Blood transfusion……………………………………………………………………………………… Hemostasis in surgery………………………………………………………………………………… Nutrition in surgery……………………………………………………………………………………. Metabolic response to trauma…………………………………………………………………… Perioperative management……………………………………………………………………….. Surgical prophylaxis………………………………………………………………………………….. SCD and surgery…………………………………………………………………………………………. Diabetics and Surgery ………………………………………………………………………………. HIV and the surgeon ………………………………………………………………………………… Obesity and surgery………………………………………………………………………………….. Surgery in the elderly ………………………………………………………………………………. Surgical hypertension………………………………………………………………………………. Asepsis in surgery…………………………………………………………………………………….
  3. 3. bbinyunus2002@gmail.com Page 3 Multiply Injured patient ………………………………………………………………………….. Cancer chemotherapy………………………………………………………………………………… Radiotherapy …………………………………………………………………………………………….. Use of drains in surgery…………………………………………………………………………… Diathermy…………………………………………………………………………………………………… Lacer ………………………………………………………………………………………………………… Tourniquet………………………………………………………………………………………………… Minimal access surgery…………………………………………………………………………….. Principles of neonatal surgery…………………………………………………………………… Biopsy ………………………………………………………………………………………………………. Prostate biopsy Dialysis Informed consent……………………………………………………………………………………… Day case surgery ……………………………………………………………………………………… Medical ethics ………………………………………………………………………………………….. Surgical audit……………………………………………………………………………………………. PART TWO (Principles in management) Upper GI bleeding ……………………………………………………………………………………. Urinary calculi………………………………………………………………………………………….. Calculus cholecystitis ………………………………………………………………………………. Typhoid ileal perforation…………………………………………………………………………. Surgical management of peptic ulcer disease…………………………………………. Fournier gangrene …………………………………………………………………………………..
  4. 4. bbinyunus2002@gmail.com Page 4 Benign prostatic hyperplasia……………………………………………………………………. Prostate cancer……………………………………………………………………………………….. Obstructive uropathy...……………………………………………………………………………… Gastric outlet obstruction ……………………………………………………………………….. Gastrostomy ………………………………………………………………………………………………… Hernia ………………………………………………………………………………………………………….. Intestinal fistula…………………………………………………………………………………………… Malignant ascites ……………………………………………………………………………………….. Malignant bowel obstruction …………………………………………………………………….. Malignant hyperthermia …………………………………………………………………………….. Chest trauma………………………………………………………………………………………………. Abdominal injury ………………………………………………………………………………………. Mass casualty …………………………………………………………………………………………….. Regional anaesthesia …………………………………………………………………………………. PART THREE Operatives………………………………………………………………………………………………… PART FOUR Long case …………………………………………………………………………………………………. OSCE………………………………………………………………………………………………………….. Surgical instruments…………………………………………………………………………………. Radiographs…………………………………………………………………………………………….. PART FIVE (pathology and management)
  5. 5. bbinyunus2002@gmail.com Page 5 Surgical tutor ………………………………………………………………………………………….. Past questions –  Essay  Orals SURGICAL INFECTIONS DEFINITIONS Infection in which there is anatomic or mechanical problem that must be resolved by operation or another invasive procedure to cure the infection. Antibiotic are adjunct and are not substitute for indicated surgical therapy. BACTERAEMIA; the transient invasion of the circulation by bacteria is known as bacteraemia. SEPTICEMIA; this implies prolonged presence of bacteria in the blood accompanied by severe systemic reaction. SYSTEMIC INFLAMMATORY RESPONSE SYNDROME (SIRS): The systemic inflammatory response to a wide variety of severe clinical insults manifests by 2 or more of the following conditions: • Temperature greater than 38°C or less than 36°C • Heart rate greater than 90 beats per minute (bpm) • Respiratory rate greater than 20 breaths per minute or PaCO2 less than 32 mm Hg • White blood cell count greater than 12,000/mL, less than 4000/L, or 10% immature (band) forms SEPSIS: This is a systemic inflammatory response to a documented infection. SEVERE SEPSIS: This is sepsis and SIRS associated with organ dysfunction, hypoperfusion, or hypotension. SEPTIC SHOCK: Refers to severe sepsis which is not responsive to intravenous fluid infusion for resuscitation and requires inotropic or vasopressor agent to maintain systolic blood pressure.
  6. 6. bbinyunus2002@gmail.com Page 6 CHARACTERISTICS IF SURGICAL INFECTIONS (unlike medical infections) - Damaged host defences (especially epithelial barrier) - Immunological defects are global – trauma, nutritional deficiency, etc - Pathogens are polymicrobial, both aerobic and anaerobic - Pathogens often from endogenous flora (opportunistic) as well as from exogenous. ORGANISMS COMMONLY ENCOUNTERED IN SURGICAL INFECTIONS The organisms commonly encountered in surgical infections are the:  Staphylococci; o Staph. pyogenes causes boils, carbuncle, styes, septic hand, breast abscess, osteomyelitis, wound sepsis, deep abscess, septicemia and pyaemia o Staph albus non pathogenic though can cause low grade inflammation in dead tissues  Streptococci; the haemolytic(α and β) and the anaerobic are surgical concern. The toxins produce include; haemolysin, leucocidin, fibrinolysin, erythrogenic toxin, hyaluronidase, deoxyribonuclease. Β-haemolytic strept. E.g Strep Pyogenes causes erysipelas, cellulitis, severe wound infection, tonsillitis, otitis media, scarlet fever, puerperal sepsis. Α-haemolytic eg Strept. Viriadans cause intra oral and dental infections, can contaminate burns or chronic skin ulcers, seed cardiac lesions  Pneumococci; lobar pneumonia or with other organisms causing bronchopneumonia; they may also produce otitis media, sinusitis, meningitis, acute primary peritonitis in young girls and wound infection.  Gram negative bacteria; E.coli, Pseudomonas, Proteus, Klebsiella, Haemophilus Influenzae. The intestinal bacteria commonly encountered are Escherichia coli, Pseudomonas, and Proteus organisms usually described as coliforms. In general, those bacilli which do not ferment lactose eg Pseudomonas, proteus, salmonella B.fragilis , V.cholerae are more pathogenic for man. In surgical practice, however, it is the lactose fermenters eg Klebsiella, E. coli, Enterobacter ,which predominate. o They infect wounds near the lower ileum and colon, the urinary tract and bums.
  7. 7. bbinyunus2002@gmail.com Page 7 o They are found in mixed infections and are commonly secondary invaders in infections by staphylococci and streptococci o They elaborate in their capsule a powerful endotoxin which causes pyrexia, rigors and septic shock when released into the blood stream Other gram negatives  Klebsiella organisms are gram-negative rods usually responsible for pneumonic lesions and hepatic abscesses but may produce wound infections especially after transplantation procedures.  Haemophilus influenzae often found in the healthy upper respiratory tract. It causes acute epiglottitis, meningitis and bronchitis. INFECTIONS OF SIGNIFICANCE IN SURGICAL PATIENTS SURGICAL SITE INFECTION (SSI) It is defined as infection present in any location along the surgical tract after a surgical procedure within 3odays of procedure or up to 1 year after a procedure that has involved the implantation of a foreign material. Classification  Incisional SSI o Superficial- those involving only the skin and subcutaneous tissue o Deep - those involving deep soft tissues of the incision (e.g. fascial and muscle layers)  Organ/space SSI - involves any part of the anatomy (e.g., organs or spaces) manipulated Criteria for defining an SSI as superficial 1. Infection occurs within 30 days after an operation. 2. The infection involves only the skin and the subcutaneous tissue adjacent to the incision. 3. At least one of the following is present:  a purulent discharge from the surgical site,  at least one of the signs and symptoms of infection(pain, tenderness, localized swelling, rednessor heat),  spontaneous dehiscence of the wound or deliberate opening of the wound by the surgeon (unless the culture results from the site are negative),
  8. 8. bbinyunus2002@gmail.com Page 8  an abscess or evidence of infection on direct examinationor reoperation, or histopathologic or radiological examination,  diagnosis of infection by a surgeon or attendingphysician. Deep incisional SSI Criteria: 1. They occur within 30 days after surgery with no implant (up to 1 year after surgery if an implant is left in place), 2. The infections involve deep soft tissues, fascia and muscle layers, 3. At least one of the following:  Purulent drainage/organism isolated from an aseptically obtained culture.  Fascial dehiscence or deliberate opening of the fascia by a surgeon due to signs of inflammation.  An abscess or other evidence of infection noted below the fascia during reoperation, radiological examination or histopathology.  A surgeon declares that a deep incisional infection is present. Organ/space SSI These infections involve any part of the anatomy, in organs and spaces other than the incision, which was opened or manipulated during operation. Criteria 1. The infection occurs within 30 days after surgery or within 1 year if an implant is present and the infection seems related to the operation. 2. The infection involves a joint/organ/space, or anatomic structures opened or manipulated during the operation. 3. At least one of the following:  Purulent drainage from a drain placed into the organ/space.  An organism is isolated from a culture sample obtained aseptically from joint fluid or deep tissue.  An abscess or other evidence of infection involving a joint, organ or space during reoperation, radiological examination or histopathology.  A diagnosis of an organ/space SSI by a surgeon
  9. 9. bbinyunus2002@gmail.com Page 9 RISK FACTORS FOR DEVELOPMENT OF SURGICAL SITE INFECTIONS PATIENT FACTORS Older age Immunosuppression Obesity Diabetes mellitus , malignancies, steroids Chronic inflammatory process Malnutrition Peripheral vascular disease Anemia Radiation Chronic skin disease Carrier state (e.g., chronic Staphylococcus carriage) Recent operation LOCAL FACTORS Poor skin preparation, Surgical technique Contamination of instruments Inadequate antibiotic prophylaxis Prolonged procedure Local tissue necrosis, foreign body Hypoxia, hypothermia, hematoma, MICROBIAL FACTORS Prolonged hospitalization (leading to nosocomial organisms) Toxin secretion Resistance to clearance (e.g., capsule formation) Remote site infection Bacterial number, virulence, and antimicrobial resistance Previous antibiotic therapy
  10. 10. bbinyunus2002@gmail.com Page 10 Surgical Wound Classification According to Degree of Contamination WOUND CLASS DEFINITION Clean (classI)  Surgically incised, no break of asepsis.  An uninfected operative wound in which no inflammation is encountered  lumen is not entered.  Wounds are closed primarily and, if necessary, drained with closed drainage.  Surgical wounds after blunt trauma should be included in this category if they meet the criteria  Infection rate <2%  Eg herniorrhaphy, lump excision, thyroidectomy, total joint athroplasty, lipoma excision Clean- contaminated (classII)  lumen is entered under controlled conditions and without unusual contamination or minimal spillage  rate of infection is 5-10%  Eg Cholecystectomy, elective GI surgery (not colon), bladder surgery, uninflamed appendectomy Contaminated (classIII)  Open, fresh, accidental wounds. <4h  operations with major breaks in sterile technique  gross spillage from the lumen  and incisions in which acute, nonpurulent inflammation is encountered are included in this category  Rate of infection is 15-20%  Eg appendectomy for inflamed appendix, Colorectal surgery, bowel resection for infarcted bowel, Dirty (class IV)  Old traumatic wounds with retained devitalized tissue, perforated viscera, abscess, fecal contamination, established infection b4 wound is made on skin.  Infection rate <40%
  11. 11. bbinyunus2002@gmail.com Page 11 Preventive Measures for Surgical Site Infection TIMING OF ACTION DETERMINANT IN WHICH THE PREVENTIVE MEASURE ACTS Microorganism Local Patient Preoperative Shorten preoperative stay Antiseptic shower preoperatively Appropriate preoperative hair removal or no hair removal Avoid or treat remote site infections Antimicrobial prophylaxis Appropriate preoperative hair removal or no hair removal Optimize nutrition Preoperative warming Tight glucose control (insulin drip) Stop smoking Intraoperative Asepsis and antisepsis Avoid spillage in gastrointestinal cases Surgical technique: Hematoma/seroma Good perfusion Complete débridement Dead spaces Monofilament sutures Justified drain use (closed) Limit use of sutures/foreign bodies Delayed primary closure when indicated Supplemental oxygen Intraoperative warming Adequate fluid resuscitation Tight glucose control (insulin drip) Postoperative Protect incision for 48-72 hours Remove drains as soon as possible Avoid postoperative bacteremia Postoperative dressing for 48-72 hours Early enteral nutrition Supplemental oxygen Tight glucose control (insulin drip) Surveillance programs
  12. 12. bbinyunus2002@gmail.com Page 12 ACUTE INFECTIONS Cellulitis Phlegmon Abscess Pustule, furuncle and carbuncles Hydradenitis supprativa Infective gangrene Tetanus Necrotizing Fasciitis Erysipelas CELLULITIS This is a diffuse inflammation of the subcutaneous tissue resulting from invasion by pyogenic bacteria. It spreads along subcutaneous tissues and fascial planes. Usually due to infection with ß haemolytic streptococcus- strep.pyogenes (commonest cause) or Staph. aureus .Both produce enzymes that degrade tissue and allow spread of infection. Anaerobic streptococci (peptostreptococci) are part of the normal flora of the mouth and gastrointestinal tract. In contrast to other streptococcal wound infections, these organisms produce a thin, brown discharge, often with crepitation in the infected tissue (anaerobic cellulitis). Clinical features • Cellulitis usually presents with a well demarcated area of inflammation • Redness, heat, swelling and pain are the cardinal signs of inflammation • Usually associated with malaise, fever and a raised white cell count • If not rapidly treated it can progress to lymphangitis and lymphadenitis • Localised areas of skin necrosis may occur • Predisposing factors include o Lymphoedema o Venous stasis o Diabetes mellitus o Surgical wounds Management  Rest and elevation of the affected limb andapplication of insulating dressings to prevent heat loss arecomforting  Antibiotics  May initially be given orally  Intravenous administration if no rapid improvement
  13. 13. bbinyunus2002@gmail.com Page 13  Benzylpenicillin and flucloxacillin are usually antibiotics of choice where suppuration occurs surgical d rainage is indicated. PHLEGMON occurs when inflammation is relatively diffuse, i.e. like cellulitis, yet there are small loci of necrotic tissue as well as multiple tiny pockets of pus. It is the subsequent progression shortly to innumerable microscopic abscesses which distinguishes a phlegmon from cellulitis. The usual causative organism is staph. aureus, possibly in combination with virulent strains of Strep. haemolyticus. PUSTULE, FURUNCLE AND CARBUNCLES These are forms of abscesses peculiar to the skin and result from infections of hair follicles by Staph. Pyogenes. The tiny abscess thus formed is a pustule and the inflammation may subside with egress of the bead of pus. The infection frequently spreads to the surrounding subcutancous tissue before discharge of the necrotic products and in this layer further extension may take place involving several hair follicles. This is a typical boil or furuncle with a central core of necrotic tissue which is discharged with the pus on ripening of the boil. Carbuncles also result from infection of hair follicles but in areas such as the back of the neck, back of the trunk, the hairy surfaces of the hand or fingers, the lip and scalp, well-endowed with thick columns of subcutaneous fat projecting around the follicles. Diabetics arc particularly prone to this complication. Word meaning of carbuncle is charcoal. It is an infective ga11grane of skin and subcutaneous tissue. Control of diabetes is essential using insulin. Antibiotics like penicilhns, cephalosporins or depending on C/S is given. Drainage is done by a cruciate incision and debridement or all dead tissue is done. Excision is done later. Once wound granulates well, skin grafting may be required. HYDRADENITIS SUPPRATIVA It is a chronic infective and fibrous disease of the skin bearing apocrine sweat glands. Apocrine sweat glands are coiled glands which open into the hair follicles. Site of apocrine sweat glands: • Axilla, Areola, Umbilicus, Groin, Perineum
  14. 14. bbinyunus2002@gmail.com Page 14 Aetiology • Obesity, smoking, Poor hygiene,Diabetes mellitus, Steroids. Common bacteria involved are staphylococci, streptococci, staphylococcus ~aureus, propioni-bacterium acnes. Clinical Features Common in females 4 : 1. Commonest site is axilla. Multiple discharging sinusct., with nodules in the skin which is tender. Induration due to fibrosis. Investigation: Discharge study, Biopsy. DDX: Tuberculous sinus, Malignancy (squamous cell carcinoma of skin). Treatment Antibiotics. Excision of the involved area widely followed by skin grafting or flaps (radical wound excision). Wounds in the affected area do not heal well by secondary intention. Antiandrogen drugs. ABSCESS Liquefaction of the dead tissue is produced by proteolytic enzymes contained in the polymorphonuclear leucocytes and the mass of bacteria, leucocytes, exudate and dying tissue residues thus formed is called pus. A pyogenic membrane of granulation tissue soon forms separating the suppurating mass from the contiguous normal tissues. (pyogenic abscess) Other Types Pyaemic abscess, Metastatic abscess, Cold abscess due to chronic infection like tuberculosis Bacteria causing abscess • Staph. aureus. • Strept. pyogenes • Gram-negative bacteria (E. coli, Pstudomonas, Klebsiella). • Anaerobes.
  15. 15. bbinyunus2002@gmail.com Page 15 Factors precipitating abscess formation • General condition of the patient; nutrition, anaemia, age of the patient • Associa1ted diseases: Diabetes, HIV, immununosuppression • type and virulence of the organisms • Trauma, haematoma, road traffic accidents Clinical Features Fever often with chills and rigors. Localised swelling which is smooth, soft and fluctuant Visible (pointing) pus. Throbbing pain and pointing tenderness Brawny induration around. Redness and warmth with restricted movement around the joint (Commonly cellulitis occurs first which eventually get localized to form abscess.) Treatment Abscess should be formed before draining. Exceptions for this rule are:Parotid abscess, Breast abscess, Axillary abscess, Thigh abscess, Ischiorectal abscess INFECTIVE GANGRENE Gangrene is the death of large sections of tissue with superimposed putrefaction. It is occasionally due to infection. It is either directly through microbial enzymes or indirectly through thrombotic occlusion of blood vessels. Infective gangrene is aerobic, anaerobic or synergistic. Aerobic gangrene; the causative organisms are highly virulent strains of Strep. haemolyticus often occurring in epidemic forms such as the classic hospital gangrene. A similar condition may result from certain highly virulent strains of Staph. aureus - the scalded skin syndrome. P. aeruginosa burn wound necrosis is another form of monobacterial aerobic gangrene. Treatment: appropriate bactericidal chemotherapy and wide debridement of all necrotic tissues.
  16. 16. bbinyunus2002@gmail.com Page 16 Anaerobic gangrene/ Gas gangrene it is an infective gangrene caused by clostridial organisms. The causative organisms fall into two groups: those that breakdown starch or the saccharolytic group (CI. Welchii or CI. Perfringens, Cl. novy, Cl. oedematiens, Cl. septicum) and those which break down protein or the proteolytic group (Cl. Sporogenes and CI. haemolyticus). The effects produce are as a result of exotoxins produced by organisms. It usually takes two forms; clostridium myonecrosis (attacking muscles more serious disease with high mortality) and clostridium welchii cellulitis (affecting subcutenous tissue) commoner, not associated with cardiovascular disturbances. Extensive necrosis of muscle with production of gas (hydrogen sulphide; nitrogen; carbon dioxide) which stains the muscle brown or black. Usually muscle is involved from origin to insertion. Often may extend into thoracic and abdominal muscles.When it affects the liver it causes necrosis with frothy blood-foaming liver, is characteristic. Clinical Features  Symptoms develop rapidly appearing within 10 -12 h after the injury.  Features of toxaernia, fever, tachycardia, pallor.  Wound is under tension with foul smelling discharge (sickly sweety odour).  Khaki brown colored skin due to haemolysis.  Crepitus can be felt.  Jaundice may be ominous sign and also oliguria signifies renal failure. Prevention of gas gangrene  Proper debridement of devitalised crushed wounds.  Devitalized wou11ds should not be sutured.  Adequate cleaning of the wounds with H2O 2 and normal saline.  Penicillin as prophylactic antibiotic. X-rays of the affected part may reveal in the soft tissues collections of gas which cannot be demonstrated by palpation. lnvestiga11ons X·ray shows gas in muscle plane or under the skin. LFT
  17. 17. bbinyunus2002@gmail.com Page 17 Treatment  Resuscitate; correct hypotension, anaemia  Debridement  Irrigation and pack with H2O2 soaked guaze  Exhibition of antibiotics, usually penicillin in massive doses of up to 10 million units a day is essential. Clindamycin and metronidazole together have been effective.  Administration of gas gangrene serum  Hyperbaric O2 SYNERGISTIC GANGRENE It is the result of symbiotic infections from two or more bacterial species, and the resultant lesion is far more fulminant than the regular lesion usually attributable to either individual pathogen. The anaerobic partners are usually the primary pathogens contributing the destructive enzymes. The aerobic organism extract the O2 from tissue making it conducive for the anaerobes. MeIeney's Gangrene or Cellulitis, a progressive recalcitrant ulcer produced by symbiotic infections with the anaerobe Peptostreptococcus and the common aerobe Staph. aureus. Ulcerative gingivitis; Fusiformis bacillus and a spirochete. Cancrum oris, or noma; Sets of gram-positive cocci and Bacteroides melaninogenicus Necrotizing fasciitis.; Combinations of coliforms, staphylococci, anaerobic streptococci, peptostreptococci and Bacteroides species. Fournier 's gangrene; Mixed aerobic-anaerobic organisms (including Staphylococcus, micro-aerophilic Haemolytic streptococcus, E. coli, Fusobacterium and Cl. welchi) Treatment: antibiotics, debridement and hyperbaric O2
  18. 18. bbinyunus2002@gmail.com Page 18 TETANUS This is caused by a gram positive spore-forming obligate anaerobe, C. tetani, found in the feces of humans and animals, and capable of prolonged survival in soil. Two exotoxins are produced: tetanospasmin, a neurotoxin, and tetanolysin, a hemolysin. PATHOGENESIS spores Enters wound Germinates in anaerobic media to releasing bacteria which multiply Release of exotoxins Tetanospasmin hemolysin Hemolysis Thru perineural sheath circulation Enters the CNS, blocks toxemia (thru blood) blocks the NMJ by acting on the cholinesterase at the anterior cholinesterase enzyme horn cells Causes hyperexcitability and aggravates the muscle spasm reflex spasms of muscles Once toxin fixed to the nerve tissue, can no longer be neutralized by antitoxin.
  19. 19. bbinyunus2002@gmail.com Page 19 CLINICAL FEATURES Symptoms  Jaw stiffness –lockjaw (usu the 1st symptom), pain and stiffness in the neck and back muscles  Anxiousness, sweating  Headache, delirium, sleeplessness  Dysphagia  Dyspnoea Signs  Trismus, due to spasm of masseter and pterygoids.  Risus sardonicus (smiling facies), due to spasm of the facial muscle- zygomaticus major. Looks as if patient is smiling.  Neck rigidity.  Spasm and rigidity of all muscles.  Hyperreflexia.  Respiratory changes-due to laryngeal muscle spasm, infection, aspiration.  Tonic-clonic convulsions.  Abdominal wall rigidity often with haematoma formation.  Severe convulsion may often lead to fractures, joint dislocations and tendon ruptures.  Fever and tachycardia.  Retention of urine (due to spasm of urinary sphincter), constipation (due to rectal spasm).  Rarely carditis, can cause cardiac arrest. Steroid is helpful.  Symptoms will be aggravated by stimuli like light, noise. INCUBATION PERIOD  Time between the entry of spore and appearance of first symptom.  Usually 6-10 days.  Shorter the incubation period worser the prognosis and more severe the course of the disease.
  20. 20. bbinyunus2002@gmail.com Page 20 PERIOD OF ONSET  Time between appearance of first symptom and appearance of first reflex spasm.  Shorter the period of onset worser the prognosis and vice versa.  If less than 48hrs, death is very likely TYPES  Generalized (commonest)  Localized  Cephalic  Neonatal DIFFERENT POSTURES IN TETANUS  Opisthotonus: Posterior muscles are acting more, so backward bending.  Orthotonus: Straight posture. Both front and back muscles are acting equally.  Emprosthotonus: Forward bending as front muscles are acting more.  Pleurosthotonus: lateral bending as lateral muscles act more. STAGING OF TETANUS  Mildly ill: Rigidity, spasm, trismus and different postures.  Seriously ill: Spasm, rigidity, severe respiratory infections.  Dangerously ill: Cyanosis with respiratory failure and tonic-clonic convulsions. CAUSE OF DEATH IN TETANUS  Respiratory failure with aspiration pneumonia and ARDS  Severe carditis--an ominous sign  Mortality is 45-50% PRINCIPLES FOR TETANUS PROPHYLAXIS There are two types of immunization the active and passive. The active- toxoid- the dead or modified organism introduce into the host body which stimulates the reticulo- endothelial system to produce antibodies. More effective but it takes about 2-3 months to be operational. The passive form- tetanus immune globuline- given to protect the
  21. 21. bbinyunus2002@gmail.com Page 21 victim. It neutralizes the toxin, however it is less effective and may precipitate anaphylaxis. Toxoid administration; 0.5ml subcutaneously  Traditionally ; day 1, 6weeks, 6month and every 10years  Rapid method; day 1, day 4 and day 7. Using alum-precipitated toxoid. Immunity is demonstrable in 28days. Anti-tetanus serum: given IM, after a test dose of 0.1ml or 150 IU subcutaneously  Human ATS 250IU  Equine ATS 1500IU TETANUS PROPHYLAXIS IN WOUND MANAGEMENT (see surgical prophylaxis) History of tetanus toxoid doses Clean, minor wound All other wounds Toxoid+ Immune globulin Toxoid+ Immune globulin Less than three doses or unknown Yes No Yes Yes Three or more doses++ Yes if < 10 years since last booster No Yes if ≥ 5 years since last booster No Treatment ; aims of treatment are  Halt production of toxin  Neutralize circulating toxin  Removing source of infection  Controlling convulsion or spasms
  22. 22. bbinyunus2002@gmail.com Page 22  General supportive measures and prevention of complications Treatment is multidisciplinary GENERAL MEASURES • isolation • Avoid noise and light • A TG 3,000 units 1M • ATS-50,000 IM and 50,000 IV-After test dose • Antibiotics like inj penicillin 20 lacs 6th hourly or metronidazole • Inj tetanus toxoid 0.5 ml 1M - to deltoid muscle • IV fluids with TPN • Urinary catheterization • Nasogastric tube is passed to prevent aspiration initially, later for feeding • Regular suction of throat • Nasal oxygen when required SPECIFIC MEASURES • IV diazepam 20 mg 6th hourly • IV phenobarbitone 30 mg 6th hourly • IV chorpromazine 25 mg 6th hourly • Endotracheal intubation and ventilator support or Tracheostomy if there is severe respiratory secretions • Steroids • Bronchodilators like deriphylline • Wound care- debridement, drainage, and local injection of A TG, wound is not closed primarily. ERYSIPELAS This arises from cutaneous infection with strains of Strep. Pyogenes with a predilection for the lymphatics. Rose pink rash with cutaneous lymphatic oedema develop. Vesicles are formed which form eventually ruptures discharge. Site of predilection include face, orbit, scrotum and umbilicus in infant. Toxemia is always a feature. Milian ear sign is use to differentiate it from cellulitis wherein in cellulitis the ear lobe is spared. The condition is associated with poor hygiene. Treatment is with penicillin.
  23. 23. bbinyunus2002@gmail.com Page 23 NECROTISING FASCITIS It is spreading inflammation of the skin, deep fascia and soft tissues with extensive destruction, toxaemia. Types;  Type 1-lt is due to mixed infection  Type 11- lt is due to Strep Pyogenes, usually due to minor trauma like abrasions.  Occurs in immunocompromised patients  Often diabetic, alcoholics or intravenous drug abusers  Occurs at several characteristic sites  Limbs after cuts, abrasions or bites  Around postoperative abdominal surgical wounds  In the perineum secondary to anorectal sepsis  In the male genitalia (Fournier's gangrene) • Polymicrobial infection involving the following:  Facultative aerobes  Streptococcal species or E. coli  Anaerobes  Exotoxins produce severe systemic toxicity Clinical features  Often presents similar to cellulitis  Warning features include o Severe pain - out of proportion to the clinical signs o Severe systemic toxicity o Cutaneous gangrene o Hemorrhagic fluid leaking from a wound MANAGEMENT • Requires high clinical suspicion and early diagnosis • Patients should be managed in high dependency unit • Need fluid resuscitation and organ support • Early surgical debridement is essential
  24. 24. bbinyunus2002@gmail.com Page 24 • Requires excision well into apparently normal tissue • Amputation or fasciotomies may be required • Defunctioning colostomy may be required for perineal sepsis • Antibiotic cover should include benzylpenicillin, metronidazole and gentamycin • Hyperbaric oxygen therapy may be of benefit. NOSOCOMIAL INFECTION (Hospital Acquired Infection) It is an infection acquired because of hospital stay. SOURCES • Contaminated infected wounds. • Urinary tract infection. • Respiratory tract infection. • Opportunistic infections. • Abdominal wounds with severe sepsis spreading can occur from one patient to another, through nurses or hospital staffs who fail to practice strict asepsis. It is more common in • Diabetics • Immunosuppressive individuals • Patients on steroid therapy a nd life-Supporting machines • Instrumentations (indwelling catheter, IV cannula, tracheostomy tube) • Patients with artificial prosthesis ORGANISMS  Staphylococcus aureus is the commonest organism causing hospital acquired wound infection. Others are Pseudomonas, Klebsella, E. coli, Proteus,  Strept. pneumo, Haemophilus, Herpes,Varicella, Aspergillus, Pneumocystis carinii are the commonest pathogens involved in hospital acquired respiratory tract infection which spreads through droplets.  Klebsiella is the commonest pathogen involved in hospital acquired UTI which is highly resistant to drugs.
  25. 25. bbinyunus2002@gmail.com Page 25 MANAGEMENT Most of the time, organisms involved are multidrug resistant, virulent and hence, cause severe sepsis. • Antibiotics. • Isolation. • Blood, urine, pus for culture and sensitivity to isolate the organisms. • Blood transfusion, plasma or albumin therapy. • Ventilator support. • Maintaining optimum urine output. • Nutritional support. PREVENTION • Isolation of patients with bodly infected open wounds, severe RTI/UTI. • Following strict aseptic measures in out and in ward by hospital attendants. • Proper cleaning and use of disinfectant lotions and sprays for bedpans, toilets and floor. • The precipitating causes has to be treated, along with caring for proper nutrition and improving the anaemic status by blood transfusion.
  26. 26. bbinyunus2002@gmail.com Page 26 WOUND AND WOUND HEALING Wound is a break in the integrity of the skin or tissues often which may be associated with disruption of the structure and function. CAUSES o Mechanical agents o Chemical agents o Radiation energy o Pathogenic micro-organism TYPES /CLASSIFICATION  Close- intact epithelial surface o Contusion or bruise: injury to tissue subadjacent to surface epithelium usually by blunt trauma. A subcutaneous hematoma > 1cm is Ecchymosis o Hematoma: is a localized collection of blood outside the blood vessels, liquid or clotted within the tissue.  Open- break or disruption of skin or epithelium. o Incision; a wound created with sharp instrument usually during surgery o Abrasion; loss of superficial layers of the epithelium o Laceration: irregular tear-like wounds caused by some blunt trauma or sharp instrument. o Avulsion; injuries in which a body structure is forcibly detached from its normal point of insertion. May be complete (no connection between the injured and its original site) or partial (tenuous or strands of tissue connect the tissue to site) o Puncture: caused by pointed instrument with small entry e.g. nail puncture o Penetrating or perforating ; penetrating wounds enter a body cavity such as the chest or abdomen perforating wounds entirely pass through an organ or cavity and are characteristic of firearms or missile injuries. o Amputation; o Gunshot; caused by a bullet or similar projectile driving into or through the body. There may be two wounds, one at the site of entry and one at the site of exit.
  27. 27. bbinyunus2002@gmail.com Page 27 RANK AND WAKEFIELD CLASSIFICATION o Tidy wounds o Incised o Clean o Healthy tissues o Seldom tissue loss o Untidy wounds o Crushed or avulsed o Devitalised tissues o Contaminated o Often tissue loss SURGICAL WOUNDS (see page 7) o Clean o Clean contaminated o Contaminated o Dirty ACUTE AND CHRONIC WOUNDS Acute wounds heal in a predictable manner and time frame. The process occurs with few, if any, complications, and the end result is a well-healed wound. A chronic wound is a wound that does not heal in an orderly set of stages and in a predictable amount of time the way most wounds do; wounds that do not heal within three months are often considered chronic. E.g. chronic leg ulcer SIMPLE OR COMPLEX WOUND In simple wounds, only skin is involved. Complex wounds, vessels, nerve, tendons, or bones are involved. WOUND MANAGEMENT (acute wound) o History – timing, cause, type of injury, nature of force o Examination – site, size, shape and depth, involvement of neighboring structures o Initial resuscitation may be required o Primary closure depends on the time of presentation; presentation within the “Golden hours”- 6-8hours are primarily sutured otherwise delayed.
  28. 28. bbinyunus2002@gmail.com Page 28 TREATMENT PROCEDURE o Debridement o Strict asepsis o Wound closure o Gentle tissue handling o Minimize blood loss o General measures o Tetanus prophylaxis o Immobilization and elevation o Broad spectrum bactericidal antibiotics WOUND HEALING Wound healing is the process by which damaged tissues of the body are repaired by living tissue. It is a natural restorative response to tissue injury. PHASES o HEMOSTASIS AND INFLAMMATORY o Hemostasis precedes and initiates inflammation, with the ensuing release of chemotactic factors from the wound site. o Exposure of subendothelial collagen to platelets results in platelet aggregation, degranulation, and activation of the coagulation cascade. Platelet -granules release a number of wound-active substances, such as platelet-derived growth factor (PDGF), transforming growth factor beta (TGF-b), platelet-activating factor (PAF), fibronectin, and serotonin. There is also release of basic fibroblast growth factor(b-FGF) and epidermal growth factor (EGF), VEGF, IGF-1. o The process;  Start immediately after wounding and last 4-6days  1st vasoconstriction  2nd blood clot formation  3rd platelet aggregation  4th platelet degranulation- growth factors release, serotonin and other chemo-attractants  5th vasodilatation- plasma,plasma proteins, C5a and C3a are poured into the wound  6th chemotaxis
  29. 29. bbinyunus2002@gmail.com Page 29  Granulocytes -1st 48hrs, attracted by inflammatory mediators  Monocytes –attracted by compliment, activated by fibrin, hypoxia, acidosis, foreign body. Reach maximum at 24hrs and last for weeks.  Macrophage- 3rd day. Activated macrophage are essential for proliferation, mediate angiogenesis, o DESTRUCTIVE PHASE (DEMOLITION)  Immediately follows inflammatory phase  There is removal of dead and dying tissues from the wound  Neutrophils and monocytes migrate into the wound kill bacteria, monocytes converts to macrophage.  The inflammatory and destructive phases are the LAG phases during which wound has no tensile strength. A preparation phase, where foundation of repair is laid down . 4-6days may be prolonged by infection. o PROLIFERATIVE (COLLAGEN OR FIBROBLASTIC PHASE)  Tensile strength of wound increase. Rapidly from 1-6weeks and slowly upto a year.  1st angiogenesis  2nd fibroblast formation  3rd formation of granulation tissue  4th re-epithelialization o REMODELING (MATURATION PHASE)  Start from weeks to years  Blood vessels starts to disappear(endarteritis obliterans)  The fibroblasts starts to disappear  Type III collagen is gradually been replaced by type I  Tensile strength of scar gradually increase TENSILE STRENGHT OF A WOUND; the capacity of the cut edge of a wound to hold together and resist disruption. Very slight in the lag phase(4-6days) bridge only by epithelium. It rises sharply to with peak rate at 14-15th day corresponds to fibroplasia in the wound. After 15th day, the tensile strength but at slower rate after 6th weeks, for a year. Attains 50% of pre-injury state at 3years. Lag phase of rectus sheeth is 7days. Increases steeply for 3months, then more gradually for 1 year.
  30. 30. bbinyunus2002@gmail.com Page 30 COLLAGEN; structural proteins in the extracellular space synthesis by fibroblast. Tropocollagen is the procollagen molecule. Helical structure with glycine at every third position, hydroxyproline(most abuntant) and hydroxylysine. Vitamin C is required in the hydroxylation of proline and lysine. Copper is required to hydroxylate lysine. The 4 common types; I, II, III, IV seen predominantly in ‘SCAB’ (skin, connective tissues or cartilage, arteries and basement membrane) respectively. TYPES OF WOUND HEALING Healing by primary intention Healing by secondary intention Healing by tertiary intention Healing by primary intention  Wound edges opposed.  Normal healing.  Minimal scar  Healing In a surgically incised wound ■ By secondary intention  Wound left open.  Heals by granulation, contraction and epithelialisation  Increased inflammation and proliferation  Poor scar  Healing in a wound with much tissue loss. ■ By tertiary intention  also called delayed primary intention  Wound initially left open(4-5days)  Edges later opposed when healing conditions favourable  Heavily contaminated wound
  31. 31. bbinyunus2002@gmail.com Page 31 FACTORS AFFECTING WOUND HEALING Systemic  Age  Malnutrition  Trauma  Metabolic diseases  Immunosuppression  Connective tissue disorders  Smoking  Medications; Steroids, cytotoxic. Local  Mechanical injury  Infection  Edema  Ischemia/necrotic tissue  Topical agents  Ionizing radiation  Low oxygen tension  Foreign bodies  Site of the wound; pressure, repeated movement COMPLICATIONS OF WOUND HEALING  Wound infection, septicaemia.  Chronicity  Abnormal scars: hypertrophic scar, keloid.  Contracture  hyperpigmentation  Implantation cyst  Neoplastic change  Weak scar  Cicatrization
  32. 32. bbinyunus2002@gmail.com Page 32 DIFFERENCE BETWEEN KELOID AND HYPERTROPHIC SCAR KELOID HYPRETROPHIC SCARS Genetic predisposition yes no Site of occurrence chest wall, upper arm anywhere in the body, ears, lower neck common in flexure areas Growth continues to grow without growth limits for 6 month time limit, goes beyond scar limit to scar tissue only. and extends to normal skin. Treatment poor response good response to steroid Recurrence very high uncommon Collagen synthesis 20 times more than normal 6 times than normal skin skin,(type III thick ) (type III fine collagen) Age adolescence and middle children age Sex commoner in females equal in both sex Race more in blacks (15 times) no racial relation Structure Thick collagen with increased Fine collagen with epidermal hyaluronic acid increased alpha actin Size of injury no relation, small healed scar related to size of injury and can form large keloid duration of healing. WOUND DEHISCENCE. The partial or total disruption of any or all layers of the operative wound. Define evisceration. Rupture of the abdominal wall and extrusion of the abdominal viscera. FACTORS THAT PREDISPOSE TO DEHISCENCE  Age > 60 years,  obesity and increased intra-abdominal pressure,  malnutrition,  renal or hepatic insufficiency,
  33. 33. bbinyunus2002@gmail.com Page 33  diabetes mellitus, use of corticosteroids or cytotoxic drugs, and radiation have been implicated in wound dehiscence.  Infection also plays an important role; an infective agent is identified in more than half of wounds that undergo dehiscence.  Despite these excuses, the most important factor in wound dehiscence is the adequacy of closure. Fascial edges should not be devitalized. Ideally the linea alba sutures should be placed neither too laterally nor too medially. Excessive lateral placement may incorporate the variable blood supply of the rectus abdominis muscle and compromise fascial circulation. Excessive medial placement misses the point of maximal strength at the transition zone between the linea alba and rectus abdominis sheath. In addition, sutures should be tied correctly without excessive tension, and suture material of adequate tensile strength should be chosen. WHEN DOES WOUND DEHISCENCE OCCUR It may occur at any time after surgery; however, it is most common between the 5th and 10th postoperative days, when wound strength is at a minimum. SIGNS AND SYMPTOMS OF WOUND DEHISCENCE  Normally a ridge of palpable thickening (healing ridge) extends about 0.5 cm on each side of the incision within 1 week. Absence of this ridge may be a strong predictor of impending wound breakdown.  More commonly, leakage of serosanguineous fluid from the wound is the first sign.  In some instances, sudden evisceration may be the first indication of abdominal wound dehiscence.  The patient also may describe a sensation of tearing or popping associated with coughing or retching. MANAGEMENT OF WOUND DEHISCENCE.  If the dehiscence is not associated with infection, elective reclosure may be the appropriate therapeutic course.  If the condition of the patient or wound makes reclosure unacceptable, however, the wound should be allowed to heal by second intention. An unstable scar or incisional hernia may be dealt with at a later, safer time.  Dehiscense of a laparotomy wound with evisceration is a surgical emergency with a reported mortality of 10-20%.
  34. 34. bbinyunus2002@gmail.com Page 34 o Initial treatment in this instance consists of appropriate resuscitation while protecting the eviscerated organs with moist towels; o the next step is prompt surgical closure. Exposed bowel or omentum should be lavaged thoroughly and returned to the abdomen o The abdominal wall should be closed; and the skin wound should be packed open. Vacuum-assisted wound closure may be valuable in select cases.
  35. 35. bbinyunus2002@gmail.com Page 35 SUTURES AND SUTURE MATERIALS DEFINITION A suture is a strand of material use in approximation of wound edges or ligation of blood vessel. PROPERTIES OF AN IDEAL SUTURE • Adequate tensile strength • Good knot holding property • Should be least reactive (inert) • Easy handling property • Should have less memory • Should be easily available and cost effective CLASSIFICATION  Absorbable (natural or synthetic) These are broken down in the body and eventually absorbed by digestion by lysosomal enzyme of white blood cells or by hydrolysis (synthetic absorbable sutures).  Non-absorbable (natural or synthetic) They effectively resists enzymatic digestion. They are used in tissues that heal more slowly, or if a very secure tightening is required. They are either left in the body, where they become embedded in the scar tissue, or they are removed when healing is complete. NATURAL ABSORBABLE o Catgut o Plain catgut is derived from submucosa of jejunum of sheep. o - It is yellowish white in colour. o - It is absorbed by inflammatory reaction and phagocytosis-absorption time is 7 days. o - It is used for subcutaneous tissue, muscle, circumcision in children. Chromic catgut is catgut with chromic acid salt.
  36. 36. bbinyunus2002@gmail.com Page 36 - It is brown in colour. - Its absorption time is 21 days. - It is used for suturing muscle, fascia, external oblique aponeurosis, ligating pedicles, etc. o Collagen This is produced from the collagen fibers from the bovine flexor tendon in both plain and chromic form, and can be applied in the same fields as surgical gut. SYNTHETIC ABSORBABLE o Polyglycolic acid o Dexon (Polyglycolic acid) is synthetic absorbable suture material like vicryl. It is creamy yellow in colour (braided). o It has an excellent tensile strength (remaining unchanged for about 3 weeks) and excellent knot security. It is completely absorbed in 60-90 days. o Polyglactin o Vicryl (Polyglactic acid): o - It is synthetic absorbable suture material. o - It gets absorbed in 90 days. o - Absorption is by hydrolysis. o - It is violet in colour (braided). o - It is multifilament and braided. o - It is very good suture material for bowel anastomosis, o suturing muscles, closure of peritoneum. o Poly-p-dioxanone o PDS (Poly Dioxanone Suture material) is absorbable suture material. o It is creamy in colour with properties like vicryl. o It is costly but better suture material than vicryl. o The tensile strength on day 14 is 70%. Absorption is minimal up to 90 days, but complete within 6 months. o Maxon (Polyglyconate) monofilament. o Monocryl (Polyglecaprone) monofilament. o Biosyn (Glycomer) monofilament NATURAL NON-ABSORBABLE o Silk o Silk is natural, multifilament, braided, non-absorbable suture material derived from cocoon of silkwormlarva. It is black in colour. It is coated suture material to reduce capillary action.
  37. 37. bbinyunus2002@gmail.com Page 37 o Linen o This is a twisted thread, which is weaker than silk; however, it is straightened when wet. Therefore, it must be dipped into saline solution before use. o Cotton o This is made from twisted cotton fibers. It should also be dipped into saline solution. o Stainless steel o This causes almost no tissue reaction. It is manufactured in monofilament and twisted forms. o It is rarely used because it is difficult to handle, it may break up and it can easily cut tissues. SYNTHETIC NON-ABSORBABLE o Polyesters o They give the strongest sutures, apart from surgical steel. o monofilament (Miralene or Mirafil) o braided, either uncoated (Dacron, Mersilene or Dagrofil), or coated with Teflon (Ethiflex or Synthofil) o Polyamide (Nylon) o Its tensile strength for 1 year is 80%, for two 2 years is 70% and for 11 years 66% and it causes only a minimal inflammatory response. o Polypropylene o Polypropylene (Prolene) is synthetic, monofilament suture material. o It is blue in colour. o It has got high memory. (Memory of suture material is recoiling tendency after removal from the packet. Ideally suture material should have low memory.) (Prolene mesh used for hernioplasty is white in colour). o it causes only a minimal tissue reaction, it has a high tensile strength (100% for 2 years) and it holds knots better than most other synthetic materials. o It can also be applied in infected fields. NUMBERING OF SUTURE MATERIAL 2-Thick. For pedicle ligation. 1- 0-zero. 1-zero. 2-zero. For bowel suturing. 3-zero. 4-zero. 5-zero. For vascular anastomosis.
  38. 38. bbinyunus2002@gmail.com Page 38 6-zero. 7-zero. 8-zero. 9-zero. For ophthalmic surgery. Requires operating microscope. TYPES OF SUTURING Interrupted o Simple o Vertical mattress o Horizontal mattress Continuous o Simple o Locked o Subcuticular o Purse-string TYPES OF KNOT Reef knot or Viennese knot Granny knot Surgeons knot
  39. 39. bbinyunus2002@gmail.com Page 39 CUTENEOUS ULCERS ULCER is a sustained breach in the continuity of the surface epithelium- skin and mucous membrane. PARTS 1. Margin the line of demarcation between the ulcer and the intact skin. o Healing margin shows typical bluish line of growing epithelium which is squamous without cornification. Margin of a healing ulcer shows 3 zones  Outer –white  Intermediate – blue  Inner – red o Spreading ulcer margin shows irregular in malignant and inflamed in infected. o Chronic non-healing ulcer shows fibrous thick white margin without the bluish growing epithelium. (NB; margin commonly stated in conventional books) 2. Edge is the mode of union between the floor and the margin of the ulcer.  Slopping –healing, venous ulcers.  Punched out – trophic ulcers eg syphilitic  Undermined – tuberculous  Raised – rodent or basal cell ca.  Everted – squamous cell ca. 3. Floor the exposed surface of the ulcer. i.e the part which can be seen within the edge of the ulcer.  Healing ulcer shows pink or red granular granulation tissue  Chronic ulcer shows pale flat and smooth granulation tissue  Infected ulcer shows unhealthy granulation tissue- contains slough.  Tuberculous ulcer has afloor with watery or apple jelly granulation tissue  A floor may also show hypertrophic granulation tissue- sprouting flesh. 4. Base the area on which the ulcer rest. The base is palpated through the floor of the ulcer for;  Mild induration may be felt in any chronic ulcer  Marked induration is almost diagnostic of malignant ulcer  Mobility of the ulcer over the underlying structure CLASSIFICATION Specific Non-specific Malignant
  40. 40. bbinyunus2002@gmail.com Page 40 SPECIFIC ULCERS They are caused by specific organisms e.g. mycobacterium ulcerans bacilli, treponema pallidum or Pertenue. The edge is characteristic for each type.  Tropical ulcers; synergistically by the anaerobic Fusobacteria (Bacteriodes fusiformis) and the aerobic Borrelia vincenti. Commoner in males, risk factors include malnutrition, walking bare-footed. Over 95% occur in the lower part of the leg. Organisms are transmitted by flies.  Tuberculous; mycobacterium tb  Burili ; mycobacterium ulcerans  Syphilitic; (gummatous ulcer); Treponema pallidum  Yaws; Treponema pertenue (NB; see text for details of specific ulcers ) NON- SPECIFIC They have essentially the same feature of a sloping edge, but the underlying aetiologies are varied. They are the commonest ulcers. 1. Traumatic ulcers. 2. Pyogenic ulcers. 3. Ulcers of vascular origin: (i) Venous (gravitational) ulcers. (ii) Arterial ulcers. (iii) Decubitus ulcers. (iv) Pressure sores. 4. Neurotropic (trophic) ulcers: (i) Leprosy. (ii) Diabetic neuropathy. (iii) Cord lesions. (iv) Peripheral neuropathies. (v) Syringomyelia. 5. Ulcers associated with metabolic or systemic disease: (i) Diabetic ulcers. (ii) Haemoglobinopathic ulcers. (iii) Ulcers of spherocytosis. (iv) Ulcers of ulcerative colitis. MALIGNANT ULCERS  Squamous cell ca  Malignant melanoma  Basal cell ca  Kaposi sarcoma  Penetrating malignant tumour
  41. 41. bbinyunus2002@gmail.com Page 41 PHASES A non- specific ulcer goes through the following phases I. Acute or infective phase / extension  In this the initial phase, the ulcer is painful  The sloughing floor is covered with purulent discharge in which different types of bacteria may be identified  Base is indurated and fixed  Surrounding skin is inflamed II. Transition phase  The slough separates, the pus drains,  infection subsides, granulation tissue grows and the floor becomes clean and pinkish-red.  The edge, which is sloping, has a thin bluish-white layer of young epithelium growing inwards.  The surrounding skin is slightly hyperaemic or nonnal.  Induration diminish III. Reparative or healing phase  The ulcer is now painless.  The healthy granulation tissue fills the floor and the epithelium grows from the edge at the rate of 1 mm/day to cover the floor. IV. Chronic, indolent or callous phase  Some ulcers may enter a chronic phase and remain unhealthy for a long time because of secondary infection, defective circulation, poor general condition, foreign body, lack of rest, malignant transformation.  Unhealthy granulation tissue  Offensive discharge, indurated base ragged edge and inflamed surrounding skin. COMPLICATIONS OF NON-SPECIFIC ULCERS 1. Septicaemia 2. Lymphangitis 3. Lymphadenitis 4. Wasting 5. Tetanus 6. Lymphoedema:- Recurrent lymphangitis may lead to below-knee lymphoedema of varying degrees. 7. Periostitis: - When the ulcer is close to bone, periostitis occurs and if persistent may lead to new bone format ion at the base of the ulcer. 8. Malignant change:- Long-standing ulcers and unstable scars may undergo squamous carcinomatous change. 9. Deformities of the foot or ankle may occur if deep tissues are involved in the fibrosis.
  42. 42. bbinyunus2002@gmail.com Page 42 TREATMENT OF NON-SPECIFIC ULCERS 1. ACUTE ULCERS 1. In the acute phase, the patient is admined for bed rest and the footend of the bed elevated. 2 Wound swab is done for gram staining, culture and sensitivity of any organisms cultured. 3. Broad-spectrum antibiotics are started while awaiting the results of the culture and sensitivity tests. 4. Tetanus booster dose is given to prevent tetanus infection. 5. The wound is cleansed regularly with normal saline. Acetic acid is effective for cleansing wounds suspected infected with pseudomonas. 6. Crepe bandage is applied firmly from the toes to the knee to promote lymphatic and venous drainage. 7. The affected limb is splinted in the position of function to prevent formation of contracture. 8. Physiotherapy is started early to prevent wastage of muscle and contractures. 9. Once the ulcer becomes healthy, it is grafted with split skingrart. 10. Where there is an infected slough, appropriate antibiotics are started and the slough removed either with saline soaks or by sloughectomy i.e. surgical excision of the slough. The wound is then cleansed regularly until healthy granulation tissue is formed. A wound swab is then taken for culture to rule out streptococcal infection before grafting with split skin. 2. CHRONIC ULCERS These ulcers may be excised and then grafted with split-skin graft or covered with a flap. 3. ADVICE AFTER DISCHARGE  The patient is advised on foot hygiene.  He is advised to use pressure dressing from the toes to the knee to promote lymph and venous drainage where there is excessive scarring.  Farmers are advised to wear protective clothing and boots.  The patient should seek prompt treatment for any abrasion to the affected limb. DIFFERENTIAL DIAGNOSIS OF AN ULCER The diagnosis is arrived at after: 1. Careful history. 2. Clinical examination and 3. Investigations. HISTORY Mode of onset Duration Pain Progress of the ulcer: Painful regional lymph lIodes Symptoms or past history suggestive of; Diabetes
  43. 43. bbinyunus2002@gmail.com Page 43 Tuberculosis DVT Varicose vein Haemoglobinopathy Neuropathy Yaws Syphilis EXAMINATION a. The ulcer  Number  Site  Size  Shape  Edge  Floor  Base  Discharge  Surrounding skin  State of local circulation  Arterial pulsation of the limb  State of innervation  Regional lymph node b. General physical examination INVESTIGATIONS I. Urine - for sugar and albumin. 2. Blood , (i) V.D.R.L. for syphilis. (ii) Sugar level for diabetes mellitus (iii) Haemoglobin genotype for haemoglobinopathy . (iv) Haemoglobin level to exclude anaemia. (v) Plasma protein levels (vi) Mantoux test. (vii) E.S.R. 3. Bacteriology of the ulcer - for special organisms;Mycobacteria, Fusobacteria, Borrelia 4. Radiology: (i) Plain films of ulcer to see any bony changes or calcification. (ii) Duplex Doppler scanning, arteriography or venography for vascular disorders. (iii) Plain films of the chest should be done also if tuberculosis or malignancy is suspected. 5. Biopsy of ulcer - may be the final step in definitive diagnosis. 6. Other tests may be done as indicated by the probable cause of the ulcer e.g. Lepromin test in suspected leprosy.
  44. 44. bbinyunus2002@gmail.com Page 44 FLUID AND ELECTROLYTES Fluid and electrolyte management is paramount to the care of the surgical patient. Changes in both fluid volume and electrolyte composition occur preoperatively, intraoperatively, and postoperatively, as well as in response to trauma and sepsis. BODY FLUIDS TOTAL BODY WATER- (TBW); Water constitutes approximately 50 to 60% of total body weight. It is primarily a reflection of body fat. Lean tissues such as muscle and solid organs have higher water content than fat and bone. TBW depends on age, sex, obesity. It is lower in the aged and obese. Male – 60% body weight Female -50% . TBW--60% ICF40% ECF20%  Intravascular(plasma) 4%  Extravascular 16%  Transcellular 1%  Interstitial 15% TBW in full term neonate 75%, ECF 35%. The ratio of surface area to weight in neonate is larger with more insensible loss. In preterm, TBW is 95%. By the age of 2years, it is corrected to TBW 65%, ECF 20%. BODY ELECTROLYTE INTRACELLULAR; K+ 14Ommol/l the most important cation Na+ 8mmol/l Mg2+ 15mmol/l Phosphate 26mmol/l most important anions Protein 9mmol/l EXTRACELLULAR Na+ 135-145mmol/l most important cation Mg2+ 0.7-0.9mmol/l
  45. 45. bbinyunus2002@gmail.com Page 45 K+ 3.6-5.2mmol/l Cl- 95-105mmom/l Ca2+ 2.1-2.6mmol/l HCO3 - 24-29mmol/l 24HRS FLUID AND ELECTROLYTE REQUIREMENT IN THE TROPICS FLUID  LOSS Insensible loss 1700ml Urine 1500ml Faeces 200ml Total 3400ml  GAIN Endogenous production 200ml  NET 3200ml Surgical patient usually requires parenteral and not likely to pass stool, hence 24hrs requirement is 3000ml. for 10 C rise in temperature, 12% of daily requirement is added to compensate for water loss in sweating. ELECTROLYTE Na+ 130-140mmol/l Urine 114mmol/l Sweat 10-16mmol/l Faeces 10mmol/l K+ 60mm0l/l Urine 50mmol/l Faeces 10mmol/l Sweat – negligible As surgical patient is unlikely to pass stool, daily Na+ is 130mmol and K+ 50mmol. Energy should be replace since patient is on NPO, and body store of glycogen (400g ≈1600kcal) is used up in the 1st day of starvation, then 75-90% is provided from combustion of fat and protein. 100-150g of
  46. 46. bbinyunus2002@gmail.com Page 46 exogenous glucose is given to reduce gluconeogenesis to the minimum and acidosis prevented. 2L of 5% DW contains 100g of glucose. VitC100-200g essential for wound healing and scavenger of free radicals Bcomplex aids protein and CHO metabolisms. Other mineral and trace element are add prolong treatment DISTURBANCE OF FLUID BALANCE Extracellular volume deficit is the most common fluid disorder in surgical patients and can be either acute or chronic. Acute volume deficit is associated with cardiovascular and central nervous system signs, whereas chronic deficits display tissue signs, such as a decrease in skin turgor and sunken eyes, in addition to cardiovascular and central nervous system signs. The most common cause of volume deficit in surgical patients is a loss of GI fluids from nasogastric suction, vomiting, diarrhea, or enterocutaneous fistula. In addition, sequestration secondary to soft tissue injuries, burns, and intra-abdominal processes such as peritonitis, obstruction, or prolonged surgery can also lead to massive volume deficits. Dehydration is loss of water and electrolyte especially sodium. Acute dehydration is loss of ECF as in intestinal obstruction, peritonitis, diarrhea . in chronic dehydration, there is loss of both ECF and ICF as in GOO. There is loss of large amount of K+ . Shock ensues with ECF loss ≥ 3.5L Signs and Symptoms of Volume Disturbances System Volume Deficit Volume Excess Generalized Weight loss Weight gain Decreased skin turgor Peripheral edema Cardiac Tachycardia Increased cardiac output Orthostasis/hypotension Increased central venous pressure Collapsed neck veins Distended neck veins Murmur Renal Oliguria — Azotemia GI Ileus Bowel edema Pulmonary — Pulmonary edema Extracellular volume excess may be iatrogenic or secondary to renal dysfunction, congestive heart failure, or cirrhosis. FLUID AND ELECTROLYTE THERAPY Extracellular volume deficit leads to loss of fluid and electrolyte and the principle of correction is through  Correction of deficit
  47. 47. bbinyunus2002@gmail.com Page 47  Correction of ongoing loss  Maintainace fluid  Monitoring of treatment Parenteral solutions Commonly used are; 0.9% saline Na+ 154mmol Cl- 154mmol mOsmo 308 Ringer’s lactate Na+ 130mmol K+ 4mmol Ca2+ 4mmol Cl- 111mmol HCO3 - 27mmol mOsmo 273 full strength darrows Na+ 124mmol K+ 36mmol Cl- 104mmol HCO3- 56mmol mOsmo 320 4.3% glucose in 1/5 saline Na 30.8mmol Cl 30.8mmol Glucose 43g 5% dextrose water
  48. 48. bbinyunus2002@gmail.com Page 48 50g glucose Correction of dehydration (deficit) IV access secured, blood samples taken for U/ECr, PCV Crystalloid are started ; ringers lactate, N/S IL for 30-45min Pass urethral catheter, empty the urinary bladder, then monitor urine output Then re-assess patient, if parameters(PR,BP, urine output ) inadequate, repeat IV fluid IL over 30-45min, and reassess as appropriate upto 4L, then give frusemide. Otherwise if adequate, place on maintenance of 1L 8hrly. During resuscitation, the following parameters are checked for;  Hourly urine output 30-50ml/hr (0.5-1ml/kg/min)  Half-hourly P.R and BP  Skin tugor, moistness of tongue , fill of subcutaneous veins  Frequent auscultation of the lungs and monitoring of JVP to prevent overhydration or quickly diagnose and treat if occur.  CVP 10-15mmHg Maintenance With correction of deficit and patient is making adequate urine, PR,BP,CVP all within normal limit, patient is placed on daily maintenance. 1L 8hrly, 2L of 5%DW,1L of N/S and 3g of KCL added to the fluid. However, ongoing loss is taken into consideration and added to the total maintenance fluid. Ongoing loss Ongoing GI losses such as N-G tube drainage, drainage from enterocutenous fistulae, diarrhea, vomiting are estimated and added into maintenance fluid. Monitoring  Input –out put chart  Serum U/ECr must be checked daily and deficiency corrected,12hly for critically ill patient.  Reapeat Hb/PCV after rehydration and correct if depleted.  State of hydration assessed daily; urine output of ≥ 1000ml is indicative of good hydration  Monitoring for overload o Frequent auscultation o CVP
  49. 49. bbinyunus2002@gmail.com Page 49 ELECTROLYTE DISTURBANCE SODIUM HYPONATREMIA- serum sodium level of ≤130mmol/L. Manifest clinically when serum Na<125mmol/L Symptoms; Irritability, cerebral oedema – headache, vomiting and convulsion, pulmonary congestion, convulsion is seen in severe hyponatremia < 120mmol. Causes; vomiting or N-G aspiration, diarrhea, internal fluid shift, enterocutenous fistulae, excessive sweating, polyuria. Treatment ; IV normal saline. Treat the cause. In the presence of cerebral oedema, IV diuretics is given. HYPERNATREMIA Hypernatremia results from either a loss of free water or a gain of sodium in excess of water. Like hyponatremia, it can be associated with an increased, normal, or decreased extracellular volume. Types of Hypernatremla • Euvolemic (pure water loos) • Hypovolaemic (among the loss of water and sodium, more water is lost than sodium) • Hypervolaemic (both sodium and water gain but sodium gain is more than water gain). Hypernatremia could either be hypervolemic(caused either by iatrogenic administration of sodium-containing fluids, including sodium bicarbonate. Urine Na conc. > 20mEq/L), normovolemic(result from renal causes, including diabetes insipidus, diuretic use, and renal disease) or hypovolemic(nonrenal water loss from the GI tract or skin, although the same conditions can result in hypovolemic hypernatremia<20mEq/L) Management is restriction of saline and sodium. Treatment of pulmonary oedema. Correction is slowly to prevent cerebral oedema and hyperglycemia. N/S then 1/2strength saline and later 5% dextrose.
  50. 50. bbinyunus2002@gmail.com Page 50 POTASSIUM Normal value is 3.5-5.6mmol/L Hypokalemia Can occur suddenly in a diabetic coma patient treated with insulin and saline. Gradual loss is seen in; • Diarrhoea of any causes, villous tumour of the rectum, ulcerative colitis. • After trauma or surgery. • Pyloric stenosis with gastric outlet obstruction. • Duodenal fistula, ileostomy. • After uretero sigmoidostomy. • Insulin therapy. • Poisoning. • Drugs like beta agonists Clinical Features • Slurred speech. • Muscular hypotonia. • Depressed reflexes. • Paralytic ileus. • Weakness of respiratory muscles. • Cardiac arrhythmias. • Inability to produce concentrated urine and so causes nocturia and polyuria. ECG shows prlonged QT interval, depression of the ST segment and inversion of T wave, prominent U wave, ectopic beats. Often hypokalaemia is associated with alkalosis. Serum potassium will be decreased. Treatment o Deficit ×weight ×0.6 o Using KCl in 5% dextrose or N/S slowly under ECG monitoring o Patient making adequate urine o Not > 20mmol/hr o Not > 40mmol/L o Not >120mmol/day o Not given in bolus. HYPERKALEMIA Serum K+ > 6mmol/L Causes:
  51. 51. bbinyunus2002@gmail.com Page 51 o Trauma o Burns o Sepsis o Shock o Acidosis o Massive transfusion of old blood o Excessive supplement o Drugs : K sparing diuretics, ACE inhibitors, Aminoglycoside Clinical features o Nausea, vomiting, diarrhea, muscle weakness ECG; o peak T wave, o absent P wave, o widened QRS, o ventricular arrhythmias, o fibrillation, cardiac arrest. Treatment o Under ECG monitoring o Sodium bicarbonate 80-100mmol over 10min to combat acidosis o 10% calcium gluconate to prevent cardiac arrest o Glucose under influence of insulin uses K to form glycogen; 10IU of soluble insulin in 1L of 5%dextrose is given IV or 100ml of 20% dextrose in 30min o Ion exchange resin, calcium resonium 15-30mg 6hly or 30g rectally is given to exchange Ca for K. o Β-2 agonist eg neubulised or IV salbutamol increase uptake of K o Hemodialysis or peritoneal dialysis. HYPERMAGNESAEMIA It is rare. Serum magnesium > 2.5 mEq/L Causes • Advanced renal failure treated with magnesium containing antacids, diabetic ketoacidosis. • Intentionally produced hypermagnesaemia while treating pre-eclampsia.
  52. 52. bbinyunus2002@gmail.com Page 52 Clinical Features • l.oss of tendon reflexes (commonest). • Neuromuscular depression. • Flaccid quadriplegia. • Respiratoty paralysis. • Somnolence. • Hypotension. HYPOMAGNESAEMIA • Serum magnesium< 1.5 mEq/L Causes o Malnutrition, alcohol. o Large GI fluid loss. o Patients on total parenteral nutrition. Clinical Features o Hypereflexia. o Muscle spasm. o Parasthesia. o Tetany. It mimics hypocalcaemia. It is often associated with hypokalaemia and hypocalcaemia. Two gram (16 mEq) of magnesium sulphate slow intravenously, in 10 minutes. Later maintenance dose of 1 mEq/kg/ day as slow continuous infusion is given/ oral magnesium is needed. CALCIUM The vast majority of the body's calcium is contained within the bone matrix, with <1% found in the ECF. Serum calcium is distributed among three forms: protein found (40%), complexed to phosphate and other anions (10%), and ionized (50%). It is the ionized fraction that is responsible for neuromuscular stability and can be measured directly. When total serum calcium levels are measured, the albumin concentration must be taken into consideration: Adjust total serum calcium by 0.8mg/dl for every 1g/dl decrease in serum albumin
  53. 53. bbinyunus2002@gmail.com Page 53 Unlike changes in albumin, changes in pH will affect the ionized calcium concentration. Acidosis decreases protein binding, thereby increasing the ionized fraction of calcium. Daily calcium intake is 1 to 3 g/d. Most of this is excreted via the bowel, with urinary excretion relatively low. Total body calcium balance is under complex hormonal control, but disturbances in metabolism are relatively long term and less important in the acute surgical setting. However, attention to the critical role of ionized calcium in neuromuscular function often is required HYPERCALCEMIA Hypercalcemia is defined as a serum calcium level above the normal range of 8.5 to 10.5 mEq/L (2.2- 2.6mmol/L)or an increase in the ionized calcium level above 4.2 to 4.8 mg/dL. Primary hyperparathyroidism in the outpatient setting and malignancy in hospitalized patients, from either bony metastasis or secretion of parathyroid hormone–related protein, account for most cases of symptomatic hypercalcemia. Anorexia, nausea/vomiting, abdominal pain, Weakness, confusion, coma, bone pain, Hypertension, arrhythmia, polyuria, Polydipsia ECG changes in hypercalcemia include shortened QT interval, prolonged PR and QRS intervals, increased QRS voltage, T-wave flattening and widening, and atrioventricular block (which can progress to complete heart block and cardiac arrest). Treatment ; initial therapy – fluid and diuretics, bisphosphonate and calcitonin. Treatment of the underlying cause. HYPOCALCEMIA Hypocalcemia is defined as a serum calcium level below 8.5 mEq/L or a decrease in the ionized calcium level below 4.2 mg/dL. The causes of hypocalcemia include; o pancreatitis, o massive soft tissue infections such as necrotizing fasciitis, o renal failure, o pancreatic and small bowel fistulas, o hypoparathyroidism, o toxic shock syndrome, o abnormalities in magnesium levels, o tumor lysis syndrome o malignancies associated with increased osteoclastic activity eg breast and prostate ca. o massive blood transfusion with citrate toxicity. Asymptomatic hypocalcemia may occur when hypoproteinemia results in a normal ionized calcium level. Conversely, symptoms can develop with a normal serum calcium level during alkalosis, which decreases ionized calcium. neuromuscular and cardiac symptoms do not occur until the ionized fraction falls below 2.5 mg/d.
  54. 54. bbinyunus2002@gmail.com Page 54 paresthesias of the face and extremities, muscle cramps, carpopedal spasm, stridor, tetany, and seizures. Patients will demonstrate hyperreflexia and may exhibit positive Chvostek's sign (spasm resulting from tapping over the facial nerve) and Trousseau's sign (spasm resulting from pressure applied to the nerves and vessels of the upper extremity with a blood pressure cuff).Hypocalcemia may lead to decreased cardiac contractility and heart failure. ECG changes of hypocalcemia include prolonged QT interval, T- wave inversion, heart block, and ventricular fibrillation. FLUID AND ELECTROLYTE IN; BURNS TYPHOID PERFORATION GASTRIC OUTLET OBSTRUCTION PANCREATITIS BURNS Hyponatremia : Hyponatremia is a result of decreased sodium in the blood from the destroyed tissue caused by burns on the body. Hyperkalemia; Hyperkalemia happens to burn victims as a result of the destruction of cells and tissues. TYPHOID PERFORATION Perforation is usually preceded by diarrhoea with considerable loss of potassium (20-40mmol/L) and limited intake of food. With perforation, paralytic ileus occurs with loss of more potassium in the accumulating intestinal secretions. The peritoneal exudate. which may be 2-3litres, also has increased Concentration of potassium- 10mmol/L Vomiting also causes loss of more potassium (9 mmol/L). The potassium deficit is therefore considerable although it may be masked by dehydration. This deficit should be corrected pre-operatively as soon as urine output has improved with vigorous fluid therapy. Otherwise, cardiac arrhythmias and even death on the table may result. GASTRIC OUTLET OBSTRUCTION Both E.C F. and I.C. F. are lost. Hydrogen and chloride ions are also lost. Potassium is lost not only in the vomitus but also in large amounts from the kidney as a result of increased aldosterone secretion to conserve sodium. The patient therefore has hyponatraemia, severe hypokalaemia, hypochloraemia and metabolic alkalosis in addition to water depletion. He needs dextrose saline or saline and potassium chloride later.
  55. 55. bbinyunus2002@gmail.com Page 55 PREOPERATIVE FLUID THERAPY A surgical patient without deficit, preoperatively are on NPO and hence placed on daily maintenance fluid; 3L in adult surgical patient as seen above. This is form of 2L of 5%D/W and 1L of N/S and 3g of KCl if making adequate urine. Fluid and electrolyte deficit if present is corrected before placing on maintenance. Alternatively fluid maintenance is given as; For the first 0 to 10 kg Give 100 mL/kg per day For the next 10 to 20 kg Give an additional 50 mL/kg per day For weight >20 kg Give an additional 20 mL/kg per day INTRAOPERATIVE FLUID THERAPY With the induction of anesthesia, compensatory mechanisms are lost, and hypotension will develop if volume deficits are not appropriately corrected before the time of surgery. Hemodynamic instability during anesthesia is best avoided by correcting known fluid losses, replacing ongoing losses, and providing adequate maintenance fluid therapy preoperatively. Blood loss is measured , the is third space loss. Although no accurate formula can predict intraoperative fluid needs, replacement of ECF during surgery often requires 500 to 1000 mL/hr of a balanced salt solution to support homeostasis. Maintaining acceptable vital signs and urine output. Redistributive and Evaporative Surgical Fluid Losses Degree of tissue trauma Additional fluid requirement Minimal (herniorapphy) 2 ml/kg/hr Moderate (cholecystectomy) 4 ml/kg/hr Severe (bowel resection) 6 ml/kg/hr POST OPERATIVE FLUID THERAPY Postoperative fluid therapy should be based on the patient's current estimated volume status and projected ongoing fluid losses. Any deficits from either preoperative or intraoperative losses should be corrected and ongoing requirements should be included along with maintenance fluids. In the initial postoperative period, an isotonic solution should be administered. COMPLICATIONS OF FLUID THERAPY Thrombophlebitis High osmolality
  56. 56. bbinyunus2002@gmail.com Page 56 Prolong use of same needle or cannula and vein Infection Leakage of fluid around the vein Endothelial injury Local sepsis Septicemia Overloading Air embolism Pyrogenic reaction
  57. 57. bbinyunus2002@gmail.com Page 57 SHOCK DEFINITION Shock is the clinical manifestation of failure of cellular function due to inadequate tissue perfusion and consequent cellular hypoxia resulting from a reduction in the effective circulating blood volume. It the most common cause of death amongst surgical patient. Hence every surgeon must understand the pathophysiology, diagnosis as well as priority in the management. CLASSIFICATION • Hypovolemic • Cardiogenic • Septic • Neurogenic • Anaphylactic Hypovolemic shock; There is reduction in the actual blood volume. It may result from Hemorrhagic (commonest)- could be internal or external bleeding Loss of plasma as occurs in extensive bums or peritonitis. Loss of Extracellular Fluid as occurs in intestinal obstruction, diarrhoea, peritonitis and vomiting Cardiogenic shock; Impaired function of the heart causes reduced cardiac output and so to reduced effective circulating blood volume. It is commonly due to myocardial infarction or contusion, cardiac tamponade, sepsis and obstruction to blood flow from the heart by massive pulmonary embolism or tension pneumothorax The other forms (septic, neurogenic and anaphylactic) of shock results from peripheral vasodilatation and pooling of blood resulting in reduction in effective circulating blood volume. Total spinal anaesthesia, spinal injury-vasovagal syndrome, are causes of neurogenic shock. PATHOPHYSIOLOGY The cellular changes; in shock, there is cellular hypoxia, leading to decrease ATP production (3ATP rather than 38) resulting in decrease efficacy of Na-K pump, with subsequent leakage of K out cells and movement of Na into the cells along with water and the cells swell. The concentration of cyclic AMP falls and the affect the actions of hormones on cell. With further reduced energy production, there is release of lysosomal enzymes and proteases with causes lysis of the cell with inflammatory responses.
  58. 58. bbinyunus2002@gmail.com Page 58 The stages of shock; the stages are illustrated using haemorrhagic shock Early stage; The average adult person has 4-5L of blood (75-80ml/kg) and 25 per cent (1000ml) must normally be lost before shock appears. With blood loss, there is stimulation of the baroreceptors which in turns sends inhibitory stimulus to the cardio-inhibitory (a center that reduces the activity of the heart, via reduced vagal activity) center and the vasomotor center (increases sympathic out flow via adrenaline release). There is subsequent vasoconstriction, increase venous return, increase heart rate and contraction, and bronchiolar relaxation. Middle stage; with continued bleeding or inadequate resuscitation, there is diversion of blood from peripheral and splanchnic to vital organs (heart and brain). Reduction of renal perfusion leads to release of renin from the juxaglomerular cells which causes conversion of angiotensinogen to angiotensin I, this is further converted in the epithelium of the lungs to angiotensin II. Angiotensin II – causes vasoconstriction, release aldosterone which causes reabsorption of sodium and water, release of ADH, stimulates thirst center, stimulates sympathetic out flow. Splanchnic vasoconstriction causes mucosal ischemia, with depression of the barrier and bacterial transmigration into the systemic circulation. (link between hemorrhagic and septic shock) Late stage; the stage of decompensation. Compensatory mechanisms break down and the circulation fails. Further blood loss reduce coronary and cerebral perfusion. There is cardiac failure, venous pooling of blood, capillary damage from back pressure and impaired cerebral function resulting in confusion, restlessness, coma and death. CLINICAL FEATURES 1. Rapid, weak and thready pulse 2. Low or unrecordable blood pressure 3. Skin and mucous membrane is cold and clammy (except in distributive shock where skin is warm). Mucous membrane is pale, cyanotic and collapse 4. Rapid and deep respiration (air hunger) 5. Confused, restless, apathetic or comatose, blurred vision 6. Decrease Urine output or anuria 7. Severe thirst 8. Subnormal temperature 9. MODS MANAGEMENT OF A PATIENT IN SHOCK; Categories; a) Those who respond to treatment b) Those who respond and relapse c) Those who donot respond; a and b may require surgery to control bleeding
  59. 59. bbinyunus2002@gmail.com Page 59 Resuscitation; 1. Control bleeding 2. Elevate the foot of the bed 3. Fluid replacement; secure iv access with widebore cannula. Take samples for hemogram, GXM, U/ECr.  Crystalloid (readily available); 1L of N/S or R/L is started over 30-45min, the re- assess the PR, BP, urine output, CVP, if still deranged, repeat fluid up to 4L. (blood must have been ready- in hemorrhagic shock. Otherwise septic shock in non- hemorrhagic)  Blood; in severe blood loss, crystalloid shows only transient improvement. Blood is cross matched and transfused. Occasionally uncrossed matched blood is given to save life.  Blood substitute; in absent of blood, colloids; human albumin(most physiologic), fresh frozen plasma, dextran 110 or 70, haemacel, gelofusine, and hetastarch 4. Oxygen; oxygen supplements is given. Blood gases are monitored regularly and PO2 maintained between 80-100mmHg. If PO2 falls below 60mmHg and the PCO2 rises above 45mmHg, then ventilatory support is necessary. 5. Drugs  Morphine; if patient is in pains, may be given 10mg 1v  Vasodilators; after adequate fluid therapy, and normal CVP, but perfusion remains inadequate; i. Dobutamine; b-vasodilator, decreases pulmonary and systemic resistance thereby better blood flow and O2 delivery. ii. Isoproterenol; b-adrenergic; peripheral vasodilatation, increase force of contraction of the heart. iii. Dopamine; a precursor of nor-adrenaline, it acts on b1 and a-adrenergic receptors.  Hydrocortisone  Naloxone  Mannitol  Sodium bicarbonate MONITORING 1. CLINICAL a. Sensorium b. Skin; warm and vein refill c. Pink conjunctiva d. Capillary re-fill 2. Urine output > 30ml/h 3. PR and BP every 15min
  60. 60. bbinyunus2002@gmail.com Page 60 4. CVP normal 10-15 cmH2O 5. Lungs and jugular vein 6. Blood gases NON-HAEMORRHAGIC HYPOVOLEMIC SHOCK Extracellular (extravascular) fluid loss must be at least 6% of body weight to result into shock. That is 3600ml of ECF IRREVERSIBLE SHOCK Shock that does not respond to treatment. Causes; inadequate fluid replacement, continued blood loss, undetected organ injury, metabolic acidosis, myocardial failure, septic shock, MODS.
  61. 61. bbinyunus2002@gmail.com Page 61 SEPTIC SHOCK Results from moderate to severe sepsis or tissue damage. It is considered as part of a spectrum and a progression of SIRS (systemic inflammatory response syndrome). DEFINATION OF TERMS; Bacteremia : transient invasion of circulation by bacteria Septicemia: prolonged presence of bacteria in the blood accompanied by systemic reaction SIRS (systemic inflammatory response syndrome ): it is a syndrome characterized by the presence of two or more of the following clinical criteria:  Temperature(core) >38°C or<36°C  Heart rate >90beats/min  Respiratory rate >20b/min or PaC02 <32mmHg  WBC >12000cells/ml or <4000cells/ml or >10%immature band forms.  Sepsis: SIRS with a clearly established focus of infection  Severe sepsis: sepsis associated with organ dysfunction and hypoperfusion.  Septic shock: Refers to severe sepsis which is not responsive to intravenous fluid infusion for resuscitation and requires inotropic or vasopressor agent to maintain systolic blood pressure. EPIDEMIOLOGY 4.6 cases/1000 persons in a study in US. 200,000 cases annually with 50% mortality. M>F(most studies M=52-66%). Extreme of ages are more affected. 13th leading cause of death in US. Leading cause of death in ICU. AETIOLOGY BACTERIA: gram –ve nearly 2/3, gram+ve 1/3. of the gram –ve, E.coli is the commonest. GRAM -VE  Klebsiella,  Entrobacter,  Serratia,  Proteus,  Mirabillis/Vulgari,  Pseudomonas and  Bacteroides GRAM +VE  Streptococci
  62. 62. bbinyunus2002@gmail.com Page 62  Staph  Clostridia and Pneumococci Viruses, Fungi and Parasites in a few especially the immuno-compromised. SOURCE  Endogenous –  Skin- SSI  urinary tract- UTI  respiratory tract- LRTI  GIT- bowel surgery, perforations  Exogenous.  surgical instruments  drapes  imaging machines  staff RISK FACTORS  Age (<10 >70years)  malnutrition,  anemia,  Primary disease: Malignancies, DM, CLD, CRF,  Immunosuppression, Immunosupresssive agents,  necrotic tissue  hematoma  poor surgical technique  Catheriration  Prolong hospitalisation  Major surgeries, trauma, extensive burns PATHOGENESIS Micro-organisms or products of tissue damage stimulates production of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8) which in turn stimulate production of secondary mediators (PGI2, PGE2, TXA2, LT, PAF,NO, KININS, IL-1,IL-6, OXYGEN FREE RADICAL, PROTEASES.) of inflammation in order to localize infection and limit proliferation. The production of the pro-inflammatory cytokines is regulated to limit damage. However in poorly controlled sepsis or extensive tissue damage, there is excessive inflammatory response which is poorly regulated.
  63. 63. bbinyunus2002@gmail.com Page 63 Anti-inflammatory and immunosuppressive cytokines IL-10 which aided by IL-4 inhibits the activity of the pro-inflammatory cytokines to limit damage. In severe sepsis they become immunosuppressive to patient.
  64. 64. bbinyunus2002@gmail.com Page 64 Effects of secondary mediators  Damage of vascular endothelium  Vasodilation of microvasculature  Activation of neutrophils(aggravates endothelial damage)  Diminished force of cardiac contraction  These ultimately lead to peripheral pooling of blood, extravasation of fluid, hypotension, hypoxia EFFECT OF COPLIMENT COMPONENT  vasodilatation and increase permeability  Endothelial damage  C5a causes aggregation of platelet and leucocytes thereby acting as procoagulant leading to DICnd shock
  65. 65. bbinyunus2002@gmail.com Page 65 Pro-inflammatory cytokines reduces plasma levels of thrombomodulin, coagulation inhibitors like protein S, protein C, and ATIII. Microvascular coagulatio results which worsens DIC. Hence there is acute inflammation, vasculitis, haemorrhage, capillary thrombosis and necrosis are seen in several vital organs. Net effect:  Maldistribution of blood flow at microvasculature  Arteriovenous shuting O2 utilization  Interstitial loss effective vol. Hypovolemia  Myocardial depression CLINICAL FEATURES It could be in inn patients receiving treatment for another condition EARLYSTAGE(compensated/warm shock )
  66. 66. bbinyunus2002@gmail.com Page 66  Not associated with hypovvolemia  febrile (38.2-41°C )  Shivering and malaise  warm dry and flushed skin.  hyperventilation  rapid bounding pulse  wide pulse pressure LATE STAGE (decompensated/ cold shock)  Hypovolemia with superimposed sepsis  altered sensorium  cold clammy skin  Feeble pulse  hypothermia, hypotension  Oliguria  Jaundice  upper GI bleeding  DIC LOCALISING INFECTION A good complete systemic examination is done to detect any focus of sepsis. NOTE THAT RESUSCITATION TAKES PRECEDENCE OVER INVESTIGATIONS, WHICH SHOULD NOT DELAY INTERVENTION INVESTIGATION GOES HAND-IN-HAND WITH RESUSITATION  FBC: there is leucocytosis after initial leucopenia. Throbocytopenia  Septic work up; Blood culture, Sputum m/c/s, Urine m/c/s, Wound swab m/c/s, Endocervical swab m/c/s or any exudate  Based on suspected source; CXR, Abd-X RAY, Abd-pelvic uss, CT Scan of various sites TREATMENT Septic shock is a medical emergency that requires prompt and efficient resuscitation If possible patient should be admitted to ICU AIMS:  Improve haemodynamic state  Restore tissue perfusion thereby increase O2 delivery to tissue.  Administer O2  Combat the bacteria and cytokines
  67. 67. bbinyunus2002@gmail.com Page 67  Eliminate septic focus RESUSCITATION  FLUID (see above)  Vasopressor ; After adequate fluid resuscitation or about 4L, with signs of fluid overload(basal crepitation, high CVP) and persistent hypotension. a. Norepinephrine – α & β ; 1st line for septic shock refractory to volume replacement .Vasoconstriction & reflex bradycardia 5-20mcg/min  Dopamine – systemic vasoconstriction, inotropic, renal vasodilatation 2-20mcg/m  OXYGEN ADMISTRATION In a cleared and patent airway, O2 is delivered via a face mask to increase O2 saturation. Increasing uptake and delivery to tissue.  ANTIBIOTIC Give in large doses IV to combat infection. Empirical IV Broad spectrum bactericidal & anerobe coverage (3rd generation cephalosporin) Ceftriaxone 50-100mg/kg up to 2gm daily + Metronidazole 500mg 8hrly  Steroids  NSAID  FREE REDICALS SCAVENGERS; superoxide dismutase, allopurinol, vitamin C, a- tocopherol  Glycemic control- soluble insulin (GKI) to maintain blood sugar – 80- 120mg/dl has been found to ↓morbidity/mortality.  PREVENTION OF FURTHER COAGULATION • Atiii and C₁-estrase inhibitor • Recombinant human activated protein C • inhibits thrombosis and inflammation, promotes fibrinolysis, and modulates coagulation and inflammation.  SURGERY • resuscitative & therapeutic • If septic focus is responsible for the shock it should be dealt with as soon as possible especially if respose to therapy is poor. E.g debridement, drainage of abscess
  68. 68. bbinyunus2002@gmail.com Page 68 NUTRITION IN SURGERY  Introduction  Nutritional requirements  Cause of under nutrition  Effect of malnutrition  Nutritional assessment  Nutritional support  Future trends INTRODUCTION The process of utilizing exogenous substances for the production of energy and synthesis of new tissues. It entails provision of water, electrolyte, vitamins and other nutrients. Nutritional status determines the outcome of a surgical patient. Provision of adequate nutrition requires appreciation that injured or septic patient requires higher nutrient than healthy one. Nutrition support is aimed in timely manner. It is given via the safest route to minimize complication. Terms; Resting energy expenditure (REE); the energy expended by a person at rest in a thermoneutral environment. Basal metabolic rate (BMR); the expenditure for an individual under standard condition of 12-18hours fasting, recumbent at mental rest in thermoneutral environment. REE and BMR usually differs by lessthan 10% but REE is higher because it include energy expenditure at mental activity and other expenditure. REE in newborn 55Kcal/kg/day, in adult 20-30Kcal/kg/day. NUTRITIONAL REQUIREMENT; Adult Neonate/infant Energy (kcal/kg/day) 20-25 90-120 Protein (g/kg) 0.7-1.5 2.5 Fat (g/kg) 1.5-2.0 4.0 Water(/kg) 45-50ml 125-150ml Caloric contribution; CHO 55-60%, Fat 30-35%, proteins 5-10% and 1g of CHO delivers 4kcal(17j), 1g of protein 4kcal and 1g of fat 9kcal(38j) Vitamins; vitamin A 5000iu weekly, K 5-10mg weekly, C 60-80mg daily, B12 500mcg weekly, folic acid 3-6mg daily. Fat soluble vitamins ADEC, water soluble B, C and folic acid. B is produced by gut bacteria, B12(cyanocobalamin) absorbed in the terminal ileum, folic is absorbed in the duodenum Minerals; zinc 5mg, cu 0.5-2.0mg, Mn 70-150mcg, Cr 40mcg, Se 70-150mcg
  69. 69. bbinyunus2002@gmail.com Page 69 The energy requirement is increased in catabolic states; Major elective abdominal surgeries or trauma by 10-30%, generalized peritonitis 15-50%, sepsis 50- 80% and burns 80-200%. If these requirements are not met by exogenous supplement, they will be provided from endogenous alternative ways to the deterrent of the body. Starvation; 1st 12hrs previous meal utilized and within 24 hrs body glucose store is depleted. After 24hrs fatty acids and amino acids are being broken down (gluconeogenesis).Obligate use of glucose (the CNS others; rbc, wbc, fibroblast, proximal convulated tubules) is gradually being adapted to ketones. Increased secretion of counter regulatory hormones. Exaggerated hepatic glucose production. Pro inflammatory cytokines are produced TNF, IL6. Plasma albumin concentration falls rapidly. There is increased catabolic state depending on the severity of injury/infection. 12% increase in BMR/degree rise in temperature. Trauma and sepsis; there is increased counter-regulatory hormones- adrenaline, noradrenaline and cortisone. Energy requirement increase (upto 40kcal/kg/day). N2 requirement increase. There is insulin resistance and glucose intolerance. There preferential oxidation of lipids. There is increase gluconeogenesis, loss of adaptive ketogenesis, fluid retention with hypoalbuminemia. CAUSES OF UNDERNUTRITION DECREASE INTAKE INADEQUATE ABSORBTION EXCESSIVE LOSSES EXCESSIVE DEMAND starvation poverty anorexia nervosa hyperemesis cancer sepsis liver disease dysphagia alcoholism git obstruction short bowel syndrome major gastric resection motility disorders ( irritable bowel syndrome) pseudo obstruction (ogilvie syndrome) GIT fistula malabsorbtion states inflammatory bowel disease protein loosing enteropathy Hypercatabolicstates burns sepsis trauma surgical stress
  70. 70. bbinyunus2002@gmail.com Page 70 EFFECTS OF MALNUTRITION  Impaired mental function: Apathy, fatigue, poor cognition  Impaired muscle function: Respiratory failure  Impaired immune function: Increased incidence of infection  Miscellaneous: Impaired thermogenic response, Impaired wound healing NUTRITIONAL ASSESSMENT Aim; identify patient who are at increased risk of post-operative complication due to malnutrition and where possible, to improve nutritional status through intervention. Methods; Clinical Anthropometry Laboratory evaluation Clinical detailed history and examination HISTORY Vomiting, difficulty in swallowing, diarrhea. Medical history of DM, AIDS, chronic liver dx, chronic kidney dx Surgical history of abdominal operation Drug history; chemotherapy. Dietery hx; 24hr dietery recall. CLINICAL EXAMINATION Acutely or chronically ill looking. Wasted, sunken eyes, palor, silky hair,chelosis, pedal aodema Cvs; displaced apex beat , haemic murmurs Abdomen; stomas, fistula, abdominal masses, hepatomegaly. Rectal examination; perineal fistula, pale stools Nervous system; neuropathies
  71. 71. bbinyunus2002@gmail.com Page 71 SUBJECTIVE GLOBAL ASSESSMENT 5 features in the history  Weight loss in the past 6months  Dietary intake  GI symptoms  Functional status or energy level  Metabolic demands 4 features in physical examination  Loss of subcutaneous fat  Oedema  Ascites  Muscle wasting ANTHROPOMETRIC Body mass index (BMI); 18.5-24.9kg/m2 Interpretation  Severely underweight-<16.5  Underweight-16.5-18.4  Normal weight-18.5-24.9  Overweight-25-29.9  Obesity grade 1; 30-34.9  Obesity grade 2; 35-39.9  Obesity grade 3; >40  Superobesity >50 Ideal body weight; using Devine formula  Men:50kg+ 2.3kg for every inch over 5ft  Women:45.5kg +2.3kg for every inch over 5ft. Mid arm circumference, Triceps skin fold thickness, waist hip ratio, LABORATORY EVALUATION 1. Serum protein concentration a. Total protein b. Albumin; <3.5g/dl, t ½ 21days c. Prealbumn; for acute changes t ½ 3days

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