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Gastrointestinal and abdominal problems angina pectoris

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Gastrointestinal and abdominal problems angina pectoris Powered By Docstoc
					GASTROINTESTINAL AND ABDOMINAL PROBLEMS
The enlarged synopsis of the course 6, module C, cycle II of the reformed curriculum
of the Third Faculty of Medicine, Charles University
J. Horák, J. Fanta
Abbreviations:
DD ……..differential diagnosis
Def………definition
Dg…………….diagnosis
Et……………..etiology
Ci……………..contraindications
Lab…………. laboratory findings
Th…………….. therapy


1. INTRODUCTION - problem delineation, definition, clinical importance
The gastrointestinal tract and other organs of the abdominal cavity may become a
source of numerous subjective and objective problems of the patient. The causes of
these problems may be functional, i.e. without a definable morphological or
biochemical cause, or organic, where a cause can be established. Diseases of the
gastrointestinal tract and other organs of the abdominal cavity have a bearing on many
clinical specialties (gastroenterology and hepatology, nephrology, urology,
gynecology and obstetrics, oncology, infectious diseases, angiology, rheumatology,
hematology, endocrinology etc.). Their clinical importance covers the whole spectrum
of problems from subjective complaints that impair the quality of life of the affected
patients but do not have any apparent consequences nor do they threaten the life of the
patients (e.g., irritable colon) up to dramatic situations conveying high mortality (e.g,
acute hepatic or renal failure). The appropriate medical approach must establish the
right diagnosis as fast as possible, introduce an effective treatment, remove all risk
and complicating factors, initiate preventive measures and establish prognosis. At the
same time, the physician must gain confidence and collaboration of the patient
necessary in chronic disease and last but not least he must take into account also the
economic aspects of his activities. It is sometimes very difficult to bring all these
requirements into harmony, yet to do is an imperative that we under all circumstances
must meet to the highest degree.


2. MAIN GASTROINTESTINAL AND ABDOMINAL PROBLEMS
2.1. Dysphagia and the heartburn
2.1.1. Definition and clinical presentation
 Dysphagia means difficult swallowing of the meals, odynophagia painful
swallowing.
2.1.2. Etiology and pathophysiology
- anatomy of the esophagus - see textbooks of anatomy


                 -#-
- physiology of swallowing
Swallowing (deglutition) begins with the voluntary (oral) phase, during which the
bolus is advanced into the pharynx by the tongue. There the bolus activates the
involuntary contraction of the pharyngeal muscles, i.e. the swallowing reflex. This is
designed to ensure the passage of bolus through the esophagus at the same time
inhibiting the bolus entry into the airways.
Dysphagia caused by a large bolus or by a narrowing of the esophagus lumen is called
mechanical dysphagia whereas difficult swallowing due to impaired muscle
coordination or weak peristalsis is called motoric dysphagia. The upper part of
esophagus contains striated muscle innervated by n. vagus. The motoric neurons are
cholinergic and excitatory. Motoric dysphagia of the pharynx may be the result of
neuromuscular disorders causing muscle paralysis, non-peristaltic contractions or of
the loss of the opening function of the upper esophageal sphincter. Clinical
manifestation of the pharyngeal dysphagia usually overshadows impaired function of
the cervical esophagus.
The musculature of the thoracic esophagus and of the lower esophageal sphincter
(LES) is smooth and is innervated by preganglionic vagal fibers and postganglionic
neurons from plexus myentericus. Vagal fibers are here both excitatory (mediator
acetylcholine) and inhibitory (mediator nitric oxide). Dysphagia results if the
peristalsis is weak or ineffective (e.g. in sclerodermia) or when the LES fails to open
as in achalasia.
Oropharyngeal dysphagia (oropharyngeal paralysis)
- etiology: myasthenia gravis, polymyositis, cerebral ischemia
- symptoms and signs: dysphagia, nasal outpouring of meal, aspiration
- auxilliary examination: X-ray - barium meal - disorder of the oral phase of
swallowing, aspiration
Esophageal dysphagia:
- primary motility disorders: achalasia, esophageal spasm
Achalasia:
Def: motoric disorder of the esophageal smooth muscle, LES does not relax during
swallowing
Pathogenesis: loss of intramural neurons of the myenteric plexus in the distal part of
the esophagus
- primary - etiology unknown
- secondary - infiltrating carcinoma, lymphoma etc.
Sy: dysphagia, regurgitation, chest pain
Complication: aspiration
Dg: plain chest pain - gastric bubble is missing, occassionally dilated esophagus with
the hydroaeric phenomenon can be seen
Barium meal swallowing: the patient is swallowing an X-ray contrast meal, during
which he is examined both in the vertical and horizontal position. Side projection is a
necessity. X-ray is indispensible for swallowing examination. It clearly shows


                 -#-
esophageal stenoses, diverticula and hiatal hernia. In achalasia, esophageal dilatation,
loss of peristalsis of the distal esophagus and its narrowing are present.
Th: - semiliquid diet
- pharmacotherapy: nitrates improve the esophageal passage (sublingual nitroglycerin
up to 0.5 mg or isosorbid dinitrate 10 - 20 mg per os before meals). Anticholinergic
agents are usually ineffective
- dilatation
- endoscopic treatment
- surgery (myotomy)
Esophageal spasm
Def: motoric disorder of esophageal smooth muscle, leading to numerous
incoordinated contractions
- cause is unclear, histologically focal degeneration of neural fibers is found
Sy: retrosternal pain lasting seconds to minutes that may immitate pain of angina
pectoris or reflux esophagitis, dysphagia
Dg: X-ray of the esophagus - uncoordinated simultaneous esophageal contractions,
sometimes the so-called cork-screw esophagus, LES opens normally
Th: sublingual nitroglycerin, isosorbid dinitrate p.o., niphedipin before meals
- secondary motility disorders: benign stenoses, tumors, esophageal rings,
compression from outside
Dg: X-ray, endoscopy
Th: according to etiology
- sclerodermia: weakness of the lower two thirds of the esophagus, incompetence of
LES
Sy: dysphagia following solid meals, on lying even after liquids, sometimes heartburn
X-ray: dilatation and loss of peristalsis of the distal esophagus
Th: ineffective, only the reflux esophagitis is amenable to treatment
- globus hystericus (pharyngeus)
Sy: lasting feeling of a lump in the throat, swallowing is not hampered
X-ray is normal
Th: psychotherapy
2.1.3. Diagnosis and differential diagnosis
- history: correctly taken history allows to presume dysphagia in more than 80% of
cases. If problems are caused by solid meals only, mechanic dysphagia with moderate
nerrowing of the lumen is present. If also liquids cause dysphagia, the stenosis is
advanced. On the other hand, in motor dysphagia in achalasia and diffuse esophageal
spasms the patient from the beginning has the same problems on swallowing solid
meals and liquids. Patients with sclerodermia suffer from dysphagia that follows solid
meals independently on body position, dysphagia following liquids is present on lying
but not on standing.


                  -#-
Imaging and other diagnostic methods:
X-ray: vide supra
Esophagoscopy: it allows for direct visualization and biopsy of the esophageal
mucosa. It enables to diagnose Barrett‘s esophagus, esophageal varices, stenosis,
esophagitis, diverticula, hiatal hernia, and esophageal ulcer.
Manometry: contemporary pressure registration in several parts of esophagus by
means of pressure sensors.
Upper esophagus manometry enables differentiation among dysphagia resulting from
CNS lesions, primary esophageal muscle lesions and cricopharyngeal dystonia.
Lower esophagus manometry is helpful in diagnosing achalasia, esophageal spasms
etc.
Esophageal pH-metry and perfusion (Bernstein) test with 0.1N HCl: they are helpful
in diagnosing gastroesophageal reflux disease
DD: stenocardia, pleuritis, pericarditis, vertebrogenic pain
2.1.4. Treatment
- treatment of underlying disease
- nutrition by means of a tube or gastrostomy (complication: aspiration)
- pharmacotherapy - vide supra
- dilatation
- endoscopic treatment
 A new treatment option in esophageal achalasia is local injection of botulotoxin A.
Botulotoxins selectively inhibit acetylcholine liberation from cholinergic nerve
endings on muscle plates. Irreversible chemical denervation of muscle fibers follows.
Due to regeneration processes the muscle function starts to appear again
approximately after three months and its restitution is complete in another three
month time. However, in clinical setting the therapeutic effect lasts considerably
longer. The use of botulotoxin is limited by its high cost.
- surgical procedures
2.1.5. Preventive, prognostic and opinion aspects
2.1.6. Gastroesophageal reflux
- reflux of the gastric contents into the esophagus damages esophageal mucosa (reflux
esophagitis)
- pathogenesis: weakening of LES
- anatomy and physiology of LES
Et: - increased volume of gastric contents (after the meals, pylorostenosis, gastric
hypersecretion)
- influence of body position (lying, recumbent)
- hiatal hernia
- increase of gastric pressure (obesity, ascites, gravidity)



                   -#-
- reflux esophagitis:
- moderate (histologically infiltration with granulocytes or eosinophils)
- erosive - endoscopically apparent
 - scarring and stenosis of the esophagus - caused by esophageal wall fibrosis in
chronic esophagitis
 - Barrett‘s esophagus - intestinal metaplasia (replacement of normal squamous
epithel by cylindrical epithel) - increased risk of esophageal adenocarcinoma
Sy: heartburn, chest pain (occassionally simulating pain of angina pectoris),
dysphagia in stenosis
- risk of aspiration
Dg: - history
- endoscopy + biopsy
- scintigraphy of the esophagus
- pH-metry
- perfusion test with 0.1 N HCl
Th: weight reduction, head elevation during the sleep, smoking ban, remove factors
impairing LES tonus (fatty meals, alcohol, coffee, orange juice etc.).
- pharmacotherapy: H2 blockers, metoclopramid, cisaprid, protone pump inhibitors
(omeprazol). In reflux esophagitis the treatment lasts everal months.
- follow-up and repeated endoscopies in Barrett‘s esophagus
- dilatation of stenoses
- surgical treatment: fundoplication


2.1.7. Esophageal diverticula
- pulse (upper and lower esophagus) and traction (middle esophagus) diverticula
- Zenker‘s diverticulum (dorsal wall of hypopharynx)
Sy: small diverticula are asymptomatic, in large - dysphagia, vomiting of older meals
Dg: history, X-ray, endoscopy


2.1.8. Esophageal webs and rings
Plummer-Vinson syndrome: hypopharyngeal web with dysphagia and sideropenic
anemia
Schatzki‘s ring: localized in LES area, presents with dysphagia


2.1.9. Hiatal hernia
- sliding - gastric fundus ascends above the diaphragm, it becomes more frequent with
age and may cause reflux



                 -#-
- paraesophageal - risk of strangulation, treatment is surgical


2.2. Nausea and vomiting
2.2.1. Definition and clinical picture
Nausea is defined as a feeling of imminent vomiting. Vomiting means evacuation of
gastric contents by mouth. Usually, nausea precedes vomiting and is accompanied by
signs of parasympathetic activation (pale skin, perspiration, salivation, ev.
hypotension and bradycardia).
2.2.2. Etiology and pathophysiology
- coordinated activity of striated muscle and autonomous nervous system
- chemoreceptors
- mechanism of vomiting: center for vomiting is localized in dorsolateral part of
reticular formation. In integrates and controls the act of vomiting. The center gets
afferent stimuli from the GIT, from higher stem and cortical centers, from labyrinth
and chemoreceptor triggering zone in area postrema in the floor of the IVth ventricle.
Efferent fibers lead from the centre of vomiting via n. phrenicus, spinal nerves and n.
vagus. During vomiting, LES and gastric fundus are relaxed and pylorus is contracted.
Intraabdominal pressure increases markedly owing to forceful contraction of the
diaphragm and abdominal wall muscles. The gastric contents enters esophagus, from
where it is expelled by increased intrathoracic pressure into the mouth. Esophageal
antiperistalsis may contribute to this act. During vomiting, the soft palate is elevated,
the glottis is closed and breathing stops, which prevents gastric contents from entering
nasopharynx and trachea.
- etiological factors: kinetosis, psychic factors (mental anorexia), intracranial
processes, drugs, metabolic causes, local factors
- GIT diseases: inflammations (acute gastritis, cholecystitis, appendicitis, pancreatitis,
peritonitis), obstruction (ileus, pylorostenosis), gastroparesis
- CNS diseases: Meniere‘s disease, kinetosis, migraine, meningitis
- drugs: apomorphin and other opiods, digitalis, L-dopa, cytostatics
- metabolic causes: uremia
- others: acute myocardial infarction, advanced tumours
2.2.3. Diagnosis and differential diagnosis
- history and physical findings
- time relation to meal intake (vomitus matutinus in early pregnancy, early vomiting
after a meal - pylorostenosis, late vomiting – Zenker‘s diverticulum, achalasia)
- vertigo and tinnitus – Meniere‘s disease
- alleviation of pain following vomiting - peptic ulcer
- auxilliary examinations - vide supra
Complications:
Regardless of the underlying cause, vomiting can lead to severe conseqeunces such as
esophageal wall rupture, Mallory-Weiss syndrome etc.


                 -#-
DD: regurgitation, rumination, singultus
2.2.4. Treatment
- symptomatic
- causal
2.2.5. Preventive, prognostic and opinion aspects


2.3. Upper-type dyspepsia
2.3.1. Definition and clinical picture
Heterogeneous group of problems (pain, pressure, feeling of fullness in the
epigastrium) arising in relation to food intake
2.3.2. Etiology nad pathophysiology
anatomy and clinical physiology of the stomach, duodenum, biliary tree and pancreas
functional disorders: a functional problem can be presumed whenever a structural or
biochemical underlying cause of the patient‘s problems cannot be proved. The very
term "functional disorder" implicates favorable prognosis so that the patient will not
be damaged if the cause of his troubles cannot be established. However, prognosis is
favorable only quoad vitam, whereas it is mostly gloom quoad sanationem - the
patient‘s problems usually last for years and pose a burden for the patients as well as
the health-care system. The likelihood of a functional disorder increases with time and
absence of serious disease manifestations. Functional gastrointestinal disorders can be
divided according to site of presumed origin into esophageal, biliary, intestinal,
anorectal and chronic abdominal pain.
Functional dyspepsia of the upper type is characterized by pressure, feeling of fullness
or straightforward pain in epigastrium lasting more than three months without clinical,
biochemical, endoscopic or sonographic proof of an organic disease. Dyspepsia may
be further specified as reflux (with burning in epigastrium), dysmotility (uncertain
pressure without a clear-cut pain), ulcer (pain in epigastrium) biliary (pressure, pain or
even colic under the right costal margin) or unspecified, which evades the described
types. This division, however, is of limited clinical importance. In some patients, the
symptoms of upper-type dyspepsia may mingle with those of irritable colon (vide
infra).
Pathophysiology of functional gastrointestinal problems
Important factors for the origin functional GIT problems are dysmotility and
decreased level for perception of intestinal distension (increased visceral sensibility).
Other factors worth mentioning are infectious diarrhoea (in some patients symptoms
of irritable colon may last for months) and the syndrome of bile-acid loss, which is
frequent esp. following cholecystectomy. Bile acids enter increasingly into the colon,
whose mucosa they irritate and thus cause the symptoms of irritable colon mainly
with diarrhoea. In the pathogenesis of functional GIT disorders also abnormal
evaluation of peripheral impulses in CNS, psychic disorders (depression, anxiousness,
stress) and acquired behaviour of the patient in the sense of unintended aggravation
take part.




                   -#-
DD: gastroesophageal reflux, H. pylori infection, lambliasis or amebiasis,
duodenogastric reflux, motility disorders of the gallbladder and Oddi sphincter,
lactose intolerance, food allergy, inflammation and tumours.
For practical reasons, it is not possible to examine thoroughly every patient presenting
with functional gastrointestinal disorders. An individual approach is necessary. The
more demanding examination procedures are indicated especially in cases suspect of a
possible organic disease. A therapeutic test may be helpful. E.g., protone pump
inhibitors can be tried in suspected reflux, prokinetics in feeling of fullness,
antispasmodics in spasms and psychotherapy and antidepressants in psychic lability.
Helicobacter pylori infection
The importance of Helicobacter pylori in the pathogenesis of GIT diseases may be
exaggerated. It seems likely that H. pylori does not act as a direct etiological factor
but contributes to GIT diseases as one of many other factors, moreover acting on the
mucosa already damaged by other influences.
2.3.3. Diagnosis
- history and physical findings
- auxilliary examinations
- laboratory methods
- sonography
- endoscopy: esophagogastroduodenoscopy
 - ERCP (endoscopic retrograde cholangiopancreaticography). Indications: obstructive
icterus, choledocholithiasis, cholangitis, acute biliary pancreatitis, suspicion on a
tumor of bile ducts or pancreas, cholestasis of unclear etiology (stenosis of the papilla,
suspicion on primary sclerosing cholangitis etc.), examination preceding a planned
endoscopic intervention such as drainage
 Ci: cardiorespiratory failure, shock, stenosis of the esophagus, pylorus or duodenum,
coagulopathy, disagreement or lack of collaboration from the side of the patient
- PTC - percutaneous transhepatic cholangiography
 Indications: unavailability or previous        failure of ERCP, preparation for
cholangioscopic intervention
- radiology
DD: gastroesophageal reflux, motility disorders, ulcer disease, diseases of the
gallbladder, pancreatitis, malabsorption, inflammatory bowel disease, abdominal
angina


2.3.4. Differential diagnosis of dyspeptic disorders
Helicobacter pylori infection
- microaerophilic Gram-negative bacillus in the mucus layer
- it does not invade mucosa
- it produces proteins (urease, chemotactic proteins for neutrophils, platele activating
factor, proteases, phospholipases) → damage to the mucus


                   -#-
- the prevalence of H. pylori increases with age
- direct transfer from man to man (fecal-oral, oral-oral)
- the majority of infected persons will never develop an ulcer
- diagnosis: - histology
- cultivation
- urease test
- breath test (production of radioactive CO2 from isotope-marked urea given p.o.)
- serology
- treatment: tripple combination (omeprazole 2x20 mg + clarithromycin 2x250 mg +
metronidazole 2x500 mg or amoxycillin 2x1 g for one week)
- effect: H. pylori eradication, decrease in ulcer recidives
Peptic ulcer
Def.: defect of gastric or duodenal mucosa reaching into submucosa
Etiopathogenesis: dysbalance of protective (gastric mucus, NaHCO3 secretion,
prostaglandins, blood perfusion) and aggressive (HCl, pepsin) factors
drugs - non-steroidal antiinflammatory drugs
Zollinger-Ellison syndrome
A. Duodenal ulcer
In 95% in duodenal bulb. The highest incidence is in the 5th decenium, both sexes are
affected
Risk factors (appart from those mentioned above):
- genetic factors (blood group 0, antigen HLA-B5)
- smoking
- alcoholic cirrhosis
- chronic renal failure
Sy: - epigastric pain, typically 90 or even more minutes following a meal
- the pain often wakes up the patient, is alleviated by meals and antacids
- some ulcers are asymptomatic
- complications:
- bleeding
- penetration
- perforation
- pylorostenosis
- physical findings: epigastric pain on palpation
- auxilliary examinations:
- X-ray with baryum meal


                   -#-
- gastroduodenoscopy
- gastric secretion - today in suspicion on Z. - E. syndrome only
- serum gastrin concentration
Th:
- eradicate H. pylori
- auxilliary treatment:
 - diet: no dietetic manipulation has been shown to accelerate ulcer healing. We can
recommend ban on coffee, alcohol and substances that are not tolerated by the patient
 - antacids (a mixture of aluminium hydroxide and magnesium hydroxide, calcium
carbonicum, NaHCO3)
- antagonists of H2 receptors (cimetidine, ranitidine, famotidine)
- anticholinergic agents (pirenzepin) - low efficacy
- sucralfate - it blocks H-ions access to the ulcer base
 - colloidal bismuth - it creates a defence layer on the mucosa, suppresses H. pylori
and treats gastritis
 - prostaglandins - alone are not used in the treatment, PGE1 analogue misoprostol is
used in prevention of NSAID-induced ulcers but it is very expensive
- proton pump inhibitors - omeprazol, pantoprazol, lansoprazol - are very effective
- evaluation of effectivity of any treatment is complicated by high tendency to
spontaneous healing and frequent recidives
- surgical treatment: nowadays of limited importance
 - various types of vagotomy - preferably superselective vagotomy, sometimes in
combination with pyloroplasty
- gastric resection type Billroth I and II
B. Gastric ulcer
The highest incidence is in the 6th decade with slight prevalence of males
Severe gastritis is usually found in the adjacent mucosa
Benign ulcers are found predominantly in the antrum, nearly always associated with
H. pylori infection
Secretion of HCl is normal or decreased, gastric evacuation is slow
Up to 25% of gastric ulcers are due to NSAIDs.
Sy: - epigastric pain – soon following a meal, some patients vomit without having
pylorostenosis
Complications: bleeding, perforation, penetration, pylorostenosis
Dg: - history – often atypical
-     gastric X-ray
-     gastroscopy – it is necessary to take at least 6 bioptic samples from the ulcer
      margins to exclude a malignancy


                   -#-
-   test for H. pylori infection
Th: - stop NSAIDs
-   if H. pylori tests positive – eradicate using triple therapy
-   protone pump inhibitors
-   H2-blockers and carbenoxolone have limited efficacy
-   if the ulcer does not heal or at least markedly diminishes within two months, it us
    suspect of malignity
-   surgical treatment: Billroth I resection (today performed exceptionally)
Complications of surgical treatment:
-   relapse of the ulcer
-   reflux gastropathy
-   afferent loop syndrome
-   dumping syndrome
-   anemia (sideropenic or from lack of vitamin B12)
-   postvagotomic diarrhoea
-   osteoporosis and osteomalacia
-   steatorrhoea
-   development of gastric cacinoma


Acute and chronic gastritis
Gastritis = inflammation of gastric mucosa of various etiology
Acute gastritis
-   H. pylori - induced
-   caused by other bacteria (phlegmonous – staphylococci, streptococci)
-   viral (herpes simplex, cytomegalovirus)
-   parasitic
-   mycotic
Tendency to spontaneous healing
Chronic gastritis is divided into two types:
Type A (autoimmune) – it affects gastric fundus and body only. Typically found in
pernicious anemia. Laboratory findings: achlorhydria and low pepsinogen-1
concentration, high serum gastrin concentration. Antibodies against parietal cells and
intrinsic factor may be present. Infection with H. pylori may occassionally be found.
In patients with pernicious anemia gastric glands disappear. Because intrinsic factor is
produced in parietal cells, anemia ensues.




                   -#-
Type B (non-autoimmune) is more frequent than type A. At the beginning antrum is
affected, later whole stomach is involved. It is caused by H. pylori infection. The end
result is atrophic gastritis with low serum gastrin concentration.
Both gastritis types pose an increased risk of gastric carcinoma. H. pylori infection
may be an independent risk factor for gastric carcinoma.
MALTomas – lymphomas of the gastric wall (Mucosa Associated Lymphoid Tissue)
are apparently caused by chronic H. pylori infection
Treatment of chronic gastritis:
-   in pernicious anemia, life-long treatment with vitamin B12
-   if peptic ulcer or MALToma is not found, no other treatment including H. pylori
    eradication is recommended


Ménétrier’s disease
gastric mucosa hyperplasia, often with exudative enteropathy
Th: anticholinergic agents, H2-blockers, gastrectomy


Zollinger-Ellison syndrome
multiple peptic ulcers, often in atypical localization and gastric hypersecretion
It is caused by gastrinoma (tumour from delta-cells of pancreatic islets)
Sy: peptic ulcers, diarrhoea caused by gastric hypersecretion
Dg: - BAO > 15 mmol/h
-   hypertrophic mucosal folds and multiple ulcers on endoscopy and X-ray
-   hypergastrinemia
-   secretin test (gastrinemia increase following i.v. secretin application)
-   imaging methods (CT, arteriography) often fail to visualize a tumour
Th: - H2 receptor antagonists
-   proton pump inhibitors (treatment of choice)
-   tumour resection
-   gastrectomy


Drug-induced gastropathy
Non-steroidal antiinflammatory drugs (NSAIDs) come among medicaments most
commonly prescribed. Typical examples are acetylosalicylic acid, ibuprofen,
indomethacine, diclophenac, piroxicam and nowadays also the selective
cyclooxygenase II inhibitor nimesulid (Aulin). NSAIDs suppress formation of
prostaglandins from arachidonic acid by means of cyclooxygenase. The result is their
analgetic, antipyretic and antiinflammatory effect. These beneficial effects are,
however, accompanied by their untoward effects, in the first place gastropathy.
Protaglandins have important gastroprotective properties. NSAIDs application may


                  -#-
cause various forms of gastric and duodenal mucosa damage (hyperemia, petechias,
erosions and ulcers with a potential for bleeding, penetration and perforation). Before
starting a protracted NSAIDs treatment it is therefore necessary to search the patient’s
history for peptic ulcer, upper GIT bleeding and current use of corticosteroids. In
some cases it will be useful to perform gastroscopy prior to the start of the treatment.
If endoscopy reveals an active mucosal lesion, NSAIDs are contraindicated and can
be used after healing the lesion only, preferably with contemporary anti-ulcer
treatment (proton pump inhibitors omeprazol or pantoprazol, H2 antagonists
famotidin or ranitidin). If present, H. pylori infection must be eradicated.
Cytoprotective prostaglandin analogues such as misoprostol have not gained clinical
acceptance. Theoretical advantages of selective COX-II inhibitors (nimesulid) have
not yet been proven by clinical studies.
-   H. pylori infection can be found in some patients but etiological relation has not
    been established
Cholelithiasis and cholangitis
Pancreatitis and its sequelae
Tumours


2.3.4. Treatment
-   symptomatic
-   causal


2.3.5. Preventive, prognostic and opinion aspects


2.4. Abdominal distension, bloating and flatulence
2.4.1. Definition and clinical presentation
-   abdominal volume enlargement from various causes
-   increased gas contents in the intestines
-   increased passage of gas through the anus
-   mechanical difficulties up to limitation of ventilation


2.4.2. Etiology and pathophysiology
-   abdominal distension due to accumulation of fluid, gas or fat (obesity)
-   fluid: - free (ascites, bleeding, peritonitis)
-   confined (cysts, pancreatic pseudocysts, abscesses, dilated stomach or urinary
    bladder)
-   gas – intraluminal (bloating, ileus)
    - free (viscus perforation)
    - intramural (pneumatosis cystoides intestinalis)


                   -#-
2.4.3. Diagnosis and differential diagnosis
-   history and physical findings
-   laboratory – hypoproteinemia, signs of an iflammation
-   fluid – sonography
-   CT, cavography, arteriography
-   puncture, catheter or tube insertion
-   examination of ascites (chemistry, cytology, culture)
-   laparoscopy
-   gas – X-ray examination on standing and lying


2.4.4. Treatment
-   ascites – evacuation
-   dietary intervention (salt and water restriction)
-   drug treatment (diuretics, antibiotics, chemotherapeutics, cytostatics, albumin
    etc.)
-   TIPS (transjugular intrahepatic portosystemic shunt), ascites reinfusion, LeVeen’s
    shunt, liver transplantation)
-   gas – intraluminal – conservative treatment (think of ileus)
         -     free – surgery
         -     intramural – conservative treatment
2.4.5. Preventive, prognostic and opinion aspects


2.5. Abdominal pain
2.5.1. Definition
Pain is an unpleasant perceptual and emotional feeling connected with a real or
potential tissue damage. There are two basic forms of pain: acute and chronic. Acute
pain is short-lived with time and causal relation between tissue damage and feeling of
pain. Chronic pain lasts long, longer than the respective wound healing and often no
clear cause can be discerned.


In abdomen, two distinct types of pain can be differentiated:
a) visceral pain;         b) somatic pain.


A constant presenting feature of acute abdomen, pain may originate from the
abdominal viscera (visceral pain) or from the parietes (somatic pain). Visceral and
somatic pain differ from each other in character, localization, and in the effective
stimulus required for evoking a response.




                    -#-
Visceral pain is dull in character, poorly localized, diffusely felt, and projected more
often to the anterior rather than to the posterior abdominal wall. In contrast, somatic
pain is sharp in character, well localized, and is felt directly over the area of parietal
peritoneal irritation.


NEUROANATOMIC CONSIDERATIONS


Autonomic nervous system. The autonomic nervous system includes that portion of
the central and peripheral nervous system which is primarily concerned with
regulation of visceral function in contrast to the somatic nervous system, which
controls the function of voluntary muscles and innervates skin through which
different forms of sensation are appreciated.
Anatomically, the autonomic nervous system is divided into craniosacral and
thoracolumbal outflow. The cell bodies of craniosacral outflow are located in the
brain stem and in the second, third, and fourth sacral spinal segments; the cell bodies
of thoracolumbal outflow are located in all the thoracic and first two lumbar segments
of the spinal cord.
Functionally, the autonomic nervous system is divided into parasympathetic and
sympathetic divisions; the parasympathetic division corresponds to craniosacral
outflow and the sympathetic to thoracolumbar outflow.
Both these divisions supply the same organ and exert opposite effects.


Both visceral and somatic pain impulses are carried to the brain over multisynaptic
relay. The primary afferents transmit impulses from the receptor site to the spinal
cord, the secondary neurons from the spinal cord to the thalamus, and tertiary neurons
from the thalamus to the cerebral cortex.


PAIN STIMULI. Normal viscera are sensitive to many stimuli which when applied to
the surface of the body evoke a painful response. An effective stimulus for eliciting
pain in a hollow viscus is its distension or forced contraction. As for solid organs,
pain fibres are present in their capsule, and stretching of the capsule by distension and
the degree of distensibility of the capsule determine the intensity of pain. Ischemia is
also believed to be a potent pain stimulus.


REFERRED PAIN. The phenomenon of pain in area other than where the painful
impulses originate is referred pain, a good example being the pain experienced over
the ispilateral shoulder caused by irritation of the under surface of the diaphragm.
Pain arising from a viscus is referred to the skin with the corresponding nerve supply.
The primary afferents from stomach, duodenum, pancreas, gallblader, hepatic capsule
etc. enter the spinal cord from the sixth to eights thoracic segments, and the pain
originating from these structures is referred to the epigastrium, which is supplied by
spinal nerves of the same segments. Pain is referred to the periumbilical area from
structures whose afferents enter the ninth and tenth thoracic segments, which include
the distal duodenum, jejunum, ileum, appendix, ovaries, testes, upper ureter, and



                 -#-
pancreas. Pain arising from the colon, bladder, rectum, lower ureter, and uterus,
whose afferents enter the eleventh and twelfth thoracic and first two lumbar segments,
is referred to the hypogastrium.


PAIN THRESHOLD. The degree of painful stimulation required to produce an
awareness of pain is the pain threshold. The pain threshold differs from person to
person, and differs in the same person from time to time, depending on various
factors. Pain perceived and the reaction to that perception cannot be measured; a
given individual´s reaction to pain depends not only on the painful stimulus, but also
on his physical and psychological state.


REFLEX MANIFESTATIONS. Anorexia, nausea, vomiting, diaphoresis, abdominal
wall rigidity, changes in heart rate and blood pressure, and altered gastrointestinal
motility – all of which may accompany acute abdominal conditions – are reflexly
produced.


2.5.2. PRESENTATION
Abdominal pain is the main symptom of ACUTE ABDOMEN. Diagnosing acute
abdomen may be compared to solving a jigsaw puzzle; the pieces of the puzzle must
fit together properly for the problem to be solved. History, physical examination, and
laboratory findings, as well as the information gained from imaging techniques such
as X rays, sonography, computer tomography etc. often are pieces joined in solving
the puzzle of acute abdomen.


Of the presenting symptoms, pain is a constant feature (in acute abdomen), whereas
disturbances in gastrointestinal function such as anorexia, nausea, and vomiting are
inconstant. The patient should be carefully questioned regarding the onset of pain and
its duration, location, radiation, and character, as well as factors that aggravate or
relieve the pain, since these details provide important diagnostic clues.


Onset. Pain that awakens a patient is very significant and is almost always due to an
organic problem. The onset of pain in individuals with a perforated ulcer is
dramatically sudden – so dramatic that the majority recollect the details of their
activity up to the moment of perforation. Occasionally the onset of pain
accompanying pancreatitis mimics that of ulcer perforation in suddenness. Colic pain
occurs fairly suddenly, whereas with inflammation the onset of pain is usually
gradual.


Duration. Until otherwise proven, pain of 6 hours´ duration or more should be
attributed to an acute abdomen. The duration of pain gives a clue as to the progression
of the disease. For example, the inflammation in acute appendicitis of less than 24
hours is usually confined to the viscus, whereas the inflammation will have spread
beyond the confines of the viscus in appendicitis of longer than 48 hours duration.




                -#-
Location. Pain of visceral origin is poorly localized and is referred to the dermatome
with corresponding nerve supply. Pain of early acute appendicitis is referred to the
periumbilical area, and pain of acute cholecystitis is referred to the epigastrium or
right hypochondrium. Once inflammation has spread to the adjacent parietal
peritoneum, the pain becomes sharp and localizes to the area of parietal peritoneal
irritation. For this reason, as inflammation progresses periumbilical pain of early
acute appendicitis shifts to the right lower quadrant; epigastric pain of acute
cholecystitis shifts to the right upper quadrant.


Radiation. In some instances radiation of pain is characteristic enough to enable
accurate localization of its source. Biliary colic pain typically radiates to the right
scapular area and pain of ureteral colic to the ipsilateral groin. Pain of diaphragmatic
irritation is referred to the shoulder.


Character. Pain of colic is intermittent and sharp. Between attacks, the patient may
be free from pain. Continuous, sharply localized pain results from irritation of the
parietal peritoneum. Patients often characterize the pain as gnawing, tearing, or
stabbing; these descriptive terms are of occasional diagnostic value. The pain of an
abscess is often throbbing, the pain of friction between two inflamed surfaces is
stabbing, and the pain of a dissecting aneurysm is tearing in character.


Factors aggravating or relieving pain. Movement aggravates pain in patients with
peritonitis. Stretching of muscles contiguous to inflammation aggravates pain; when
an acutely inflammed appendix apposes the iliopsoas muscle, the thigh is held in a
position of flexion and attempts at extension cause pain. Pain aggravated by
micturition suggests the presence of an inflamed viscus in intimate contact with the
bladder. Changes in posture may relieve pain; in pancreatitis the pain is somewhat
eased by leaning forward and pain at the shoulder tip from irritation of the
undersurface of the diaphragm caused by extravasated blood is sometimes relieved
when the patient assumes a semiupright position. Vomiting relieves the pain of gastric
outlet obstruction and, not surprisingly, patients often voluntarily induce vomiting to
obtain relief.



2.5.3. PHYSICAL EXAMINATION


General examination. Time permitting, the physical examination must be thorough,
including not only examination of the abdomen, but also of the patient as a whole.
The patient´s physical appereance may provide valuable clues in diagnosis and must
be carefully observed while taking the history. The patients with peritonitis remain
immobile, or move very cautioously when they must, since movements aggravate the
pain. In contrast, patients with colic are restless, frequently changing position in bed.
Rapid breathing, pallor, and beads of perspiration on the forehead are indicative of
hemorrhage. Rapid breathing in the absence of other signs of hemorrhage may be a
clue in the diagnosis of pneumonia. Patients with acute cholecystitis, cholangitis, and


                 -#-
pancreatitis may be jaundiced. Some patients complain little and look surprisingly
well despite the presence of a serious intraabdominal condition. Therefore, one should
not dismiss the possibility of an acute abdomen solely based on appereance.
Temperature, pulse, and blood pressure should be routinely checked in every patient.


Examination of the abdomen
INSPECTION. The abdomen should be completely exposed and observed under
adequate light – if it is not, important findings are apt to be missed. The abdomen
should be inspected for restricted respiratory movements, scars, rash, discoloration,
distension, masses, and abdominal pulsations.


PALPATION. Prior to palpation, patients should be asked to locate the site of
maximum pain. Patients with pain of visceral origin find it difficult to localize the
area of maximum pain and not uncommonly place the whole hand over an area of the
abdomen. In contrast, the patients with pain arising from irritation of the parietal
peritoneum readily locate the area of maximum pain with the tip of a finger.
Palpation should be caried out with utmost gentleness using the palmar surface of the
fingers. Pressing the abdomen with the tips of fingers should be avoided. Cold hands
placed on the abdomen cause the muscles to contract reflexly, rendering palpation less
satisfactory. During palpation, it is always preferable to start at a site farthest from the
area of maximum pain and work gradually toward it. By this maneuver, the patient is
reassured that he will not be subjected to unnecessary discomfort. Signs to look for
during palpation are tenderness, rebound tenderness, rigidity, and masses.
Tenderness is present thorought the abdomen in general peritonitis. Localized
tenderness, which is due to irritation of the underlying peritoneum, assists in diagnosis
by its location. Tenderness in the right lower quadrant is most commonly due to acute
appendicitis, in the right upper quadrant to acute cholecystitis, in the epigastrium to
acute pancreatitis, and in the left lower quadrant to sigmoid diverticulitis.
Rebound tenderness is pain produced by friction between two inflamed peritoneal
surfaces. It can be produced by several maneuvers, the simplest being to instruct the
patient to cough; pain thus aggravated is a sign of rebound tenderness. Rebound
tenderness can also be elicited by gradually applying pressure over the area of
tenderness and then suddenly releasing the pressure; friction between the inflamed
surfaces with the sudden release of pressure produces pain (Blumberg´s sign).
Rebound tenderness can also be elicited by displacing the inflamed structure through
the application of pressure at a site away from the area of involvement (Rovsing´s
sign). For example in acute appendicitis pressure over the left lower quadrant
aggravates pain in the right lower quadrant by displacing the viscera.
Rigidity of the abdominal wall is caused by the reflex or involuntary muscle
contraction produced by irritation of the parietal peritoneum. The boardlike rigidity of
a perforated ulcer is so striking that, once palpated, it is never again mistaken.
However, in other conditions, where rigidity is not so striking, differentiation from
voluntary muscle contraction may be difficult. Rigidity may be absent in patients who
are moribund, toxemic or take corticosteroids.




                 -#-
Masses felt during abdominal examination are always significant. The mass may be
intraperitoneal or extraperitoneal and should be evaluated as to location, consistency,
mobility, tenderness, and presence or absence of pulsation.


Percussion. This is useful in differentiating the causes of abdominal distension and in
delineating the borders of palpable masses. The abdomen distended with gas is
tympanic, whereas that distended with fluid is dull to percuss. When a large amount
of fluid is present, a fluid wave can be elicited by tapping one flank and feeling the
transmitted impact by the other hand placed on the opposite side. Dullness which
shifts with the change of position of the patients is useful in demonstrating fluid of
lesser amount. Solid viscera are dull to percuss. Normal liver dullness is obliterated
when sufficient air escapes into the peritoneal cavity following perforation of a
hollow viscus. Liver dullness may also be absent because of interposition of colon
between liver and diaphragm (Chilaiditi‘s syndrome).


Auscultation. This is helpful in detecting changes in bowel sounds, presence of
friction rub and vascular bruit. The bowel sounds in mechanical intestinal obstruction
are high-pitched and hyperactive, whereas in gastroenteritis they are hyperactive but
not high-pitched. In paralytic or adynamic ileus, bowel sounds are absent; one must
listen for at least one minute to confirm their absence. When two inflamed surfaces
rub against one another friction rub is produced, but the findings is rare. In elderly
patients vascular bruits secondary to arteriosclerotic narrowing of the visceral arteries
are not uncommon, and the presence of a bruit by itself is not of diagnostic value
except as an indicator of a narrowed vessel. With complete obstruction the bruit
disappears; the disappearance of a previously known bruit may have significance
when bowel ischemia is suspected.
Rectal and pelvic examination. Examination of a patient with acute abdomen is
incomplete without a rectal examination; rectal examination provides important
diagnostic clues which may not be apparent on abdominal examination alone, and
therefore should never be omitted. As in abdominal palpation, one must palpate for
the presence of tenderness, masses, and fluid in the cul-de-sac. Masses, when present,
are often better evaluated by bimanual examination.
In female patients, pelvic examination supplements rectal examination. Discharge
from vagina and tenderness in the region of Bartholin glands should be noted.
Tenderness elicited on pelvic examination may be due to salpingitis, pelvic
appendicitis, or torsion of an ovarian cyst. Movement of the uterus in the presence of
pelvic peritonitis is painful. As in rectal examination, pelvic masses must be examined
bimanually for more accurate delineation.



2.5.4. IMAGING PROCEDURES


X-Ray studies. Of the various imaging procedures available for the examination of
patients with an acute abdomen, plain X rays of the abdomen usually are readily
obtainable and provide significant information within a short period. In interpreting


                 -#-
the films one should systematically study general appereance, position of the
diaphragm, size, and location of the solid organs (liver, kidney, and spleen), gas
pattern of the gastrointestinal tract (absence, excess, and displacement), presence of
air in unusual locations (peritoneal cavity, retroperitoneal space, biliary passages,
portal venous system, bowel wall, urinary tract, and abscess cavity), clarity of psoas
shadows, abnormal soft tissue masses, radioopaque densities, and the bony structures
(vertebral column, pelvis, and lower ribs).
The presence of air outside the lumen of gastrointestinal tract is abnormal.
Pneumoperitoneum (free air in the peritoneal cavity) most frequently is the result of
gastrointestinal perforation, resulting from perforated gastroduodenal ulcer, sigmoid
diverticulitis, or appendicitis. Free air is best demonstrated under the diaphragm in
upright films of the abdomen and chest.
Gas within the gastrointestinal tract is increased from aerophagia and intestinal
obstruction; with aerophagia gas fills the lumen but air-fluid levels are absent,
whereas in intestinal obstruction air-fluid levels are typically present – these occur
proximal to an obstruction because of the accumulation of gastrointestinal secretions
and swallowed air. The bowel distal to an obstruction remains collapsed after
emptying its contents. Air-fluid levels in both the large and small bowel are seen in
adynamic ileus.
Sonography. The addition of sonography to the diagnostic armamentarium has many
advantages. Because of its noninvasiveness it can be repeated several times without
discomfort to the patient, nor does the success of the test depend on the function of
the organ to be visualized. The danger of allergic reaction is nonexistent since no
contrast materials are needed. Sonography has been found particularly useful in
detecting gall stones, lesions of the liver, pancreatic edema, phlegmon, pseudocyst
and abdominal aortic aneurysms; it is also useful in detecting ectopic pregnancy,
ovarian cysts, uterine pregnancy, and in differentiating solid from cystic masses.
Ultrasonography has a diagnostic sensitivity of about 80% for acute appendicitis. It
has good sensitivity also in diagnosis of free blood (fluid) in peritoneal cavity.


CT. It is particularly helpful in pancreatic and retropancreatic lesions and any severe
localized infections (acute diverticulitis). CT is absolutely significant in detection of
liver and spleen traumatic ruptures.


ENDOSCOPY
Gastroduodenoscopy. It is indicated in patients with the bleeding from upper part of
gastrointestinal tract.
Proctosigmoidoscopy, colonoscopy. Indications: suspection from bowel obstruction,
bloody stools, rectal mass.


Laparoscopy. Laparoscopy has an established role prior to laparotomy in women in
whom the diagnosis of appendicitis is uncertain.


2.5.5. PARACENTESIS



                 -#-
The findings of free blood or infected ascites on abdominal paracentesis is invaluable
in patients with free peritoneal fluid. Aspiration of blood, bile, or bowel contents is
indication for urgent laparotomy.



2.5.6. LABORATORY INVESTIGATIONS
Urine. Urinalysis must be performed in every patient. Unsuspected diabetes may be
uncovered by the presence of glycosuria. Ketone bodies appear in the urine of patients
with diabetic ketoacidosis and starvation. Pus cells indicate a urinary tract infection.
Red blood cells appear in the presence of infections, stones, and tumors of the urinary
tract. Crystals readily explain pain of ureteral colic.


Blood. Determination of hemoglobin and hematocrit levels by itself is of limited use.
The levels remain unchanged soon after hemorrhage, then gradually decline as
compensatory hemodilution progresses; normal levels therefore do not exclude
bleeding, for which a serial drop is a more reliable indicator. When low hemoglobin
and hematocrit levels are found at the onset of an acute abdominal condition, a
chronic underlying process should be suspected. Thus, in anemic patients presenting
with intestinal obstruction, one should suspect gastrointestinal malignancy.
Leukocytosis is usually associated with inflammatory conditions, but its absence does
not exclude inflammation, since it may be absent in the early stages of an
inflammatory process as well as in debilitated, moribund patients. An increase in band
forms of polymorphonuclear leukocytosis – even when the total count is normal – is a
significant indicator of severe inflammation. A gradually increasing white cell count
is evidence of advacing inflammatory changes. With parasitic infections and allergic
conditions the oesinophil count increases. Leukopenia is a usual finding in typhoid
fever and in viral infections.
Serum amylase and lipase levels are useful in the diagnosis of acute pancreatitis;
however, it must be pointed out that normal levels do not exclude the diagnosis, nor
are increased levels pathognomonic of the condition. Serum amylase and, to a lesser
extent serum lipase increase in conditions other than pancreatitis, including mumps,
parotid duct obstruction, intestinal obstruction, perforated ulcers, pseudocyst of the
pancreas, ruptured ectopic pregnancy, and macroamylasemia. The urinary amylase
level remains elevated for a longer period and hence is more accurate in the diagnosis.
Elevated levels of serum glutamic oxaloacetic and serum pyruvic transaminases are
indicative of liver damage and provide a clue in diagnosing hepatitis in patients
presenting with right upper quadrant pain and tenderness.


Stools. Examination of stools for blood, ova, and parasites should not be neglected.
Blood appears in stool in the presence of neoplastic, ulcerative, and ischemic lesions
of the gastrointestinal tract.


2.5.7. ACUTE PERITONITIS




                 -#-
Of the four pathologic processes – inflammation, hemorrhage, torsion, and colic –
responsible for an acute abdomen, inflammation is by far the most common. Specific
conditions such as acute appendicitis, acute cholecystitis, and perforated duodenal
ulcer are associated with peritoneal inflammation, the extent and severity of which
varies. Regardless of the underlying conditions responsible for peritonitis, the features
of peritoneal irritation remain the same: pain, tenderness, rebound tenderness and
muscle spasm. Identifying the area of peritoneal irritation provides a clue to the
probable structure involved in the inflammatory process. For example, inflammation
resulting from causes as diverse as acute appendicitis, cecal diverticulitis, perforation
of cecal carcinoma, Meckel´s diverticulitis, and acute regional enteritis of the terminal
ileum is associated with pain, tenderness, rebound tenderness and muscle spasm in the
right lower quadrant. Signs of inflammation in the right upper quadrant should lead
one to suspect that the problem arises from the gallbladder, liver, duodenum, head of
pancreas, hepatic flexure of the colon, or right kidney – structures normally present in
that area.


Localization of inflammation. Peritonitis may be either localized or generalized.
The factors responsible for localization of the inflammation are both anatomic and
pathologic.
Anatomic factors. The peritoneal cavity is divided into a greater and a lesser sac;
these communicate with each other through the foramen of Winslow. The greater sac
is further divided into a supracolic and an infracolic compartment by the mesentery of
the transverse colon. The mesentery of the small bowel, which extends from the left
upper quadrant to the right lower quadrant, divides the infracolic compartment into a
right and left half. These peritoneal folds subdivide the peritoneal cavity into
compartments and deter the spread of infection from one compartment to another.
Pathologic factors. When the inflammation responsible for acute abdomen progresses
slowly, there will be sufficient time for adhesions to form between the inflamed organ
and adjacent structures, thus confining the inflammation. In contrast, when the
inflammation is sudden in onset and is associated with massive contamination of the
peritoneal cavity (as in a perforated ulcer) there is not enough time for adhesions to
form and confine the inflammation, and diffuse peritonitis ensues. The greater
omentum plays an important role in confining inflammation by enveloping and
adhering to the inflamed structure. In children this structures is not well developed,
and the barrier formed against the spread of infection is less effective. Therefore,
children are more prone to develop generalized peritonitis and at a much earlier stage
of the disease than are adults. With the onset of peritonitis, peristaltic activity in the
adjacent coils of the intestine ceases – this again helps form an effective barrier the
spread of infection. Stimulation of peristalsis, either by ingested food or by ill-advised
administration of cathartics, would interfere with nature´s attempt to confine the
inflammation.


Etiology and pathophysiology. The causative agents of acute peritonitis are
primarily bacterial and chemical. Even when peritonitis is chemical in origin (as in a
perforated ulcer or intraperitoneal rupture of the bladder), bacteria sooner or later
colonize the peritoneal cavity, so that for all practical purposes acute peritonitis is
indeed acute bacterial peritonitis.



                 -#-
Bacteria may invade the peritoneal cavity through:
1. Direct invasion
       a) Through perforation of a part of the gastrointestinal tract
       b) Through intraperitoneal rupture of the urinary tract
       c) Through the fallopian tubes
       d) Through accidental or surgical wounds of the abdominal wall
2. Local extension
              a) From an inflamed organ such as acutely inflamed appendix or
                  gallbladder
              b) Transmigration of bacteria across gangrenous bowel wall
3. The bloodstream

Primary peritonitis. Peritonitis occuring without an obvious source of contamination
is referred to as primary peritonitis. Unlike secondary peritonitis, in which the
infection is polybacterial, the infection in primary peritonitis is monobacterial. How
the bacteria enter the peritoneal cavity to produce the infection is still a matter of
speculation; they may reach the peritoneal cavity through the blood stream, through
the fallopian tubes, by transmigration (translocation) across the intact gastrointestinal
tract, or by way of the lymphatics across the diaphragm. Primary peritonitis is
predominately a disease of children; those suffering from nephrosis or cirrhosis are
particularly vulnerable. Primary peritonitis in adults, once considered rare, is
diagnosed with increasing frequency in cirrhotics.
Since the advent of antibiotics there has been a change in the bacteriologic findings in
this condition. In the preantibiotic era gram-positive cocci, pneumococcus in
particular, were the chief offending organisms. At present, gram-negative bacteria,
particularly Escherichia coli, Klebsiella, have superseded the gram-positive
organisms as the etiologic agent.
Diagnosis of primary peritonitis is difficult and is essentially a diagnosis of exclusion;
surgical exploration often is necessary to exclude other causes of peritonitis.
However, certain features are of help in diagnosing the condition with reasonable
certainty. Sudden onset of peritonitis followed by rapid progression in a patient who
has either nephrosis or cirrhosis is highly suggestive of the condition.


Secondary peritonitis. The initial features of secondary peritonitis are those of the
underlying disease, such as acute appendicitis or perforated ulcer. Pain, the most
common presenting feature, may be sudden or gradual in onset, often accompanied by
nausea and vomiting. The cardinal physical findings of peritoneal irritation are
tenderness, rebound tenderness, and involuntary muscle spasm; the area over which
these are found depends on the extent of peritonitis. In generalized peritonitis
tenderness, rebound tenderness, and muscle spasm will be present over the whole of
the abdomen, whereas in localized peritonitis these findings will be confined to a part
of the abdomen. The maximum tenderness and muscle spasm, usually, will be over
the area of the initial irritation. Abdominal rigidity may be absent in moribund
patients, and when inflammation is confined to the pelvis, lesser sac, and
subdiaphragmatic space.
Changes in pulse and temperature are variable. Beginning may not be associated with
significant changes in either pulse or temperature. In later stages tachycardia and



                 -#-
fever are invariably present. As peritonitis progresses, fluid exudes into the peritoneal
cavity, resulting in a loss of vascular volume; this loss, unless compensated by the
administration of fluids and electrolytes, results in dehydration and hypovolemic
shock. Adynamic ileus accompanying peritonitis results in regurgitant vomiting,
abdominal distention, and decreased or absent bowel sounds.


Management. Management of patient with peritonitis consists of providing general
supportive measures and correcting the underlying cause. Derangements in fluid and
electrolyte balance need correction. Monitoring of central venous pressure, pulmonary
wedge pressure, and urinary output, as well as serial determination of serum
electrolytes, blood urea nitrogen, and hematocrit levels assist in restoring the balance
as quickly as possible.
Necessary to decompress the stomach and decrease abdominal distension, nasogastric
suction also minimizes vomiting and aspiration of the vomitus into respiratory
passages.
Intravenous antibiotics are useful in controlling infection. More often than not,
bacterial culture and sensitivity studies will not be available at the time treatment is
initiated; for this reason, antibiotics effective against a wide spectrum of organism
should be chosen – including agents effective against anaerobic organisms.
Operation – although it is generally agreed that the peritoneal cavity should be cleared
of all contaminants once the primary cause has been dealt with, there is no uniformity
of opinion on how to accomplish this – the procedures followed include irrigation of
the peritoneal cavity with saline and antibiotic – containing solutions and radical
mechanical debridement of all fibrinous material. Localized abscesses (when present)
are drained, but effective drainage of the general peritoneal cavity is not possible
since adhesions formed around the drain isolate it from the rest of the peritoneal
cavity.

2.6. ABDOMINAL MASSES
2.6.1. Definition and presentation
- palpable abnormal mass
- often an unexpected finding, sometimes various unspecific symptoms
2.6.2. Etiology and pathophysiology
- solid tissue – enlargement of a solid organ (liver, spleen, kidney, lymphatic
     nodes, testis)
- tumors (benign or malignant)
- gravidity
- scybala
- hernia
- increased volume of hollow organs (gallbladder, urinary bladder, stomach,
     intestine, hydrocele)
2.6.3. Diagnosis and differential diagnosis
- history and physical findings
- laboratory findings
- imaging procedures – sonography, X-ray, endoscopy
- biopsy (blind, guided)
- probatory laparotomy



                 -#-
- cannulation, tube insertion
2.6.4. Treatment
- removal of the obstacle from hollow organs
- correction of fluids and electrolytes
- surgery
- symptomatic and palliative procedures
2.6.5. Preventive, prognostic and opinion aspects

2.7. GASTROINTESTINAL BLEEDING
2.7.1. Definition
 - loss of more than a few mililiters of blood into the GIT
 - occult blood loss (loss of up to 50 ml blood daily)
 - melaena (partially digested blood in the stools)
 - enterorrhagia (undigested blood in the stools)
2.7.2. Etiology and pathophysiology
 - upper part of the GIT (oral cavity, esophagus, stomach, duodenum)
 - middle part (jejunum, ileum)
 - lower part (colon, rectum and anus)
 - hemocoagulation disorders – source may be anywhere
 - melena – source in esophagus – varices, ulcer, tumor
     - source in stomach – ulcer, tumor, gastritis
     - source in duodenum - ulcer
     - source in small intestine – vascular malformation, tumor
- enterorrhagia – proctocolitis, tumors (benign, malignant), vascular malformation,
hemorrhoids
 - occult bleeding – source anywhere
 2.7.3. Clinical presentation
 Quantitative aspect – occult bleeding
                       - massive bleeding
  Type of bleeding: - hemateméza
                         - enterorrhagia
                         - melena
In chronic bleeding (even if occult) anemia is common, in massive bleeding the
patient is threatened by a hemorrhagic shock.
2.7.4. Diagnosis and differential diagnosis
 - history
 - physical findings
 - auxilliary metods:
          - fibroscopy
          - X-ray, angiography, CT scan, sonography
         - rectoscopy, sigmoidoscopy, colonoscopy
          - laboratory findings

Differential diagnosis of the bleeding from:
  - upper part of the GIT
  - lower part of the GIT
  - GIT, lungs, other sources
 - hemobilia
  - hemoperitoneum
  - hemoptysis, hemoptoe


                 -#-
   - hematometra
   - hematuria
 2.7.5. Treatment
 - conservative pharmacotherapy (terlipressin)
 - balloon tamponade in esophageal varices
- endoscopical invasive therapy
 - surgical treatment
- circulatory stabilization, general supportive measures
         - bleeding termination, volume repletion
        - drug treatment
       - endoskopical methods – sclerotization, electrocoagulation
        - balloon tamponade
        - TIPS
- definitivne treatment
        - repeated esophageal sclerotization
        - peptic ulcer or proctocolitis treatment
        - endoscopical polypectomy
        - surgical treatment
        - treatment of hemorrhoids
        - liver transplantation

2.7.6. Preventive Measures. Prognosis.

2.8. MAIN HEPATOBILIARY SYNDROMES
2.8.1. Icterus and cholestasis
2.8.1.1. Definition and clinical presentation
- icterus – yellow discoloration of the skin, mucosal membranes and sclerae, which
     appears at the increase of bilirubinemia to about twice the upper limit of normal,
     i.e. approximately 35 µmol/l
- cholestasis is defined as an impairment of bile production and secretion
- the start is variable (asymptomatic, sudden or gradual, following an abdominal
     colic, drugs or hunger, influenza-like symptoms, intoxication, acute liver failure)
2.8.1.2. Etiology and pathophysiology
- icterus
     - prehepatic (hemolysis, Gilbert’s syndrome)
     - hepatocellular (lesion of liver parenchyma]
     - obstructive (stone, tumour, inflammatory stenosis, pancreatic head
          enlargement)
2.8.1.3. Diagnosis and differential diagnosis
- history and physical findings
- laboratory
- sonography
- X-ray (ERCP, PTC, CT)
- cholescintigraphy

Differential diagnosis of icterus
type of the icterus            prehepatic    hepatocellular          obstructive
bilirubin total                + to ++       + to ++++               + to ++++
       direct                  n             + to +++                + to +++
ALT, AST                       n             ++ to ++++              n to ++


                 -#-
ALP, GMT                       n               n to ++                ++ to ++++
urine: bilirubin               negat.          + to ++++               + to ++++
       urobilinogen            negat. to +     ++ to ++++             negat. to +
stools colour                  dark            hypocholic             acholic*
cholesterolemia                n               n to decreased         + to ++++
pruritus                       negat.          rare, transient        frequent
+ to ++++ = degree of increase, n = normal value
 * acholic stools is seen in complete biliary obstruction only; in incomplete
obstruction the stools is either hypocholic or of normal colour

2.8.1.4. Treatment
- according to etiology
- in biliary obstruction endoscopic and surgical procedures

2.8.1.5. Preventive, prognostic and opinion aspects

2.8.2. Portal hypertension and esophageal varices bleeding
- normal pressure in the portal vein is about 7 – 10 mmHg, i.e. 10 – 15 cm of water.
    Pressure higher than twice this value means portal hypertension.
- classification of portal hypertension
a) prehepatic (portal vein obstruction)
b) intrahepatic
- presinusoidal (e.g. in schistosomiasis)
- sinusoidal (typically in liver cirrhosis)
- postsinusoidal (e.g. in venoocclusive disease)
c) posthepatic – in hepatic vein thrombosis (Budd – Chiari syndrome), constrictive
    pericarditis, congestive heart failure
Portal pressure can be measured by a catheter obturating a hepatic vein (wedged
hepatic vein pressure)
Long-lasting portal hypertension leads to the development of collateral circulation
(intra- and extrahepatic portosystemic shunts)
Esophageal varices bleeding is manifested usually by hematemesis followed by
melena, occassionally by a circulatory shock
Treatment of bleeding esophageal varices
- aim: to stop bleeding, to stabilize circulation and to prevent hepatic
    encephalopathy
- control of bleeding:
    - endoscopic (sclerotization of varices)
    - Sengstaken-Blakemore balloon tube
    - substances with vasoconstrictive effect in portal circulation (vasopressin and
         its analogues such as terlipressin and somatostatin or its derivative octreotid)
    - TIPS (transjugular intrahepatic portosystemic shunt)
    after the bleeding has been stopped, we must set up a therapeutic plan:
- repeated variceeal sclerotization
- pharmacological decrease of the portal pressure with beta-blockers (these two
    options can be combined)
- surgical creation of a portosystemic shunt (usually the distal splenorenal
    anastomosis)
- TIPS



                -#-
2.8.3. Retention of fluid and ascites
2.8.3.1. Pathofysiology of ascites formation has not been satisfactorily clarified.
Contributing factors:
- portal hypertension
- decreased plasma albumin concentration and subsequent changes of the renin-
    aldosterone system (secondary hyperaldosteronism)
- peripheral vasodilatation due to nitric oxide hyperproduction
- lymphatic hypertension

2.8.3.2. Diagnosis of ascites
- abdominal sonography
- probatory paracentesis with biochemical, cytological and cultivation examination
    of the aspired fluid
- counting the leukocytes is the most sensitive marker of spontaneous bacterial
    peritonitis. Counts higher than 250 granulocytes per microliter are diagnostic
2.8.3.3. Treatment of cirrhotic ascites
- bed rest, salt restriction
- potassium-sparing diuretics
- hydrochlorothiazide (25 – 50 mg) or furosemide (40 – 80 mg)
- if the effect is unsatisfactory, it is necessary to restrict water intake to 1000 ml/24
    hrs
- in case of mechanical problems (compromised ventilation) large-volume
    paracentesis is indicated
- peritoneovenous (LeVeen) shunt and ascites reinfusion have virtually been
    abandoned
- TIPS

Treatment of spontaneous bacterial peritonitis
- it is usually caused by intestinal Gram-negative bacteria
- third-generation cephalosporins (cephotaxim, cephtriaxon) or chinolons
    (norfloxacine, ciprofloxacine)

2.8.4. Disorders of hematopoiesis and hemocoagulation
- anemia (usually macrocytic), leukopenia and thrombocytopenia
- folic acid deficit is frequent, esp. in alcoholics
2.8.4.1. Pathogenesis
Hypersplenism, hypovitaminoses, decreased hematopoiesis in liver insufficiency
- hemocoagulation disorders

2.8.4.2. Treatment
- of limited effectivity
- in cholestasis, parenteral vitamin K administration
- supplementation of blood cells and/or hemocoagulation factors (blood and
    platelet transfusions, cryoprecipitate, single hemocoagulation factors)
- liver transplantation

2.8.5. Hepatic encephalopathy
definiton: neuropsychiatric syndrome caused by severe liver disease
2.8.5.1. Clinical presentation
Four-degree classification:


                 -#-
I.     Mood changes, euphoria or depression, attention disorders, irritability
II.    Slow mentation, lethargy, marked personality changes, inappropriate
       behaviour, intermittent desorientation
III.   Somnolence, marked desorientation, amnesia, blurred speach
IV.    Coma

2.8.5.2. Diagnosis of hepatic encephalopathy (HE) is easy in advanced cases.
Subclinical HE is diagnosed on the ground of typical findings on physical
examination (foetor hepaticus, flapping tremor), pathological results of
electrophysiological examination (electroencephalography, evoked stem potentials)
and/or some simple tests such as constructive apraxia and the number-connection test.
Classification of HE:
- according to duration – acute and chronic
- according to cause – exogenous (due to GIT bleeding) and endogenous (without
    apparent cause)
2.8.5.3. Pathogenesis
- toxic products of protein metabolism arising in the gut by the activity of intestinal
    bacteria (ammonia, biogenic amines – octopamine, phenylethanolamine,
    mercaptans, gamma-aminobutyric acid)
- dysbalance in plasmatic amino acids (increased concentration of aromatic and
    decreased concentration of branched-chain amino acids)
- short-chain fatty acids
- endogenous ligands of the central benzodiazepine receptors (endozepines)

2.8.6. Acute liver failure
Def.: severe impairment of liver functions directly threatening life of the patient that
appeared within 10 weeks since the beginning of liver disease in a patient without
previous liver lesion.
2.8.6.1. Clinical presentation
- hepatic encephalopathy
- disorders of hemocoagulation
- various metabolic changes (metabolic acidosis or alkalosis, hyponatremia,
    hypokalemia,           hypomagnesemia,     hypofosfatemia,      hyperammonemia,
    hypoglycemia. hyperaminoacidemia, hypocholesterolemia, increased free-fatty
    acid plasma concentration)
- brain edema
- impairment of both cellular and humoral immunity with frequent pneumonias and
    other infectious complications
- functional renal failure (hepatorenal syndrome)

2.8.6.2. Tretament of acute liver failure
- oral protein intake limitation, administration of neomycin by a tube and high
    enemas and laxatives (preferably magnesium sulphate) to suppress production of
    nitrogen metabolites in the intestine,
- parenteral nutrition including corection of internal environment,
- prophylactic broad-spectrum antibiotics administration (e.g. cephalosporin +
    aminoglycoside)
- administration of H2-antagonists (famotidine, ranitidine) or proton-pump
    inhibitors (omeprazole) for prevention of stress peptic ulcer



                 -#-
Prognosis is poor with mortality of about 80%. The most effective tretament is urgent
liver transplantation.

2.8.7. Chronic hepatic insufficiency
Def.: severe impairment of liver functions due to a long-standing liver disease. The
syndrome includes:
- hepatic encephalopathy,
- disorders of hemocoagulation,
- fluid retention,
- portal hypertension with splenomegaly, hypersplenism and the risk of esophageal
    varices bleeding,
- impairment of both cellular and humoral immunity with frequent infectious
    complications including tuberculosis and other
- malnutrition often with marked muscle atrophy,
- hyperdynamic circulation,
- characteristic skin changes,
- endocrine changes,
- corresponding laboratory findings

2.8.8. Functional renal failure (hepatorenal syndrome)
Def.: progressive azotemia and oliguria with marked sodium retention, complicating
ascitic liver cirrhosis or acute liver failure
Pathogenesis: renal hemodynamic changes with decreased blood flow through the
renal cortex. Contributing factors: decreased synthesis of renal prostaglandins,
increased sympathetic tone, thromboxane, renin-aldosteron mechanism, adiuretin,
atrial natriuretic factor
Lab.: Urine sodium concentration is lower than 5 mmol/l, also hyponatremia is
frequent, urinary sediment is normal. Prognosis is very poor, nearly all patients will
die due to liver failure or esophageal varices bleeding but not because of uremia.
Occassionally patients have been saved by urgent liver transplantation or TIPS
insertion.

2.8.9. Biliary dyspepsia and colic
Def.: biliary dyspepsia – vaguely defined complex of problems such as pressure or
pain in the right hypochondrium, often accompanied by nausea or vomiting, or
occassionally by meteorism and obstipation, which appears following fat or aromatic
meals and lasting more than 15 to 30 minutes. Biliary dyspepsia is not relieved by gas
or stools evacuation.
Pathogenesis: biliary dyskinesia
Biliary colic – pain caused by sudden obstruction of choledochus or the cystic duct. It
is brought about by increased pressure in the bile ducts and their dilatation. The pain
is wave-like and lasts several hours.
Dg: history, physical findings, sonography
Th: antispasmodics, elective cholecystectomy, in selected cases peroral stone
dissolution or extracorporeal wave lithotripsy.

2.9. Diarrhoea
2.9.1. Definition and clinical manifestation
- increased frequency, volume and water contents of the stools
- acute – lasting up to two weeks


                -#-
- chronic – lasting more than two weeks
2.9.2. Etiology and pathophysiology
- bacterial growth (shigella, salmonella….)
- bacterial exotoxins (staphylococci, clostridia, vibria …)
- viruses (adevirus, rotavirus …)
- parasites (lamblia, entamoeba, tape worms …)
- drugs (laxatives)
- inflammatory bowel disease
- gluten enteropathy
- malabsorption syndrome
- irritable colon
- endocrinopathies (thyreotoxicosis, diabetes mellitus, hyperparathyreoidism,
    endocrine active tumours of the GIT)
- uremia
- intestinal resection
- Whipple’s disease

2.9.3. Diagnosis and differential diagnosis
- history and physical findings
- laboratory examination (culture, stool examination for blood or parasites,
    metabolic abnormalities, gliadin antibodies, enterobiopsy)
- endoscopy, X-ray
Malabsorption syndrome
Def.: decreased intestinal absorption of nutrients with their loss in the stools.
Digestion of fat is usually impaired first, which leads to steatorrhea.
Etiological classification:
A. Maldigestion
- deficit or inactivation of pancreatic lipase
- pancreatic external secretion insufficiency
- gastrinoma
- postgastrectomy steatorrhea
B. Bile salts depletion
- liver disease
- damaged enterohepatic circulation of bile acids
- drugs (cholestyramine, colestipol, neomycine, calcium carbonate)
- blind-loop syndrome
C. Reduction in resorptive area
- intestinal resection, bypass or fistula
D. Lymphatic obstruction
- intestinal teleangiectasia
- lymphomas
E. Cardiovascular disease
- right heart failure
- abdominal angina
- vasculitis
F. Diseases of intestinal mucosa
- inflammation, infiltration, infection (Crohn’s disease, amyloidosis, salmonellosis)
- toxic and genetic disorders (sprue, lactase deficit etc.)
G. Endocrine and metabolic diseases
- diabetes mellitus


                -#-
- thyreotoxicosis
- carcinoid
Clinical presentation:
- influenced by etiology
- diarrhoea, steatorrhoea, creatorrhoea, malabsorption of vitamins, calcium and
    other minerals
- malnutrition, hypo- to avitaminoses, osteopenia
Dg: steatorrhea > 6 g/24 hrs, muscle fibers and starch granules in the stools
- etiological diagnosis
Th: if possible causal, MCT fats if needed, maltodextrin, supplementation of
vitamins, calcium and trace elements, pancreatic enzymes

Inflammatory bowel disease
Two basic entities: Crohn’s disease and idiopathic (ulcerative, hemorrhagic) colitis
Epidemiology: the white race is most affected, esp. Jews, both sexes, commonly in
the age of 15 – 35 years
- the prevalence of ulcerative colitis is about 70 – 150/100000, that of Crohn’s
    disease 20 – 40/100000
- etiology is unclear; genetic and environmental influences
Pathology:
- ulcerative colitis – continuous damage of the mucosa, inflammation, hyperemia,
    hemorrhage, crypt abscesses, the inflammation does not reach beyond the
    submucosa. Rectum is nearly always involved and the inflammation reaches
    higher into the colon, with involvement of whole colon up to the distal ileum
    (backwash ileitis). Development of pseudopolyps and dysplasia with risk of
    carcinoma
- Crohn’s disease – the inflammation encompasses the whole width of intestinal
    wall and extends to the adjacent mesentery and regional lymph nodes. Thickening
    of the wall leads to intestinal stenoses. Fistulas and abscesses are readily formed.
    Healthy and involved parts of the intestine alternate. Most commonly, the distal
    ileum is involved (terminal ileitis) but the disease may attack any part of the
    digestive tube. Microscopically, granulomatous inflammation is found;
- in some patients it is not possible to differentiate between the Crohn’s disease and
    ulcerative colitis.
Clinical findings
A. ulcerative colitis
- diarrhoea with admixture of blood, abdominal pain, in severe cases fever and
    weight loss, toxic megacolon
- laboratory: nonspecific signs of inflammation – increased erythrocyte
    sedimentation rate, anemia, leukocytosis
B. Crohn’s disease
- abdominal pain, diarrhoea (usually without blood), fever, weight loss
- formation of fistulas, fissures and abscesses
- ileus
- nonspecific signs of inflammation
Course: chronic, clinical remissions of varying length
Diagnosis:
- history
- clinical findings
- rectosigmoidoscopy, irrigography


                -#-
- in suspected Crohn’s disease enteroclysis
Systemic complications
- malnutrition, anemia
- arthralgia, arthritis, spondylitis
- liver lesion (primary clerosing cholangitis, reactive hepatitis)
- thrombosis, thromboembolism
- eye involvement (iritis, uveitis)
Treatment
A. Ulcerative colitis
- sulfasalazine
- mesalazine (5-aminosalicylic acid)
- prednisone
- in predominantly rectal involvement clysma and suppositories
- colectomy in toxic megacolon
- prognosis usually good
B. Crohn’s disease
- treatment as in ulcerative colitis, the effect is usually worse
- surgical treatment in complications (intestinal obstruction, fistulas, abscesses –
   about 70% of patients)
- prognosis is worse, risk of peritonitis and sepsis, frequent relapses

Whipple’s disease (intestinal lipodystrophy)
A rare disease occuring mostly in males who develop arthritis, prolonged diarrhea,
malabsorption and weight loss. Arthritis is acute in onset; symptoms are migratory.
Diagnosis is based on the finding of PAS-positive bacilliform structures in
macrophages from duodenal mucosa or other tissues. The etiologic agent is
uncultivable bacterium Tropheryma whippelii that can now be diagnosed by means of
a polymerase-chain reaction (PCR). Treatment is with antibiotics such as tetracycline,
erythromycine etc. However, Tropheryma whippelii has been found also in healthy
people and therefore its finding is not sufficient for the diagnosis of Whipple’s disease
or antibacterial treatment (Ehrbar, H. - U. et al.: Lancet, 353, 1999, No 9171, p.
2214).

Irritable colon
 This term denotes abdominal problems such as feeling of pressure or pain lasting
 longer than three months, which
 - improve or disappear with defecation and/or
 - are accompanied with change in stool frequency or
 - are accompanied with change in stool consistency.
 Most common is obstipation or diarrhea or their interchange, defecation urgency and
 feeling of incomplete evacuation, bloating and mucus in the stools. Irritable colon is
 sometimes divided into three types – with predominant diarrhoea, with predominant
 constipation and the painful type. It is apparent that differentiation between irritable
 colon and functional diarrhoea or habitual constipation is often unclear or right
 impossible.
 Treatment
 - psychotherapy
 - pharmacotherapy
 Prevention
 Prognosis and opinion aspects


                 -#-
2.9.4. Treatment
- diet
- symptomatic treatment
- antimicrobial treatment
- other
- 2.9.5. Preventive, prognostic and opinion aspects

2.10. Constipation
2.10.1. Definition and clinical picture
- decreased frequence and water contents of the stools
- difficult bowel emptying which bothers the patient
2.10.2. Etiology and pathophysiology
- decreased intestinal motility
- life-style changes
- low fibre intake
- abuse of laxatives
- drugs (opiods, anticholinergics, antacids, diuretics etc.)
- metabolic and endocrine disorders (hypokalemia, hypercalcemia, hypothyreosis,
    diabetes mellitus, amyloidosis)
- neuromuscular disorders (irritable colon, Hirschprung’s disease, CNS diseases,
    anxiety and depression, sclerodermia, diverticulosis)
- vascular diseases (mesenteric artery obstruction)
- anorectal disorders
- fissures
- hemorrhoids
- stenoses
- abscesses
- proctitis
- rectokele
- intestinal obstruction
- tumours
- volvulus
- invagination
- incancerated hernia
- rectal mucosa prolaps
2.10.3. Diagnosis and differential diagnosis
- history and physical findings
- laboratory examination (serum minerals, blood count, thyroid hormones,
    glycemia)
- rectoscopy, colonoscopy, mucosal biopsy, plain X-ray, irrigography, sonography,
    CT, arteriography

Colorectal carcinoma
Colorectal carcinoma is the second most frequent neoplasm in both sexes in the Czech
Republic. Its incidence in CR is the highest in the world (75.5 newly diagnosed cases
per 100000 inhabitants in 1997).
Genetic influences: familiar adenomatous polyposis caused by mutation of the APC
gene (tumour-suppressing gene on the 5th chromosome), the Lynch syndrome
(hereditary nonpolypous colorectal carcinoma). Recently new genetic deviations have



                -#-
been found – DNA mismatch gene mutations of genes hMSH1 and hMSH2 in
Afroamericans with an early form of colorectal carcinoma.
Clinical manifestation:
 - depending on localization - constipation to ileus, intestinal bleeding, diarrhoea,
     anemia, weight loss, abdominal mass, liver and other organ metastases
 Diagnosis:
- occult blood in stools, rectal examination, rectoscopy, colonoscopy
Treatment:
- surgical (radical, palliative)

2.10.4. Treatment of constipation
- diet, psychotherapy, lifestyle changes
- avoidance of harmful drugs
- internal environment modification
- treatment of local diseases of the rectum and anus
- removal of intestinal obstruction
- laxatives as the last resort only
2.10.5. Preventive, prognostic and opinion aspects

2.11. Anorectal problems
2.11.1. Definition
- surgical anatomy of the anorectal region
- anorectal function
2.11.2. Etiology and pathophysiology
- injuries, foreign bodies
- hemorrhoids, hemorrhoidal thrombosis, anal fissura
- abscess, fistula, sinus
- proctitis
- tumours
2.11.3. Clinical picture
- bleeding
- pruritus
- pain
- prolaps
- incontinence and stenosis
- tenesmus

2.11.4. Diagnosis and differential diagnosis
- history
- rectal examination
- anoscopy, rectoscopy, sigmoidoscopy
- irrigography
- sonography
- stool examination
- biopsy etc.
Hemorrhoids
- external and internal
- bleeding, thrombosis, pain, prolaps, anal pruritus
Dg: inspection, palpation, anoscopy



                -#-
Th: treatment: - conservative (sitting bath, suppositories, ointments, stool
lubrification)
- bandage, sclerotization
- surgery

2.11.5. Treatment
- pharmacotherapy: ointments, suppositories, microenemas. Anal fissure can be
    treated with an injection of botulotoxin into the internal anal sphincter. Similar
    effect can be achieved with local application of nitrates as ointments;
- physical therapy (eg. laser)
- endoscopic treatment
- surgery

2.11.5. Preventive, prognostic and opinion aspects

2.12. Gastro-, jejuno-, ileo- and colostomy

2.12.1. Definition and Problem Specification
2.12.2. Pathophysiological Basis and Justification of Stomas
2.12.3. Indications for Jejunostomy, Ileostomy, Colostomy:
     - acute – emergent (ileus, inflammation, haemorrhage, injury, insufficiency of
         anastomosis, atresia)
     - planned – elective (undernourishment, fistulae, inflammations, tumours,
         incontinence, malformations and others)
2.12.4. Kinds of Stomas:
     - Jejunostomia nutritiva
     - Ileostomia terminalis
     - Ileostomia axialis
     - Coecostomia
     - Transversostomia
     - Sigmoideostomia axialis
     - Colostomia terminalis
2.12.5. Complications Connected with Stoma
2.12.6. Care of Stomas. Aids, Diet Modification
2.12.7. Prognosis. Indications for Stoma Closure


2.12.1. Definition and Problem Specification

The concept of stoma is generally used for a communication created between the
bowel lumen and the body surface. This communication can be created by a direct
junction of the bowel lumen with the skin or indirectly by means of a drain.

2.12.2. Pathophysiological Basis and Justification of Stomas

The reason for establishing a stoma (fistula, stoma) can be a disease of the alimentary
canal or the organs which are functionally connected with it (liver, pancreas),
compression of the alimentary canal by neighbouring structures and other indications
(urological, gynaecological, etc.).



                 -#-
2.12.3. Indications for Jejunostomy, Ileostomy, Colostomy
     - acute (ileus, inflammation, haemorrhage, injury, insufficiency of
         anastomosis, atresia)
     - elective (undernourishment, fistulae, inflammation, tumours, incontinence,
         malformations and others)

Indications can be divided into 2 basic groups:
1. conditions in which it is necessary to reach a decompression of the bowel or a
derivation of the bowel content
2. conditions in which it is desirable to ensure the entry into the alimentary canal
because of nutritive or curative reasons. A stoma can be created as a temporary or
permanent one.

2.12.4. Kinds of Stomas

Jejunostomia nutritiva

This stoma is established in the case of patients where it is necessary to exclude from
the passage more proximal parts of the alimentary canal for a long period of time (e.g.
in conditions following gastrectomy with the insufficiency of gastrojejuno- or
gastroduodenoanastomosis, and the like) or to administer alimentation for a long
period of time in the case of the patient‘s lack of cooperation (gastrostomy is more
often used here). A jejunostomy is also established in the operations on the bile ducts
and pancreas, when the drains from the ductus pancreaticus and the bile ducts are led
out in this way. It is also used in the treatment of meconium ileus or in the treatment
of duodenal atresia.

Stoma technique: according to Witzel (stoma created on the drain), enterostoma
according to Bischop-Koop – terminal jejunostomy with enteroenteroanastomosis
end-to-side), percutaneous endoscopic jejunostomy and others.

Ileostomia terminalis

A terminal ileostomy is indicated in proctocolectomy. The most frequent indications
are idiopathic proctocolitis resistant to conservative treatment, toxic megacolon, m.
Crohn with the affection of the colon and the rectum, familiar polyposis with the
malignant affection of the distal rectum and others.
 Stoma technique: a terminal ileostoma is localized into the rigth underbelly; the most
frequently used methods are the Brooks method with the eversion of final part (3-6
cm) of the ileum or a continent stoma according to Kock where a pouch (reservoir)
with a ventil mechanism is created from the distal ileum before the stoma itself.

Ileostomia axialis

An axial (loop) ileostomy is used for the derivation or decompression of the large
intestine as a temporary protection of ileoanal or another risky anastomosis or
anastomosis with a pouch after a total proctocolectomy.
Stoma technique: the so-called „loop ileostomy“ is mostly used where one keeps the
continuity of the back wall of an ileal loop and creates an everted part of stomy on the



                 -#-
proximal loop. This loop is shifted out above the level of the abdominal wall, while
the orifice of the distal loop remains at the level of the skin.

Coecostomia

A wall colostoma is almost exclusively performed on the coecum, less on the
transverse colon, as a rule as a temporary stomy. It is rarely established and indicated
as a decompression stomy, when it is impossible to establish a loop colostomy, or for
other weighty reasons.
Stoma technique: a stomy can be created by means of a drain or a catheter (Foley)
which is introduced into the colon lumen, the front wall of the colon is fixed to the
peritoneum in the place of the introduced drain and the drain is led out through the
abdominal wall, further on it is possible to suture the bowel wall directly to the skin
and/or it is possible to perform a percutaneous endoscopic coecostomy.

Transversostomia

A loop transversostomy is most frequently used as a decompression or diverting
stomy in the case of obstruction caused by the stenotic process on the left colon
(tumour, diverticulitis, etc.), in the case of colon perforations and the insufficiency of
anastomosis on the left colon and the rectum.
Stoma technique: the determination of a suitable place for a stomy (already before the
opeation by applying a colostomic planchet to the standing or sitting patient, further
on it is suitable not to place a stomy into the area of an operation wound), a circular
excision of the skin in the extent of approximately a ten-crown coin, an excision or
unfolding of the fatty tissue a cross incision of the fascia and after the muscle stretch
out an incision of the peritoneum and drawing of the bowel loop over level of skin.
The support is drawn into the created canal in the mesocolon closely under the bowel
and the edges of the bowel are fixed to the edges of the skin by means of a suture. It
was the Czech surgeon Maydl who described the first loop colostomy in the literature
(1888).

Sigmoideostomia axialis

A loop sigmoideostomy is indicated – apart from the above-mentioned indications in
the case of a transversostomy – in rectum tumours (a palliative operation), anorectal
malformations, perianal, rectovaginal and other fistulae, anal incontinence, injuries of
the rectum, post-irradiation proctitis, large perianal inflammatory processes,
hydrosadenitis, etc./.
Stoma technique: it is practically the same as in the case of a transversostomy, only
the placement is in the left meso- till hypogastric region.


Colostomia terminalis

A terminal colostomy is most frequently established on the sigmoid colon. It is
performed as definitive in the case of exstirpation of the rectum (Miles procedure),
discontinuous resections of the left colon and the rectum (Hartmann´s type or the type
of a terminal stomy and a mucous fistula). These operations are mostly indicated for



                 -#-
the tumorous diseases of the rectum and the rectosigmoid, perforated diverticulitis or
devastating injuries in the area of the rectum and the sigmoid colon.
Stoma technique: after the colon interruption the proximal part of the bowel is led out
in the previously marked place as a terminal colostomy (a technique corresponding to
the procedure of a loop stomy), the distal part is either exstirpated (Miles´ excision of
the rectum) or blindly closed (Hartmann‘s resection) or led out as a stomy (mucous
fistula) in another place.

2.12.5. Complications Connected with Stoma

1. Early complications

- Necrosis of the bowel orifice due to blood supply failures
- Stoma retraction
- Infection in the wound around the stoma
- Stoma prolapse
- Prolapse of the bowel loops parastomally with the possibility of their strangulation

2. Late complications
 - Stenosis of the stoma orifice (mostly scarred)
 - Stoma prolapse (particularly in an loop ileostomy or a transverostomy)
 - Parastomal hernia
 - Perforation of the proximal loop (mostly mechanically during irrigation)

2.12.6. Care of Stomas, Aids, Diet Modification

The care of a stomy is for a great part performed by the patient himself. Stoma nurses
are trained in the hospital as well as in the field; they acquaint the patient with the
problems of stoma care and help the patient in the case of his/her technical
difficulties. Publications with the themes of stoma treatment, the use of stoma care
and diet in the case of a stoma are published for the people with a stoma.
One-part and two-part stoma care aids are accessible in the Czech Republic
(particularly the planchet and the stoma pouch), most stoma care aids are delivered by
the companies Convatec and Coloplast.

2.12.7. Prognosis. Indications for Stoma Closure

 The prognosis of patients with a stoma depends on the basic disease for which the
stoma was created. The stoma can be closed, as far as the reason ceased which had led
to its creation (removal of stenosis in the distal part of GIT, healing of anastomosis,
healing of inflammation, etc.).

Recommended Literature:
Černý J.: Chirurgia trávicej rúry, Martin, Osveta. 1998 p.512
Černý J.: Špeciálna chirurgia – chirurgia brušných orgánov a retroperitonea, Martin,
Osveta, 1992, p.584
Novák J.: Základy proktologie, Praha, Avicenum, 1985, p. 254-262
Niederle B., Šebek V.: Operace náhlých příhod břišních, Praha, Státní zdravotnické
nakladatelství, 1968, p.488
Tošovský V.: Náhlé příhody břišní u dětí, Praha, Avicenum, 1981, p.448


                 -#-
Corman M.L.: Colon and Rectal Surgery, Philadelphia, J.B.Lippincott comp., 1993,
p.1077-1149
Kremer K.,Grewe M.E.: Atlas chirurgických operací, Praha,. Avicenum, 1987, p.724


2.13. ABNORMAL LABORATORY FINDINGS
For the covered topic, following tests are of major importance:
- so-called liver function tests and viral hepatitis markers
- serum proteins
- amylase, lipase
- urea, creatinin, serum minerals, acid-base balance
- laboratory findings in autoimmune diseases
- others (indices of the metabolism of iron, copper, porphyrins, purines and amino
acids, deficit od alpha-1 antitrypsin, tumour markers, blood count, hemocoagulation,
urine and urinary sediment)

2.13.1. History, physical findings and complementary examination
The finding of a pathological result of a laboratory test, for which there is no apparent
explanation, is a common clinical problem. Typical example from the field of
hepatogastroenterology is the finding of isolated hyperbilirubinemia; however, any
test may be involved. In this situation the following approach can be recommended:
a) repeat the test after some time (one must bear in mind a possibility of a laboratory
mistake, sample interchange etc.)
b) complete the patient's history and check once more the appropriate area
c) order complementary laboratory and imaging tests
d) unclear cases must be followed-up in the long term as laboratory changes may
precede clinical manifestation of a disease. E.g., rising alpha-fetoprotein
concentration may herald the development of hepatocellular carcinoma that will be
diagnosed by the imaging procedures only several months later).

2.13.2. Differential diagnosis and prognosis
2.13.3. If no cause of a pathological laboratory test result can be discerned, it is
necessary to take into account the clinical state of the patient and time evolution of the
finding. With time the problem will usually be solved either by evolution of a hitherto
unrecognised disease or by normalization of the pathological finding. On the other
hand, there are patients in whom a pathological finding such as an extreme elevation
of the erythrocyte sedimentation rate lasts many years without any apparent reason. In
similar cases, the prognosis is always uncertain.


                                    --------------------




                 -#-

				
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