UNIVERSITY OF MEDICINE AND PHARMACY OF CRAIOVA

IInd GENERAL SURGERY CLINIC

 THE ABSCESS
DEFINITION:
• well defined encapsulated
puss collection, localized in
tissues or anatomical areas.
ETIOLOGY:
• “HOT” ABSCESS:
– staphylococcus, rarely
streptococcus.
– Deep intraabdominal
abscesses are usually
determined by enteral Gram-
negative germs (E. Coli) and
anaerobe germs etc.
• “COLD” ABSCESS:
– mycobacterium tuberculosis
PATHOLOGY

• Abscess wall
– pyogenic membrane with 3 layers internal ( fibrin, microbes and leukocyte) ,
middle layer (granulation tissue), outer layer (scleral tissue).

• The abscess contain pus:

– Alive and dead microbes, dead leucocytes, blood cells, death tissue.

• Pus:
Creamy, odorless: staphylococcus;
Fluid, serous purulent: streptococcus;
Creamy, green: pneumococcus;
Gray, fluid, intensely fetid: anaerobe germs.
 DIAGNOSIS
• Local signs and symptoms:
– Acute inflammation signs:
• Swelling, redness, local heat and pain, fluctuation
• General signs and symptoms:
– Septic syndrome:
• intermittent fever, chills, tachycardia, altered general
status.
• Leukocytosis
• Local puncture - Pus.
• Bacteriologic examination of pus:
– involved microorganism(s);
– Antibiotic sensitivity.
Clinical Forms:
– Buttock abscess: secondary to an intramuscular
injection in which the asepsis isn’t respected;
– Mammary abscess: acute mastitis;
– Perianal abscess.
EVOLUTION
• Fistulas formation: spontaneous eviction of pus
– An external fistula formation
– an internal fistula formation into an organ or a serous cavity in deep
intra abdominal abscesses.
• healing
• or the transformation in a chronic suppuration.
TREATMENT
• Invasion stage:
– General treatment: antibiotics, non-steroidal anti-inflammatory drugs;
– Local: antiseptics, cold applications (ice) (prevent pus accumulation) of
heat (favor the pus accumulation and drainage).
• Collection stage:
• Incision, pus eviction, drainage, local antiseptic dressings;
• Antibiotics: in severe sepsis.
 THE PHLEGMON
DEFINITION
• An acute diffuse infection of the subcutaneous
tissue, with extensive tendency, accompanied by a
severe septic syndrome.
ETIOLOGY
– Hemolytic streptococcus – most frequent;
– Staphylococus Aureus;
– Gram-negative aerobe and anaerobe bacteria.

 Usually an entrance gate is present: accidental or

operatory wounds, sting or bite wounds.
DIAGNOSIS
• The invasion period (1-2 days)
– Local signs (are those of an acute inflammation): the
affected tissue is swollen, infiltrated due to interstitial
exudate. The skin is shiny, congestive, with livid areas.
• The pus is missing at this stage.
– General signs: sepsis signs; can evolve to severe
sepsis, MODS and death.
• The extensive tissue necrosis period (2-4 days)
– Local signs: serous or purulent phlyctenae above an
ulcerated skin;
– General signs: severe sepsis, septic shock and MODS.
• The suppuration stage (5-8 days)
– massive suppuration with abundant pus and dead
tissue discharged through fistulous orifices.
– The process is diffuse along superficial fascia, with
intra-muscular lodges.
– Pus elimination is followed by a clinical
improvement.

• The healing stage:

– is long and characterized by the occurrence of
large retractile scars, limiting the functionality of
the affected segment.
COMPLICATIONS
– local: vascular thrombosis, large muscular destructions,
extensive scars
– general: metastatic abscesses, MODS, death.
TREATMENT
• LOCAL Treatment:
– Invasion stage: non-steroidal anti-inflammatory drugs,
antiseptics, cold dressings;
– Suppuration stage: large incision, excision of dead tissue,
drainage, irrigation with antiseptics.
• General treatment:
– antibiotics: G penicillin in large doses,
– blood and plasma transfusions,
– volemic rebalancing,
– shock treatment.
 NECROTIZING SURGICAL INFECTIONS
DEFINITION
– Severe surgical infections, characterized by the presence of
the necrotic tissue, and the lack of the specific boundaries
(extensive character).
ETIOLOGY
• Clostridial necrotizing infections – gas gangrene (clostridial
myonecrosis)
– Involves the muscle and the underlying soft tissues (fascia,
subcutaneous, skin)
• Non-clostridial necrotizing infections – necrotizing fasciitis
– Involves the fascia and the subcutaneous tissue, leaving the
muscular tissue uninvolved.
CLASSIFICATION

a) Posttraumatic Gangrene: most often affects the lower limbs,

after major injury and muscle damage associated with
vascular lesions (ischemia).
– Therapeutic mistakes can promote post therapeutic gangrene:
hermetic wound suturing, compressing bandages.

b) Postoperative Gangrene: after arteritis surgery or after

operation in which the gastrointestinal tract is opened.
– It is favored by diabetes, ischemic muscle mass, emergency
interventions (intestinal obstruction), but it can appear also after
“clean” interventions.

c) Non-trauma and non-surgery related Gangrene: after

intramuscular or intravenous injection, infection of an
arterial or venous ulcer, perineal suppuration complicating
chronic perineal fistula or perineal abscesses.
DIAGNOSIS

• Incubation: few hours to several days.

• Pain early and constant.
• Skin: cold, pale, with ecchymosis. Erythema may be
absent or if present is mild.
• Swelling is mild to moderate in clostridial gas
gangrene, while in non-clostridial infections is
moderate to severe.
• Gaseous crepitus are rarely missing, and present the
significance of the necrosis with subsequent dead
tissue (consequence of the anaerobic metabolism).
• General signs: severely altered general status, Fever
(2% < 38 C; chills; Septic shock, MODS, death (25 –
45%)
• On surgery, after the incision a fetid smell is noticed,
with the fascia necrotic and swollen.
• Subcutaneous tissue is edematous, filled with grey,
fetid liquid.
• The infection extends through the fascia.
• If myonecrosis exists, the muscle is pale, swollen,
doesn’t shrink after section.

• Bacteriological diagnosis: most often are

multimicrobial infections, and Aerobic Gram negative
germs (O2 consumption) favor anaerobic infections.
– Anaerobic germs are rarely detected in culture from the
wound or blood cultures.
– A smear of the wound is more useful for bacteriological
orientation.
 TREATMENT
• Prophylaxis
– Open-wounds in contaminated cases (in limb
amputations for arteritic gangrene)
– Preoperative antibioprophylaxis
– “clean” surgery
• Curative treatment:
– Great emergency (45% mortality after 12 hours from
the onset)!
– Antibiotics: Penicillin G 200,000 u/kg/day; 3rd
generation cephalosporines, clindamycine
– Aggressive surgery: large incisions and debridement of
the necrotic tissue, amputations, antiseptics (H2O2 3%)
 THE TETANUS
DEFINITION
• an acute poisoning caused by the Bacillus tetani (Clostridium tetani)
toxins.
ETIOLOGY
• The germ remains stuck at the entrance gate where it secrets two
toxins:
– A hemolysin (tetanolysin) which action is at the entering gate
favoring the growth condition;
– a neurotoxin (tetanospasmin) that runs the body and is fixed on
the central nervous system – responsible for the symptoms.
• The onset of the disease involves a combination of several favorable
conditions: deep puncture wounds, anfractuous wounds with tissue
devitalization, the retention of foreign bodies, dirt.
• Tetanus occurs often due to
the neglected minor wounds.
• May occur in neonates,
postabortum, postpartum.
DIAGNOSIS

• Traumatic history establishes the infection gateway.

Between wound contamination and the onset is
running a variable time of 2-50 days (incubation
period) – a shorter incubation period means a poorer
prognosis.
• At the onset symptoms are non specific:
– wound pain, muscle spasms of the lesion,
insomnia, restlessness, headache, fever.
– In progression appear lingual paraesthesia, spams
and then paralysis of the jaw muscles (trismus).
• During the active stage (12-24 hours after the onset)
are characteristic contractions of the striated
muscles:
• dysphagia, photophobia, asphyxia.
• The failure of fluid intake and high fever lead to
dehydration.
• The muscle contractions are painful, permanent,
with intermittent clonic spasms determining specific
body positions:
• characteristic expression of the face: risus
sardonicus.
• generalized contractions of the muscles fixates the
body in specific positions, in hyperextension
(opisthotonos).
• The contracture of the diaphragm is installed in the
last phase and is followed by asphyxia and death.
• Clonic seizures are triggered by exciting bright,
acoustic or mechanical factors.
• High fever, > 40 0C, has a severe prognostic, and it is
caused by the action of the neurotoxin upon the
thermo regulation sensor in the hypothalamus.
• The patient presents hypotension, due to
hypovolemia (dehydration) and vasodilatation
mechanism, and reactive tachycardia.
• In the terminal period the patient develops
circulatory failure, pneumonia (esophago-tracheal
reflux).
• Mortality is around 50 % and increases when the
wound is closer to the head and the incubation
period is short.
TREATMENT
• Prophylaxis: vaccination.
• Curative treatment – objectives:
– neutralizing circulating toxin before it is attached to
the nervous system (after which cannot be
neutralized) with antitetanic serum and human
immune globulin in high, repeated, doses.
– Respiratory support: tracheostomy or intubation and
assisted ventilatory support.
– Antibiotics: Penicillin G in doses 20-40 MU/day
prevents the release of neurotoxin and the super
infection with vegetative forms of the bacteria.
– Surgical treatment aims to suppress the infectious
focus (wide debridement, excision, amputation if
necessary).
 THE ANTHRAX
DEFINITION
• an acute, necrotizing infection produce by the Bacillus
anthracis (coal Bacillus).
ETIOLOGY
• the vegetative form or spores of the bacillus have been
used as an biological weapon.
• Usually the bacillus source are infected animals.
• Contamination can be dermal (contact) and rarely by
respiratory or digestive tract.
Cutaneous form: the malignant pustule (the most
common form);
Respiratory form: a hemorrhagic pneumonia and
pleurisy  mediastinitis  high mortality
DIAGNOSIS OF THE CUTANEOUS FORM
• The contamination is made starting from a minor,
superficial wound;
• The onset is marked by mitigate general signs:
– Headache
– Low fever (subfebrility)
– Altered general status,
• Rarely high fever, chills, poor general status.
• Locally:
– A painless, itchy papule  hemorrhagic vesicle surrounded by
small similar vesicles with an important edema and regional
lymphadenopathy  sore (local necrosis of the skin)
– After several weeks the sore eliminates  a permanent scar.
TREATMENT
• Antibiotics: Penicillin G in high doses;
cephalosporines;
• Volemic rebalancing;
• Respiratory support;
• Local antiseptics.
 SURGICAL SITE INFECTIONS

DEFINITION
• Infections with onset between the 1st and the 30th
day postoperatively, located anywhere along the
surgical tract after a surgical procedure.
Wound infection (incisional infection)
Superficial incisional infection (involves skin and
subcutaneous tissue)
Deep incisional infection (involves fascial and muscular
plane)
Organ-related infection (intraperitoneal abscess)
ETIOLOGY
• The wound infection appear as an interaction between 3
factors:
– Bacterial factors: most often encountered Staphylococcus,
Escherichia coli, Enterobacter;
– Wound-related factors: the anatomical region of the operation,
the type of surgery (clean, clean-contaminated, contaminated,
dirty), a long preoperative stay in the hospital;
• Hair removal on the operating field to early favor wound
infection  the skin will be shaved just before the incision.
– Patient-related factors: age, poor immunity (malignancy,
cashexia, steroids, chemotherapy), diabetes, obesity.
DIAGNOSIS
• The clinical onset: usually after 3-5 days postoperatively.
– Severe streptococcal and clostridial infection may start from the
1st day/hours postoperatively.
• Signs and symptoms:
– Postoperative fever (usually on the 3rd - 5th postoperative day);
– Local increasing pain: after 24 hours the pain tends to alleviates;
in case of wound infection the pain remain or increase in intensity.
– Local edema, redness, heat.
• Surgical exploration (removal of sutures, opening the wound) (on
the first suspicion!!!) allow to notice the modified aspect of the skin
and subcutaneous tissue, and the presence of an wound secretion:
serous, seropurulent or purulent.
• Must be followed by a bacteriological examination of the
secretion.
PREVENTION
• Rigorous asepsis and antisepsis measures;
• Antibioprophylaxis at risk-patients, one hour before
surgery;
• Shaving of the operative field just before the incision;
• A clean surgery, with atraumatic gestures, good
hemostasis;
• Avoiding the closure of the intense contaminated wounds
(ischemic limbs, peritonitis, severe acute intraabdominal
infections – gangrenous appendicitis – gross spillage of
digestive content intraoperatively);
• Good anesthesia (good oxygenation and hemodinamic
stability intraoperatively).
TREATMENT
• Removal of 1-2 sutures immediate at suspicion and
surgical exploration of the wound;
• If the infection is confirmed removal of the sutures in
order to ensure a good eviction of the pus;
• Antiseptics lavage of the wound, 1-2 times per day,
or continuous irrigation in severe infections;
• Curative antibiotics in extensive, severe infections;
• General supportive treatment in severe sepsis;
• Drainage (CT- or ultrasonographycally guided) or
surgical drainage of profound or serous collections.