GASTROINTESTINAL AND ABDOMINAL PROBLEMS

The enlarged synopsis of the course 6, module C, cycle II of the new curriculum of the Third Faculty of Medicine, Charles University J. Hork, J. Fanta, J. Strnad, J. Faltn, M. Urban Abbreviations: DD .. differential diagnosis Def definition Dg diagnosis Et etiology Ci.contraindications Lab. laboratory findings Ththerapy 1. INTRODUCTION problem outline, 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 defined. 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 must under all circumstances 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 motor dysphagia. The upper part of esophagus contains striated muscle innervated by n. vagus. The motoric neurons are cholinergic and excitatory. Motor 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: motor 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: motor 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 the 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, mechanical 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 direct visualization and biopsy of the esophageal mucosa. It enables to diagnose Barretts 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 restituion 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 - Barretts 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 (omeprazole). In reflux esophagitis the treatment lasts everal months. - follow-up and repeated endoscopies in Barretts esophagus - dilatation of stenoses - surgical treatment: fundoplication 2.1.7. Esophageal diverticula - pulse (upper and lower esophagus) and traction (middle esophagus) diverticula - Zenkers 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 Schatzkis 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: Menieres 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 Zenkers diverticulum, achalasia) - vertigo and tinnitus Menieres disease

- alleviation of pain following vomiting - peptic ulcer - auxilliary examinations - vide supra Complications: Regardless of the underlying cause, vomiting can lead to severe consequences 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 patients 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 patients 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 - omeprazole, pantoprazole, lansoprazole - 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 malignancy surgical treatment: Billroth I resection (today exceptionally performed)

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

Mntriers 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 patients 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 omeprazole or pantoprazole, 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, meteorism 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 (meteorism, ileus) free (viscus perforation)

intramural (pneumatosis cystoides intestinalis)

2.4.3. Diagnosis and differential diagnosis

history and physical findings laboratory hypoproteinemia, signs of an inflammation 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, LeVeens shunt, liver transplantation) gas intraluminal conservative treatment (think of ileus)
o o

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 parieties (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 phenomen 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 individuals 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 patients 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 posiibility of an acute abdomen solely based on appereance. Temperature, pulse, and blood presure 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 carired 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 produce pain (Blumbergs 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 (Rovsings 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 (Chilaiditis 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 leukocytes 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 eosinophil 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, Meckels 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 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 natures 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. b. c. d. Through perforation of a part of the gastrointestinal tract Through intraperitoneal rupture of the urinary tract Through the fallopian tubes Through accidental or surgical wounds of the abdominal wall

1. 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. Beggining 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 correctiong 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 determanation 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) tumours (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 and problem specification Gastrointestinal bleeding may be divided as follows: A) anatomically as: 1. bleeding above the duodeno-jejunal flexure (pharynx, oesophagus, stomach, duodenum) 2. bleeding below the duodeno-jejunal flexure (jejunum, ileum, colon, rectum, anus). B) according to the severity (amount) and speed of bleeding as: 1. chronic (occult) bleeding, with losses of up to 50 ml per day 2. acute (massive) bleeding. Gastrointestinal bleeding may manifest itself as: A) haematemesis: the vomiting of either altered ("coffee grounds

vomitus") or unaltered blood. B) melaena (the passage of black, tarry stools). C) enterorrhagia (the passage of unalterd blood, with or without stools). 2.7.2 Aetiology and pathophysiology Acute gastrointestinal bleeding is usually unexpected and sudden and its source is usually unknown (history: peptic disease, liver cirrhosis). It is difficult to determine immediatelly the volume of blood lost and the extent of the continuing haemorrhage. D.R.Kafonek et al found that in 2225 patients, the source of upper gastrointestinal bleeding was: - in 24,3% - duodenal ulcer - in 23,4% - haemorrhagic gastritis - in 21,3% - gastric ulcer - in 10,3% - oesophageal varices - in 7,2% - Mallory-Weiss syndrome - in 6,3% - oesophagitis - in 5,8% - erosive duodenitis - in 2,9% - neoplasm - in 1,8% - mouth ulceration - in 1,7% - oesophageal ulceration (Barrets ulcer) - in 6,3% - others (peptic jejunal ulcer, ulcer in anastomosis, hiatal hernia, haemangioma, Curlings ulcer in burns, benign tumours, neurinomas). A) In upper gastrointestinal bleeding: - peptic ulcers: there is usually a history of peptic disease, non-steroid anti-inflammatory drug use (NSAIDs), glucocorticoid

use, stress, - haemorrhagic gastropathy: alcohol abuse, NSAIDs, trauma, surgery, serious medical conditions (stress), - oesophageal varices: portal hypertension (mainly in liver cirrhosis), - Mallory-Weiss syndrome: (a longitudinal rupture of the mucosa at the gastrooesophageal junction) - forceful vomiting, Differential diagnosis: Boerhaavs syndrome = rupture of the oesophagus. B) Sources of bleeding in the middle stratum (jejunum, ileum) may include: Crohns disease, invagination, angiodysplasia, diverticles (Meckels, Grasers), inflammatory intestinal disease, neoplasm (benign: polyp, lipoma, leiomyoma, fibroma, or malignant: carcinoma, sarcoma). C) The most frequent sources of bleeding (usually in the form of enterorrhagia or occult bleeding) in the lower stratum (colon, rectum, anus) include: haemorrhoids, malignant tumours, benign tumours (polyps, adenomas), diverticles, invaginations, specific (tbc) and non-specific inflammation (ulcerous colitis, Crohns disease), acute occlusion of the mesenteric arteries, vascular malformations. CAVE: in approximately 10% of cases, 20-30% of patients bleed from two or more lesions! Half the patients with liver cirrhosis bleed from peptic ulcers and gastric erosions, and not from oesophageal varices! The source of occult bleeding may be practically anywhere! 2.7.3. Clinical aspects Occult bleeding: weakness, paleness, chest pain (patients are often admitted to cardiology ICUS with suspected myocardial infarction).There is no hypotension or tachycardia. The blood count shows low haematocrit and haemoglobin. Test sets (e.g. Haemoccult) give false negative results in 20% and false positive results in 10% of cases. Massive bleeding: shock (pale skin, cold sweat, tachycardia, hypotension, low haematocrit and haemoglobin, possibly leukocytosis). In upper GIT bleeding, there is massive haematemesis and, eventually, enterorrhagia, with melaena appearing later on. Bleeding from the middle or lower stratum manifests as enterorrhagia 2.7.4 Diagnosis and differential diagnosis

History: we search for the following: 1. Treated or untreated peptic ulcer 2. Past hepatitis infection or treatment for liver disease (cirrhosis) 3. Alcohol abuse 4. Drugs (antipyretics, anti-rheumatics, anticoagulants) Physical findings: we look for signs of chronic liver disease (spider haemangiomas, palmar erythema, hepatomegaly, splenomegaly, jaundice and ascites). On abdominal palpation, we search for palpable pathological masses. During rectal examination, we note the presence of haemorrhoidal nodes and pathological masses in the ampula recti. Additional examinations: In upper GIT bleeding, urgent fibroscopy (oesophago-gastro-duodenoscopy) represents the most useful first study. It is not only diagnostic, but also therapeutic (see 2.7.5). CT or US scans may confirm the presence of pathological masses and fluids (ascites) in the abdominal cavity. By determining liver density, these methods may confirm suspected liver steatosis, or cirrhosis. In lower GIT bleeding, which is rarely massive, colonoscopy represents the most useful study. Selective angiography of the upper and lower mesenteric artery may reveal the source of bleeding, especially in the middle stratum - small intestine and the lower stratum - large intestine - in cases of arterial bleeding. A normal haematocrit in the first hours of massive bleeding does not rule it out: blood dilution from the extravascular compartment requires several hours. Differential diagnosis: 1. Upper GIT: a) vomiting of blood swallowed during bleeding from the nose, mouth and pharynx, b) haemoptysis: the vomiting of light, frothy blood (moist rales on auscultation of the lungs), c) vomiting in haemobilia. 2. Middle and lower GIT:

a) melaena-like stools may also appear following the oral administration of iron preparations, carbo adsorbens, bismuth, or after eating blueberries or spinach, b) haematuria or metrorrhagia (menstruation, cervical or uterine carcinoma) may imitate enterorrhagia. 2. 7. 5 Treatment: Evaluation and treatment of acute GIT bleeding may be divided into three related phases: 1. Supportive phase: a) estimating blood loss and securing adequate volume replacement (erythrocyte concentrates, fresh frozen plasma), b) placing a nasogastric tube, with nothing per os (following endoscopic examination and after ruling out oesophageal varices), inserting a central venous catheter, c) oxygen as required (e.g. 3 l/minute), d) intensive haemodynamic monitoring, e) if agitated, the patient should be tranquillised (Diazepam 5 mg iv.), f) laboratory tests: blood type, blood count, coagulation studies (APTT, Quick, platelets, fibrinogen), liver tests (AST, ALT, GMT, bilirubin, protein electrophoresis), electrolytes, urea, creatitine, blood glucose, Hct and Hb should be monitored in 4 hour intervals. 2. Diagnostic phase:- determining the source of bleeding (see 2.7.4) 3. Therapeutic phase: I. Acute GIT bleeding A. In cases of peptic ulceration, we rely on Forrests classification. Stage 1a: spurting arterial bleeding, usually from the posterior wall of the duodenal bulbus (a. gastroduodenalis), requires emergency surgery. Stage 1b: permeating bleeding may be stopped using endoscopic electrocoagulation, laser techniques, or injections of adrenaline (1:1000) or absolute alcohol. Stage 2a: localised bleeding without a visible vessel: as in 3.

Stage 2b: a visible bleeding vessel requires early surgery because of the risk of rebleeding. Stage 3: ulcer with no signs of bleeding: prevention of recurrence (conservative treatment of peptic disease). B. In cases of bleeding oesophageal varices. 1. If possible, urgent sclerotisation of the bleeding varices is performed (CAVE: ethoxysclerol is a powerful cardiopressoric agent). If this is not possible or if bleeding persists, then compression using the Sengstaken-Blakemore balloon tube or the Linton-Nachlas tube is indicated, the latter is more effective in varices located in the gastric fundus. 2. Apart from basic supportive care (see 2.7.5), we administer electrolyte infusions with terlipressin (Remestyp), at a dose of 2 mg in 400 ml of normal saline for 30 minutes every 4 hours. If signs of hepatic insufficiency are present (decompensation of liver cirrhosis), medicamental support of liver functions is indicated (see chapter dealing with liver cirrhosis). II. Treatment of chronic bleeding (occult bleeding, development of chronic anaemia). This depends on the cause of bleeding. The most frequent causes include: a) bleeding from chronic gastroduodenal ulcers b) bleeding from polyps of the large intestine (endoscopic polypectomy) c) bleeding from a malignant blastoma of the large intestine (radical or palliative surgery - see tumours of the GIT) d) haemorrhoidal bleeding (surgical treatment, laser therapy, cryotherapy). 2. 7. 6 Prevetion. Prognosis Prevention of recurrent bleeding from gastroduodenal ulcers consists of strict adherence to dietary regimens, intensive conservative treatment (medication), and surgery after a second episode of bleeding. Prevntion of oesophageal varices consists of conservative treatment (medication) of the underlying disease (usually liver cirrhosis), regimen adherence (absolute

absention from alcohol), repeat sclerotisation in 10 to 20-day intervals until varices disappear. Prevention of bleeding from blastoma involves early surgical removal of the tumour, either radically or palliatively. The prognosis of peptic disease is good if preventive measures are observed. In the case of blastomas, prognosis depends on how advanced the disease is (metastases). In the case of oesophageal varices, it depends on liver function, assessed according to Childs criteria: bilirubin (above 50 mol/l), albumin (below 30 g/l), the existence of irreversible ascites and the presence of neuropsychiatric symptoms. If these are met, than the prognosis is fatal. In general, 80% of GIT bleeding ceases when treated conservatively. 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 mol/l cholestasis is defined as an impairment of bile production and secretion the onset 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, Gilberts syndrome) hepatocellular (lesion of liver parenchyma] obstructive (stone, tumour, inflammatory stenosis, pancreatic head enlargement)

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 2.8.1.3. Diagnosis and differential diagnosis

history and physical findings laboratory sonography X-ray (ERCP, PTC, CT) cholescintigraphy

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)

a. 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 varices 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. Count higher than 250 leukocytes per microliter is diagnostic

2.8.3.3. Treatment of cirrhotis 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. II. III. IV. Mood changes, euphoria or depression, attention disorders, irritability Slow mentation, lethargy, marked personality changes, inappropriate behaviour, intermittent desorientation Somnolence, marked desorientation, amnesia, blurred speach 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 freefatty 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 ancephalopathy, 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 prostaglandines, 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 Whipples 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 isufficiency 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

C. Lymphatic obstruction

intestinal teleangiectasia lymphomas

C. Cardiovascular disease

right heart failure abdominal angina vasculitis

C. Diseases of intestinal mucosa

inflammation, infiltration, infection (Crohns disease, amyloidosis, salmonellosis) biochemical and genetic disorders (sprue, lactase deficit etc.)

C. 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, calsium and trace elements, pancreatic enzymes INFLAMMATORY BOWEL DISEASE Two basic entities: Crohns 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 Crohns 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 Crohns 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 Crohns 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

A. Crohns 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 Crohns 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

A. Crohns 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

Whipples 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 Whipples 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, meteorim 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, Hirschprungs 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 localisation constipation to ileus, intestinal bleeding, diarrhoea, anemia, weight loss, abdominal mass, liver and other organ metastases. it is apparent that due to its protean symptomatology colorectal carcinoma could be included also in other chapters of symptomatic division of abdominal problems GIT bleeding, abdominal mass, diarrhoea or abnormal laboratory tests.

Dg: physical examination including examination per rectum, rectosigmoidoscopy, colonoscopy, irrigography Th: in all operable cases surgery. Palliative treatment aims mainly at maintaining intestinal passage. Prognosis: about 50% of operated patients survive 5 years 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

The anal canal is about 3 cm long. It points toward the umbilicus and forms a distinct angle with the rectum in its resting state. During defecation, the angle straightens out. At the superior boundary of the anal canal is the anorectal juncture mucocutaneous juncture, pectinate, or dentate line. blood supply: inferior hemorrhoidal arteries, inferior hemorrhoidal veins lymphatics inervation: the nerve supply of the rectum is derived from the sympathetic and parasympathetic systems.

anorectal function

2.11.2. Etiology and pathophysiology

injuries, foreign bodies hemorrhoids, hemorrhoidal thrombosis, anal fissure abscess, fistula, sinus proctitis tumours

2.11.3. Clinical presentation

bleeding pruritus pain prolaps incontinence and stenosis tenesmus

2.11.4. Diagnosis and differential diagnosis Most disorders affecting the anorectum can be diagnosed by history and physical examination, including perianal inspection and palpation, digital rectal examination, anoscopic examination, and proctosigmoidoscopic examination. Necessity to exluded cancer of anus or rectum- as a minimum rigid rectoscopy and double contrast barium enema, optimum- total colonoscopy DISEASES OF THE ANORECTUM HEMORRHOIDS /PILES/ INTERNAL AND EXTERNAL HEMORRHOIDS Ist degreeIInd degree- temporary prolaps IIIrd degree - fixed prolaps Essentials of diagnosis

history - rectal bleeding, protrusion, discomfort, thrombosis, pain, prolaps, anal pruritus mucoid discharge from rectum possible secondary anaemia rectal examination: inspection, palpation, anoscopy - characteristic findings on external anal inspection and anoscopic examination anoscopy, rectoscopy, sigmoidoscopy irrigography sonography stool examination biopsy etc.

Hemorrhoids

external and internal

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) injection treatment rubber band ligation cryosurgery hemorrhoidectomy - different type: Whitehead, Milighan Morgan., de Longo

2.11.6. Preventive, prognostic and opinion aspects ANAL FISSURE (Fissura-in-Ano, Anal Ulcer) Essentials of Diagnosis

Rectal pain related to defecation. Bleeding. Constipation. Spasm of sphincters. Anal tenderness. Ulceration of anal canal. Stenosis. Hypertrophic anal papilla. Sentinel pile.

Dd: cave anal cancer Th: medical - anaesthetic and analgetic suppository surgical ANORECTAL ABSCESS Dg:

Persistent throbbing rectal pain. External evidence of abscess, such as palpable induration and tenderness, may or may not be present. Systemic evidence of infection.

CLINICAL FINDINGS

COMPLICATIONS sepsis, formation of anorectal fistulas

Th: surgery, antibiotics ANORECTAL FISTULAS communication between anus or rectum and perianal skin 80% cryptogenic fistulas TYPE OF FISTULA I marginal, II transphincteric III suprasphincteric, IV high.

A/ SYMPTOMS AND SIGNS B/ SPECIAL EXAMINATIONS: fistulography, transrectal ultrasound examination Dd: M Crohn, cancer of rectum treatment: surgery

PRURITUS ANI cave parasites Haemorrhoids are not a cause of pruritus ani RECTAL PROLAPSE Essentials of Diagnosis

Protrusion of the rectum through the anus. Partial or complete faecal incontinence. Rectal bleeding and discharge.

SOLITARY RECTAL ULCER FECAL INCONTINENCE Essentials of Diagnosis

Loss of voluntary control of passage of faeces from anus. Faecal soiling of clothing.

CLINICAL FINDINGS: status of sphincter, EMG of sphincter, ultrasound examination PREVENTION TREATMENT - surgical ANAL STENOSIS MALIGNANT TUMORS OF THE ANAL CANAL AND PERINEUM EPIDERMOID CARCINOMA OF THE ANORECTUM

SQUAMOUS CELL CARCINOMA

MALIGNANT MELANOMA BOWENS DISEASE EXTRAMAMMARY PAGETS DISEASE BASAL CELL CARCINOMA MALIGNANT TUMORS: KAPOSIS SARCOMA 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 patients 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 an 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 (Hartmanns 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 (Hartmanns 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 supplied 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.). 2.13. DISCHARGE FROM URETHRA AND VAGINA 2.13.1. Definition and clinical presentation discharge from urethra secretion from urethra apart from voiding and ejaculation mainly in males acute inflammation of the male urethra a) specific b) nonspecific sexually transmitted disease prostatourethritis Terminology: dysuria, stranguria, polyuria, polakisuria, nycturia, oliguria, anuria, urine retention Definition and clinical picture of lower urinary obstruction discharge from vagina 2.13.2. Etiology and pathophysiology urethral discharge infection gonococcal urethritis (N. gonorrhoeae) nongonococcal urethritis (chlamydia, Ureaplasma urealyticum, Trichomonas vaginalis, herpesviruses) benign prostatic hypertrophy, prostatic cancer, urethral stricture

2.13.3. Diagnosis and differential diagnosis history and physical findings Gram stain culture of the secretion urinalysis prostate examination further findings Reiters disease Etiology and pathogenesis Clinical presentation Diagnosis Treatment 2.13.4. Treatment antimicrobial other actions (identification and treatment of sexual partners) treatment of benign prostatic hypertrophy treatment of prostatic cancer treatment of urethral stricture 2.13.5. Preventive, prognostic and opinion aspects 2.14. PROBLEMS WITH VOIDING 2.14.1. Definition and clinical presentation Urinary incontinence is defined as involuntary flow of urine, which can be objectively proved and causes social or hygienic problems to the patient. Incontinence is either true, in which urine flows out of the urethra, and false or extraurethral. The cause of incontinence

may be either hyperactivity of the detrusor, lowering of the closing intraurethral pressure or distension of the urinary bladder. Hyperactivity of the detrusor is caused by increased irritability of the urinary bladder. The patient suffers from voiding urgency, which is rapidly followed by spontaneous outflow of urine (urgent incontinence). The contents of the urinary bladder is small. If the closing urethral pressure decreases below the intravesiceal pressure only during a strain, we speak about the stress incontinence. Total incontinence means complete loss of miction control, e.g. in advanced dementia. The term ischuria paradoxa is used for spontaneous urine outflow in retention and vesical distension. Most frequent is the mixed incontinence, which is a mixture of urgent and stress incontinence. Predisposing factors for urinary incontinence are advanced age, obesity, immobility, some diseases as cerebral atherosclerosis, Alzheimer and Parkinson disease, urinary tract infection, prostate hypertrophy and diabetes mellitus and some drugs (diuretics, beta-sympatolytics and mimetics, alpha-sympatolytics and mimetics, antidepressants). In women come to this list also mulitple pregnancies and strenuous physical work. Untoward sequelae of urinary incontinence are medical (perineal dermatoses, urinary tract infections), psychological (feeling of uncertainty to anxiety, insomnia, depression), social (isolation or institutionalization of the patient, extra load on the attending personel) and economic (increased tending costs). 2.14.2. Diagnostics properly taken history, ultrasonography, urodynamic examination. 2.14.3. Treatment adjustment of drinking regimen (limitation of water intake in the evening with preservation of the total daily water intake) support of the overall physical activity availability of a WC strengthening of the pelvic floor (important especially in women) pharmacotherapy is useful especially in urgent and mixed incontinence. Parasympatholytics and spasmolytics (oxybutinin Ditropan, Cystrin), tricyclic antidepressants (imipramin) and alpha-sympatholytics (Hytrin, Xatral) are used. In urinary tract infection, antibiotics are used; surgical treatment may be useful in stress incontinence; if the described treatment is not effective, it is necessary to use incontinence aids. In males a condome urinal is used, in both sexes absorbing disposable aids. Use of

a permanent urinary catheter always causes urinary tract infection and as a standard solution is unacceptable. 2.14.4. Preventive, prognostic and opinion aspects 2.15. IMPOTENCE 2.15.1. Definition anatomy of male sexual organs function of penis: a) voiding b) erection c) ejaculation 2.15.2. Etiology and pathophysiology Organic causes of impotence: vascular cause of impotence filling disorder vascular cause of impotence storing disorder impotence in a combined disorder of both filling and storing the blood impotence caused by an endocrine disease effect of drugs and medicines on the potence impotence following surgery Peyrons disease priapism impotence caused by a trauma neurogenic disorders renal diseases Psychogenic impotence Organic impotence

Mixed impotence 2.15.3. Diagnosis clinical examination: NPT (nocturnal penile tumescence monitoring) test registering nocturnal erections snop gang test device measuring erection and rigidity of the penis sleep laboratory blood examination doppler ultrasound arteriography cavernosogram neural examination the papaverin test 2.15.4. Treatment Psychologic, psychotherapeutic, medical, penile prostheses 2.15.5. Prevention 2.16. 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)

2.16.1. 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) to repeat the test after some time (one must bear in mind a possibility of a laboratory mistake, sample interchange etc.) b) to complete the patient's history and check once more the appropriate area c) to 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) 2.16.2. Differential diagnosis and prognosis 2.16.3. 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. 2.17. RENAL SYNDROMES Diagnostics and treatment of renal diseases belongs to two medical specialties: the medical part is taken care of by nephrology, the surgical part by urology. Diseases of the kidneys and urinary tracts are commonly manifested by several typical syndromes (i.e., grouped symptoms and signs). Therefore, when examining a new patient the physician usually first sets up a syndromological diagnosis and on its basis by means of further examination he tries to identify the etiology of the problem in question. The most common renal syndromes are as follows: 2.17.1. Abnormal urinalysis (asymptomatic) - microscopic hematuria

- proteinuria - leukocyturia - bacteriuria - casts usually accompany some of the above findings 2.17.2. Nephrotic syndrome - cf. cycle II, module C, course No 8 2.17.3. Acute and rapidly progressing renal failure Etiology and classification A. Prerenal azotemia - hypovolemia (dehydration, bleeding, burns, vomiting, diarrhoea) - decreased cardiac output (myocardial diseases, valvular diseases, arrhytmias, cardiac tamponade) - renal hemodynamics changes (sepsis, antihypertensives, hypercalcemia, renal vasoconstriction, hepatorenal syndrome, cyclooxygenase inhibitors, ACEinhibitors) - hyperviscosity syndrome B. renal failure - renovascular obstruction (renal arteries or veins) - glomerular diseases (acute glomerulonephritis, hemolytic-uremic syndrome) - acute tubular necrosis (renal ischemia, nephrotoxins, hemolysis, rhabdomyolysis) - interstitial nephritis (allergic, infectious) - tubular obstruction (urates, globulins in myeloma) - rejection of a transplanted kidney C. Postrenal azotemia (urinary tract obstruction) - at the level of ureters (stones, blood clots, tumours, retroperitoneal fibrosis)

- at the level of the bladder neck (enlarged prostate, tumour, blood clots, stone) - in the urethra (stenosis, phimosis) Dg: - history - physical examination - oliguria to anuria - decrease in glomerular filtration - increase in serum creatinine and urea concentration - urinary sediment examination - others (sonography, X-ray etc.) Stepwise approach: a) syndromological diagnosis and treatment b) etiological diagnosis c) removal of the underlying cause and start of the specific treatment d) prevention and treatment of uremia 2.17.4. Chronic renal failure

low glomerular filtration lasting at least three months it usually develops over several years decreased size of the kidneys

Et. (according to frequency) - diabetes mellitus - hypertension - chronic nephritis - polycystic renal disease - unclear cuase

Uremic toxins: - urea - guanidine derivatives including creatinine - urates and hippurates - end-products of metabolism of nucleis acids, aliphatic amines and aromatic amino acids - glycosylated metabolites etc. Lab: - anemia - hypocalcemia - hyperphosphatemia - broad casts in the sediment - acidosis Sy: - uremic syndrome - renal osteodystrophy - hypertension - polyuria or oliguria 2.17.5. Acute nephritis A. glomerulonephritis - inflammation mainly of the glomeruli Et: poststreptococcal Sy: hypertension and edema due to extracellular volume increase Lab: hematuria, poteinuria, glomerular filtration decrease, increased serum creatinin and urea B. acute tubulointestitial nephritis - inflammation of tubules and interstitium

Et: bacterial, metabolic, toxic Lab: leukocyturia, slight hematuria, proteinuria is never massive 2.17.6. Urinary tract infection - presence of pathogenic microorganisms in urine - bacteria (bacteriuria > 105/ml) or yeasts Et: E. coli, Klebsiella, Enterobacter, Proteus Sy: dysuria, polakisuria DD: interstitial nephritis 2.17.7. Hypertension - blood pressure higher than 140/90 mmHg - renovascular or nephrogenic DD: essential hypertension, other types of secondary hypertension 2.17.8. Nephrolithiasis Sy: renal colic, hematuria, flank pain, dysuria Lab: hematuria, bacteruria, crystaluria Dg: history, clinical presentation, sonography, plain abdominal X-ray, intravenous urography 2.17.9. Urinary tract obstruction Et: stone, blood clot, prostate hypertrophy, urethral stenosis Sy: palpable urinary bladder, oligoanuria, urinary retention, enlarged prostate Lab: azotemia, large kidneys, urinary tract dilatation 2.17.10. Renal tubular defects a) anatomic (inherited - renal polycystosis) b) transport disorders (inherited or acquired) -----------------------------

Further reading Balaz V et al: Speciln chirurgie II, Avicenum, 1985 Corman M.L.: Colon and Rectal Surgery, Philadelphia, J.B.Lippincott comp.,1993, p.1077-1149 ern J.: Chirurgia trvicej rry, Martin, Osveta. 1998 ern J.: pecilna chirurgia chirurgia brunch orgnov a retroperitonea, Martin, Osveta, 1992, p.584 Harrisons Principles of Internal Medicine, 14th Edition, McGraw Hill 1998 Harvey A. McG et al: The Principles and Practice of Medicine. Appleton and Lange, 1998, 22nd edition. Kremer K.,Grewe M.E.: Atlas chirurgickch operac, Praha,. Avicenum, 1987, p.724 Niederle B., ebek V.: Operace nhlch phod binch, Praha, Sttn zdravotnick nakladatelstv, 1968, p.488 Novk J.: Zklady proktologie, Praha, Avicenum, 1985, p. 254-262 Schaffler A, Braun J, Renz U: Vademecum lekare, Galen 1993 Toovsk V.: Nhl phody bin u dt, Praha, Avicenum, 1981, p.448 --------------------