Surgical infections

Dr Gersam
Objectives
 Describe the pathogenesis of surgical
infection
 Describe the prevention and treatment of
surgical infections
 Discuss some of the common surgical
infections
Historical Background
 1846, Ignaz Semmelweis – maternity ward
 Louis Pasteur- S.aureus
 Joseph Lister – antisepsis
 Robert Koch – 4 postulates
 Charles McBurney – source control
 In 1928, Sir Alexander Fleming - penicillin
 William Osler: "Except on few occasions, the patient
appears to die from the body's response to infection
rather than from it."
Basic definitions
 Contamination – colonization without
inflammation
 Inflammation – host’s response
 Infection – inflammation in response to
contamination
 Surgical infection
◦ Any infection that follows contamination of
damaged tissue after operative or
accidental trauma
Pathogenesis of Infection (Host
defense)
Host defense: Several layer
 Skin:
◦ physical barrier by the epithelial surface
◦ “colonization resistance”
 Staphylococcus and Streptococcus, as well as Corynebacterium and
Propionibacterium species.
◦ chemicals that sebaceous glands secrete
◦ constant shedding of epithelial cells
 Respiratory tract
◦ mucus traps larger particles including microbes; ciliary
movement pushes them up and gets coughed out
◦ phagocytosis by pulmonary alveolar macrophages
 GIT
◦ the highly acidic, low-motility environment
Pathogenesis of Infection (Host
defense)
◦ Once microbes enter a sterile body
compartment – additional host defense
 lactoferrin and transferrin
 Fibrinogen
 Omentum - wall off infection
 resident macrophages and low levels of
complement (C) proteins and immunoglobulins (Ig,
antibodies).
 C5a, microbial cell wall, and cytokines such as IL-8
attract PMN cells
Pathogenesis of Infection
 The magnitude of the response and
eventual outcome generally are related to
 the initial number of microbes
 the rate of microbial proliferation in relation to
containment and killing by host defenses
 microbial virulence, and
 the potency of host defenses.
Pathogenesis of Infection
 Possible outcomes
◦ Eradication

◦ Containment - locoregional infection , or

◦ systemic infection
Local phase of infection

 If the extent of tissue injury and number

of bacteria exceed the capacity of the
host to terminate an infection locally, an
abscess may form
Systemic phase of infection
 If local circumscription of infection is
impossible – bactremia and Sepsis

 Severe sepsis is characterized as sepsis

combined with the presence of new-
onset organ failure.
 Septic shock
◦ mortality rate of 60 to 80%
Risk factors for infection
Patient related
Malnutrition
Immune compromise
Obesity
Renal insufficiency
Pulmonary dysfunction
Cardiovascular disease
Endocrine and metabolic disorders

Injury related
Location, extent

Environment related
Contamination, superinfection
Hygiene
Long-term stay in intensive care unit
 Prevention
 General guidelines - Prophylaxis
◦ hair removal using a clipper rather than a
razor
◦ Bowel preparation before surgery on colon
and rectum
◦ Scrubbing; sterilization of equipment
◦ Pre op antimicrobial agent
◦ Cleaning with antiseptic agent
Prevention
◦ Tissue should be handled gently

◦ Devitalized tissue, debris, and traumatic

foreign bodies should be removed.

◦ Complete hemostasis

◦ Blood supply should not be impaired.

Prevention
◦ Formation of dead space should be avoided
during closure.

◦ The wound may be irrigated with liberal

amounts of sterile saline/Ringer's lactate
solution prior to closure

◦ The wound should be closed by layer-to-layer

approximation without tension.

◦ Operative time should be kept to a minimum

Treatment
 Source control
◦ consists of
 drainage
 debridement
 removal of foreign bodies

◦ Antimicrobial therapy is effective only in

conjunction with operative reduction of the
bacterial inoculum
Appropriate antibiotic use
 Prophylaxis,

 Empiric therapy or

 Definitive therapy
Bacteria on Gram
Source Initial calculated antibiotic therapy
stain
In chains, Gram +ve Penicillin G (high dose; 10 million units 8-
Soft tissue
cocci hourly)
In clusters, Gram +ve Penicillin G (high dose; 10 million units 8-
Soft tissue
cocci hourly)
Clindamycin or methicillin
Gram –ve rods Abdomen Cefotaxime
Table 3 Initial empiric therapy for surgical infections
Pulmonary Ceftriaxone
Biliary tract Ciprofloxacin or other quinolones
Penicillin G (high dose; 10 million units 8-
Gram +ve rods Soft tissue
hourly)
Mixed Gram +ve and Cefotaxime + metronidazole, or ampicillin–
Intra-abdominal abscess
–ve sulbactam
Multiple injuries,
Cefotaxime + clindamycin
especially extremities
EXAMPLES OF
INFECTIONS OF
SIGNIFICANCE IN
SURGICAL PATIENTS
Surgical site infection
 Defn
 Classification
◦ Superficial/deep incisional and
◦ organ specific
 related to four factors:
◦ Patient factor
◦ Anesthesia factor
◦ Wound factor, and
◦ Surgeons factor
How to prevent
◦ Hair removal – clipping, or depilatory cream or
no hair removal
◦ Skin preparation – soap+alcohol, iodine,
chlorhexidine
◦ Surgical hand preparation: alcohol vs water
◦ Antibiotic prophylaxis
◦ Postponement of elective surgeries on the face of
active remote infection
◦ Maintain appropriate blood sugar control in
diabetic patients in the perioperative period
◦ Expertise of the surgeon: technique
Diagnosis and Treatment
 Diagnosis
◦ Clinical + microbiologic
 Drainage
◦ “Don’t let the sun set on an abscess”
◦ Look for Necrotizing infection
 Drainage of clear brownish fluid (dish water)
 Dark brown discoloured sub cut
 Easily separating tissue planes
 Subcut vessel thrombosis
Intra-Abdominal
Infections/peritonitis
 Primary
◦ in those individuals
 ascites, and
 who are being treated for renal failure via
peritoneal dialysis.
◦ These infections invariably are monomicrobial
and rarely require surgical intervention
◦ Dx – clinical and lab
 the presence of more than 100 WBCs/mL, and
 Gram's stain from peritoneal paracentesis;
◦ Rx - antibiotic
Secondary peritonitis
 Secondary
◦ contamination of the peritoneal cavity
 perforation of GIT (e.g PUD perforation) or
 infection of an intra-abdominal organ (e.g.
appendicitis, diverticulitis)
◦ Approach
 Hx and Px
 Ix (Lab and Xray)
◦ Rx- Effective source control and antibiotic
therapy
Tertiary peritonitis

◦ Progressive peritonitis despite initial control

◦ Occult sepsis without evidence of infection

◦ Due to poor host defense

◦ Difficult to manage
Hepatic abscesses
 Pyogenic abscesses - 80%;
 Parasitic and fungal – 20%;
 worldwide – amebic liver abscess is the
commonest
Pyogenic liver abscesses
 Etiologies:
◦ impaired biliary drainage,
◦ hematogenous (IV drug users, bacterial
endocarditis),
◦ local extension (diverticulitis, crohn’s)
 Single or multiple; monobacterial or
polybacterial
◦ Gram neg bacteria like Ecoli, S Fecalis, Klebsiella;
◦ anearobes like Bacteroides
 Mainly the right lobe of the liver
Pyogenic liver abscesses
 Presentation: Fever and RUQ pain
◦ Jaundice in one third
 Lab
◦ Leukocytosis,
◦ ESR increased,
◦ ALP increased;
◦ other liver enzymes are usually normal
Pyogenic liver abscesses
 US – hypoechoic well demarcated lesions;
if multiple and coalesing look like “honey
comb”
 CT/MRI
 Management –
◦ drainage (percutaneous or surgical) and
antibiotics for at least 8 weeks
◦ Small (<1cm) – no need for drainage
Amebic liver abscess
 E Hystolytica
◦ from colon via the portal system
 Superior and anterior part of rt lobe
usually
 The abscess is thick reddish brown;
likened to chocolate sauce or Anchovy
paste
Amebic liver abscess
 Presentation – RUQ pain, fever and
hepatomegaly
◦ Lab similar to Pyogenic abscess; jaundice is
not common
◦ Serology – antibody test for E histolytica
positive
◦ US, CT
 Management – Metronidazole 750mg tid
for 7-10days;
◦ drainage not needed in most
Hydatid disease
 E Granulosus;
◦ dogs are the final host;
◦ humans and sheep are intermediate hosts
 Liver is affected in 70%; also affect
◦ Lung,
◦ spleen,
◦ Brain,
◦ bones
 Right lobe of liver
Hydatid disease
 Presentation –
◦ Silent; RUQ pain and abd distension; can also
be superinfected or rupture and present with
anaphylaxis
 Lab and imaging
 Serology – ELISA for echinococcal antigen
 Eosinophilia >7% - 20-30%
Hydatid disease
◦ US, CT
 Hypodense lesion with distinct wall; Pericyst
calcification; daughter cysts/scolices
◦ Management
 Mainly surgical unless the cyst is small and patient
not fit
 Complete cystectomy and scolicidal injection
 Albendazole
◦ Complications if ruptures during surgery –
anaphylactic reaction and peritoneal seeding
References
 Schwartz Principle of Surgery
 Surgical site infection, surgery in Africa
monthly review
 ACS surgery principles and practice