patho sheet # 10

VASCULAR DISORDERS


Ischemic Bowel Disease

Ischemic lesions may be restricted to the small or large intestine or may affect both, depending on the particular vessel or vessels involved. Acute occlusion of one of the three major supply trunks of the intestines-celiac, superior, and inferior mesenteric arteries-may lead to infarction of extensive segments of intestine. However, insidious loss of one vessel may be without effect, thanks to the rich anastomoses between the vascular beds. Lesions within the end-arteries that penetrate the gut wall produce small, focal ischemic lesions. The severity of injury ranges from transmural infarction of the gut, involving all visceral layers(mucosa, submucosa, muscular wall), to mural infarction of the mucosa and submucosa, sparing the muscular wall, to mucosal infarction, if the lesion extends no deeper than the muscularis mucosae.

Almost always, transmural infarction is caused by acute occlusion of a major mesenteric artery.
The three forms of ischemia are as follows:

Arterial thrombosis: severe atherosclerosis (usually at the origin of the mesenteric vessel), systemic vasculitis, dissecting aneurysm, angiographic procedures, aortic reconstructive surgery, surgical accidents, hypercoagulable states, and oral contraceptives
-Angiographic procedure : medical imaging of the blood by adding dye but it’s dangerous and may cause thrombosis.

Arterial embolism: cardiac vegetations (as with endocarditis, or myocardial infarction with mural thrombosis), angiographic procedures, and aortic atheroembolismVenous

Venous thrombosis: hypercoagulable states induced, for example, by oral contraceptives or antithrombin III deficiency, intraperitoneal sepsis, the postoperative state, vascular-invasive neoplasms (particularly hepatocellular carcinoma), cirrhosis, and abdominal trauma.

Nonocclusive ischemia: cardiac failure, shock, dehydration, vasoconstrictive drugs (e.g., digitalis, vasopressin , propranolol)
-it is not due occlusion in the vessel rather than it happens due to decrease in pressure because of shock, deyahdration etc….., which leads to decrease of blood supply to the intestine.

Miscellaneous: radiation injury, volvulus, stricture, and internal or external herniation.

Morphology :
Transmural intestinal infarction may involve a short or long segment, depending on the particular vessel affected and the patency of the anastomotic supply. Whether the ---- -occlusion is arterial or venous, the infarction always has a dark red hemorrhagic appearance because of reflow of blood into the damaged area.
The ischemic injury usually begins in the mucosa and extends outward; within 18 to 24 hours there is a thin, fibrinous exudate over the serosa.
-With arterial occlusion the demarcation from adjacent normal bowel is fairly sharply defined, but with venous occlusion the margins are less distinct. Histologically, the changes are typical of ischemic damage with marked edema, interstitial hemorrhage, necrosis, and sloughing of the mucosa. Within 24 hours intestinal bacteria produce outright gangrene and sometimes perforation of the bowel.
- Mural and mucosal infarctions are recognized by multi-focal lesions interspersed with spared areas.
- Histologic features are those of acute injury: edema, hemorrhage, and outright necrosis of the affected tissue layers, Inflammation develops at the margins of the lesions, and an inflammatory fibrin-containing exudate (pseudomembrane), usually secondary to bacterial superinfection, may coat the affected mucosa. Alternatively, chronic vascular insufficiency may produce a chronic inflammatory and ulcerative condition, mimicking idiopathic inflammatory bowel disease.

Clinical features :

-Ischemic bowel injury is most common in the later years of life. With the transmural lesions, there is the sudden onset of abdominal pain, often out of proportion to the physical signs. Sometimes the pain is accompanied by bloody diarrhea. The onset of pain tends to be more sudden with mesenteric embolism than with arterial or venous thrombosis.

-The mortality rate with infarction of the bowel approaches 90%, largely because the window of time between onset of symptoms and perforation caused by gangrene is so small.

- mural and mucosal ischemia may appear only as unexplained abdominal distention or gastrointestinal bleeding, sometimes accompanied by the gradual onset of abdominal pain or discomfort. Suspicion is raised if the individual has experienced conditions that favor acute hypoperfusion of the bowel, such as an episode of cardiac decompensation or shock. Mucosal and mural infarctions are not by themselves fatal, and, indeed, if the cause or causes of hypoperfusion can be corrected, the lesions may heal.

Angiodysplasia

-Tortuous dilations of submucosal and mucosal blood vessels are seen most often in the cecum or right colon, usually only after the sixth decade of life. They are prone to rupture and bleed into the lumen. Such lesions account for 20% of significant lower intestinal bleeding. The hemorrhage may be chronic and intermittent and only cause severe anemia, but rarely it is acute and massive
- These lesions sometimes are part of a systemic disorder such as hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome) or limited scleroderma, sometimes called the CREST syndrome.

Hemorrhoids

- Hemorrhoids are variceal dilations of the anal and perianal submucosal venous plexuses. They are common after age 50 and develop in the setting of persistently elevated venous pressure within the hemorrhoidal plexus. Common predisposing conditions are straining at stool in the setting of chronic constipation and the venous stasis of pregnancy in younger women. More rarely, hemorrhoids may reflect portal hypertension, usually resulting from cirrhosis of the liver

- Varicosities in the superior and middle hemorrhoidal veins appear above the anorectal line and are covered by rectal mucosa (internal hemorrhoids). Those that appear below the anorectal line represent dilations of the inferior hemorrhoidal plexus and are covered by anal mucosa (external hemorrhoids). Both are thin-walled, dilated vessels that commonly bleed, sometimes masking bleeding from far more serious proximal lesions. They may become thrombosed, particularly when subject to trauma. from passage of stool. Finally, internal hemorrhoids may prolapse during straining at stool and then become trapped by the compressive anal sphincter, leading to sudden, extremely painful, edematous hemorrhagic enlargement or strangulation


COLONIC DIVERTICULOSIS


-A diverticulum is a blind pouch that communicates with the lumen of the gut. Congenital diverticula have all three layers of the bowel wall (mucosa, submucosa, and most notably the muscularis propria) and are distinctly uncommon. The prototype is Meckel diverticulum.

-Virtually all other diverticula are acquired and either lack or have an attenuated muscularis propria. Acquired diverticula may occur anywhere in the alimentary tract, but by far the most common location is the colon, giving rise to diverticular disease of the colon, also called diverticulosis. The colon is unique in that the outer longitudinal muscle coat is not complete but is gathered into three equidistant bands (the taeniae coli). Focal defects in the muscle wall are created where nerves and arterial vasa recta penetrate the inner circular muscle coat alongside the taeniae. The connective tissue sheaths accompanying these penetrating vessels provide potential sites for herniations

- Colonic diverticulosis is relatively infrequent in native populations of non-Western countries. Although unusual in Western adults younger than 30 years of age, in those older than the age of 60 the prevalence approaches 50%. This high prevalence is attributed to the consumption of a refined, low-fiber diet in Western societies, resulting in reduced stool bulk with increased difficulty in passage of intestinal contents.
Morphology:

- Most colonic diverticula are small, flasklike or spherical outpouchings, usually 0.5 to 1 cm in diameter). They are located in the sigmoid colon in approximately 95% of patients

- Inflammatory changes may supervene to produce both diverticulitis and peridiverticulitis. Perforation may lead to localized peritonitis or abscess formation

Clinical Features:


-In only about a fifth of the cases does intermittent cramping or sometimes continuous left-sided lower quadrant discomfort appear, with a sensation of never being able to completely empty the rectum. Superimposed diverticulitis accentuates the symptoms and produces left lower quadrant tenderness and fever

- A high-fiber diet is recommended on the theory that the increased stool bulk reduces the exaggerated peristalsis


BOWEL OBSTRUCTION

- Although any part of the gut may be involved, because of its narrow lumen, the small bowel is most commonly affected. Four entities-hernias, intestinal adhesions, intussusception, and volvulus-account for at least 80% of the cases

- Hernias, a weakness or defect in the wall of the peritoneal cavity, may permit protrusion of a pouchlike, serosa-lined sac of peritoneum, called a hernial sac

- Hernias are of concern because segments of viscera frequently intrude and become trapped in them (external herniation).

- Pressure at the neck of the pouch may impair venous drainage of the trapped viscus. The ensuing stasis and edema increase the bulk of the herniated loop, leading to permanent trapping (incarceration). Further compromise of its blood supply and drainage leads to infarction of the trapped segment (strangulation).

- Surgical procedures, infection, and even endometriosis often cause localized or general peritoneal inflammation (peritonitis). With healing, adhesions may develop between bowel segments or the abdominal wall and the operative site. These fibrous bridges can create closed loops through which the intestines may slide and become trapped (internal herniation). The sequence of events is much the same as with external hernias.

-Volvulus refers to twisting of a loop of bowel or other structure (e.g., ovary) about its base of attachment, constricting the venous outflow and sometimes the arterial supply as well. Volvulus affects the small bowel most often and rarely the redundant sigmoid. Intestinal obstruction and infarction may follow


ENTEROCOLITIS (DIARRHEAL DISEASES)

- Although a precise definition of diarrhea is elusive, an increase in stool mass, stool frequency, or stool fluidity is perceived as diarrhea by most persons. For many individuals, this consists of daily stool production in excess of 250 gm, containing 70% to 95% water. More than 14 L/day of fluid may be lost in severe cases of diarrhea, equivalent to the circulating blood volume! Diarrhea is often accompanied by pain, urgency, perianal discomfort, and incontinence. Low-volume, painful, bloody diarrhea is known as dysentery.

- The major types of diarrheal diseases are:
Secretory diarrhea: net intestinal fluid secretion that is isotonic with plasma and persists during fasting
Osmotic diarrhea: excessive osmotic forces exerted by luminal solutes that abate with fasting
Exudative diarrhea: output of purulent, bloody stools that persists on fasting; stools are frequent but may be small or large volume
Malabsorption diarrhea: output of voluminous, bulky stools with increased osmolarity resulting from unabsorbed nutrients and excess fat (steatorrhea); it usually abates on fasting
Deranged motility diarrhea: highly variable features regarding stool output, volume, and consistency; other forms of diarrhea must be excluded


Infectious Enterocolitis

-. Infectious enterocolitis is a global problem of staggering proportions, causing more than 3 million deaths annually worldwide and accounting for up to one-half of deaths in children younger than 5 years of age in some countries

-Among the most common offenders are rotavirus, calciviruses, and enterotoxigenic Escherichia coli. However, many pathogens can cause diarrhea; the major offenders vary with the age, nutrition, and immune status of the host, environment (living conditions, public health measures), and special predispositions such as foreign travel, exposure to more virulent organisms while hospitalized, and wartime dislocation. In 40% to 50% of cases, the specific agent cannot be isolated

- Worldwide, intestinal parasitic disease and protozoal infections are also major causes of chronic or recurrent infectious enterocolitis. Collectively, they affect more than one-half of the world's population, because they are endemic in less developed nations. Of the various lower alimentary tract infections, only selected examples are described here.

- Viral Gastroenteritis

-Viral infection of superficial epithelium in the small intestine destroys these cells and their absorptive function. Repopulation of the small intestinal villi with immature enterocytes and relative preservation of crypt secretory cells leads to net secretion of water and electrolytes, compounded by an osmotic diarrhea from incompletely absorbed nutrients

- Symptomatic disease is caused by several distinct groups of viruses:

1-Rotavirus
It constitutes approximately 60% of childhood enterocolitis in the United States. The affected population is children 6 to 24 months of age; spread is by fecal-oral contamination

2- Caliciviruses, particularly the Norwalk virus, are responsible for most cases of nonbacterial food-borne epidemic gastroenteritis in older children and adults. Infection in young children is unusual

3- Additional viruses accounting for infectious diarrhea in children, almost always by person-to-person contact, include several subtypes of adenovirus (Ad40 and Ad41) and astrovirus.