• Introduction
• Most common site of acute inflammation and infection in the abdomen and the most frequent surgical emergency of the abdomen. Develops in approximately 7% of the general population. 2/3 of cases occur in 10-30 y/os.
• Pathophysiology: Obstruction followed by infection.
• (1) The lumen of the appendix becomes obstructed by: fecalith (most common cause), hyperplasia of submucosal lymphoid follicles, vegetable matter or fruit seeds, tumor (carcinoid - most common cancer of the appendix).
• (2) Mucous accumulates in the obstructed appendix with secondary infection leading to increased intraluminal pressure followed by lymphatic occlusion, venous obstruction and increasing edema and ischemia.
• (3) Bacterial invasion of the wall of the appendix occurs and acute suppuration ensues.
• (4) Venous and arterial thrombosis and gangrene occur with escape of bacteria into the peritoneal cavity followed eventually by perforation.
• Diagnosis: Acute appendicitis is primarily a clinical diagnosis.
• Symptoms. Visceral-somatic sequence of pain: patients initially complain of vague diffuse epigastric and periumbilical pain which, after ~ 8 hours, shifts to the RLQ and becomes sharp in character.
• Visceral pain is the result of stimulation of visceral afferent nerve fibers by increases in intra-abdominal pressure. The patient senses the pain in the periumbilical region. This occurs when the disease is localized to the appendix.
• Somatic pain occurs as a result of somatosensory nerve stimulation related to contact of inflamed serosa of the appendix with the parietal peritoneum producing localized pain.
• Failure to follow the classic visceral-somatic sequence occurs in up to 45% of patients with appendicitis.
• Associated symptoms: anorexia, nausea, and vomiting
• Signs
• Point localized tenderness in the right lower quadrant. Maximal tenderness is often elicited at McBurney’s point which is located two-thirds of the distance along a line drawn from the umbilicus to the right anterior superior iliac spine (marks the usual position of the appendix).
• Pt may also have muscle guarding and rebound tenderness.
• Rovsings Sign may be present (pain elicited in the right lower quadrant with palpation pressure in the left lower quadrant).
• Mean temp between 37.8 and 38.6BC. Higher temperatures occur with perforation.
• Right-sided tenderness on pelvic exam.
• As the disease progresses, a mass may be palpable which may either be a phlegmon or abscess.
• Phlegmon: an inflammatory mass consisting of the inflamed, usually non-perforated appendix with adherence of surrounding structures such as omentum, colon, small intestine, mesentery, and the right fallopian tube and ovary.
• Abscess: walled off collection of pus that results from appendiceal perforation.
• The clinical diagnosis of appendicitis is accurate in 80-85% of patients overall, but only 50-60% of women of childbearing age.
• Labs. Non-perforated appendicitis - moderate leukocytosis (10,000 to 15,000). Peritonitis – WBC >20,000.
• Abdominal imaging studies
• Plain roentgenograms may demonstrate a fecalith.
• Ultrasound exam of the pelvis is helpful in women of childbearing age to exclude gynecologic pathology.
• Helical CT scanning is now used in all patients with questionable appendicitis
• Differential diagnosis of RLQ pain is extensive: Mesenteric lymphadenitis, Pelvic inflammatory disease, Gastroenteritis, Ruptured corpus luteal cyst, Meckel’s diverticulitis, Torsion of the ovary, Regional enteritis (Crohn’s disease), Ectopic pregnancy, Right renal calculi, Endometriosis, Mittleschmertz (ruptured graffian follicle during ovulation)
• Bacteriology. Appendicitis, associated wound infections and intra-abdominal abscesses, are polymicrobic infections consisting of the combination of aerobic Gram-negative enteric organisms and anaerobes. Organisms most frequently cultured from abdominal abscess: Bacteroides fragillis, Escherchia coli, Klebsiella spp., Enterobacter spp.
• Treatment.
• (1) Volume resuscitation and correction of electrolyte abnormalities.
• (2) Surgical antimicrobial prophylaxis – general principles of antimicrobial prophylaxis:
• antibiotic administration within 30 minutes of incision
• adequate concentrations for duration of operation – redisoing a 2x the T1/2 of thedrug
• postoperative doses rarely necessary
• doses beyond 24 hrs postoperatively provide no additional benefit
• (3) Appendectomy
• Morbidity and Mortality – Risk of perforation is highest in patients at the extremes of age (infants and the elderly)

• Introduction
• Colonic diverticula are saccular outpouchings of mucosa and submucosa herniating through the colonic wall at sites of penetration of segmental blood vessels. Because they do not contain all layers of the bowel wall, they are referred to as pseudodiverticula. The incidence of diverticulosis increases linearly with age. It affects one-third of the population older than 45 years and two-thirds older than 85 years. The sigmoid colon is the most frequent site of involvement (95%). It is typically a disease of western countries.
• Diverticulitis, or inflammation of diverticuli, occurs in 10-25% of people with diverticulosis. Sigmoid colon is involved in >90% of cases of diverticulitis. 20% of all patients with diverticulitis will require surgical intervention.
• Pathogenesis
• Inflammation in a single diverticulum, (because of stasis of colonic contents) Þ obstruction and perforation of the diverticulum Þ peridiverticulitis.
• Perforation of a diverticulum may be contained within the mesocolon, developing into a phlegmon (inflammatory mass usually comprised of the inflamed sigmoid colon, adjacent omentum and often small bowel with little or no gross purulence) or an abscess, or free perforation into the peritoneal cavity may occur.
• Diagnosis of diverticulitis is based largely on clinical findings
• The classic presentation consists of LLQ pain and tenderness, fever, and leukocytosis. Patients may have an associated illeus with nausea, vomiting, and abdominal distention, LLQ mass.
• A history of previous episodes of diverticulitis or known diverticulosis is helpful but not always present
• Proctosigmoidoscopy or barium enema should not be performed during the acute stage because of the risk of precipitating or exacerbating a perforation and producing barium peritonitis.
• CT should be done when: an associated abscess is suspected, the diagnosis is unclear or, there is failure to improve with medical management. CT findings suggestive of diverticulitis include: localized thickening of sigmoid colon and increased density of the pericolic fat.
• Differential Diagnosis includes: colon carcinoma, PID, inflammatory bowel disease, appendicitis, ischemic colitis, pyelonephritis
• Treatment
• Medical Management: bowel rest, nasogastric suction for patients who are vomiting, intravenous fluids, and parenteral antibiotics. 45% will have a recurrent attack of diverticulitis.
• Surgical Management is indicated for: failure to respond to medical management and complications. Surgical therapy consists of: sigmoid resection, abscess drainage, end colostomy and Hartmann pouch (connect bowel to abdominal wall for colostomy) versus primary anastamosis.
• Complications of Diverticulitis
• Abscess formation – most common complication of diverticulitis
• Obstruction – repeated episodes of diverticulitis heal with residual fibrosis and scarring leading to obstruction
• Fistula – forms as a result of abscess rupture into a contiguous viscus. Colovesicle fistula is the most common (stool in urine).
• Free perforation

• Microbiology
• The gallbladder and bile ducts are normally sterile, but may become colonized in the presence of stones, ductal obstruction, or biliary-enteric anastamoses. Bugs gain entry from the duodenum or via the portal circulation.
• Causative organisms in biliary tract infections are principally Gram-negative aerobes, most commonly E. coli, and Klebsiella species, and Gram-positive cocci, most commonly enterococcus and staphylococcus species.
• Anaerobes are a rare cause for infections in the biliary tract.
• Acute cholecystitis
• Pathogenesis: 85-95% of patients have cystic duct obstruction by gallstones (Þ inflammation and bacterial overgrowth)
• Risk factors for cholelithiasis: fat, female, forty, fertile
• Biliary stasis and ischemia are the potential pathophysiologic factors involved in acute cholecystitis especially acalculous cholecystitis. Acalculous cholecystitis accounts for 5% of all cases of acute cholecystitis.
• Diagnosis
• Symptoms: RUQ pain, nausea, and vomiting
• Signs: fever, RUQ tenderness, Murphy’s sign (Ý tenderness and inspiratory arrest occurring with palpation of the right upper quadrant), palpable gallbladder.
• Labs: Leukocytosis, elevation of serum alkaline phosphatase, bilirubin, and liver transaminases. Ultrasound - diagnostic modality of choice for evaluating the gallbladder - 95% accurate in detecting stones. Acute cholecystitis is suggested by: wall thickness >3mm, pericholecystic fluid, intramural gas, and subserosal edema.
• Treatment
• Initial management consists of parenteral antimicrobial therapy, IV fluid hydration, correction of electrolyte abnormalities, and narcotic analgesics (avoid morphine or fentanyl which may worsen pain by causing spasm of the sphincter of Oddi).
• Cholecystectomy - definitive treatment
• Complications of acute cholecystitis: empyema of the gallbladder, gangrene, perforation, abscess
• Cholangitis
• Pathogenesis: secondary to obstruction of the common bile duct (CBD) from: stones, stricture, neoplasm, stents, or Mirizzi’s syndrome (extrinsic compression of the CBD by a cystic duct stone of an inflamed gallbladder).
• Diagnosis:
• Charcot’s triad: RUQ pain, fever, and jaundice. (<50% of patients manifest all 3)
• Reynold’s pentad: Charcot’s triad + hypotension and mental status change. (Indicative of suppurative cholangitis which requires urgent drainage of the CBD)
• Labs: Ý bilirubin and alkaline phosphatase levels, Ý liver transaminases, leukocytosis, positive blood cultures, ultrasound exam, Endoscopic retrograde cholangiopancreatography (ERCP)
• Treatment:
• (1) IV fluid hydration and parenteral antimicrobial therapy
• (2) CBD drainage, clearance of CBD stones, and cholecystectomy

• Clinical manifestations: Abrupt onset of severe generalized pain, Diffuse tenderness, involuntary guarding, rebound tenderness, and muscle rigidity, Fever, Tachycardia, Hypotension, Dehydration, Upright chest x-ray will usually demonstrate free air beneath one or both diaphragms.
• Etiology: Perforated peptic ulcer - most common cause, perforated sigmoid diverticulitis, colonic perforation, small intestinal perforation from strangulated obstruction, penetrating trauma, blunt trauma, and foreign bodies, perforated appendicitis.
• Microbiology of ensuing intra-abdominal infection: Polymicrobial with a predominance of anaerobic isolates along with facultative Gram-negative enteric organisms. Reflects the source of contamination. Anaerobic organisms, principally B. fragillis, are the most common organisms in the distal ileum and colon. E. coli is the principal facultative bacterium recovered from the distal small intestine and colon.
• Treatment:
• (1) Vigorous volume resuscitation to correct hypovolemia prior to operation.
• (2) Empiric broad spectrum antibiotics to cover the enteric Gram-negative bacilli and anaerobes
• (3) Exploratory laparotomy with control of contamination and drainage of infected intra-abdominal fluid collections.

Postoperative Infections – and common clinical situations in which they occur

• Wound Infection
• Definition: drainage of pus from an operative incision or growth of organisms from a culture of fluid from a wound that was primarily closed. Major cause of nosocomial infection in the surgical patient resulting in delayed recovery, prolonged hospital stay, and increased medical costs.
• Development of wound infection is dependent on: the pathogenicity of the bacteria involved, the magnitude of the bacterial inoculum, the local wound environment, and host defense mechanisms.
• Group A Streptococcus and C. perfringens are two examples of highly virulent bacteria that may cause wound infection within 48 hours of operation. Virulence is related to exotoxin production.
• The greater the number of bacteria in the wound at operation, the more likely that infection will develop.
• Local wound factors such as hematoma, seroma, devitalized tissue, foreign bodies including drains, and hemorrhagic shock, reduce the size of the bacterial inoculum necessary to produce infection.
• Host factors associated with an Ý incidence of wound infection include: age >60 years, malnutrition, obesity, a remote site of infection at time of operation, steroids or other immunosuppressive drugs, shock, malignancy, uremia, diabetes mellitus and other systemic diseases.
• The probability of developing wound infection was Ý in patients undergoing abdominal procedures, procedures lasting longer than two hours, and in patients with three or more concomitant systemic diseases.
• Wound Classification Criteria
• (1) Clean Surgery – elective surgery where the skin incision is closed primarily, there is no inflammation and no entry into the gastrointestinal, oropharyngeal, genitourinary, biliary or tracheobronchial tracts; and there are no breaks in sterile technique. (Examples: hernia repair, breast biopsy, thyroidectomy).
• (2) Clean contaminated surgery – includes urgent or emergent cases that would otherwise be considered clean; when there is elective, controlled opening of the gastrointestinal, oropharyngeal, genitourinary, biliary, or tracheobronchial tracts; when there is minimal spillage and/or a minor break in technique; when there is a re-operation via a "clean" incision within 7 days; or in the presence of blunt trauma with intact skin and negative exploration. (Examples: removal of a normal appendix or an uninflammed gallbladder or vagotomy and pylorplasty).
• (3) Contaminated surgery – the presence of acute, non-purulent inflammation; a major break in sterile technique, or a major spill from a hollow organ; penetrating trauma <4 hours old; or chronic open wounds to be closed or covered with soft tissue. (Examples: Cholecystectomy for acute cholecystitis or appendectomy for appendicitis).
• (4) Dirty surgery – characterized by the presence of purulence or abscess; preoperative perforation of the gastrointestinal, oropharyngeal, genitourinary, biliary, or tracheobronchial tracts, or the presence of penetrating trauma >4 hours old. Because of the high incidence of wound infection in dirty cases, these wounds should be left open and managed by delayed primary closure or closure by secondary intention.
• Top 3 bacteria causing wound infection: S. aureus, E. coli, Enterococci
• Endogenous sources of bacteria: normal flora from the skin, anterior nares, and the site of operation.
• Exogenous sources of bacteria (are less common causes for wound infection): break in sterile technique.
• most wound infections manifest themselves on the 4th to the 7th postoperative day with a variable presence of fever, incisional pain and tenderness, erythema, and fluctuance.
• Treatment: open the operative incision to drain the underlying pus.
• Intra-abdominal Abscess
• Definition: localized, walled off collection of pus that may be single or multiple and located within the peritoneal cavity, a viscus, or the retroperitoneum.
• Arises as a result of:
• (1) a perforation of the GI or biliary tracts which is walled off by peritoneal defense mechanisms
• (2) the resolution and healing of generalized peritonitis
• Bacteriology: Polymicrobic infection, Anaerobes are the predominant organisms (Bacteriodes species and anaerobic streptococci). Most common organisms recovered: Bacteriodes fragillis, Eschericia coli, Enterococcus faecalis and other streptococci, Klebsiella species and Enterobacter species.
• Signs and Symptoms:
• Fever - initially spiking Þ persistent with abscess maturity.
• Chills and tachycardia as a result of transient bacteremia
• Anorexia, nausea, vomiting and abdominal distention secondary to paralytic ileus
• Diarrhea and Abdominal pain and tenderness
• Leukocytosis with a left shift
• Diagnosis: CT is the diagnostic modality of choice with an accuracy greater than 95%.
• Sites of pus accumulation and typical clinical situations:
• Intraabdominal abscesses – in physiologic drainage basins of the peritoneal cavity. Pus is directed by gravity.
• Pelvic abscess – commonly the result of perforated appendicitis, perforated sigmoid diverticulitis, and PID.
• Left subphrenic abscess may occur as a complication of splenectomy or pancreatitis.
• Right subphrenic abscess – secondary to rupture of an intrahepatic abscess or to operation on the stomach or duodenum.
• Right subhepatic abscess – most commonly occurs as a result of emergency operations for peptic ulcer disease, biliary tract procedures and colonic surgery.
• Lesser sac abscesses – most commonly occur as a result of pancreatic abscess or an infected pancreatic pseudocyst. They may also occur as a complication of diseases of the stomach, duodenum, and pancreas.
• Interloop abscesses – are locations of pus between loops of bowel, mesentery, the abdominal wall and omentum. Usually the result of generalized peritoneal contamination.
• Visceral abscesses:
• Pancreatic abscess -– pancreatitis is the antecedent cause
• Hepatic abscess – Most common antecedent is cholangitis secondary to choledocholithiasis. 2nd most common cause is hematogenous spread.
• Splenic abscess – usually occurs following bacteremia emanating from a remote site of infection.
• Treatment:
• (1) fluid resuscitation
• (2) drainage and control of contamination
• (3) antimicrobial therapy.
• Host consequences of intra-abdominal infection: septic shock, Adult respiratory distress syndrome (ARDS), Multiple organ system failure (MOSF). Mortality varies from 5-40%.