Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_2826_Библиотеки_им_академика_М_И_Перельмана.pdf
The Colon and Rectum 113
Ischaemic colitis
Blood supply to the colon is from the superior and inferior mesenteric arteries. Watershed areas in the splenic flexure and caecum are most susceptible
to ischaemia. Ischaemic colitis is most common in the elderly and related
to underlying atherosclerosis and vessel occlusion. It also occurs in a
younger population associated with use of contraceptives, thrombophilia and
vasculitis. Presentation is with abdominal pain and rectal bleeding, and occasionally shock. Sigmoidoscopy is often normal apart from blood. Treatment
is symptomatic, although surgery may be required for gangrene, perforation
or stricture formation.
Colon polyps and the polyposis syndromes
A polyp is an abnormal growth of tissue projecting into the intestinal lumen
from the normally flat mucosal surface. Polyps may be single or multiple and
are usually asymptomatic. Most polyps in the colon are adenomas, which are
the precursor lesions of most colorectal cancer (CRC). Other types are hyperplastic, inflammatory (in patients with IBD) and hamartomatous, of which only
the latter carry a malignant potential.
Adenomatous polyps
These are tumours of benign neoplastic epithelium and are more common
with increasing age. The aetiology is unknown, although genetic and environmental factors are implicated. They rarely produce symptoms, although
large polyps can bleed and cause anaemia, and large villous adenomas
can occasionally present with diarrhoea and hypokalaemia. Although most
adenomas do not become malignant during the patient’s lifetime, they are
removed at endoscopy to reduce the risk of developing CRC. The risk of
malignant change in a polyp increases with:
• Size >1 cm
• Sessile polyps (base attached to colon wall) > pedunculated polyps
(mucosal stalk is interposed between polyp and colon wall)
• Severe dysplasia > mild dysplasia
• Villous histology > tubular
• Polyp number: multiple > single
About 5% of CRCs occur on a background of a genetic syndrome
associated with colonic polyps and an increased risk of colon cancer
(Table 3.14). A family history suggestive of one of these syndromes
may lower the threshold for investigation in a patient presenting with
gastrointestinal symptoms. In addition, referral for genetic testing may be
appropriate in a patient with colonic polyps or cancer when one of these
syndromes is suspected (e.g. young age at diagnosis <50 years, affected
family members, other associated cancers).
114 Gastroenterology and nutrition
Table 3.14 The family colon cancer syndromes
Name Mutated
HNPCC
(Lynch’s
syndrome)
Familial
adenomatous
polyposis
(FAP)
MYH-
associated
polyposis
Peutz–
Jeghers
syndrome
All are autosomal dominant inheritance, other than MYH-associated polyposis.
CRC, Colorectal cancer; HNPCC, hereditary non-polyposis colorectal cancer.
gene(s)
DNA mismatch
repair genes
APC gene Numerous colorectal
Base- excision
repair gene
STK-11 Numerous pigmented
Description Cancer risk
Accelerated
progressionfrom
adenoma to CRC.
Increased risk of
several extracolonic
malignancies;
endometrial is
commonest
polyps (>100) develop
in teenage years
Increased risk of
extracolonic
malignancies. FAP
variants are Turcot’s
(with brain tumours),
Gardner’s (with
desmoid tumours,
skull osteomas) and
attenuated FAP (fewer
polyps at a later age)
Multiple polyps (>15)
at a young age
(<50 years)
spots on lips and
buccal mucosa.
Multiple hamartomas,
polyps. Small intestinal
polyps may bleed,
obstruct or cause
intussusception
Over half develop
CRC, onset in
fourth decade
100% lifetime risk
of CRC, onset in
young adults
Increased risk
of CRC, onset in
fourth decade
Increased risk
of non-gastrointestinal and
gastrointestinal
cancer (through
adenomatous
change in polyps)
Colorectal cancer
Most colorectal cancers occur sporadically. Family colon cancer syndromes
(see Table 3.14) or cancers occurring on a background of long-standing
colitis account for a small percentage.
The Colon and Rectum 115
Epidemiology
CRC is the third most common cancer worldwide and the second most common cause of cancer deaths in the UK. Increasing age is the greatest risk
factor and the average age at diagnosis is 60–65 years. Family history, next
to age, is the most significant risk factor. In the West, the lifetime risk of CRC
is 1 in 50, increasing to 1 in 17 in those with one affected first-degree relative and greatly increased in the family cancer syndromes ( see Table 3.14).
Colon cancer is rare in Africa and Asia, largely because of environmental
differences. A diet high in meat and animal fat and low in fibre is thought to
be one aetiological factor.
Inheritance
In sporadic CRC, a stepwise accumulation of abnormalities in a number of
critical growth regulating genes drives the progression from normal mucosa
to adenoma to invasive cancer. These include the activation of tumourpromoting genes or oncogenes, e.g. K-ras, and the inactivation of tumour
suppressor genes.
Pathology
Spread is by direct invasion through the bowel wall, with later invasion of
blood vessels and lymphatics and spread to the liver and lung. Mortality of
CRC is related to the TNM stage at presentation (Table 3.15). Synchronous
(i.e. more than one) tumours are present in 2% of cases.
Table 3.15 TNM staging of colon cancer
TNM stage Description 5-year
Stage 0 Tumour confined to the mucosa
Stage 1
Stage II
Stage IIIa
Stage IIIb
Stage IIIc
Stage 4
Tumour invades submucosa (T1) or
muscularis propria (T2). No involved nodes
(N0) or distant metastases (M0)
Tumour invades into subserosa (T3) or
directlyinto other organs (T4). No involved
nodes (N0) or distant metastases (M0)
T1/T2 and 1–3 regional lymph nodes
involved(N1)
T3, N1 or T4, N1
Any T, ≥ 4 regional lymph nodes (N2)
Any T, any N + distant metastases
survival (%)
>95
80–95
65–85
55–65
35–42
25–27
5–7
116 Gastroenterology and nutrition
Clinical features
Most tumours are in the left side of the colon. They cause rectal bleeding
and stenosis, with symptoms of increasing intestinal obstruction such as
an alteration in bowel habit and colicky abdominal pain. Carcinoma of the
caecum and ascending colon often present with iron deficiency anaemia or
a right iliac fossa mass. Clinical examination is usually unhelpful, although a
mass may be palpable transabdominally or in the rectum. Hepatomegaly may
be present with liver metastases.
Investigation
The purpose of investigation is to confirm the diagnosis and stage the tumour.
Colonic examination Colonoscopy, CT colonography and barium enema
are all used to examine the colon in suspected CRC but colonoscopy and
biopsy of lesions remains the gold standard.
Blood tests A full blood count may show anaemia, and abnormal serum
liver biochemistry suggests the presence of liver metastases. Serum levels of
the tumour marker carcinoembryonic antigen (CEA) are often raised in CRC
but are more commonly used in follow-up (rising levels suggest recurrence)
rather than diagnosis.
Radiology CT scan of the chest, abdomen and pelvis is the initial staging
investigation to look for local spread and metastatic disease. PET scanning is
often used for evaluation of suspicious lesions found on CT. MRI and endoanal
ultrasound are used to locally stage rectal cancer.
Faecal occult blood tests These tests are used in population screening
studies (see below) and are not of value diagnostically.
Management
Treatment of CRC is surgical, with tumour resection and end-to-end anastomosis of bowel if possible. In very low rectal cancers abdominoperineal
resection with permanent end colostomy is necessary. Post-operative (adjuvant) chemotherapy increases survival in stage III and selected stage II
tumours. Pre-operative radiotherapy improves survival in some patients
with rectal cancer, and radiotherapy can also offer effective palliation in
patients with locally advanced disease. Patients with up to two or three liver
metastases confined to one lobe of the liver may be offered hepatic resection.
Patients with unresectable metastatic disease are commonly offered palliative
chemotherapy, which increases median survival and improves quality of life.
Prognosis
This is related to tumour stage at presentation (see Table 3.15).
Screening
High-risk individuals, e.g. from family colon cancer syndromes or those with a
first-degree relative with colon cancer aged <45 years, are offered screening
Diarrhoea 117
colonoscopy. Many countries now have population screening programmes to
detect early-stage cancer and improve outcome. In the UK, screening with
biannual faecal occult blood tests (with colonoscopy when positive) for individuals 60–69 years is predicted to reduce CRC mortality by 16%.
DIARRHOEA
Diarrhoea is a common complaint in clinical practice.
Acute diarrhoea is usually due to infection or dietary indiscretion.
Stool cultures (× 3 for ova, parasites and cysts) are sent and a flexible
sigmoidoscopy with colonic biopsy is performed if symptoms persist and no
diagnosis has been made. Treatment is symptomatic to maintain hydration.
Antibiotics may be indicated if the cause is infective. Antidiarrhoeal agents
may be used for short-term relief.
Chronic diarrhoea is defined as diarrhoea persisting for more than
14 days. Organic causes (resulting in stool weights >250 g) have to be
distinguished from functional causes (frequent passage of small volume
stools with stool weights <250 g) which can usually be done from the history.
Sometimes faecal markers of intestinal inflammation are used to differentiate
functional disorders from organic disease.
Mechanisms of diarrhoea
Osmotic diarrhoea
Large quantities of non-absorbed hypertonic substances in the bowel lumen
draw fluid into the intestine. The diarrhoea stops when the patient stops eating or the malabsorptive substance is discontinued. The causes of osmotic
diarrhoea include:
• Ingestion of non-absorbable substance, e.g. a laxative such as
magnesium sulphate
• Generalized malabsorption so that high concentrations of solute (e.g.
glucose) remain in the lumen
• Specific malabsorptive defect, e.g. disaccharidase deficiency.
Secretory diarrhoea
In secretory diarrhoea there is active intestinal secretion of fluid and electrolytes as well as decreased absorption. Secretory diarrhoea continues when
the patient fasts. Causes of secretory diarrhoea include:
• Enterotoxins, e.g. from Escherichia coli, cholera toxin
• Hormone-secreting tumours, e.g. VIPoma
• Bile salts (in the colon) following ileal disease, resection or idiopathic bile
acid malabsorption
• Fatty acids (in the colon) following ileal resection
• Some laxatives.
118 Gastroenterology and nutrition
Inflammatory diarrhoea (mucosal destruction)
Damage to the intestinal mucosal cell leads to loss of fluid and blood and
defective absorption of fluid and electrolytes. Common causes are infective
(e.g. Shigella, salmonella) and inflammatory conditions (e.g. UC and CD).
Motility related
Abnormal motility often produces frequency rather than true diarrhoea.
Causes are thyrotoxicosis, diabetic autonomic neuropathy and post-vagotomy.
Approach to the patient with diarrhoea
An assessment of the likely cause of diarrhoea is initially made on the history:
Step 1 Determine if the diarrhoea is likely to have an organic or
functional basis. Frequent passage of small-volume stools (often formed)
points to a functional cause; the exceptions are distal colon cancer and
proctitis – organic causes that present with stool frequency and normal stool
volumes. Symptoms suggestive of an organic cause include large-volume
watery stools, nocturnal diarrhoea, bloody stools, weight loss or a stool
description suggesting steatorrhoea.
Step 2 Distinguish malabsorptive from colonic/inflammatory forms
of diarrhoea. Colonic, inflammatory and secretory (see below) causes of
diarrhoea typically present with loose liquid or watery stools. Inflammatory
diarrhoea is associated with blood or mucous discharge. Malabsorption is
often accompanied by steatorrhoea.
Step 3 Rarely, measurement of stool weight by a 3-day stool collection
as a hospital inpatient may be necessary where differentiation between
organic and functional bowel disease is difficult. Occasionally diarrhoea is
factitious due to surreptitious laxative ingestion, or the patient deliberately
dilutes the faeces by adding water or urine.
Investigation
Chronic diarrhoea of likely organic origin always requires investigation.
Fig. 3.4 outlines an approach to investigation. Laxative abuse must be
excluded as a cause. Patients taking anthraquinone purgatives, e.g. senna,
develop pigmentation of the colonic mucosa (melanosis coli) which may be
seen at sigmoidoscopy. Other laxatives may be detected in the stool or urine.
Treatment of chronic diarrhoea depends on the cause.
FUNCTIONAL BOWEL DISORDERS
This is a large group of gastrointestinal disorders that are termed ‘functional’
because symptoms occur in the absence of any demonstrable abnormalities in the digestion and absorption of nutrients, fluid and electrolytes, and
no structural abnormality can be identified in the gastrointestinal tract.
Functional Bowel Disorders 119
Chronic diarrhoea
P
H
stool cultures including a search for unusual organisms.
Stool culture and baseline
bloods: FBC, ESR, B
folate, coeliac serology, TFT
Watery stool
+/– blood
Colonoscopy with ileal
and colonic biopsies
If normal may need SBFT,
serum gut hormones,
urine collection for 5-HIAA
atients with presumed functional diarrhoea, based on history, age and normal baseline
investigations (FBC, ESR coeliac serology) are excluded from this algorithm.
igh-risk patients (immunosuppressed, recent travel or antibiotics) should have multiple
folate/ MCV
,
12
Steatorrhoea or baseline
bloods suggest malabsorption
+ve coeliac
serology
OGD with D2
biopsy and
jejunal aspirate
(for Giardia)
Hb
SBFT
Fig. 3.4 Approach to the investigation of chronic diarrhoea. B12, Vitamin
B12; CT, Computed tomography; ESR, erythrocyte sedimentation rate; FBC,
full blood count; hb, haemoglobin; HIAA, hydroxyindoleacetic acid; MCV, mean
corpuscular volume; MRCP, magnetic resonance cholangiopancreatography; OGD,
oesophagogastroduodenoscopy; SBFT, small bowel follow-through; TFT, thyroid
function test.
Functional bowel disorders are extremely common worldwide, accounting
for up to 80% of patients seen in the gastroenterology clinic. Rather than
a diagnosis of exclusion after normal investigations (as the definition would
suggest), this is frequently a positive diagnosis made in a patient with
symptoms suggestive of a functional gastrointestinal disorder (Table 3.16).
It is estimated that only 25% of persons with this condition seek medical
care for it, and studies suggest that those who seek care are more likely to
have behavioural and psychiatric problems than those who do not seek care.
Altered bowel motility, visceral hypersensitivity (they have a lower pain
threshold when tested with balloon distension of the rectum), psychosocial
factors, an imbalance in neurotransmitters and gastrointestinal infection have
all been proposed as playing a part in the development of functional bowel
disorders. Common functional gastrointestinal disorders are listed below.
• Functional oesophageal disorders occur in the absence of dysphagia,
pathological gastro-oesophageal reflux disease or other oesophageal
disorder. They include globus (a sensation of a lump in the throat
Normal bloods
CT pancreas
Pancreatic
function tests
MRCP
120 Gastroenterology and nutrition
Table 3.16 Chronic gastrointestinal symptoms suggestive of a
functional gastrointestinal disorder
Nausea alone
Vomiting alone
Belching
Chest pain unrelated to exercise
Post-prandial fullness
Abdominal bloating
Abdominal discomfort/pain (right or left iliac fossa)
Passage of mucus per rectum
Frequent bowel actions with urgency first thing in the morning
persisting between meals), regurgitation and midline chest pain.
Sometimes these symptoms will respond to high-dose acid suppression
or antidepressants, e.g. amitriptyline or citalopram.
• Functional dyspepsia is associated with symptoms including epigastric
pain or discomfort, early satiety, bloating and nausea. Symptoms are
sometimes similar to peptic ulceration. Investigation is frequently
unnecessary in younger people (<55 years) but endoscopy is usually
required in older people or in those with ‘alarm symptoms’ (for
management of dyspepsia, see p. 86). Management is mainly by
reassurance and lifestyle changes (reducing intake of fat, coffee,
alcohol and cigarette smoking). PPIs help some patients with epigastric
pain. Prokinetic agents such as metoclopramide and domperidone are
sometimes helpful, particularly in those with fullness and bloating.
Eradication of H. pylori is helpful in some patients.
• Irritable bowel syndrome (IBS) can result in crampy abdominal pain
relieved by defecation or the passage of wind, altered bowel habit, a
sensation of incomplete evacuation, abdominal bloating and distension.
Subtypes of IBS can be identified according to the predominant stool
pattern: IBS with constipation, IBS with diarrhoea and mixed IBS with
alternating diarrhoea and constipation. In other patients with IBS,
diarrhoea without pain (formed stools followed by loose mushy stools
mainly in the morning) or abdominal pain without alteration in bowel
habit are the major symptoms.
Symptoms are more common in women than men, and the history is
usually prolonged. Characteristically the patient looks healthy. Examination is
usually normal, although sigmoidoscopy and air insufflation may reproduce
the pain. If frequency of defecation is a feature, a rectal biopsy should
be performed to exclude IBD. Investigation depends on the individual
patient. Young patients with classic symptoms need only simple blood
tests (full blood count, C-reactive protein and coeliac serology) to look for
evidence of other gastrointestinal diseases that present similarly, e.g. IBD
The Acute Abdomen 121
and coeliac disease. Onset of symptoms in an older patient (>50 years)
should be investigated further, e.g. colonoscopy, to exclude other pathology.
Management of functional disorders is largely reassurance, with a discussion
of lifestyle and diet. Initial treatment is symptom based with soluble fibre
supplements for constipation, e.g. ispaghula husk and antidiarrhoeal drugs,
e.g. loperamide for bowel frequency. Smooth muscle relaxants, such as
peppermint oil and mebeverine, are useful in some patients with abdominal
pain. Second-line treatment is with low-dose amitriptyline or citalopram.
Psychological interventions (hypnotherapy, cognitive behavioural therapy and
psychotherapy) are used for patients with resistant symptoms.
THE ACUTE ABDOMEN
Most patients with an acute abdomen are admitted under the care of the
surgical team and some will need a laparotomy. Medical conditions that present as an acute abdomen include diabetic ketoacidosis, myocardial infarction
and pneumonia. IBS occasionally presents with acute severe abdominal pain.
A leaking abdominal aortic aneurysm may present similarly to renal colic
and should be considered in the over 50 s presenting with apparent colic.
Mesenteric ischaemia is easily missed and should be considered in a patient
presenting with abdominal pain and prior weight loss. A plain abdominal
X-ray and erect chest X-ray are appropriate initial investigations but the
most useful imaging modalities are ultrasound (for cholangitis, cholecystitis,
appendicitis, gynaecological conditions) and CT (site and cause of intestinal
obstruction, renal colic, acute pancreatitis).
History
The history, including gynaecological and urinary symptoms, will often point
to the cause of the pain.
• Onset of pain may be sudden or gradual. Sudden-onset pain suggests
perforation of a viscus (e.g. duodenal ulcer), rupture of an organ
(e.g. aortic aneurysm) or torsion (e.g. ovarian cyst). The pain of acute
pancreatitis often begins suddenly. Ruptured ectopic pregnancy, rupture
or torsion of ovarian cysts and acute salpingitis cause lower abdominal
pain in women.
• Site of pain and radiation must be noted. In general, upper abdominal
pain is produced by pathology of either the upper abdominal viscera
— e.g. acute cholecystitis, acute pancreatitis — or the stomach and
duodenum. The pain of small bowel obstruction is often in the centre of
the abdomen. A common cause of acute right iliac fossa pain is acute
appendicitis. Pain from acute pancreatitis, rupture of an aortic aneurysm
or renal tract disease often radiates to the back.
• Pain may be intermittent or continuous. Intermittent (colicky) pain
describes pain that occurs for a short period (usually a few minutes)
and is interspersed with pain-free periods lasting a few minutes or up to
122 Gastroenterology and nutrition
Table 3.17 Some causes of mechanical intestinal obstruction
Small intestinal obstruction
Adhesions (80% in adults)
Hernias
Crohn’s disease
Intussusception
Obstruction due to extrinsic involvement by cancer
Colonic obstruction
Carcinoma of the colon
Sigmoid volvulus
Diverticular disease
half an hour. This is characteristic of mechanical obstruction of a hollow
viscus, e.g. ureteric calculus or bowel obstruction (Table 3.17). Additional
symptoms of bowel obstruction, which may or may not be present, are
abdominal distension, vomiting and absolute constipation (i.e. failure to
pass flatus or stool). Biliary pain (previously called biliary colic) resulting
from obstruction of the gall bladder or bile duct is not colicky but usually
a constant upper abdominal pain.
• Continuous pain is relentless with no periods of complete relief. It occurs
in many abdominal conditions.
Examination
• The presence of shock (pale, cool peripheries, tachycardia, hypotension)
suggests rupture of an organ, e.g. aortic aneurysm, ruptured ectopic
pregnancy. It also occurs in the later stages of generalized peritonitis
resulting from bowel perforation (see below).
• Fever is common in acute inflammatory conditions.
• The signs of peritonitis are tenderness, guarding (involuntary contraction
of the abdominal muscles when the abdomen is palpated) and rigidity on
palpation. Bowel sounds are absent with generalized peritonitis.
• Mechanical bowel obstruction produces distension and active ‘tinkling’
bowel sounds. A strangulated hernia may produce obstruction, and the
hernial orifices must always be examined.
A rectal and pelvic examination should be performed in most patients
with an acute abdomen.
Investigations
• Blood tests will demonstrate an elevated white cell count in inflammatory
conditions. The serum amylase is raised in any acute abdomen, but
levels greater than five times normal indicate acute pancreatitis.
• Urinalysis may show evidence of infection or blood in renal colic. Women
of childbearing age should have a pregnancy test.