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Major Clinical Syndromes






The Acute Abdomen

The term 'acute' or 'surgical' abdomen is used to designate a great number of acute conditions associated with the diseases of abdominal organs that may be regarded as a direct indication for emergency surgery. This term is however only used in preliminary (provisional) diagnosis, while deciding whether the patient should or should not be taken to hospital, when an accurate diagnosis at patient's bedside is not possible.

The diseases, that can be manifested by the clinical picture of the acute abdomen may conventionally be classed into the following four groups:

1. Perforation of hollow organs, e.g. the stomach, the intestine, the gall
bladder, with discharge of their contents into the abdominal cavity.
Peritoneal irritation evokes severe stabbing pain and collapse with subse
quent acute peritonitis.

2. Acute inflammatory diseases: acute appendicitis, acute cholecystitis,
acute pancreatitis, acute adnexitis, gastric phlegmon, etc. As the disease
progresses, it is attended by extensive purulation, necrosis of the organ
(pancreas), or its wall (appendix, gall bladder), escape of pus into the ab
dominal cavity with local or diffuse acute serous or purulent peritonitis.
The clinical picture is characterized by rapidly purulent peritonitis. The
clinical picture is characterized by rapidly aggravating abdominal pain, in
flammatory symptoms, and toxaemia.

3. Intestinal obstruction by strangulation or obturation, strangulation
of internal or external hernia, necrosis of the intestinal wall. The intestine

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Chapter 7. Digestive System



 


necrotizes in all these cases, except in obstruction; peritonitis is likely to develop. Severe abdominal pain, vomiting and meteorism are characteristic.

4. Occult bleeding into the abdominal cavity (due to rupture of the uterine tubes in ectopic pregnancy, apoplexy of the ovary, rupture of the spleen or liver due to injury, etc.). The main symptoms are severe abrupt abdominal pain that can gradually abate, and circulatory collapse.

Clinical picture. Each specific disease that presents as the acute abdomen is characterized by a variety of clinical symptoms some of which are common for all of them and may be used to establish a provisional diagnosis.

1. The main symptom is a paroxysm of severe abdominal pain. Some
times it develops suddenly and manifests as a severest attack of stabbing
pain (in perforation of the gastric or intestinal wall). In other cases pain
is first relatively mild but its intensity rapidly increases to become severe
(in inflammation of the abdominal organs; colics).

2. Symptoms of peritoneal irritation. The symptoms are severe and per
sistent in perforation of the hollow abdominal organs, acute bleeding into
the peritoneal cavity, acute inflammation of the abdominal organs. Local
or diffuse muscular strain in the anterior abdominal wall (muscular
defense) can also be seen. Perforated peptic ulcer may be manifested by
board-like rigidity of the abdomen. Respiratory excursions of the abdomen
are either limited or absent. The Shchetkin-Blumberg sign is positive.

3. A group of symptoms demonstrating severely disordered peristalsis
and tone of the digestive tract: nausea, vomiting, pronounced meteorism,
constipation and passage of flatus. These symptoms may mostly be due
to organic causes such as intestinal obstruction, or they may arise by reflex.
In obturating or strangulating intestinal obstruction, the abdomen is inflat
ed unevenly. The inflation combines with a severe abdominal pain and visi
ble wave-like peristaltic protrusions and retractions on the abdomen (Wahl's
symptom). Percussion of the abdomen over the inflated zone reveals tympa-
ny; X-ray examination reveals multiple air-fluid levels (Kloiber's symptom).

4. Circulatory collapse: pallor, syncope, cold sweat, rapid and weak
pulse, low arterial pressure, pinched face (fades Hippocratica). These sym
ptoms are either due to massive blood loss or develop by reflex due to perfo
ration, inflammation of the abdominal organs, acute intestinal obstruction,
or peritonitis.

5. General rapidly progressing signs of inflammation: fever, neutrophilic
leucocytosis, and accelerated ESR combined with severe abdominal pain
and symptoms of peritoneal irritation. These are characteristic of gastroin
testinal perforation or obstruction with subsequent peritonitis and also
acute inflammation of the abdominal organs.

In typical cases, the symptoms of the acute abdomen are so specific


that findings of the examination, palpation and percussion of the abdomen, as well as questioning of the patient are sufficient to diagnose the acute abdomen, although it is often difficult to establish the underlying cause. The condition is an emergency and requires rapid correction since irreversible changes may rapidly develop. The patient must therefore be taken to hospital in the presence of at least one sign of the acute abdomen. The necessary examinations must be urgently conducted at hospital to establish the diagnosis and to decide on surgical or therapeutic tactics.

The patient's condition permitting, the first necessary examinations at a hospital include hourly taking body temperature, total blood counts, ECG, radiographic examination of the abdomen (roentgenoscopy and roentgenography) with the patient in an upright position (in the absence of suspicion for myocardial infarction). Other examinations may also be performed depending on the specific character of each particular case.

Treatment. It is necessary to remember, that some symptoms of the acute abdomen may be quite misleading. Thus, some 'obvious' cases of the acute abdomen may not require operative intervention, while even the 'mildest' abdominal pain may sometimes require an urgent surgical correction. Before the patient is delivered to hospital, spasmolytics (baralgin) may be given parenterally to alleviate pain. Preparations correcting the cardiovascular function should be given whenever necessary. Narcotics may be given only in special cases to control shock during patient's transportation. Undue administration of narcotics may cause transient improvement of the patient's condition but mask the symptoms of peritoneal irritation thus making the diagnosis difficult. Laxatives are absolutely contraindicated. A precise record of the drugs administered before hospitalization should be made. The exact time of administration should also be indicated.

Inadequate Digestion Syndrome

This is a symptom complex characterized by digestive disorders in the gastrointestinal tract. Disorders can be associated with upset cavital digestion, i.e. in the stomach and the intestine (dyspepsia), and parietal digestion. Mixed forms also occur.

Aetiology and pathogenesis. Dyspepsia. This occurs due to non-
compensated secretory insufficiency of the stomach, exocrine dysfunction
of the pancreas, upset secretion of bile, disordered passage of chyme
through the gastrointestinal tract (stasis, congestion due to stenosis and
compression of the intestine, or accelerated passage due to intense peristal
sis). Intestinal infection, dysbacteriosis, and alimentary disorders (overeat
ing, diet rich in proteins, fats, or carbohydrates, intake of large amounts
of fermented drinks) are also important. Dyspepsia may be functional, but
commonly it is due to a digestive tract disease.'.: ,


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Pathogenesis: incomplete breakdown of food particles, active propagation of bacterial flora in the intestine with its invasion of the proximal parts of the small intestine, dysbacteriosis, abnormally high activity of bacteria in the enzymatic decomposition of food with formation of toxins (ammonia, indole, low-molecular fatty acids, etc.) that irritate the intestinal muco-sa, intensify peristalsis, and cause symptoms of toxaemia due to their penetration into the blood.

Clinical picture. Gastric dyspepsia. This condition occurs in ach-lorhydria and achylia, long-standing decompensated pyloric stenosis, atrophic gastritis, and cancer of the stomach. The disease is characterized by the feeling of discomfort, pressure or distension in the epigastrium after meals, frequent eructation, regurgitation (often with acid or fetid odour), unpleasant taste in the mouth, nausea, and poor appetite. Achylous diarrhoea and meteorism are not infrequent. Examination of the gastric juice reveals achlorhydria or achylia (both hydrochloric acid and pepsin are absent from the gastric juice).

Intestinal dyspepsia occurs in the presence of exocrine dysfunction of the pancreas, chronic inflammatory diseases of the small intestine, and some other conditions. It presents as inflation and rumbling in the abdomen (borborygmus), intensive passage of flatus, diarrhoea with putrefactive or acid smell and (in rare cases) constipation. Coprologic findings: steator-rhoea, amylorrhoea. X-ray findings: accelerated passage of the barium meal through the small intestine. Studies of the secretory function of the pancreas, aspiration biopsy, determination of enterokinase and alkaline phosphatase in the intestinal juice, and other tests help verify the cause of intestinal dyspepsia. Tests for hyperglycaemia with an oral starch load and radionuclide studies with glycerol trioleate, sunflower-seed or olive oil are used to estimate the degree of the cavital digestion derangement. The study of intestinal microflora is also important.

Treatment. This, in the first instance, is aimed at eradication of the underlying disease. Symptomatic therapy includes special diets and medication for diarrhoea; enzyme preparations (pancreatin, abomin, festal), astringents, and carbolen are also administered.

Inadequate parietal digestion can be seen in congenital secretory insufficiency of the intestinal wall (disaccharidase deficit enteropathy) and in chronic diseases of the small intestine attended with dystrophic, inflammatory, and sclerotic changes in its mucosa, upset structure of the villi and microvilli, and their decreasing number, deranged intestinal peristalsis (enteritis, sprue, intestinal lipodystrophy, exudative enteropathy, etc.).

The symptoms, course, and clinical picture are the same as in intestinal dyspepsia and in the malabsorption syndrome (see below).

The diagnosis is established on the basis of determination of enzymes


(amylase, lipase) during their desorption in homogeneous preparations of the small-intestine mucosa specimens taken by aspiration biopsy. The glycaemic curve drawn after oral intakes of disaccharides and monosaccha-rides helps differentiate the syndrome of inadequate parietal digestion (flat curve after the intake of maltose, saccharose, lactose; normal curve after the glucose and galactose intake) from lesions of the small intestine that are attended with malabsorption of the products of food decomposition in the small intestine. After an intake of polysaccharides (starch) this syndrome may be differentiated from inadequate cavital digestion. Aspiration biopsy reveals atrophy of the intestinal mucosa (indirect sign).

Treatment is aimed at the main disease. For methods of management of malabsorption syndrome see below. Symptomatic therapy includes enzyme preparations (abomin, festal) and astringents (tannalbin, albin). The drugs are given per os.

Malabsorption Syndrome

This symptom complex is due to upset absorption in the small intestine. The syndrome often develops in combination with the syndrome of inadequate digestion. Primary and secondary malabsorption syndromes are distinguished.

Malabsorption is probably explained by congenital disorders in the fine structure of the intestinal mucosa and genetically determined intestinal en-zymopathy. The onset of the secondary malabsorption syndrome is due to acquired structural changes in the intestinal mucosa evoked by acute and chronic enteritis, sprue, intestinal lipodystrophy, exudative enteropathy, lesions of the small intestine in amyloidosis, systemic scleroderma, and other disease conditions attended with digestive disorders. The upset intestinal digestion and accelerated passage of chyme through the intestine are decisive in acute and subacute diseases. In chronic conditions the decisive factors are dystrophy and atrophic fibrous changes in the mucosa of the small intestine, shortening and levelling of the villi and crypts, significant reduction of the microvilli number, fibrous tissue formation in the intestinal wall with impairment of blood and lymph circulation, and disordered parietal digestion. All these changes limit absorption of the products of hydrolysis of proteins, fats, and carbohydrates, and of mineral salts and vitamins in the intestinal wall (see Alimentary dystrophy).

Clinical picture. Course. Gradual wasting, symptoms of metabolic disorders of all types (protein, fat, vitamin, water-salt), dystrophic changes in the internal organs with their subsequent dysfunction, and also constant steatorrhoea, creatorrhoea, and amylorrhoea are characteristic. Hypo-proteinaemia develops (mostly at the expense of reduction of the serum


       
   
 
 

 

Special Part

albumin level); hypocholesterolaemia, hypocalcaemia, and moderate hypoglycaemia occur. Hypoproteinaemic oedema develops in the presence of hypoproteinaemia below 40-50 g/1. The characteristic symptoms of poly-hypovitaminosis are osteoporosis, anaemia (hypochromic anaemia in predominant malabsorption of iron, and hyperchromic anaemia in upset absorption of vitamin B12), trophic changes in the skin, nails, progressive atrophy of the muscles, signs of polyglandular insufficiency, weakness, and (in severe cases) acidosis and cachexia.

Diagnosis. Laboratory examinations determine hypoproteinaemia, hypocholesterolaemia, hypoglycaemia, and other disorders due to malabsorption.

Coprologic studies reveal increased content of undigested food in the faeces and also increased excretion of the products of enzymic decomposition of food. Enterobiopsy reveals atrophic changes in the mucosa of the proximal parts of the small intestine. Since the walls of the small intestine absorb great amounts of various substances, different methods are used to study their absorption. These are tests with carotine, folic acid, galactose, D-xylose absorption test, etc. Caseine, albumin, oleic acid, methionine, gly-cine, vitamin Bi2, folic acid, and other substances labelled with radioactive isotopes have recently beed used. The method is based on the determination of concentration of labelled substances and the time of their appearance in the blood, their excretion with the urine or faeces, and assessment of residual radioactivity of faecal masses that is indicative of the amount of unabsorbed substances. Determination of the absorbed nutrients is based on the study of the chemical composition of food and stools during a certain period of time.

The course of the disease depends on the underlying condition and prospects for its cure. The prognosis is unfavourable in severe cases.

Treatment. The underlying disease should be treated. Symptomatic treatment: parenteral nutrition, administration of vitamins, plasma, protein hydrolyzates, glucose, nutrient enema, correction of electrolyte metabolism.

Prophylaxis includes timely treatment of diseases that usually concur with the malabsorption syndrome.


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