Wound infection

Wound infection is always a major complication of surgery & trauma. It has been documented for 4000-5000 years. Wound can be caused by almost any injurious agent and can involve any tissue.

INFLAMMATION

It is vascular response in leaving subject to some stimuli; clinical features are originally described by CELSUS (Roman surgeon 25 B.C-50 A.D) –

1.   Calor (Heat)

2.   Rubor (Redness)

3.   Dolor (Pain)

4.   Tumor (Swelling)

5.   Functio Laesa (Loss of function).

INFECTION

Invasion of microorganism and production of s/s in leaving subjects by their toxins and enzyme (local & systemic).

KOCH’S POSTULATION

In 1882: postulates that (Prof. of Hygiene & Bacter, Berlin-Germany).

·       It must be found in considerable numbers in the infective focus.

·       It should be possible to culture in a pure form from that infective focus.

·       It should be able to produce similar lesions when injected into another host.

CELLULITIS

Non suppurative invasive infection of tissue (localized & spreading) by the organism B-hemolytic streptococci, staphylococci & C.perfringens due to release of streptokinase, hydrouridase & proteases.

LYMPHANGITIS

Presents as painful, red streaks in affected lymphatics. Lymphangitis is often accompanied by painful lymphnode groups (lymphadenitis) in the related draining area.

Features of cellulitis & lymphangitis:

·       Non suppurative poorly localized, commonly caused by Sterptococcus Staphylococcus or Clostridia.

·       SIRS is common.

·       Blood cultures are often negative.

BACTEREMIA & SEPTICEMIA

Bacteremia is the presence of bacteria in blood. Usually associated during instrumentation of infected bile & urine but usually cleared rapidly & harmless except in patient with damaged heart valves, cardiac , vascular or with prosthesis or impaired immunity.

SEPTICAEMIA

When the systemic response results from infection.

·       Bacteraemia is dangerous in the patient has prosthesis.

·       Septicemia is common after anastomotic breakdown.

·       Septicaemia may be associated with MSOF.

ABCESS

Localised collection of pus lined by pyogenic membrane.

PYOGENIC MEMBRANE

Fibrin and inflammatory cells in acute conditions. For chronic, the membrane consists of connective tissue.

ANTIBIOMA

When the cavity contains sterile pus surrounded by unhealthy granulation (connective tissues & chronic inflammatory cells).

PUS

Contains dead bacteria, dead WBC, cytokines (tissue exudates) & O2 free radicles.

PYAEMIA

Portal pyeamia as a complication of appendicitis.

SIRS

MODS

MSOF

ADVANCES IN CONTROL OF INFECTION IN SURGERY

§       Asceptic technique

§       Antibiotics

§       Delayed closure in contaminated wound

PHYSICAL FACTORS

ü   Low gastric pH

ü   Humoral: Ab complement & opsonin

ü   Cellular: Phagocytic cells, macrophages, polymorphs & killer lymphocytes.

CAUSES OF REDUCED REGISTANCE TO INFECTION

Ø   Metabolic: Malnutrition, diabetes, uraemia, jaundice.

Ø   Disseminated disease: Cancer & AIDS.

Ø   Iatrogenic: Steroids, Radiotherapy & Chemotherapy.

RISK FACTORS FOR INCRESED OF WOUND INFECTION

§       Malnutrition: Obesity, weight loss

§       Metabolic disease: D.M, Uraemia, Jaundice

§       Immunosuppression: Ca, MDS, Steroids, C.T, R.T

§       Colonisation & translocation in GIT: Intestinal obstruction

§       Poor perfusion: Systemic shock & local iscaemia

§       F.B implants

§       Poor surgical technique: Dead space, hematoma

SPREAD OF SURGICAL INFECTIONS

Surgical infection usually originates as a single focus and become life threatening by spreading & releasing toxins.

Spreading occurs by several mechanisms-

A.  Necrotising infections- Spread along anatomical paths, poorly perfused fascial canal, subcuteneous planes. Its toxin causing thrombosis even of large vessels- creating more ischemia & vulnerable tissue.

B.  Abcess- If not promptly drained abcess enlarges, killing more tissue in the process. Leukocytes contribute to necrosis by releasing lysosomal enzymes during phagocytosis. Natural boundaries may be breached that is enterocutenious fistula may be penetrated.

C.  Phlegmons & superficial infections- Contain small pus but much edema. They spread fat planes & by contiguous necrosis as in retro peritoneal peri pancreatic inflammation or infections. Superficial infection may spread along skin not only by contiguous necrosis but also by metastasis.

D. Spread via lymphatics: Lymphangitis produces red streaks in the skin & travels proximally along major lymph vessels. It may occur in hidden places such as the retroperitoneal space in puerperal sepsis.

Spread via blood stream: Empyema and endocarditis commonly may cause by I/V injections contaminated drugs. Brain abscess from infection like face. Also spreads from infection elsewhere in the body especially occurs in liver & diabetics. Liver abscesses may complicate appendicitis and inflammatory bowel disease, sometimes pylaephlebitis.

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