on 29-Sep-2021 (Wed)

The cause of an anal fissure, and particularly the reason why the posterior midline is so frequently affected, is not com- pletely understood. Classically, acute anal fissures arise from the trauma caused by the strained evacuation of a hard stool or, less commonly, from the repeated passage of diarrhoea. The location in the posterior midline perhaps relates to the exagger- ated shearing forces acting at that site at defaecation, combined with a less elastic anoderm endowed with an increased density of longitudinal muscle extensions in that region of the anal circumference. Anterior anal fissure is much more common in women and may arise following vaginal delivery. Perpetuation and chronicity may result from repeated trauma, anal hyperto- nicity and vascular insufficiency, either secondary to increased sphincter tone or because the posterior commisure is less well perfused than the remainder of the anal circumference

Decreased dietary fibre and increased consump- tion of refined carbohydrates may be important. As with colonic diverticulitis, the incidence of appendicitis is lowest in societies with a high dietary fibre intake.

improved hygiene and a change in the pattern of childhood gastrointestinal infection related to the increased use of antibiotics may be responsible.

While appendicitis is clearly associated with bacterial pro- liferation within the appendix, no single organism is respon- sible. A mixed growth of aerobic and anaerobic organisms is usual. The initiating event causing bacterial proliferation is controversial. Obstruction of the appendix lumen has been widely held to be important, and some form of luminal obstruction, either by a faecolith (Figure 72.5) or a stricture, is found in the majority of cases.

A faecolith (sometimes refered to as an appendicolith) is composed of inspissated faecal material, calcium phos- phates, bacteria and epithelial debris (Figure 72.6). Rarely, a foreign body is incorporated into the mass.

A fibrotic stricture of the appendix usu- ally indicates previous appendicitis that resolved without sur- gical intervention.

Obstruction of the appendiceal orifice by tumour, particularly carcinoma of the caecum, is an occasional cause of acute appendicitis in middle-aged and elderly patients.

Intestinal parasites, particularly Oxyuris vermicularis (pin- worm), can proliferate in the appendix and occlude the lumen

Lymphoid hyperplasia narrows the lumen of the appendix, leading to luminal obstruction. Once obstruction occurs, con- tinued mucus secretion and inflammatory exudation increase intraluminal pressure, obstructing lymphatic drainage. Oedema and mucosal ulceration develop with bacterial trans- location to the submucosa. Resolution may occur at this point either spontaneously or in response to antibiotic therapy. If the condition progresses, further distension of the appendix may cause venous obstruction and ischaemia of the appendix wall. With ischaemia, bacterial invasion occurs through the muscularis propria and submucosa, producing acute appendi- citis (Figure 72.7). Finally, ischaemic necrosis of the appen- dix wall produces gangrenous appendicitis, with free bacterial contamination of the peritoneal cavity.

the greater omentum and loops of small bowel become adherent to the inflamed appendix, walling off the spread of peritoneal contamination and resulting in a phlegmonous mass or para- caecal abscess. Rarely, appendiceal inflammation resolves, leaving a distended mucus-filled organ termed a mucocele of the appendix. It is the potential for diffuse peritonitis that is the great threat of acute appendicitis. Peritonitis occurs as a result of free migration of bacteria through an ischaemic appendicular wall, frank perforation of a gangrenous appendix or delayed perforation of an appendix abscess.

The classical features of acute appendicitis begin with poorly localised colicky abdominal pain. This is due to mid-gut vis- ceral discomfort in response to appendiceal inflammation and obstruction. The pain is frequently first noticed in the periumbilical region and is similar to, but less intense than the colic of small bowel obstruction.

Central abdominal pain is associated with anorexia, nausea and usually one or two episodes of vomiting that follow the onset of pain (Murphy). Anorexia is a useful and constant clinical feature, particularly in children. The patient often gives a history of similar dis- comfort that settled spontaneously.

With progressive inflammation of the appendix, the parietal peritoneum in the right iliac fossa becomes irritated, producing more intense, constant and localised somatic pain that begins to predominate. Patients often report this as an abdominal pain that has shifted and changed in character. Typically, coughing or sudden movement exacerbates the right iliac fossa pain.

Atypical presentations include pain that is predominantly somatic or visceral and poorly localised.

An inflamed appendix in the pelvis may never produce somatic pain involving the anterior abdominal wall, but may instead cause suprapubic discomfort and tenesmus.

An inflamed appendix in the pelvis may never produce somatic pain involving the anterior abdominal wall, but may instead cause suprapubic discomfort and tenesmus. In this circumstance, tenderness may be elic- ited only on rectal examination and is the basis for the recom- mendation that a rectal examination should be performed on every patient who presents with acute lower abdominal pain.