Surgery(surgical infections) 1-2


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Surgery(surgical infections) 1-2

  1. 1. Surgical Infections Dr. Zaid Muwafaq MRCS .England FJMC/ Surgery. Jordan HSM/Surgery .Jordan
  2. 2. Definition Infection : Invasion of microorganism to the healthy tissue producing inflammatory reaction
  3. 3. Pathogenesis and bacteriology Microorganisms usually prevented from causing infection in tissues by intact epithelial surface, mainly the skin. Protective mechanism includes: 1- Chemicals: low PH gastric juice. 2- Humoral: antibodies, complements and opsonin. 3- Cellular: phagocytic cells, macrophages, polymorphnuclear cells and killer lymphocytes.
  4. 4. Host response can be weakened by several factors: 1-Metabolic: malnutrition (including obesity), diabetes, uremia and jaundice. 2- Disseminated disease: cancer and acquired immune deficiency syndrome(AIDS). 3- Iatrogenic: radiotherapy, chemotherapy and steroids.
  5. 5. The chance of developing infection is also determined by: 1-the pathogenicity of the organisms present and the size of bacterial inoculum. 2- Devitalized tissues, excessive dead space or hematoma, all the result of poor surgical technique increases the chance of infection.
  6. 6. Diagnosis 1-History 2-Clinical examination Clinical features of acute inflammation : calor(heat) +rubber (redness), dolour (pain)+ tumour (swelling) + function laesa (loss/impairment of function) 3-Laboratory investigation / Radiology imaging.
  7. 7. Complication An infection may resolve spontaneously, or it may 1- destruct tissues. 2- abscess, which may rupture spontaneously. 3- sinus or fistula formation. 4- spreading infection death of tissue(gangrene), with it systemic effect. 5- bacteremia, septicaemia, septic shoch, multiorgan failure ,disseminated intravascular coagulopathy and death.
  8. 8. Treatment Source Control: - draining an abscess - resecting or débriding dead tissue - diverting bowel, relieving obstruction, and closing a perforation. Antibiotic treatment of a surgical infection without this mechanical solution will not resolve the infection. (adjunctive therapies).
  9. 9. 1- Acute nonspecific surgical infection
  10. 10. . wound infection: invasion of organisms through tissues following breakdown of local or systemic host defense. SSI Are infection of the tissues, organs, or spaces exposed by surgeons during performance of an invasive procedures. Post operative wound infection, Surgical Site Infection(SSI)
  11. 11. Classification Superficial surgical site infection: infection of surgical wounds. Deep surgical site infection: infection in the deeper musculofascial layer or organ spaces infection.
  12. 12. Major surgical site infection: discharge significant quantities of pus either spontaneously or need surgical drainage +local signs of infection patient + systemic signs; tachycardia, pyrexia and raise WBC count. Minor surgical site infection: may discharge pus or infected serous fluid (-ve systemic signs).
  13. 13. Treatment of surgical site infection Minor may resolve spontaneously by frequent dressing change ,may require drainage. Major :drainage of pus, May require debridement (removal of dead devitalized tissue) +Systemic antibiotic.
  14. 14. Cellulitis and Lymphangitis - Is non suppurative invasive infection of tissues with poor locatization + cardinal signs of inflammation. -It is spreading infection (B-haemolytic streptococci , staphylococcus , C. perfringens). -Tissue destruction, gangrene and ulcer may follow which are caused by release of proteases and allow spread of infection.
  15. 15. Clinical features . well demarcated area of inflammation (hot ,red ,tenderness ,swelling and impairment of function) • malaise, chills,fever,rigors and a raised white cell count • If not rapidly treated it can progress to lymphangitis and lymphadenitis
  16. 16. • Localized areas of skin necrosis may occur
  17. 17. Predisposing factors include: o Lymphoedema o Venous stasis o Diabetes mellitus o Surgical wounds Management • Rest and elevation of the affected limb • Antibiotics (orally/ intravenous) (Benzylpenicillin and flucloxacillin) Lymphangitis is part of a similar process and presents as painful red streaks in affected lymphatics.It is associated with painful lymph node groups in the related drainage area.
  18. 18. Erysipelas Erysipelas is a sharply demarcated streptococcal infection of skin, usually associated with broken skin on the face . The area affected is erythematous and oedematous. fever+leukocytosis. broad-spectrum antibiotics
  19. 19. Boils A boil, also called a furuncle, is a deep folliculitis, infection of the hair follicle. -Staphylococcus aureus
  20. 20. Boils are red lumps around a hair follicle that are tender, warm, and very painful (signs of inflammation). - pea-sized to golf ball-sized. - yellow or white point at the center of the lump / discharge pus. severe fever, swollen lymph nodes, and fatigue. chronic furunculosis is recurring boil + Systemic factors that lower resistance : diabetes, obesity, and hematologic disorders.
  21. 21. Treatment Antibiotics against Staphylococcus aureus . small boil burst and drain spontaneously recurrent boils a systemic cause should be looked for and treated.
  22. 22. Carbuncle(A carbuncle is made up of several skin boils) A carbuncle is a deeper skin infection that involves a group of infected hair follicles in one skin location. -back of the neck, shoulders, hips and thighs. -diabetes -Staphylococcus aureus, or Streptococcus pyogenes.
  23. 23. swelling + signs of inflammation + one or more openings draining pus. fatigue, fever and a general discomfort.
  24. 24. Treatment Antibiotic against gram positive bacteria, incision and drainage of pus collection followed by frequent dressing.
  25. 25. Hidradenitis suppurativa This is a chronic inflammatory disease of the apocrine gland containing skin(axillary and groin ). Less common sites :scalp, breast, chest and perineum. Hidradenitis suppurativa +obesity and smoking. Women are 4x. The pathophysiology involves follicular occlusion followed by folliculitis and secondary infection with skin flora (usually Staphylococcus aureus and Propionibacterium acnes).
  26. 26. Clinically,patients develop tender, subcutaneous nodules which may not point and discharge, but usually progress to cause chronic inflammation , suppurative skin abscesses, sinus tracts .
  27. 27. Management Patients should be -advised to stop smoking and lose weight -Symptoms can be reduced by the use of antiseptic soaps, tea tree oil, non- compressive and aerated underwear. -Medical treatments include topical and oral antibiotics and anti-androgen drugs. -if abscess developed ,need drainage.
  28. 28. In selected cases, patients may require radical excision of the affected skin and subcutaneous tissue+ skin grafting or flap transposition .
  29. 29. Abscesses • An abscess is collection of pus within soft tissues Pathology • An abscess contains bacteria, acute inflammatory cells, protein exudate and necrotic tissue,It is surrounded by granulation tissue (the 'pyogenic membrane') The pus is composed of dead and dying white blood cells • In superficial abscesses o Staph. Aureus o Strep. pyogenes • In deep abscesses o Gram negative species (e.g. E. coli) o Anaerobes (e.g. Bacteroides)
  30. 30. Clinical features 1- Superficial abscesses include infected sebaceous cysts, breast and pilonidal abscesses. superficial abscess shows cardinal features of inflammation - calor, rubor, dolor, tumor(Heat,Redness,Pain,Swelling) After few days superficial abscess usually 'point' and are fluctuant
  31. 31. 2-Deep abscesses like; diverticular abscess, subphrenic abscess and anastomotic leaks(inside the abdomen) • Patients shows signs of inflammation o Swinging pyrexia o Tachycardia o Tachypnoea • Physical signs are otherwise difficult to demonstrate • Site of abscess may not be clinically apparent
  32. 32. Radiological imaging(Ultrasound and/or CT scan) often required to make the diagnosis
  33. 33. Treatment (adequate drainage) • Should be performed under general anaesthesia • Antibiotics have little to offer as tissue penetration is usually poor • Prolonged antibiotic treatment can result in a chronic inflammatory mass (an 'antibioma') • Superficial abscesses open drainage • For deep abscesses closed drainage
  34. 34. Open Technique • Superficial abscesses can usually be drained through a cruciate incision • Position of incision may allow depended drainage • Pus should be sent for microbiology • Loculi should be broken down and necrotic tissue excised • A dressing should be inserted into the wound
  35. 35. Closed Techniques • Deep abscess can be treated by ultrasound /CT guided drainage
  36. 36. Definitions of infected states _ SSI(surgical site infection) is an infected wound or deep organ space _ SIRS(systemic inflammatory response syndrome) is the body’s systemic response to severe infection SIRS when Two or more of: hyperthermia (>38°C) or hypothermia (<36°C) tachycardia (>90/min, no b-blockers) tachypnoea (>20/min) or Paco2<32 mmHg or mechanical ventilation white cell count >12 × 109/l or <4 × 109/l Sepsis is SIRS with a documented infection Severe sepsis or sepsis syndrome is sepsis with new onset organ failures (respiratory (acute respiratory distress syndrome), cardiovascular ,renal (acute tubular necrosis), hepatic, blood coagulation systems or central nervous system) septic shock = sever sepsis + hypotension (follows compromise of cardiac function and fall in peripheral vascular resistance) multiorgan dysfunction syndrome= acute potentially reversible dysfunction of 2 or more organs
  37. 37. Bacteraemia and sepsis Bacteraemia : presence of bacteria in the blood stream. Sepsis(septicaemia): proliferation of bacteria in blood stream producing systemic inflammatory response syndrome. Bacteraemia occur : 1-anastomotic breakdown (deep space SSI). 2-procedures undertaken through infected tissues (particularly instrumentation in infected bile or urine). 3- bacterial colonisation of indwelling intravenous cannulae. Sepsis accompanied by MODS may follow anastomotic breakdown. Aerobic Gram-negative bacilli are mainly responsible, but S. aureus and fungi may be involved, particularly after the use of broad- spectrum antibiotics .
  38. 38. Bacteraemia is important when a prosthesis has been implanted, as infection of the prosthesis can occur.
  39. 39. 2-Acute specific surgical infections A-Gas gangrene This is caused by C. perfringens. Gram-positive, anaerobic, spore-bearing bacilli in soil and faeces. -military , traumatic surgery and colorectal operations. Risk factor for development of gas gangrene: 1- immunocompromised,diabetic 2- have malignant disease ,particularly if they have wounds containing necrotic or foreign material, resulting in anaerobic conditions. 3- Military wounds The cavitation which follows passage of a missile through the tissues causes a ‘sucking’ entry wound, leaving clothing and environmental soiling in the wound in addition to devascularised tissue.
  40. 40. Clinical Picture Infected wound with severe local wound pain and crepitus (gas in the tissues). The wound produces a thin, brown, sweet- smelling exudate. Oedema and spreading gangrene follow the release of collagenase, hyaluronidase, other proteases and alpha toxin. Early systemic complications with circulatory collapse and MSOF follow if prompt action is not taken
  41. 41. Diagnosis mainly clinical . XR may show gas in the tissue, gram stain of the discharge show the bacteria. Treatment Aggressive debridement of affected tissues (this may be repeated as required)+ large doses of intravenous penicillin
  42. 42. In neonate (tetanus neonaturum) following the use of cow dung on the umbilicus B-Tetanus following deep or penetrating (civilian/military) wound and burn . -developing countries.
  43. 43. Microbiology • Due to Clostridium tetani,Gram-positive spore forming rod. Widely found in the environment and soil.It is strict anaerobe that produces a powerful exotoxins Typically Infection produces few signs of local inflammation.
  44. 44. Pathogenesis • Germination of spores in wounds releases the exotoxin(tetanospasmi n). The toxin affects nervous system and reaches CNS via the peripheral nerves. It acts on presynaptic terminals of nerves (myoneural junctions and the motor neurones of the anterior horn of the spinal cord) and reduces the release of inhibitory neurotransmitters (e.g. glycine) resulting in excess activity of motor neurones produces muscle spasm.
  45. 45. Clinical features The entry wound may show a localised small area of cellulitis+/- exudate A short prodromal period, which has a poor prognosis, leads to spasms in the distribution of the short motor nerves of the face followed by the development of severe generalised motor spasms including : Facial muscle spasm produces trismus Typical facial appearance = 'risus sardonicus', Back muscle spasm produces opisthotomous Eventually exhaustion and respiratory failure leads to death A longer prodromal period of 4–5 weeks is associated with a milder form of the disease.
  46. 46. Prevention • Tetanus can be prevented by: o Active immunisation with tetanus toxoid with booster every 5-10 years o Adequate wound toilet of contaminated wounds any patient with open traumatic wound (if not immunized) should receive toxoid with benzylpenicillin. If immunized should receive a booster of toxoid (if last immunisation >5 years).
  47. 47. Treatment • In suspected cases: o Passive immunisation with anti-tetanus immunoglobulin o Adequate wound debridement o Intravenous benzylpenicillin o Relaxants may also be required, and the patient may require mechanical ventilation in severe forms, which may be associated with a high mortality in Intensive care support o Despite the use of ITU mortality is about 50% The diagnosis is essentially clinical, Exudate from the wound can be stained to show the presence of Gram- positive rods
  48. 48. C-Necrotising fasciitis Necrotising fasciitis results from a polymicrobial, synergistic infection, most commonly a streptococcal species (group A b haemolytic) in combination with Staphylococcus, Escherichia coli, Pseudomonas, Proteus, Bacteroides or Clostridia. 80%have a history of previous trauma/infection and over 60 % commence in the lower extremities. Meleney’s synergistic gangrene(abdominal wall) and Fournier’s gangrene(perineum) are all variants of a similar disease process . Predisposing conditions include: • diabetes; • smoking; • penetrating trauma; • pressure sores; • immunocompromised states; • intravenous drug abuse; • perineal infection (perianal abscess, Bartholin’s cysts); • skin damage/infection (abrasions, bites, boils).
  49. 49.  Classical clinical signs include: oedema extending beyond visible skin erythema; a woody hard texture to the subcutaneous tissues; an inability to distinguish fascial planes and muscle groups on palpation; disproportionate pain in relation to the affected area with associated skin vesicles and soft tissue crepitus . Early on, patients may be febrile and tachycardic, with a very rapid progression to septic shock. Radiographs should not delay treatment but if taken, they may demonstrate air in the tissues.
  50. 50. Treatment 3- debridement as soon as possible until viable, healthy, bleeding tissue is reached. Early re-look and further debridement is advisable together with the use of vacuum-assisted dressings. Early skin grafting in selected cases may minimise protein and fluid losses. Mortality of between 30 and 50 per cent can be expected even with prompt operative intervention. 1-urgent fluid resuscitation, monitoring of haemodynamic status 2-administration of high-dose broad-spectrum intravenous antibiotics.
  51. 51. Thank you
  52. 52. Exam. picture 1 What is the diagnosis? Treatment?
  53. 53. Picture 2 Diagnosis?
  54. 54. Picture 3 Diagnosis? Treatment?
  55. 55. 3- Chronic specific infection A-Tuberculosis Tuberculosis(Mycobacterium tuberculosis or Mycobacterium bovis) is common throughout the world. It Causes significant morbidity and mortality particularly in Africa and Asia . Primary tuberculosis • Usually a respiratory infection that occurs in childhood, results in sub-pleural Ghon focus and mediastinal lymphadenopathy (primary complex).Symptoms are often few,resolution of infection usually occurs. • Complications include: o Haematogenous spread causing miliary TB affecting lungs, bones, joints, meninges. o Direct pulmonary spread resulting in TB bronchopneumonia
  56. 56. Post-primary tuberculosis Occurs in adolescence or adult life, due to reactivation of infection or repeat exposure. Reactivation may be associated with immunosuppression (e.g. drugs or HIV infection) It Results in more significant symptoms. Pulmonary infection accounts for 70% of cases of post- primary TB. Clinical features include cough, haemoptysis, malaise, weight loss and night sweats. Infection of lymph glands results in discrete, firm and painless lymphadenopathy. Confluence of infected glands can result in a 'cold' abscess. Infection of the urinary tract can cause haematuria and 'sterile pyuria'
  57. 57. Investigations If discharging sinus,discharge sent for ZN stain and culture. • Repeated samples may be required Microscopy stained by Ziehl-Neelsen stain • Negative microscopy does not exclude tuberculosis Culture Collect adequate specimens (e.g. early morning urine x3),Concentration of specimen (e.g. centrifugation). o Culture on Lowenstein-Jensen method at 35-37° for at least 6 weeks Histology • caeseating necrosis • Tuberculous follicle consists of central caseaous necrosis surrounded by lymphocytes, multi-nucleate giant cells and epitheloid macrophages Multinucleated (Langhan’s) giant cell.
  58. 58. Skin tests • Delayed hypersensitivity reaction used to diagnose tuberculosis.The two commonest tests are the Mantoux and Heaf test. • Positive skin test are indicative of active infection or previous BCG vaccination Treatment • First line chemotherapeutic agents are rifampicin, isoniazid and ethambutol • Given as 'triple therapy' for first 2 months until sensitivities available • Rifampicin and isoniazid are the usually continued for further 7 months • Less than 5% of organisms are resistant to first-line agents • Second line treatment includes pyrazinamide
  59. 59. B-Syphilis Syphilis is a systemic sexually transmitted disease (STD) caused by the spirochete, Treponema pallidum. Stages of syphilis: 1-Primary Stage One or more chancres (usually firm, round,small, and painless) appear at the site of infection (most often the genital area) 10 to 90 days after infection .The chancres heal on their own in 3-6 weeks.Patient is highly infectious in the primary stage. 2- Secondary Stage Rashes occur as the chancre(s) fades or a few weeks after the chancre heals. Rashes typically appear on the palms of the hands, the soles of the feet, or on the face,but also may appear on other areas of the body. Sometimes wart-like “growths” may appear in the genital area. Rashes and syphilitic warts tends to clear up on their own within 2-6 weeks,but may take as long as 12 weeks.Patient is highly infectious in the secondary stage.
  60. 60. Latent stage: patient is serosensitive ,has no symptoms. within one year of onset of infection,(Early latent stage )the patient is potentially infectious. more than one year after onset of infection(Late latent stage), patient is not infectious at this stage. 3-Tertiary stage(late stage) Lesion in the skin and bone(gummas), internal organs, central nervous system, and cardiovascular system. Signs and symptoms of late stage of syphilis include difficulty coordinating muscle movements, paralysis,numbness,gradual blindness and dementia. This damage may be serious enough to cause death.the patient is not infectious at the late stage. Syphilitic ulcers are typically painless, rubbery , indurated, punched out ulcer.
  61. 61. Diagnosis : -Dark-field examinations or direct fluorescent antibody tests of chancre tissue are the definitive methods for diagnosing primary and secondary syphilis. -sequential serologic tests (e.g. VDRL, RPR). Treatment is by use of a long-acting penicillin.
  62. 62. Actinomycosis Chronic infectious inflammatory condition originating in the tissues adjacent to mucosal surfaces caused mostly by infection with A. israelii ,but others, A. naeslundii, A. odontolyticus, A. viscosus, A. meyeri also can cause human actinomycosis. most common recognized infections: oral and cervicofacial regions. The thoracic region, abdominopelvic region, and the CNS also frequently can be involved. Actinomyces is normal inhabitants of some areas of the GI tract of humans and animals from the oropharynx to the lower Bowel. Lesions: induration and sinuses , abscess , tissue fibrosis. In pus, the most characteristic form is the sulfur granule . The firm, fibrous masses are often initially mistaken for a malignancy
  63. 63. Diagnosis: (Identification of microorganism is difficult) -History : slowly progressive lesion with history of trauma predispose to mucosal invasion by actinomyces. -Biopsies for culture and histopathology (multiple sections ) Treatment Treatment of choice: Penicillin G. Other antimicrobics (tetracycline, erythromycin, clindamycin) are active in vitro and have shown some clinical effectiveness High doses of penicillin must be used and therapy prolonged for 4 to 6 weeks or longer before any response is seen.