Inquiry and general inspection of patients with diseases

Inquiry and general inspection of patients with diseases

of digestive system.

Inspection and superficial palpation of an abdomen.

Percussion ans auscultation of an abdomen.

Methods of determination of ascites.

Deep sliding methodical palpation of parts of intestine and stomach, a liver, spleen and kidneys.

Examination of patients with digestive tract disorders

OESOPHAGUS

           Complaints. Dysphagia (difficult passage of food via the oesophagus) is the most frequent symptom of oesophageal pathology. The patient feels difficulty in swallowing (mostly solid food); the food bolus sometimes stops in the oesophagus and the patient feels pain and oesophageal disten­tion. Dysphagiaucan be due to organic or functional narrowing of the oesophagusfOrganic stenosis develops gradually and progresses in cancer, and cicatricial stenosis of the oesophagus. Solid food first passes with dif­ficulty, then the patient feels difficulty in swallowing soft, and then liquid food. When cancer tumour disintegrates, patency of the oesophagus may be restored almost completely. Dysphagia develops immediately in the presence of a foreign body or if the oesophagus is burnt. Dysphagia may also develop due to compression from outside by an aortic aneurysm or mediastinal tumour.

         Functional narrowing of the oesophagus is explained by muscular spasms caused by reflex disorders in innervation of the oesophageal muscles, or by neurosis. As distinct from organic dysphagia, functional dysphagia more often occurs in paroxysms when food passes the oesophagus. Sometimes solid food passes more readily than liquid.

Pain occurs in acute inflammation of the oesophageal mucosa (oesophagitis) and in burns. The patient usually feels pain by the course of the entire oesophagus, both with and without swallowing; pain may radiate into the interscapular region.

         Patients with achalasia of the cardia (cardiospasm) may have spontaneous attacks of pain, usually during night. Pain is quite severe; it radiates into the back, upwards by the oesophagus, into the neck, the jaws, and continues for minutes and even hours. In the presence of hiatus hernia and gastroesophageal reflux, pain may radiate into the left side of the chest and simulate heart diseases.

         Oesophageal vomiting occurs in considerable narrowing of the oesophagus. Food is accumulated over the constricted point, in the wider portion of the oesophagus, and is expelled by antiperistaltic contractions of the muscles. Oesophageal vomiting differs from gastric vomiting in the following: it occurs without nausea and is preceded by the feeling of food retained behind the sternum the vomitus includes unaltered (non-digested) food which  contains neither hydrochloric acid (gastric juice) nor pepsin; the vomitus containing food that has been taken long time ago has foulodour; taken food can be retained for long periods  in the presence of oesophageal diverticulum or degrading cancer.

         Regurgitation is the return of swallowed food into the mouth due to    oesophageal  obstruction. Regurgitation sometimes occurs ieuropathic patients in whom it becomes a habitual symptom or a result of cardiospasm.

         Hypersalivation occurs in oesophagitis, cicatricial narrowing of the oesophagus or in cancerous stenosis as a result of the oesophagosalivary reflex.

A foul breath may be due to a cancer tumour of the oesophagus or congestion and decomposition of food in cardiospasm.

         Heartbearn (pyrosis) is a specific burning sensation  behind the sternum associated with regurgitation of gastric contents into the inferior portion of the oesophagus. This is the cause of the so-called reflux oesophagitis.

         Haemorrhage can be due to uicer of the  oesophagus,  injury to the oesophagus by a foreign body, degradation of a tumour, bleeding of dilated oesophageal veins (which occurs in congestion of blood in the portal vein system) and also  bleeding of the mucosa due to small lacerations of the vessels in the oesophagogastric junction in straining and vomiting (Mallory- Weiss syndrom)

 

STOMACH

         Complaints. Patients with diseases of stomach complain of poor appetite, perverted taste, regurgitation, heartbearn, nausea, vomiting, and  the feeling of overfilled stomach after meals are the group of the so-called dyspeptic complaints. These symptoms may be observed in diseases of some other organs and systems. Determining the specific character of each symptom is important during inquiry of the patient.

         Deranged (poor or increased) appetite occurs in infectious diseases,metabolic disorders, ets.poor appetite or itscomplete absence (anorexia)is usually characteristic of gastric cancer. This symptom is often an early sign of cancer. Appetite often increases in peptic ulcer, especially in duodenal ulcer. Loss of appetite should be differentiated from cases when the patient abstains from food for fear of pain (cibophobia)/ This condition often occurs in subjects with  gastric ulcer, though their appetite is increased.

         Perverted appetite thet sometimes occurs in patients is characterized by the desire to eat inedible materials such as charcoal, chalk, kerosine, ets.

Appetite is perverted in pregnant women and in persons suffering from achlorhydria. Some patients with cancer of the stomach or some other  organs often feel aversion to meat. The developmental mechanism of appetite is connected with excitation of the food centre (according to Pavlov).Excitation or inhibition of this centre depends on impulses arriving from the cerebral cortex, on the condition of the vegetative centres (excitation of the vomiting centre causes loss of appetite), and on reflex effects from the alimentary organs. The multitude of factors that act on the food centre account for the high  variation in appetite.

         Taste may be perverted due to the presence of unpleasant taste in the mouth and partial loss of taste in an individual. It can often be associated with some pathology in the mouth, e.g. caries or chronic tonsillitis. A coated tongue can be another cause of unpleasant taste in the mouth.

         Regurgitation usually implies two phenomena: a sudden and sometimes loud uprise of wind from the stomach or oesophagus (eructation), and the return of swallowed food into the mouth (sometimes together with air). Regurgitation depends on contraction of the oesoohageal muscles with the openn cardia. Regurgitation may be due to air swallowing (aerophagy). It is heard at a distance and occurs in psychoneurosis. In the presence of motor dysfunction of the stomach, fermentation and putrefaction of food with increased formation of gas occur in the stomach (the phenomenon otherwise absent iorm). In abnormal fermentation in the stomach, the eructated air is either odourless or smells of bitter oil, which is due to the presence of butyric, lactic and other organic acids that are produced during fermentation in the stomach. In the presence of abnormal putrefaction, the helched air has the odour of rotten eggs (hydrogen sulphide). Bitter belching indicates intensive degradation of proteins. Belching is characteristic of stenosed pylorus with great distention of the stomach and significant congestion in it. Acid regurgitation is usually associated with hypersecretion of gastric juice and occurs mostly during pain attacks in ulcer. But it can also occur iormal or insufficient secretion of the stomach in the presence of insufficiency of the cardia (when the stomach contents are regurgitated into the oesophagus). Bitter regurgitation occurs in cases with belching up of bile into the stomach from the duodenum, and also in hyperchlorhydria; bitterness depends on the bitter taste of peptones.

         Pyrosis is otherwise known as heartburn, i.e. burning pain in the epigastric and retrosternal region. Heartburn arises in gastro-oesophageal reflux, mostly in the presence of gastric hyperacidity in various diseases of the alimentary tract (e.g. peptic ulcer or cholecystitis), hiatus hernia, and sometimes in pregnancy. Heartburn in healthy subjects can be due to hypersensitivity to some foods.

         Nausea, the reflectory act associated with irritation of the vagus nerve, is an indefinite feeling of sickness and sensation of compression in the epigastrium. Nausea is often attended by pallidness of the skin, general weakness, giddiness, sweating, salivation, fall in the arterial pressure, cold in the limbs, and sometimes semisyncopal state. Nausea often (but not necessarily) precedes vomiting. The mechanism of nausea is not known. Its frequent association with vomiting suggests that it might be the early sign of stimulation of the vomiting centre. The leading role in the development of nausea is given to the nervous system and also the tone of the stomach, the duodenum, and the small intestine. Nausea may develop without any connection with diseases of the stomach, e.g. in toxaemia of pregnancy, renal failure, deranged cerebral circulation, and sometimes in healthy peo­ple in the presence of foul odour (or in remembrance of something unplea­sant). Some diseases of the stomach are attended by nausea, e.g. acute and chronic gastritis or cancer of the stomach. Nausea associated with gastric pathology usually occurs after meals, especially after taking some pungent food. Nausea often develops in secretory insufficiency of the stomach.

         Vomiting (emesis) occurs due to stimulation of the vomiting centre. This is a complicated reflex through the oesophagus, larynx and the mouth (sometimes through the nose as well). Vomiting may be caused by ingestion of spoiled food, by seasickness, or irritation arising inside the body (diseases of the gastro-intestinal tract, liver, kidneys, etc.). In most cases vomiting is preceded by nausea and sometimes hypersalivation. Factors causing the vomiting reflex are quite varied. This can be explained by the numerous connections that exist between the vomiting centre (located in the medulla oblongata, in the inferior part of the floor of the 4th ventricle) and all bodily systems. Depending on a particular causative factor, the following can be differentiated: (1) nervous (central) vomiting; (2) vomiting of visceral aetiology (peripheral or reflex); (3) haematogenic and toxic vomiting.

         Vomiting is an important symptom of many diseases of the stomach, but it can be regarded as the symptom of a particular disease only in the presence of other signs characteristic of this disease. Vomiting of gastric aetiology is caused by stimulation of receptors in the gastric mucosa by in­flammatory processes (acute or chronic gastritis), in ingestion of strong acids or alkalis, or food acting on the gastric receptors by chemical (spoiled food) or physical (overeating or excessively cold food) routes. Vomiting can also be caused by difficult evacuation of the stomach due to spasms or stenosed pylorus.

         If the patient complains of vomiting, the physician should inquire about the time when the vomiting occurred, possible connections with meals, association with pain, the amount and character of the vomited material. Morning vomiting (on a fasting stomach) with expulsion of much mucus is characteristic of chronic gastritis, especially in alcoholics. Hyperacid vomiting in the morning indicates nocturnal hypersecretion of the stomach. Vomiting occurring 10-15 minutes after meals suggests ulcer or cancer of the cardial part of the stomach, or acute gastritis. If vomiting occurs 2-3 hours after meals (during intense digestion) it may indicate ulcer or cancer of the stomach body. In the presence of ulcer of the pylorus  or duodenum, vomiting occurs 4-6 hours after meals. Expulsion of food taken a day or two before is characteristic of pyloric stenosis. Patients with peptic ulcer often vomit at the height of pain htus removing it, which is typical of the disease. The odour of the vomit is usually acid, but it can often be fetid (putrefactive processes in the stomach); the odour may be even faecal (in the presence of a faecal fistula between the stomach and the transverse colon).

         The vomited material may have acid reaction (due to the presence of hydrochloric acid, in hyperchlorhydria), neutral (in achylia), or alkaline (in the presence of ammonia compounds, in pyloric stenosis, hypofunction of renal function, and also in regurgitation of the duodenal contents into the stomach). Vomitus may contain materials of great diagnostic importance, e.g. blood, mucus (in chrome gastritis), ample bile (narrowing of the duodenum, gastric achylia), and faecal matter. Vomiting may attend acute gastritis, exacerbation of chronic gastritis, gastric neurosis, peptic ulcer, spasm and organic stenosis of the pylorus, and cancer of the stomach.

         Pain is the leading symptom in diseases of the stomach. Epigastric pain – not obligatory connected with diseases of the stomach. It should be remembered that the epigastrium is the “site of encounter” of all kinds of pain. Epigastric pain may be due to diseases of the liver, pancreas, and due to hernia of the linea alba. Epigastric pain may develop in diseases of other abdominal organs (sometimes of organs located outside the abdomen) by the viscerovisceral reflex (acute appendicitis, myocardial infarction, affec­tion of the diaphragmatic pleura, etc). In order to locate correctly the source of pain, the physician should ask the patient (1) to show exactly the site of pain; (2) to characterise the pain which may be periodical or parox­ysmal (at certain time of the day); permanent or seasonal (in spring or autumn); (3) to describe the connection (if any) between pain and meals, the quality of food and its consistency; (4) to indicate possible radiation of pain (into the back, shoulder blade, behind the sternum, left hypochoa-drium); (5) to describe conditions under which pain lessens (after vomiting, after taking food or baking soda, after applying hot-water bottle or taking spasmolytics); (6) to describe possible connections between pain and physical strain (weight lifting, traffic jolting, etc.), or strong emotions tensity and character of pain are also important diagnostically. The pain may be dull, stabbing, cutting, etc. Pain in hollow organs with smooth muscles (e.g. stomach) is provoked by spasms (spastic pain), distension the organ (distensional pain), and by its motor dysfuncion.

         Paroxysmal, periodical epigastric pain is due to the spasm of the pylorus muscles. It arises under the influence of strong impulses arriving from vagus nerve centre in cerebral cortex dysfunction. The spasm of the pylorus is stimulated by the hyperacidity of gastric juice due to hyperstimulation of the vagus. Depending on the time of paroxysmal pain (after meals), il be early (occurring 30—40 min after meals), late (90—120 min after meals), nocturnal, and hunger pain (which is abated after taking food). If pain occurs after meals stimulating secretion of gastric juice (bitter, pungent, spicy or smoked foods), this indicates the leading role of hypersecretion in its aetiology. The pain then localizes in the epigastrium, radiates to the back, and is rather intense; it is abated after vomiting and taking alkali or foods that decrease acidity of gastric juice, and also after taking antispastic preparations and applying hot-water bottle (which removes spasms)

         A seasonal character of pain, i.e. development of periodic pain duringl spring and autumn, is characteristic of peptic ulcer, especially if the process is localized in the peripyloric region. Permanent boring pain is usually caused by stimulation of the nerve elements in the mucous and submucousuii layer of the stomach; the pain is usually intensified after meals and is characteristic of exacerbation of chronic gastritis or cancer of the stomach.

         Perigastritis (chronic inflammation of the peritoneum overlyin, stomach and its adhesion to the neighbouring organs) is manifested I developing immediately after taking much food (irrespective of its quality). The full stomach distends to stimulate nerve fibres in the adhesions. In the presence of perigastritis and adhesions between the stomach and the adjacent organs, pain may be caused by any physical strain and when the patient changes his posture.

         Gastric haemorrhage is a very important symptom. It manifested by vomiting of blood (haematemesis) or by black tarry stools (melaena). Gastric haemorrhage is usually manifested by the presence of blood in the vomitus. The colour of the vomitus depends on the time duing which the blood is present in the stomach. If the blood wos in the stomach for a long time, the blood reacts with hydrochloric acid of the gastric juice to form haematin hydrochloride. The vomitus looks like coffee  grounds. If haemorrhage is profuse (damage to a large vessel) the vomitus contains much scarlet (unaltered) blood. Haematemesis occurs in peptic ulcer, cancer, and polyps, in erosive gastritis, rarely in ssarcoma,tuberculosis and syphilis of the stomach, and in varicosity of the oesophageal veins/ Tarry stools are not an obligatory sign of gastric haemorrage.

INTESTINE

         Complaints. The main complaints with intestinal diseases are pain, meteorism (intlation of the abdomen), motor dysfunction of the intestine (constipation and diarrhoea), and intestinal haemorrhage.

         Pain. If the patient complains of pain in the abdomen, the following should be established: location of pain, its radiation, intensity, character, duration, and means by which it is lessened. The general signs by which in­testinal pain may be differentiated from gastric one are: (1) absence of regular dependence of pain on food taking; the only exception is inflamma­tion in the transverse colon (transversitis): pain develops immediately after meals; the pathogenesis of this pain is connected with reflex peristaltic con­tractions of the transverse colon when food enters the stomach; (2) close association of pain with defaecation: pain occurs before, during, and (rare­ly) after defaecation; (3) pain relief after defaecation or passage of gas.

         Pain may be boring and spasmodic (intestinal colic). Colicky pain is characterized by short repeated attacks which arise and disappear quite of a sudden. Pain may very quickly change its location, the main site being round the navel. Sometimes pain may arise in other areas of the abdomen. Boring pain is sometimes permanent; it intensifies during cough, especially in the mesenterium or peritoneum are involved. Pain is characteristic of inflammatory diseases of the intestine. As inflammation extends onto the peritoneum, pain is attended by a pronounced muscular defence.

         Exact location of the source of pain is very important. Pain in right iliac region occurs in appendicitis, tuberculosis, cancer, or inflammation of the caecum (typhlitis). Acute pain in the left lower abdomen occurs in intestinal obstruction and inflammation of the sigmoid (sigmoiditis).Pain in the umbilical region occurs in inflammation of small intestine (enteritis) and inflammation or cancer of the colon. Pain in the perineal region, and especially during defaecation (with the presence of blood in faeces), is characteristic of the rectum diseases (proctitis, cancer). Pain in intestinal  pathology may radiate into the chest; pain associated with affection of the spleen angle of the descending large intestine radiates into the left side of the chest (it is sometimes mistaken for pain attacks of angina pectoris); colics of appendicitic origin radiate into the right leg.

         In acute affection of the left portions of the large intestine (dysentery) pain radiates into the sacral area. Thermal procedures, spasmolytycs, passage of gas, and emptying of the bowels can relieve pain or remove it completely.

Intestinal pain is caused by obstruction of intestinal patency and  upset motor function. Intestinal pain is mostly caused by spasms ( spasmodic contraction of smooth muscles; hence spastic pain), or by distension  of the intestine by gases. Both mechanisms often become involved.

         Spastic pain can be due to various causes. Individual predisposition to spastic contractions in general (vegetoneurosis) may be as impotant  as irritation originating in the intestine proper, e.g. in enteritis, intestinal tumour, poisoning with arsenic or lead, and also in diseases of the central nervous system (posterior spinal sclerosis).

         Pain arising due to intestinal distension by gases, and associated with tension and irritation of the mesentery, differs from spastic pain (1) by the absence of periodicity; it is long-standing and gradually lessens in prolonged inflation; and (2) by exact localization. In intestinal obstruction (complete or partial) colicky pain is combined with almost permanent pain in the abdomen. It is characterized by exact and permanent location ( the umbilical region and large intestine). The pain intensifies with intestynal peristalsis.

         Appendicular colic first localizes round the navel and the epygastrium  but in several hours (or even on the next day) it descends to the right iliac region where it intensifies gradually. Sometimes the pain arises straight the right iliac region.

         Rectal colic, or tenesmus, is also known. It occurs in frequent and painful tenesmus to defaecate and is associated with spasmodic contractions of the intestine and the sphincter ani. Only clots of mucus are sometimes expressed  of actual defaecation. Tenesmus occurs in dysentery and other  inflammatory or ulcerous diseases, and in cancer of the rectum. Pain  associated with defaecation depends on many factors. Pain preceding defaecation is associated with the disease of the descending colon or sigmoid colon. Pain during defaecation is characteristic of haemorrhoids, anal fissures, and cancer.

         Meteorism. The patient feels flatulence, inflation, and boring disten­tion of the abdomen. The causes of meteorism are (1) excessive gas formation in the intestine due to ingestion of vegetable cellular tissue and easily tormented food (peas, beans, cabbage, etc.); (2) intestinal motor dysfunc-tion due to decreased tone of the intestinal wall or intestinal obstruction; (3) lowered absorbability of gases by the intestinal wall, the process of gas formation being normal; (4) aerophagia, i.e. excess swallowing of air, with its subsequent propulsion to the stomach and the intestine; (5) hysterical meteorism: the abdomen is rapidly inflated to the size of the abdomen of a pregnant woman at her last weeks; this nervous mechanism is very com­plicated.

         When inquiring the patient, the physician should ask about the character of his nutrition and the site of abdemen inflation (the entire ab­domen or only its limited part may be inflated). If inflation is local, it is necessary to ask the patient whether or not inflation occurs always at one and the same area. In intestinal obstruction, the patient feels rumbling sounds inside the abdomen, feels movement of liquid in the intestine, and intense peristaltic movements above the point of obstruction.

         Diarrhoea. Frequent and liquid stools is a common sign of intestinal pathology. Diarrhoea occurs in acute and chronic intestinal infections (enteritis, enterocolitis, sigmoiditis, proctitis), in various exogenous intox­ications (poisoning with arsenic or mercury), endogenous intoxications (uraemia, diabetes, gout), in endocrine disorders (adrenal dysfunction, thyrotoxicosis), and in hypersensitivity to some foods (allergy).

         The mechanism of diarrhoea is very complicated. Different pathogenic factors may prevail in various pathological conditions. Accelerated move­ment of the liquefied food in the intestine due to peristalsis is among them. Almost undigested food can thus be evacuated. Another factor is disordered absorptive function of the intestine. Affection of the intestinal wall, disordered mechanisms regulating absorption, purgatives and upset water metabolism produce a marked change in the absorption process and are the cause of diarrhoea.

The third cause of liquid stools is inflammation of the intestine. Large quantities of inflammatory secretion stimulating the intestinal receptors are released into the lumen of the intestine to intensify its peristalsis and to impair its absorptive function.

         Paradoxical diarrhoea occurs in prolonged constipation due to mechanical irritation of the intestinal wall by hard faecal masses.

         Upset equilibrium between the fermentative and putrefactive flora of the intestine is another important factor in the aetiology of diarrhoea. If fermentative flora prevails, fermentative dyspepsia occurs which is characterized by flatulence of the abdomen and semiliquid acid faeces (2— 3 stools a day); the faeces contaiumerous gas bubbles, numerous starch grains, vegetable cellular tissue, and iodophilic microbes. Fermentative dyspepsia develops in connection with deranged digestion of car­bohydrates, if they are ingested in excess.

         Putrid dyspepsia more often occurs in secretory hypofunction of the stomach. The absence of bactericidal action of gastric juice is connected with the absence of hydrochloric acid; rapid passage of insufficiently digested food from the stomach to the intestine has a negative effect in the first instance on digestion of proteins. This in turn provokes putrid dyspep­sia. It is characterized by liquid dark excrements containing clots of un­digested food; the faeces react alkaline and have a foul putrid smell. Microscopy of faeces reveals much fats, muscular fibres with vivid transverse and longitudinal striation and even ends (creatorrhoea). The content of organic compounds in the faeces is increased. The iodophilic flora is absent.

         Diarrhoea occurring in organic affections of the large intestine is most­ly of the inflammatory character. It is not copious, nor does it produce strong negative effect on the patient’s general condition (as compared with affections of the small intestine which is attended by profuse diarrhoea associated with deranged motor and absorption function of the intestine). The pronounced disorder in digestion causes some metabolic disorders in the patient (impaired absorption of proteins, iron, vitamins, and elec­trolytes).

         Obstipation. This is obstinate constipation during which faeces are long retained in the intestine (for more than 48 hours). But the duration of con­stipation is only relative, because in many cases it is not the result of pathology but of the living conditions and nutrition. If vegetable food dominates in the diet, the subject may defaecate two or three times a day. Stools become rarer if the diet is rich in meat. A radical change iutrition can remove constipation. Limited mobility of the subject, hunger, and ir­regular defaecations (during the day) may prolong pauses between defaeca­tion. The main factor determining defaecation is the condition of intestinal motor function. Bowel contents are retained in the large intestine and the rectum during constipation.

         Organic and functional constipation is differentiated. Organic con­stipation is usually associated with mechanical obstruction, such as nar­rowing of the intestinal lumen due to a tumour, scar, adhesion, and also abnormalities in the intestine (megacolon, dolichosigmoid, megasigmoid, diverticulosis).

Functional constipation is subdivided into: (1) alimentary constipation; it occurs due to ingestion of easily assimilable foods, which leave small residue and normally stimulate peristalsis of the intestine by irritating its nervous receptors; (2) neurogenic constipation due to dysfunction of the intramural nervous apparatus or vagus nerve; these are the so-called dyskinetic constipation, caused by the reflex action on the intestinal motor function of another affected organ (cholecystitis, adnexitis, prostatitis, etc.), or by organic affections of the central nervous system (tumours of the brain, encephalitis, posterior spinal sclerosis); (.3) constipation associated with inflammatory affections, mainly of the large intestine (dysentery); (4) toxic constipation occurring in exogenous poisoning with lead, morphine, or cocaine; (5) constipation of endocrine aetiology, occur­ring in thyroid or pituitary hypofunction; (6) constipation caused by lack of physical exercise; (7) constipation caused by flaccidity of the prelum.

         Intestinal haemorrhage often occurs in ulcerous affections of the alimentary system. It develops in the presence of tumour, protozoal and helminthic invasions, acute infections (typhoid fever, bacillary dysentery), in thrombosis of mesenteric vessels, ulcerous non-specific colitis, etc.

LIVER AND BILE DUCTS

         Complaints. Patients with disorders of the hepatobiliary system usually complain of abdominal pain, dyspepsia, skin itching, jaundice, enlarge­ment of the abdomen, and fever.

         Pain is localized in the right hypochondrium and sometimes in the epigastrium and differs depending on the cause. Pain may be persistent and dull, or it may be severe and occur in attacks. Persistent pain is usually bor­ing, or the patient feels pressure, heaviness, or distension in the right hypochondrium. Pain may radiate to the right shoulder, scapula, and in    interscapular  space  (in  chronic  cholecystitis,  perihepatitis  and pericholecystitis, i.e. when the process extends onto the peritoneum overlying the liver and the gall bladder, and also in rapid and considerable enlargement of the liver which causes distension of Glisson’s capsule). This radiation of pain is quite characteristic of many diseases of the liver and gall bladder, because the right phrenic nerve, innervating the capsule in the region of the falciform and the coronary ligaments of the liver and the extrahepatic bile ducts, originates in the same segments of the spinal cord where the nerves of the neck and shoulder originate as well. Pain usually becomes more severe in deep breathing; in adhesion of the liver or the gall bladder to the neighbouring organs, pain is also intensified when the pa­tient changes his posture, and sometimes during walking.

         Attacks of pain (biliary or hepatic colics) develop suddenly and soon become quite severe and unbearable. The pain is first localized in the right hypochondrium but then spreads over the entire abdomen to radiate up­wards, to the right, and posteriorly. An attack of pain may continue from several hours to a few days during which pain may subside and then inten­sify again; the attack ends as suddenly as it arises; or pain may lessen gradually. Attacks of pain occur mostly in cholelithiasis. They are provok­ed by jolting (as in riding) or by fatty food. Pain attacks occur also in hypermotoric dyskinesia of the gall bladder and bile ducts. Pain usually develops quite unexpectedly due to spastic contractions of muscles of the gall bladder and large bile ducts caused by irritation of their mucosa by a stone, and due to comparatively rapid distension of the gall bladder in con­gestion of bile (e.g. due to obstruction of the common bile duct by a stone). Warmth applied to the liver (provided the attack is not attended by con­siderable fever) and also administration of cholino- and myospasmolytics (atropine sulphate, papaverin hydrochloride, etc.) remove pain characteristic of the colic. An attack of hepatic colic can be attended by subfebrility (fever develops with pain and subsides with alleviation of pain), which is followed by a slight transient subicteric colour of the sclera or pronounced jaundice in obstruction of the common bile duct by a stone.

         Pain developing in dyskinesia of the bile ducts is associated with upset coordination between contractions of the gall bladder and of the Oddi sphincter under the effect of increased tone of the vagus nerve. As a result, bile congests in the ducts, and the gall bladder is no longer emptied. This causes its convulsive contraction. Dyskinetic pain is characterized by the absence of signs of inflammation (leucocytosis, ESR, etc.).

         Dyspeptic complaints include decreased appetite, often bitter taste in the mouth, eructation, nausea, vomiting, distension of the abdomen and rumbling, constipations or diarrhoea. These complaints are characteristic not only of diseases of the hepatobiliary system but also of other parts of the digestive system. Causes of these symptoms in diseases of the liver and bile ducts are explained by deranged secretion of bile (and hence impaired digestion of fats in the intestine) and derangement of the detoxicating func­tion of the liver.

Fever occurs in acute inflammatory affection of the gall bladder and bile ducts, in abscess and cancer of the liver, in hepatitis, and active cir­rhosis.

         Skin itching attends hepatic or obstructive jaundice. It can develop without jaundice, as an early forerunner of the liver disease. Itching is caused by accumulation in the blood of bile acids which are otherwise ex­creted together with bile, or by stimulation of sensitive nerve endings in the skin. Itching is usually persistent and is a great annoyance to patients dur­ing night sleep (to cause insomnia). Severe itching causes scratching of the skin with its subsequent infection.

         Icteric colouration of the skin and the visible mucosa (jaundice) is due to accumulation of bile pigments in the blood and tissues. Jaundice may develop unnoticeably to the patient and only the surrounding people may pay attention to the icteric colouration of the sclera and then the skin. In other cases jaundice can occur all of a sudden, following an attack of hepatic colics (in obstruction of the common bile duct by a stone in cholelithiasis). Jaundice may persist for months or even years, only slightly changing in intensity (chronic hepatitis and cirrhosis of the liver, benign bilirubinaemia). For details of the mechanism of developing jaundice and its diagnostic importance see below.

         Enlargement of the abdomen (sometimes rapid) can be due to ac­cumulation of ascitic fluid in the abdominal cavity (in obstructed blood outflow from the intestine via the portal vein), in considerable meteorism (due to deranged digestion in the intestine in upset bile excretory function), or in pronounced hepato- or splenomegaly. Vany chronic diseasemare attended by general wtacnes< non-motivated fatigue< and decreased work capacity.

PANCREAS

         Pain, dyspepsia, jaundice, general weakness and wasting are the main complaints of patients with diseases of the pancreas.

         Pain may vary in intensity and character. Attacks of paroxysmal pain, like in biliary colic, arising 3-4 hours after meals (especially after taking fatty food) are characteristic of calcareous pancreatitis. Pain is usually localized in the epigastrium or left hypochondrium to radiate into the back. Pain is sometimes so severe that can only be removed by spasmolytics co-evearcotics.

Pain is especially severe in acute pancreatitis. It develops suddenly and persists for a few hours or days and even weeks. The pain is usually localiz­ed in the upper abdomen and is often girdling in character. Severe pain and its vigorous onset in acute pancreatitis are explained by a sudden obstruc­tion of the main pancreatic duct as a result of spasm and inflammatory oedema with subsequent sharp increase in pressure in small pancreatic duc­tules and irritation of the solar plexus.

         Pain is very severe and prolonged in tumours of the pancreas. If the head of the pancreas is affected, pain is localized in the right hypochondrium and radiates into the back. If the tumour extends onto the body i tail of the pancreas, pain is felt in the entire epigastrium, left hypoclm drium, and its character may be girdling. Pain is intensified when the tient is in the recumbent position because the tumour presses on the so plexus. The patient would therefore assume a forced (half-bent) posture lessen the pain. Boring pain is characteristic of chronic pancrealiil although this form of the disease may be attended by severe pain as well.

         Nausea and vomiting more frequently attend acute pancreatitis and are of reflex character. Chronic pancreatitis and tumour of the pancreas and are characterized by dyspepsia which is due to upset enzymatic activity ol il pancreas. Patients with chronic pancreatitis often complain of poor appetite, aversion to fatty foods, nausea, meteorism, diarrhoea with ample quid lustrous (fatty) and fetid faeces. Upset intestinal digestion can rapid cachexia and general weakness.

         Cancer of the head of the pancreas is characterized by the following symptoms:

         Jaundice is of the obstructive type, progressive; the skin is dark-brown (with a greenish hue); there are severe itching, and haemorrhaesg.  The tumour presses the terminal portion of the common bile duct to obstruct bile outflow. Jaundice may develop in sclerosis of the head of the pancreas as well. This is the result of chronic pancreatitis.

                  

General inspection

         Mouth and throat. The major structure of the exterior of the mouth is the lips. The doctor should note the presence of painful, inflamed, and dried cracks or fissures of the lips, called cheilitis. These may be caused by exposure to harsh climatic conditions, habitual licking or biting of the lips, mouth breathing from respiratory distress, or dehydration, particularly with fever in systemic disease. Cheilosis, or angular stomatitis, is fissuring at the angles or comers of the lips and may indicate vitamin deficiencies of riboflavin or niacin.

         Any lesions on the lips are noted. The herpes simplex virus produces singular or clusters of vesicular eruptions on the lip, which are often called “cold sores”. The lip may also be the site of a primary syphilitic chancre, which appears as a firm nodule that ulcerates and crusts. If one suspects a chancre, it is examined with a gloved hand for the doctor’s protection.

         The doctor asks the patient to open his mouth wide, requests that he move his tongue in different directions for full visualization, and has him say “ahh” in order to depress the tongue for full view of the back of the mouth (tonsils, uvula, oropharynx). For a closer look at the buccal mucosa or lining of the cheeks, the doctor can ask the patient0 to use his fingers to move the outer lip and cheek to one side. The tongue blade is placed along the side of the tongue, not the center back area where the gag reflex is elicited.

         All areas lined with mucous membranes (inside the lips and cheeks, gingiva, underside of tongue, palate, back of pharynx) are inspected, noting color, any areas of white patches or ulceration, bleeding, sensitivity, and moisture. The membranes should be bright pink, smooth, glistening, uniform, and moist. Any deviations are noted. For example, reddened areas with white ulcerated centers may be canker sores (aphthae), which may be caused by trauma to the gums during toothbrushing or chewing.

         As the doctor observes the lining of the mouth, any odor (halitosis) is noted. Mouth odors are characteristic of a number of important health problems, such as poor dental hygiene, gingival disease, chronic constipation, dehydration, malnutrition, or systemic illness. A sudden, foul odor in the mouth may indicate a foreign body in the nose, particularly a bean or pea. The doctor should inspect the nose carefully and, if possible, remove the object with tweezers.

         The teeth are inspected for number in each dental arch, hygiene, and occlusion or bite.. Discoloration of tooth enamel with obvious plaque (whitish coating on the surface of the teeth) is a sign of poor dental hygiene and indicates a need for dental counseling. Brown spots in the crevices of the crown of the tooth or between the teeth may be caries. Teeth that appear greenish black may be stained from oral ingestion of supplemental iron. Although unsightly, this disappears after the iron is no longer given.

         Tooth Abscess: Tooth abscess involving left molar region. Associated inflammation of left face can clearly be seen.

         Malocclusion or poor biting relationship of the teeth is evaluated in terms of (1) how the jaws relate to each other in vertical, transverse, and anteroposterior directions, for example, the “bucktoothed” appearance that results when the maxilla is forward in relation to the mandible, (2) how the teeth are aligned, and (3) how the teeth interdigitate when in occlusion.

         The gums surrounding the teeth are examined. The color is normally coral pink, and the surface texture is stippled, similar to the appearance of orange peel. In dark-skinned individuals the gums are more deeply colored and a brownish area is often observed along the gum line.

         The tongue is inspected for the presence of papillae, small projections that contain several taste buds each and give the tongue its characteristic rough appearance. Changes in the surface texture are noted, such as (1) “geographic tongue”, unusual patterns of papillae formation and denuded areas, (2) coated tongue, such as in thrush, or (3) an exceptionally beefy red and swollen tongue, which is a sign of various systemic diseases

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Examination of the tongue is useful in diagnostics of the following conditions:
1. Irritation (pointer medial fold).

2. Spinal cord deviation in lumbar region.

3. Spinal cord deviation in thopracic region.

4. Spinal cord deviation in cervical region.

5. Chronic enterocolitis, dyspepsia (teeth signs on the lateral parts of the tongue).

6. Thyrotoxicosis, neurasthenia, alkoholism (tremor of the tongue).
7. Chronic disease of the large bowel (a lot of amall folds).
8. Kidney disfunction.
9. Large bowel disfunction.
10. Intoxication generates in the large bowel.
11. Intoxication generates in gastrointestinal tract.
12. Cardiac disfunction.
13. Chronic bronchitis.
14. Pneumonia folloved by intoxication (brown coating).
15. Pulminary emphysema.

         The doctor also notes the size and mobility of the tongue, especially protrusion, which is frequently seen in children with mental retardation. Normally the tip of the tongue should extend to the lips. If the patient is unable to move the  tongue forward to this point, the frenulum, or central band of mucous membrane, which attaches the tongue to the floor of the mouth, may be too short. “Tongue-tie” can result in speech problems.

         The roof of the mouth consists of the hard palate, near the front of the cavity, and the soft palate, toward the back of the pharynx, which has a small midline protrusion called the uvula. Both are carefully inspected to be sure that they are intact. Sometimes there is a pinpoint cleft in the soft palate, which may go undetected unless carefully inspected. Such a cleft is especially important if the uvula is bifid or separated into two appendages. A submucosal cleft may result in speech problems later on, since air cannot be effectively trapped for vocalization. The arch of the palate should be dome shaped. A narrow-flat roof or high-arched palate affects the placement of the tongue and can cause feeding and speech problems. Movement of the uvula is tested by eliciting a gag reflex. It moves upward to close off the nasopharynx from the oropharynx.

         As the recesses of the oropharynx are inspected, the size and color of the palatine tonsils are also noted. They are normally the same color as the surrounding mucosa, glandular, rather than smooth in appearance, and barely visible over the edge of the palatoglossal arches. Enlargement, redness, and white patches on the tonsils and surrounding area are recorded. Such signs are indicative of suppurative tonsillitis or pharyngitis.

 

Left Peritonsilar Abscess. Note deveiation of uvula towards right.

 

          The roof of the mouth consists of the hard palate, near the front of the cavity, and the soft palate, toward the back of the pharynx, which has a small midline protrusion called the uvula. Both are carefully inspected to be sure that they are intact. Sometimes there is a pinpoint cleft in the soft palate, which may go undetected unless carefully inspected. Such a cleft is especially important if the uvula is bifid or separated into two appendages. A submucosal cleft may result in speech problems later on, since air cannot be effectively trapped for vocalization. The arch of the palate should be dome shaped. A narrow-flat roof or high-arched palate affects the placement of the tongue and can cause feeding and speech problems. Movement of the uvula is tested by eliciting a gag reflex. It moves upward to close off the nasopharynx from the oropharynx.

         As the recesses of the oropharynx are inspected, the size and color of the palatine tonsils are also noted. They are normally the same color as the surrounding mucosa, glandular, rather than smooth in appearance, and barely visible over the edge of the palatoglossal arches. Enlargement, redness, and white patches on the tonsils and surrounding area are recorded. Such signs are indicative of suppurative tonsillitis or pharyngitis.

         Auscultation. Each of the four quadrants should be auscultated using the diaphragm and bell chestpieces. Unlike listening to the heart or lungs, in which the stethoscope rests gently on the skin, to hear bowel sounds the stethoscope must be pressed firmly against the abdominal surface. With the diaphragm chestpiece this usually presents no difficulty, but with the bell chestpiece, especially one with a short cone, the skin may occlude the opening and prevent transmission of sound.

         The most important sound to listen for is peristalsis, or bowel sounds, which sound like short metallic clicks and gurgles. Loud grumbling noises, known as borborygmi, are the familiar “stomach growls” usually denoting hunger. A sound may be heard every 10 to 30 seconds and its frequency per minute should be recorded (for example, 5 bowel sounds/minute). However, the nurse may need to listen for several seconds before audible peristalsis can be heard. Bowel sounds may be stimulated by stroking the abdominal surface with a fingernail. Absent bowel sounds or hyperperistalsis is recorded and reported, since either usually denotes abdominal disorder.

         Various other sounds may be heard in the abdominal cavity. Normally the pulsation of the aorta is heard in the epigastrium. Sounds that resemble murmurs (called bruits), hums, or rubs are always referred for further evaluation.

         Percussion. Percussion of the abdomen is performed in the same manner as percussion of the lungs and heart. Normally dullness or flatness is heard on the right side at the lower costal margin because of the location of the liver. Tympany is typically heard over the stomach on the left side and usually in the rest of the abdomen. An unusually tympanitic sound, like the beating of a tight drum, usually denotes air in the stomach, a common cause of which is mouth breathing. However, it can also denote a pathologic condition such as low intestinal obstruction or paralytic ileus. Lack of tympany may occur normally when the stomach is full after a meal, but in other situations it may denote the presence of fluid or solid masses.

Exam of the Abdomen

         The major components of the abdominal exam include: observation, auscultation, percussion, and palpation. While these are the same elements which make up the pulmonary and cardiac exams, they are performed here in a slightly different order (i.e. auscultation before percussion) and carry different degrees of importance. Pelvic, genital, and rectal exams, all part of the abdominal evaluation, are discussed elsewhere.

         Think Anatomically: When looking, listening, feeling and percussing imagine what organs live in the area that you are examining. The abdomen is roughly divided into four quadrants: right upper, right lower, left upper and left lower. By thinking in anatomic terms, you will remind yourself of what resides in a particular quadrant and therefore what might be identifiable during both normal and pathologic states.

Quadrants of the Abdomen

Topical Anatomy of the Abdomen

 

         By convention, the abdominal exam is performed with the provider standing on the patient’s right side.

 

Inspection.

         Much information can be gathered from simply watching the patient and looking at the abdomen. This requires complete exposure of the region in question, which is accomplished as follows:

         Ask the patient to lie on a level examination table that is at a comfortable height for both of you. At this point, the patient should be dressed in a gown and, if they wish, underwear.

         Take a spare bed sheet and drape it over their lower body such that it just covers the upper edge of their underwear (or so that it crosses the top of the pubic region if they are completely undressed). This will allow you to fully expose the abdomen while at the same time permitting the patient to remain somewhat covered. The gown can then be withdrawn so that the area extending from just below the breasts to the pelvic brim is entirely uncovered, remembering that the superior margin of the abdomen extends beneath the rib cage.

         The patient’s hands should remain at their sides with their heads resting on a pillow. If the head is flexed, the abdominal musculature becomes tensed and the examination made more difficult. Allowing the patient to bend their knees so that the soles of their feet rest on the table will also relax the abdomen.

Keep the room as warm as possible and make sure that the lighting is adequate. By paying attention to these seemingly small details, you create an environment that gives you the best possible chance of performing an accurate examination. This is particularly important early in your careers, when your skills are relatively unrefined. However, it will also stand you in good stead when examining obese, anxious, distressed or otherwise challenging patients.

         While observing the patient, pay particular attention to:

         Appearance of the abdomen. Is it flat? Distended? If enlarged, does this appear symmetric or are there distinct protrusions, perhaps linked to underlying organomegaly? The contours of the abdomen can be best appreciated by standing at the foot of the table and looking up towards the patient’s head. Global abdominal enlargement is usually caused by air, fluid, or fat. It is frequently impossible to distinguish between these entities on the basis of observation alone (see below for helpful maneuvers). Areas which become more pronounced when the patient valsalvas are often associated with ventral hernias. These are points of weakening in the abdominal wall, frequently due to previous surgery, through which omentum/intestines/peritoneal fluid can pass when intra-abdominal pressure is increased.

         Presence of surgical scars or other skin abnormalities.

Patient’s movement (or lack thereof). Those with peritonitis (e.g. appendicitis) prefer to lie very still as any motion causes further peritoneal irritation and pain. Contrary to this, patients with kidney stones will frequently writhe on the examination table, unable to find a comfortable position.

         The contour of the abdomen is inspected while the patient is erect and supine. The usual male and female contours of the pelvic cavity change the shape of the abdomen to form characteristic curves, especially in the female.The size and tone of the abdomen also give some indication of general nutritional status and muscular development. A large, prominent, flabby abdomen is often seen in obese patients, whereas a concave abdomen is frequently suggestive of undernutrition.

Draping the Abdomen

 

However, careful note is made of a protruding abdomen, which may indicate pathologic states such as abdominal distention, ascites, tumors, or organomegaly. A protuberant abdomen with spindly extremities and flat, wasted buttocks suggests severe malnutrition that may occur from inadequate nutritional intake such as kwashiorkor or from diseases such as cystic fibrosis. Likewise, a scaphoid abdomen may indicate dehydration or diaphragmatic hernia, in which the abdominal organs rise into the thoracic cavity, or a “scaphoidlike” abdomen that only appears sunken in relationship to pneumothorax or high intestinal obstruction. A midline protrusion from the xiphoid to the umbilicus or pubic symphysis is usually diastasis recti, or failure of the rectus abdominis muscles to join in utero. A tense, boardlike abdomen is a serious sign of paralytic ileus and intestinal obstruction.

         The doctor also notes the condition of the skin covering the abdomen. It should be uniformily taut, without wrinkles or creases. Sometimes silvery, whitish striae are seen, especially if the skin has been stretched as in obesity or with distention resulting from ascites. Any scars, ecchymotic areas, excessive hair distribution, or distended veins are noted.

         Movement of the abdomen is observed. Visible peristaltic waves most often indicate pathologic states, particularly intestinal obstruction such as pyloric stenosis.

         A doctor may observe pulsation of the descending aorta in the epigastric region (midline and below the xiphoid). Although visible pulsations are normally seen, especially in thin patients, the doctor should auscultate and palpate the aorta for any evidence of an aneurysm, a saclike enlargement of the vessel.

         If a hemiation is present in umbilical  region, the sac is palpated for abdominal contents and the approximate size of the opening is estimated. ernias are common in infants, especially in black children. Hernias are looked for elsewhere on the abdominal wall, such as in the inguinal or femoral region. An inguinal hernia is a protrusion of peritoneum through the abdominal wall in the inguinal canal. It most often occurs in males, is frequently bilateral, and may be visible as a mass in the scrotum. It is palpated by sliding the little finger into the external inguinal ring at the base of the scrotum and asking the child to cough. If a hernia is present, it will hit the tip of the finger.

         A femoral hernia is felt or seen as a small mass on the anterior surface of the thigh just below the inguinal ligament in the femoral canal (a potential space medial to the femoral artery). Its location can be estimated by placing the index finger of the right hand on the patient’s right femoral pulse (left hand for left pulse) and the middle ring finger flat against the skin toward the midline. The ring finger lies over the femoral canal, where the hemiation occurs. Palpation of hernias in the pelvic region, particularly inguinal ones, is often part of the examination of genitalia.

Various Causes of Abdominal Distension

Obese abdomen

Hepatomegaly

         Splenomegaly: Massively enlarged spleen, the result of extramedullary hematopoiesis, is outlined above. This patient’s left upper quadrant appears more full than the corresponding area on the right.

Ascites

Markedly enlarged gall bladder
(labeled “GB”)

Umbilical Hernia

Same umbilical hernia while patient
performs valsalva maneuver.

 

Abdomen Caput Medusa

         Auscultation. Each of the four quadrants should be auscultated using the diaphragm and bell chestpieces. Unlike listening to the heart or lungs, in which the stethoscope rests gently on the skin, to hear bowel sounds the stethoscope must be pressed firmly against the abdominal surface. With the diaphragm chestpiece this usually presents no difficulty, but with the bell chestpiece, especially one with a short cone, the skin may occlude the opening and prevent transmission of sound.

         The most important sound to listen for is peristalsis, or bowel sounds, which sound like short metallic clicks and gurgles. Loud grumbling noises, known as borborygmi, are the familiar “stomach growls” usually denoting hunger. A sound may be heard every 10 to 30 seconds and its frequency per minute should be recorded (for example, 5 bowel sounds/minute). However, the nurse may need to listen for several seconds before audible peristalsis can be heard. Bowel sounds may be stimulated by stroking the abdominal surface with a fingernail. Absent bowel sounds or hyperperistalsis is recorded and reported, since either usually denotes abdominal disorder.

         Various other sounds may be heard in the abdominal cavity. Normally the pulsation of the aorta is heard in the epigastrium. Sounds that resemble murmurs (called bruits), hums, or rubs are always referred for further evaluation.

 

Abdominal Auscultation

         What exactly are you listening for and what is its significance? Three things should be noted:

1.  Are bowel sounds present?

2.   If present, are they frequent or sparse (i.e. quantity)?

3.  What is the nature of the sounds (i.e. quality)?

         As food and liquid course through the intestines by means of peristalsis noise, referred to as bowel sounds, is generated. These sounds occur quite frequently, on the order of every 2 to 5 seconds, although there is a lot of variability. Bowel sounds in and of themselves do not carry great significance. That is, in the normal person who has no complaints and an otherwise normal exam, the presence or absence of bowel sounds is essentially irrelevant (i.e. whatever pattern they have will be normal for them). In fact, most physicians will omit abdominal auscultation unless there is a symptom or finding suggestive of abdominal pathology. However, you should still practice listening to all the patients that you examine so that you develop a sense of what constitutes the range of normal. Bowel sounds can, however, add important supporting information in the right clinical setting. In general, inflammatory processes of the serosa (i.e. any of the surfaces which cover the abdominal organs….as with peritonitis) will cause the abdomen to be quiet (i.e. bowel sounds will be infrequent or altogether absent). Inflammation of the intestinal mucosa (i.e. the insides of the intestine, as might occur with infections that cause diarrhea) will cause hyperactive bowel sounds. Processes which lead to intestinal obstruction initially cause frequent bowel sounds, referred to as “rushes.” Think of this as the intestines trying to force their contents through a tight opening. This is followed by decreased sound, called “tinkles,” and then silence. Alternatively, the reappearance of bowel sounds heralds the return of normal gut function following an injury. After abdominal surgery, for example, there is a period of several days when the intestines lie dormant. The appearance of bowel sounds marks the return of intestinal activity, an important phase of the patient’s recovery. Bowel sounds, then, must be interpreted within the context of the particular clinical situation. They lend supporting information to other findings but are not in and of themselves pathognomonic for any particular process.

         After you have finished noting bowel sounds, use the diaphragm of your stethoscope to check for renal artery bruits, a high pitched sound (analogous to a murmur) caused by turbulent blood flow through a vessel narrowed by atherosclerosis. The place to listen is a few cm above the umbilicus, along the lateral edge of either rectus muscles. Most providers will not routinely check for bruits. However, in the right clinical setting (e.g. a patient with some combination of renal insufficiency, difficult to control hypertension and known vascular disease), the presence of a bruit would lend supporting evidence for the existence of renal artery stenosis. When listening for bruits, you will need to press down quite firmly as the renal arteries are retroperitoneal structures. Atherosclerosis distal to the aorta (i.e. at the take off of the Iliac Arteries) can also generate bruits. Blood flow through the aorta itself does not generate any appreciable sound. Thus, auscultation over this structure is not a good screening test for the presence of aneurysmal dilatation.

         Percussion: The technique for percussion is the same as that used for the lung exam. First, remember to rub your hands together and warm them up before placing them on the patient. Then, place your left hand firmly against the abdominal wall such that only your middle finger is resting on the skin. Strike the distal interphalangeal joint of your left middle finger 2 or 3 times with the tip of your right middle finger, using the previously described floppy wrist action (see under lung exam). There are two basic sounds which can be elicited:

1. Tympanitic (drum-like) sounds produced by percussing over air filled structures.

2. Dull sounds that occur when a solid structure (e.g. liver) or fluid (e.g. ascites) lies beneath the region being examined.

         Special note should be made if percussion produces pain, which may occur if there is underlying inflammation, as in peritonitis. This would certainly be supported by other historical and exam findings.

 

Abdominal Percussion

         What can you really expect to hear when percussing the normal abdomen? The two solid organs which are percussable in the normal patient are the liver and spleen. In most cases, the liver will be entirely covered by the ribs. Occasionally, an edge may protrude a centimeter or two below the costal margin. The spleen is smaller and is entirely protected by the ribs. To determine the size of the liver, proceed as follows:

1. Start just below the right breast in a line with the middle of the clavicle, a point that you are reasonably certain is over the lungs. Percussion in this area should produce a relatively resonant note.

2. Move your hand down a few centimeters and repeat. After doing this several times, you will be over the liver, which will produce a duller sounding tone.

3. Continue your march downward until the sound changes once again. This may occur while you are still over the ribs or perhaps just as you pass over the costal margin. At this point, you will have reached the inferior margin of the liver. The total span of the normal liver is quite variable, depending on the size of the patient (between 6 and 12 cm). Don’t get discouraged if you have a hard time picking up the different sounds as the changes can be quite subtle, particularly if there is a lot of subcutaneous fat.

4. The resonant tone produced by percussion over the anterior chest wall will be somewhat less drum like then that generated over the intestines. While they are both caused by tapping over air filled structures, the ribs and pectoralis muscle tend to dampen the sound.

5. Speed percussion, as described in the pulmonary section, may also be useful. Orient your left hand so that the fingers are pointing towards the patients head. Percuss as you move the hand at a slow and steady rate from the region of the right chest, down over the liver and towards the pelvis. This maneuver helps to accentuate different percussiootes, perhaps making the identification of the liver’s borders a bit more obvious.

         Percussion of the spleen is more difficult as this structure is smaller and lies quite laterally, resting in a hollow created by the left ribs. When significantly enlarged, percussion in the left upper quadrant will produce a dull tone. Splenomegaly suggested by percussion should then be verified by palpation. The remainder of the normal abdomen is, for the most part, filled with the small and large intestines. Try percussing each of the four quadrants to get a sense of the normal variations in sound that are produced. These will be variably tympanitic, dull or some combination of the above, depending on whether the underlying intestines are gas or liquid filled. The stomach “bubble” should produce a very tympanitic sound upon percussion over the left lower rib cage, close to the sternum.  

 

 

 

 

 

 

 

 

 

          To detect an enlarged spleen, percuss the lowest interspace in the left anterior axillary line. Ask the patient to take a deep breath and repeat. A change from tympany to dullness suggests splenic enlargement.

            Percusion can be quite helpful in determining the cause of abdominal distention, particularly in distinguishing between fluid (a.k.a. ascites) and gas. Of the techniques used to detect ascites, assessment for shifting dullness is perhaps the most reliable and reproducible. This method depends on the fact that air filled intestines will float on top of any fluid that is present. Proceed as follows:

1. With the patient supine, begin percussion at the level of the umbilicus and proceed down laterally. In the presence of ascites, you will reach a point where the sound changes from tympanitic to dull. This is the intestine-fluid interface and should be roughly equidistant from the umbillicus on the right and left sides as the fluid layers out in a gravity-dependent fashion, distributing evenly across the posterior aspect of the abdomen. It should also cause a symmetric bulging of the patient’s flanks.

2. Mark this point on both the right and left sides of the abdomen and then have the patient roll into a lateral decubitus position (i.e. onto either their right or left sides).

3. Repeat percussion, beginning at the top of the patient’s now up-turned side and moving down towards the umbilicus. If there is ascites, fluid will flow to the most dependent portion of the abdomen. The place at which sound changes from tympanitic to dull will therefore have shifted upwards (towards the umbillicus) and be above the line which you drew previously. Speed percussion (described above) may also be used to identify the location of the air-fluid interface. If the distention is not caused by fluid (e.g. secondary to obesity or gas alone), no shifting will be identifiable.

         The models below should help to clarify the concept of shifting dullness. With the “patient” lying flat on their back balloons (representing the intestines)
float on the water (representing ascites). When the “patient” turns on their right side, a new air fluid level is established.

 

Shifting Dullness (real patient)

         Realize that there has to be a lot of ascites present for this method to be successful as the abdomen and pelvis can hide several hundred cc’s of fluid that would be undetectable on physical exam. Also, shifting dullness is based on the assumption that fluid can flow freely throughout the abdomen. Thus, in cases of prior surgery or infection with resultant adhesion formation, this may not be a very useful technique. Palpation can also be used to check for ascites (see below).

         Palpation: First warm your hands by rubbing them together before placing them on the patient. The pads and tips (the most sensitive areas) of the index, middle, and ring fingers are the examining surfaces used to locate the edges of the liver and spleen as well as the deeper structures. You may use either your right hand alone or both hands, with the left resting on top of the right. Apply slow, steady pressure, avoiding any rapid/sharp movements that are likely to startle the patient or cause discomfort. Examine each quadrant separately, imagining what structures lie beneath your hands and what you might expect to feel.

            It is necessary that the abdominal cavity should be accessible to palpa­tion, i.e. that its muscles (prelum) be relaxed and that the examiner should not provoke their straining by his manipulations. The patient should relax in his bed. (The bed should not be too soft.) His legs should be stretched and the arms flexed on the chest. The patient’s breathing should not be deep; his head should rest against a small firm pillow. This position ensures relaxation of the abdominal muscles. The physician takes his place by the right side of the bed, facing the patient. The chair should be firm and level with the patient’s bed. The ambient temperature should be comfortable for the patient, and the hands of the doctor should be warm and dry.

         The examining movements should be careful and gentle so as not to hurt the patient. Touching the abdomen roughly with cold hands will cause reflex contraction of the prelum to interfere with palpation of the abdomen. The patient with distended abdomen should first be given cathartics or enema to empty the bowels. These are the conditions for palpation of the patient in the recumbent position. But some organs or their parts can only be palpated when they hang by gravity with the patient in the erect position. Thus the left lobe of the liver, the lesser curvature of the stomach, the spleen, the kidneys, the caecum, or tumours can become palpable. The epigastrium and the lateral parts of the abdominal cavity should also be palpated with the patient in the erect position.

         Palpation is used to establish normal topographic relations between the abdominal organs and their normal physical condition; the other object is , to detect any possible pathology that changes the morphological condition of the organs and their topographic relations responsible for their dysfunc­tion, to locate the defect, and to determine its nature. Surface and deep palpation are used. Deep palpation gives information on the physical and sometimes functional condition of the organs and also on their position in the abdominal cavity. In other words, deep palpation gives information on the topography of the abdominal cavity (topographic palpation).

         Surface tentative palpation. The physician assumes his position by the bedside as described above and places his right hand flat on the abdomen of the patient (the fingers may be slightly flexed) to examine carefully and gradually the entire abdomen without trying to penetrate the deep parts of the abdomen. By this examination the physician should establish the strain of the prelum, its tenderness, and location of the painful site. The left in­guinal area should be examined first, provided the patient does not com­plain of pain in this region. Palpation is then continued by examining sym­metrical points of the abdomen on its left and right sides to end in the epigastric region. If the patient complains of pain in the left inguinal area, the sequence of palpation should be so changed that the least painful site on the anterior abdomen should first be examined. The physician should simultaneously assess the condition of the abdominal skin and sub­cutaneous connective tissue, the strain of the abdominal wall, the zones of superficial and deeper painful areas to locate them accurately. Hernial separation of muscles and protrusions, and also other anatomical changes should be revealed, if any. Resistance and marked strain of muscles of the abdominal wall are usually palpated over the organ affected by inflamma­tion, especially so if the peritoneum is involved. In the presence of acute in­flammation of the peritoneum (local inflammation included, e.g. in purulent appendicitis, cholecystitis, and the like), local pressure causes strong pain but it becomes even more severe when the pressure is released (Shchetkin-Blumberg symptom). In the presence of pronounced enlarge­ment of the parenchymatous organs, in strained abdomen or intestinal loops, and also in the presence of large tumours, even surface palpation can give much diagnostic information. But only deep systematic palpation can give full information about the condition of the abdominal cavity and its organs, as well as their topography.

         Deep sliding palpation (according to Obraztsov and Strazhesko). When starting deep palpation the examiner should always be aware of the anatomical relations in the abdominal cavity, the shape and physical pro­perties of the organs, their supporting structures and possible deviations in topographical relations that may depend on the constitution of the patient, his special condition, nutrition, relaxation of the abdominal muscles, etc.

         Obraztsov used the double-checking principle in his examinations. For example, in order to make sure that a given section of the intestine is ac­tually ileum terminale it is necessary to locate the caecum; to determine the size of the stomach, the palpatory findings are checked by percussion and percussive palpation of the stomach. Respiratory excursions of the organs should be taken into consideration during palpation according to a strictly predetermined plan, beginning with more readily accessible parts. The following sequence is recommended: the sigmoid, the caecum with the ap­pendix, pars coecalis ilii, the ascending and descending colon, the stomach with its parts, the transverse colon, the liver, the spleen, the duodenum, the pancreas, and the kidneys.

         Success of palpation depends on strict observation of the rules. The posture of the patient and the physician should be the same as in surface palpation. Palpation should be carried out by the apt hand. In some cases the other hand should be placed on the examining hand to increase pressure. Palpation can also be bimanual (palpation with both hands simultaneously). If only one hand is used,, the other hand presses the prelum laterally to the palpated zone in order to lessen or overcome resistance of the abdominal wall and hence to promote relaxation of the prelum in the palpated zone. The other hand can be used to move the palpated organ closer to the examining hand or in order to perform bimanual palpation.

The palpation technique includes the following four steps. First: proper positioning of the physician’s hands. The right hand is placed flat on the anterior abdominal wall, perpendicular to the axis of the examined part or the edge o\ the examined organ. Second: formation of a skin fold to facilitate further movements of the examining hand. Third: moving the hand inside the abdomen. Deep palpation is when the fingers are moved gradually, with  each expiration, into the abdomen when the abdominal wall is relaxed. The examining hand thus reaches the posterior wall of the abdomen or the underlying organ. Fourth: sliding movement of the finger­tips in the direction perpendicular to the transverse axis of the examined organ. The organs pressed against the posterior wall and the examining finger? continue moving over the examined intestine or the stomach cur­vature, depending on the position of the organ, the sliding movement should be either from inside, in the outward direction (the sigmoid, caecum) or in the downward direction (the stomach, transverse colon); the movements should then be more oblique in accordance with the deviation of the organ from the horizontal or-vertical course. The examining hand should always move together with the skin and not over its surface.

         By palpating the intestine, the physician establishes its localization, mobility, tenderness, consistency-, diameter, the condition of the surface {smooth, tubercular), the absence or presence of rumbling sounds during palpation. Ail these signs indicate the presence or absence of pathology.

         The sigmoid is palpated from top right to medial left, downward and laterally, perpendicularly to the axis of the intestine which runs obliquely in the left iliac space at the border of median and the outer third of the linea umbilico-iliacae. Palpacion is carried out by four fingers, placed  together and slightly flexed, or by the ulnar edge of the right little finger. The fingers are immersed medially of the expected position of the intestine and as soon as the posterior wall of the abdomen is reached, the fingers slide along the intestine in the given direction, i.e. laterally and downward. The intestine is pressed against the posterior wall and first slides along it (to the extern allowed by the mesenteric length) but later it slips from under the examining fingers. The sigmoid can be palpated by the described technique in 90-95 % of cases.

 

Palpation of the sigmoid

The sigmoid is only impalpated in excess inflation of the abdomen and in obese patients. If the sigmoid is not found where it belongs, it may be displaced to some other location because of long mesenterium which accounts for the high sigmoid mobility.  It is then usually displaced closer to the navel and to the right. The sigmoid can usually be found by deep palpation of the infraumbilical and suprapubic areas. Normally the sigmoid can be palpated over the length of 20-25 cm as a smooth firm cylinder, its thichness being that of a thumb or an index finger; the sigmoid is painless to palpation, it does not produce rumbling sounds, its peristalsis is rather flaccid and infrequent. The sigmoid can be displaced 3-5 cm to either side.

         The caecum is palpated by the same technique, except that the direction is different. Since the caecum is situated at the border of the median and lateral third of the umbilico-iliac line (5 cm by the iliac spine), the palpation is carried along this line or parallel to it. Palpation is used not only to locate the caecum but also a certain part of the ascending colon (10-12 cm of its length), i.e. the part of the large intestine which is known in the clinic as typhlon. A normal caecum can be palpated in 80-85 per cent of cases as a moderately strained cylinder (widening to the round bot­tom), 2-3 cm in diameter; when pressed upon, it rumbles. Palpation is painless. It reveals a certain passive mobility of the caecum (to 2—3 cm).

Palpation of the caecum 

         The lower edge of the caecum is 0.5 cm above the bi-iliac in man and 1—1.5 cm below it in women. Further palpation of the right iliac region gives (in 80—85 per cent of cases) information on the 15-20 cm length of the ileum which ascends from the small pelvis to the right, to be connected with the large intestine (ileum terminate). This section of the intestine extends most­ly upward and to the right and palpation should therefore be carried out almost parallel to the umbilico-iliac line (but below it). The terminal end of the ileum can be palpated in the depth of the right iliac space as a soft, easi­ly peristalting and passively mobile cylinder, the thickness of the little finger (or a pencil); it slips out from under the examining fingers and rumbles distinctly. When the terminal end of the ileum is found, the ver­miform process can be found above or below  it. It is found easier if the bel­ly of the psoas muscle is first found. The location of this muscle is facilitated when the patient slightly raises his straight right leg. The ver­miform process then becomes more pronounced over the contracted belly of the psoas muscle. The vermiform process can be palpated in 20—25 per cent of cases. This is a thin (goose-feather thick) painless cylinder. When palpated the process does not change its consistency; nor does it rumble. Once the cylinder has been felt above or below the ileum, the examiner cannot be quite sure that he has found the ver­miform process because it can be simulated by mesenteric duplicature and a lymph bundle. It is difficult to find the ver­miform process also because its position varies with respect to the caecum. It becomes impalpable at all when located behind the caecum. When the process is inflamed it becomes much easier to find it because of its thickening, fixation, and consolidation.  The caecum, the terminal part of the ileum, and the ver­miform process are palpated by four fingers of the right hand; the fingers should be held together and slightly flexed.  If the prelum is tense, the muscles in the palpation zone can be relaxed by pressing the umbilical area with the radial edge of the left hand. 

         The ascending and descending colons are palpated by two hands. The   left hand is placed under the left and then the right lumbar side, while the fingers of the right hand press on the anterior wall of the abdominal cavity until the examiner feels his right and left hands meet. The examining fingers slide laterally, perpendicularly to the axis of the intestine.

 

 Palpation of the descending colon 

         The transverse colon is palpated by four fingers of the right hand held together and slightly flexed. Bimanual palpation can also be used. Since the position of the transverse colon is unstable, it is useful first to determine by percussive palpation (after Obraztsov) the lower border of the stomach, and only then to search for the colon some 2-3 cm below this border. The right hand (or both hands) is placed on the sides of the linea alba and the skin is moved slightly upwards. The examining hand is then immersed gradually during relaxation of the prelum at expiration until the posterior wall of the abdomen is felt. Once the posterior wall is reached, the examining hand should slide down to feel the intestine: this is an ar­ching (transverse) cylinder of moderate density (2—2.5 cm thick), easily movable up and down, painless and silent. If the intestine is impalpable in this region, the same technique should be used to examine the lower and lateral regions, the position of the palpating hands being changed accor­dingly. Normal transverse colon can be palpated in 60-70 per cent of cases.

Palpation of the transverse colon 

         In addition to the mentioned portions of the intestine, the horizontal parts of the duodenum and the curvature of the colon can in rare cases be palpated; an occasional loop of the small intestine that may happen in the iliac cavity can also be palpated. But the small intestine is usually im­palpable because of its deep location, high mobility, and thin walls; it can­not be pressed against the posterior abdominal wall, which is the necessary condition for palpation of normal intestine.

         The rectum can be probed by a finger after cleansing it with enema. The patient should assume the knee-chest position. The examining index finger should first be coated with vaseline oil and then introduced carefully into the rectum to the maximum possible depth. If the patient is especially sen­sitive, or the rectum and the ampulla are affected with inflammation or fissures, the sphincter and the ampulla should be anaesthetized below intervention. As the examining finger passes the sphincter, it feels anteriorly the prostate in men and the vaginal part of the uterus in women. The finger should be moved upwards to pass the sacrococcygeal plica and to reach, if possible, the terminal rectal plica that closes the entrance to the sigmoid (11-13 cm above the anus). Palpation of the rectum can be  facilitated if the patient squats and strains (makes evacuatory  efforts) After examination of the anterior wall, the posterior wall of the rectum is felt by the finger. The finger is turned through 180° and the posterosacral and then lateral walls are examined. The examiner should get an idea of the mucosa (the presence of papilloma, polyps, varicose nodes, oedema and swelling of the mucosa, cicatricial narrowings, newgrowths, etc.) and the  connective tissue surrounding the rectum, Douglass space, the prostate, the uterus and its appendages, and the pelvic bones.

Palpation of the liver

Surface palpation in diseases of the liver can reveal a tender zone in the right hypochondrium and epigastrium. Especially severe local pain (caused even by a slight touch on the anterior abdominal wall in the zone overlying the gall bladder) is observed in acute cholecystitis and biliary colic. In chronic cholecystitis slight or moderate tenderness is only revealed at the point of projection of the gall bladder fundus onto the anterior abdominal wall. In healthy subjects this point is found immediately below the right costal arch by the lateral edge of the right rectus abdominis muscle.

The liver is palpated by the Obraztsov and Strazhesko method. As the lower edge of the liver descends to meet the examining fingers during a deep inspiration it slides over the fingers and thus becomes detectable. It should be remembered that the respiratory mobility of the liver is the highest compared with that of the other abdominal organs because the liver is the closest to the diaphragm. It follows therefore that during palpation of the liver, the active role belongs to its respiratory mobility rather than to the palpating fingers (as is the case with palpation of the intestine).

The patient should stand or lie during palpation of the liver and the gall bladder. But in certain cases the liver can be easier palpated if the patient lies on his left side: the liver hangs by gravity from under the hypochon­drium and its inferio-anterior edge can thus be better palpated. Common rules should be followed during palpation of the liver and the gall bladder. Special attention should be paid to the antero-inferior margin of the liver whose properties (outlines, form, tenderness, consistency) are indicative of the condition of the liver, its position, and configuration. In many cases (especially if the liver is enlarged or lowered) the liver can be palpated not only from the left hypochondrium to the right hypochondrium, but its superio-anterior surface becomes palpable as well.

Palpation of the liver.

 

The examiner sits by the right side, facing the patient. He places four fingers of his left hand on the right lumbar region of the patient and uses his left thumb to press on the costal arch to move the liver closer to the palpating fingers of the right hand and to prevent expansion of the chest during inspiration. This stimulates greater excursions of the right cupola of the diaphragm. The palm of the right hand is placed flat on the abdomen below the costal arch in the midclavicular line. The slightly flexed fingers press lightly on the abdominal’wall. The patient is asked to take a deep breath; the liver descends to touch the palpating fingers and then slides to bypass them. The examiner’s hand remains motionless. The procedure is repeated several times, pie position of the liver margin varies depending on conditions. It is therefore necessary first to determine the lower margin of the liver by percussion before positioning the palpating fingers.

According to Obraztsov, normal liver can be palpated in 88 per cent of cases. Physical properties of the liver can be determined by palpating its lower edge (it can be soft, firm, rough, sharp, rounded, tender, etc.). The margin of an unaffected liver palpated at the height of a deep inspiration is 1-2 cm below the costal arch. It is soft, sharp, readily bending, and insen­sitive.

Palpation of the liver.

The lower edge of a normal liver is usually palpated in the right midclavicular line; the liver is impalpable to the right of this line because it  is located behind the costal arch; the liver is hardly palpable to the left of the line because of the abdominal muscles. An enlarged or consolidated liver can be palpated in all lines. The liver of patients with pronounced distension of the abdomen should be examined with the empty stomach to facilitate palpation. In accumulation of much fluid in the abdominal cavity (ascites) the liver is not always palpable if the patient is lying. The patiei should then be examined in the erect position, or he may lie on his left side. If the amount of fluid in the abdomen is very large, it should be released paracentesis.

In accumulation of much fluid in the abdominal cavity, ballotment should be used to palpate the liver. To that end the right hand (two or four flexed fingers) should be placed on the lower right part of the abdomen, perpendicularly to the expected lower edge of the liver. The abdominal wall is given a sharp tap from the palpating fingers which move upward to meet the firm object, the liver, which is first tossed to the deeper parts of the abdominal cavity but is then returned back to strike the fingers.

       Palpation is painful if the liver is inflamed and the affection extends to the liver capsule; the liver is also tender when it is distended (e.g. blood congestion due to heart failure). The liver of a healthy subject (if it is accessible to palpation) is soft; it becomes firmer in hepatitis, hepatosis and cardiac congestion. The liver is especially firm in cirrhosis. Its edge becomes sharp and the surface smooth or covered with small tubercles. The liver is also firm in the presence of tumour and multiple metastases of cancer. Its surface then becomes covered with rough tubercles (surface metastases) and the lower margin is rough. The liver is firm in amyloidosis. Comparatively small tumours and echinococcosis can sometimes be palpated. Protrusion of the lower margin of an enlarged liver is assessed with respect to the costal arch in the right anterior axillary line, right midclavicular line, right parasternal line, anterior median line, and left parasternal line. Palpation verifies the findings obtained by percussion of the liver.

The gall bladder cannot be palpated in healthy subjects because of its soft consistency and the insignificant protrusion. But if the gall bladder is enlarged (hydrops, stones in the bladder, cancer, etc.) it becomes palpable. The position of the patient for palpation of the gall bladder is the same  as in palpation of the liver. After the margin of the liver has been found, the gall bladder should be palpated at the lateral edge of the right rectus abdominis muscle. The palpation technique is the same as that for palpation of the liver. The gall bladder can easier be found by moving the palpating fingers in the direction perpendicular to the axis of the gall bladder. The bladder is felt like a pear of variable size, firmness and tenderness depen­ding on the character of pathology in the gall bladder proper or the surrounding organs (e.g. the gall bladder is enlarged, soft, and elastic in tumour-obstructed bile duct: Courvoisier- Terrier sign; the  bladder is firm and tuberous in the presence ot newgrowths in its wall, in overfilling with stones, in inflammation of the wall, etc.).

Palpation of the pancreas

Surface palpation of the abdomen of a patient with acute pancreatitis icveals tenderness and strain of the prelum muscles in the epigastrium, .’inetimes in the left hypochondrium or over the pancreas (Korte symp-10m).

Palpation of the pancreas is very difficult because of the deep position .ind soft consistency of the gland. Normal pancreas can only be palpated in 1-5 per cent of women and 1-2 per cent of men affected by cachexia with iclaxed prelum and ptosis of the internal organs. The pancreas is only palpable when enlarged considerably. Consolidated pancreas affected by cirrhosis, newgrowth, or cyst can be easier palpated.

The pancreas should be palpated in the morning, after giving purgatives (with the empty stomach). The greater curvature should first be palpated; then the position of the pylorus should be determined and the right knee of the transverse colon palpated. The horizontal portion of the duodenum should preferably be outlined by palpation in order to find the point where the head of the pancreas might be better palpated. The head of the pan­creas is easier to palpate than its body or tail because of its greater size and frequent consolidation. Palpation is deep and sliding, usually above the right pan of the greater curvature of the stomach. The Obraztsov-Strazhesko rule should be followed during palpation. The palpating hand is placed horizontally, 2-3 cm above the preliminarily found lower border of the stomach. The skin is pulled upwards and then the palpating hand presses gradually into the abdominal cavity with each expiration. As soon as the posterior wall is reached, the hand should slide in the downward direction.

A normal pancreas is a soft transverse cylinder, 1.5-3 cm in diameter. The organ is immobile and painless. In the presence of chronic pancreatitis and tumour of the pancreas, it can sometimes be palpated as a firm, ir­regular, and slightly tender band. Conclusions should be derived very carefully, because part of the stomach, the transverse colon, a pack of lymph nodes and some other formations can easily be mistaken for the pancreas.

Palpation of the kidneys

The posterior location of the kidneys, and also the absence of anterior. Upproach to them due to the interference of the costal arch, rrakes palpa-fiiun of the kidneys difficult. Relaxation of the prelum and pronounced cachexia can be attended by certain ptosis of the kidneys and make them accessible to palpation even in healthy subjects. But the results of palpation can only be reliable in considerable enlargement of the kidneys (at least 1.5—2 times, e.g. due to formation of a cyst or a tumour), or their displace­ment by a tumour, or in cases with a floating kidney. Bilateral enlargement of the kidneys is observed in polycystosis.

It is necessary to remember that the kidneys can move about in the range of 2—3 cm in the proximal and distal directions when the subject changes his position from horizontal to vertical, and also during respiratory movements of the diaphragm. Passive movements of the kidneys transmitted from the diaphragm during inspiration and expiration should be taken into consideration during palpation: the Obraztsov-Strazhesko palpation method should be used. The patient should be palpated in the lying or standing position. When the patient is in the horizontal position, his kidneys are better palpated because the strain of the prelum is absent. The movable kidney can be palpated in the stan­ding patient because the hangs by gravity and is displaced downward by the pressure of the low diaphragm.

During palpation of the patient in the lying position, his legs should be stretched and the head placed on a low pillow; the prelum is relaxed and the arms are freely placed on the chest. The physician should assume his position by the right side of the patient with his left hand under the patient’s loin, slightly below the 12th rib so that the finger tips be near the spinal column. During palpation of the left kidney, the physician’s hand should be moved further, beyond the vertebral column, to reach the left part of the lumbar region. The right hand should be placed on the ab­domen, slightly below the corresponding costal arch, perpendicularly to it and somewhat outwardly of the rectus abdominis muscles. The patient is asked to relax the abdominal muscles as much as possible and breathe deeply and regularly. The physician’s right hand should press deeper with each expiration to reach the posterior abdominal wall, while the left hand presses the lumbar region to meet the fingers of the right hand. When the examining hands are as close to each other as possible, the patient should be asked to breathe deeply by “the abdomen” without straining the prelum. The lower pole of the kidney (if it is slightly descended or enlarged) descends still further to reach the fingers of the right hand. As the physi­cian feels the passing kidney, he presses it slightly toward the posterior ab­dominal wall and makes his fingers slide over the anterior surface of the kidney bypassing its lower pole. If ptosis of the kidney is considerable, both poles and the entire anterior surface of the kidney can be palpated. The physician should assess the shape, size, surface (smooth or tuberous), tenderness, mobility, and consistency of the kidneys. Bimanual palpation of the kidney can also be done with the patient lying on his side.

In contrast to other organs, an enlarged or ptosed kidney can be ex­amined by ballottement (Guyon’s sign): the right hand feels the kidney while the fingers of the left hand strike rapidly the lumbar region in the angle between the costal arch and the longissimus thoracic muscles: the fingers of the right hand feel vibration of the kidney. In deranged urine outflow through the ureter and in pronounced distension of the renal pelvis by the accumulated urine or pus, liquid fluctuation can be felt during palpation of the kidney.

If the physician palpates some formation where he expects to find a kidney, he must check reliably if this is actually a kidney because it is easy to mistake for the kidney an overfilled and firm part of the large intestine, tumor of perirenal cellular tissue (lipoma, fibroma), an enlarged right lobe of the liver, the gall bladder (during palpation of the right kidney), or an enlarged or displaced spleen (during palpation of the left kidney). The kidney is a bean-shaped body with a smooth sin face, slipping upwards from under the palpating fingers and returning to normal position, tossed up by ballottment and giving tympany during percussion over the kidney (by overlying intestinal loops). Protein and erythrocytes appear in the urine after palpation. But all these signs are of only relative importance. For ex­ample, if a malignant tumour develops, the kidney may lose its mobility due to proliferation of the surrounding tissues; its surface becomes ir­regular and the consistency more firm; if the tumour is large, the kidney moves apart the intestinal loops and percussion gives dullness. But the kidney caevertheless be identified by the mentioned signs by difl tiating it from the neighbouring organs and other formations.

Palpation of the kidneys in the standing patient was propose S. Botkin. During palpation the patient stands facing the physicnui j sits on a chair. The prelum muscles should be relaxed and the trunk -,11 inclined forward.

Palpation can be used to diagnose ptosis of the kidneys. Three iU of nephroptosis can be distinguished: the lower pole of the kidney < palpated in cases with ptosis of the first degree; the entire kidney > palpated in the second degree; and the kidney freely moves aboui directions to pass beyond the vertebral column, to the side of thr kidney, and to sink downwards to a considerable distance, in the degree ptosis.

Palpation is also used to examine the bladder. If it contains much i especially in persons with thin abdominal wall, the urinary bladdei palpated over the pubic bone as an elastic fluctuating formation bladder is markedly distended, its superior border reaches the umlnli

Tenderness in palpation of the ureter along its course and sensitivil over the kidneys (sensitive to pressure exerted in the angle between ih# [ rib and the longissimus thoracic muscles) is of certain diagnostic h tance. The area overlying the ureter extends on the anterior abdomiiw between the superior ureter point (at the edge of the rectus abdominuj cle at the level of the umbilicus) and the inferior point (at the inter if of the bi-iliac line and the vertical line passing the pubic tubercle).

View: Location of the Kidneys

 

Examining for a fluid wave

         When observation and/or percussion are suggestive of ascites, palpation can be used as a confirmatory test. Ask the patient or an observer to place their hand so that it is oriented longitudinally over the center of the abdomen. They should press firmly so that the subcutaneous tissue and fat do not jiggle. Place your right hand on the left side of the abdomen and your left hand opposite, so that both are equidistant from the umbillicus. Now, firmly tap on the abdomen with your right hand while your left remains against the abdominal wall. If there is a lot of ascites present, you may be able to feel a fluid wave (generated in the ascites by the tapping maneuver) strike against the abdominal wall under your left hand. This test is quite subjective and it can be difficult to say with assurance whether you have truly felt a wave-like impulse.

Assessing for a fluid wave

         The abdominal examination, like all other aspects of the physical, is not done randomly. Every maneuver has a purpose. Think about what you’re expecting to see, hear, or feel. Use information that you’ve gathered during earlier parts of the exam and apply it in a rational fashion to the rest of your evaluation. If, for example, a certain area of the abdomen was tympanitic during percussion, feel the same region and assure yourself that there is nothing solid in this location. Go back and repeat maneuvers to either confirm or refute your suspicions. In the event that a patient presents complaining of pain in any region of the abdomen, have them first localize the affected area, if possible with a single finger, pointing you towards the cause of the problem. Then, examine each of the other abdominal quadrants first before turning your attention to the area in question. This should help to keep the patient as relaxed as possible and limit voluntary and involuntary guarding (i.e. superficial muscle tightening which protects intra-abdominal organs from being poked), allowing you to gather the greatest amount of clinical data. Make sure you glance at the patient’s face while examining a suspected tender area. This can be particularly revealing when evaluating otherwise stoic individuals (i.e. even these patients will grimace if the area is painful to the touch). The goal, of course, is to obtain relevant information while generating a minimal amount of discomfort.  

     Place your right hand at the inferior and lateral border of the ribs, pushing down as you push up from behind with your left hand. If the right kidney is massively enlarged, you may be able to feel it between your hands.

     Now examine the left upper quadrant. The normal spleen iot palpable.

When enlarged, it tends to grow towards the pelvis and the umbilicus (i.e. both down and across). Begin palpating near the belly button and move slowly towards the ribs. Examine superficially and then more deeply. Then start 8-10 cm below the rib margin and move upwards. In this way, you will be able to feel enlargement in either direction. You can use your left hand to push in from the patient’s left flank, directing an enlarged spleen towards your right hand. If the spleen is very big, you may even be able to “bounce” it back and forth between your hands. Splenomegaly is probably more difficult to appreciate then hepatomegaly. The liver is bordered by the diaphragm and can’t move away from an examining hand. The spleen, on the other hand, is not so definitively bordered and thus has a tendency to float away from you as you palpate. So, examine in a slow, gentle fashion. The edge, when palpable, is soft, rounded, and rather superficial. Repeat the exam with the patient turned onto their right side, which will drop the spleen down towards your examining hand.

     Exploration for the left kidney is performed in the same fashion as described for the right. Kidney pain, most commonly associated with infection, can be elicited on direct examination if the entire structure becomes palpable as a result of associated edema. This is generally not the case. However, as the kidney lies in the retroperitoneum, pounding gently with the bottom of your fist on the costo-vertebral angle (i.e. where the bottom-most ribs articulate with the vertebral column) will cause pain if the underlying kidney is inflamed. Known as costo-vertebral angle tenderness (CVAT), it should be pursued when the patient’s history is suggestive of a kidney infection (e.g. fever, back pain and urinary tract symptoms).

     Examine the left and right lower quadrants, palpating first superficially and then deeper. A stool filled sigmoid colon or cecum are the most commonly identified structures on the left and right side respectively. The smooth dome of the bladder may rise above the pelvic brim and become palpable in the mid-line, though it needs to be quite full of urine for this to occur. Other pelvic organs can also occasionally be identified, most commonly the pregnant uterus, which is a firm structure that grows up and towards the umbillicus. The ovaries and fallopian tubes are not identifiable unless pathologically enlarged.

     Finally, try to feel the abdominal aorta. First push down with a single hand in the area just above the umbillicus. If you are able to identify this pulsating structure with one hand, try to estimate its size. To do this, orient your hands so that the thumbs are pointed towards the patient’s head. Then push deeply and try to position them so that they are on either side of the blood vessel. Estimate the distance between the palms (it should be no greater then roughly 3 cm). This is, admittedly, a crude technique. Remember also that the aorta is a retorperitoneal structure and can be very hard to appreciate in obese patients. There have beeo reports of anyone actually causing the aorta to rupture using this maneuver, so don’t be afraid to push vigorously.

         Findings Commonly Associated With Advanced Liver Disease: Chronic liver disease usually results from years of inflamation, which ultimately leads to fibrosis and decline in function. Histologically, this is referred to as Cirrhosis. This can be driven by a number of different processes, most commonly chronic alcohol use, viral hepatitis (B or C) or hemachromatosis (the complete list is much longer). It’s important to realize that a cirrhotic liver can be markedly enlarged (in which case it may be palpable) or shrunken and fibrotic (non-palpable).

         After many years (generally greater then 20) of chronic insult, the liver may become unable to perform some or all of its normal functions. There are several clinical manifestations of this dysfunction. While none are pathonomonic for liver disease, in the right historical context they are very suggestive of underlying pathology. Some of the most common findings are described and/or pictured below.

1.  Hyperbilirubinemia: The diseased liver may be unable to conjugate or secrete bilirubin appropriately. This can lead to

a.  Icterus – Yellow discoloration of the sclera.

b. Jaundice – Yellow discoloration of the skin.

c. Bilirubinuria – Golden-brown coloration of the urine.

2. Ascites: Portal vein hypertension results from increased resistance to blood flow through an inflamed and fibrotic liver. This can lead to ascites, accumulation of fluid in the peritoneal cavity.

3. Increased Systemic Estrogen Levels: The liver may become unable to process particular hormones, leading to their peripheral conversion into estrogen. High levels promote:

a. Breast development (gynecomastia).

b.  Spider Angiomata – dilated arterioles most often visible on the skin of the upper chest.

c. Testicular atrophy.

4. Lower Extremity Edema: Impaired synthesis of the protein alburmin leads to lower intravascular oncotic pressure and resultant leakage of fluid into soft tissues. This is particularly evident in the lower extremities.

5. Varices: In the setting of portal hypertension, blood “finds” alternative pathways back to the heart that do not pass through the liver. The most common is via the splenic and short gastric veins, which pass through the esophageal venous plexus enroute to the SVC. This causes esophageal varices which can bleed profoundly, though these are not apparent on physical examination. A much less common path utilizes the recanalized umbilical vein, which directs blood through dilated superficial veins in the abdominal wall. These are visible on inspection of the abdomen and are known as Caput Medusae.

Icterus

Caput Medusae

  

Jaundice

Ascites

Gynecomastia

Spider

Xanthelasmas

Hyppokrate’s fingers

  

Special methods of investigation

Laboratory of examination

1. Routine blood examination

2. Urine tests (bile pigments, ketonuria)

3. Biochemical analysis of urine for diastase

4. Biochemical blood analysis (bilirubin total, unconjugated and conjugated bilirubin, protein, cholesterol, AlAT, AsAT, amylase, tripsin, lipase).

Disorders

a) Syndrome of cholistasis (increased level of total and conjugated bilirubin and cholesterol).

b) Syndrome of cytolysis (increased level of AsAT, AlAT, LDG).

c) Syndrome of dysfunction of pancreas (increased level of amylase, tripsin, lipase).

4. Chain polymerizes reaction for virus of hepatitis A, B, C.

5. Examination of feces for intestinal parasites (ascarides, lamblia cysts, enterobiosis)

6. Coprogram.

Changes from the side of koprograms:

–  indigested muscular fibers,

–  steatorrhea,

–  lientery,

–  bacteria’s in the feces.

Instrumental methods of examination

1. Esophagogastroduodenoscopy.

2. Ultrasound investigation.

3. Intragastric pH–metry.

4. Colonoscopy.

5. Procto(sigmoido)scopy.

6. Artificial contrast study of gastrointestinal system.

7. Laparoscopy.

8. Irrigoscopy and irrigography.

SECRETORY STUDIES

         There are many methods of secretory studies of stomach function by gastric intubation: the acid output is measured in response to pentagastrin, to broth, histamine, insuline.

         The acid output is measured in response to pentagastrin, a syntheric pentapeptide which exerts the biological effects of gastrin.  Preparation consists of an overnight fast. H₂-receptor antagonist drugs must be stopped for at least 48 hours before the test and omeprasole seven days before. The fasting contents of the stomach are aspirated and their volume measured; then the secretions are collected continuously for one hour. This is termed the ‘basal acid output’. Pentagastrin is then injected subcutaneously and the gastric secretions are collected for a further hour. The acid output in this hour is termed the ‘maximal acid output’.

         Total volume of 4 portions collecting for 60 minutes, after aspiration of fasting contents   50 – 100 ml

Total acidity – 40 – 60 mmol/l

Free hydrochloric acid   20 – 40 mmol/l

Fixed hydrochloric acid   10 – 15 mmol/l

Debit-hour of the free hydrochloric acid 1.5 – 5,5 mmol/hour

Debit-hour of the free hydrochloric acid 1.5 – 5,5 mmol/hour

3. Bacteriological and immunological investigation in the diseases of alimentary tract.

Helicobacter pylori infection

         Diagnosis of H.pylori infection may be made by endoscopy and biopsy, serology or ¹³C and ¹⁴C breath test

Test that measure biosynthetic function of the liver

LABORATORY TESTING

         Diagnosis in liver disease is greatly aided by the availability of reliable and sensitive tests of liver injury and function. A typical battery of blood tests used for initial assessment of liver disease includes measuring levels of serum alanine and aspartate aminotransferases (ALT and AST), alkaline phosphatase, direct and total serum bilirubin, and albumin and assessing prothrombin time. The pattern of abnormalities generally points to hepatocellular versus cholestatic liver disease and will help to decide whether the disease is acute or chronic and whether cirrhosis and hepatic failure are present. Based on these results, further testing over time may be necessary. Other laboratory tests may be helpful, such as g-glutamyl transpeptidase (GGT) to define whether alkaline phosphatase elevations are due to liver disease; hepatitis serology to define the type of viral hepatitis; and autoimmune markers to diagnose primary biliary cirrhosis (antimitochondrial antibody; AMA), sclerosing cholangitis (peripheral antineutrophil cytoplasmic antibody; pANCA), autoimmune hepatitis (antinuclear, smooth-muscle, and liver-kidney microsomal antibody). Laboratory Tests. When the physician encounters a patient with unexplained jaundice, there are a battery of tests that are helpful in the initial evaluation. These include total and direct serum bilirubin with fractionation, aminotransferases, alkaline phosphatase, albumin, and prothrombin time tests. Enzyme tests [alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase] are helpful in differentiating between a hepatocellular process and a cholestatic process, a critical step in determining what additional workup is indicated. Patients with a hepatocellular process generally have a disproportionate rise in the aminotransferases compared to the alkaline phosphatase. Patients with a cholestatic process have a disproportionate rise in the alkaline phosphatase compared to the aminotransferases. The bilirubin can be prominently elevated in both hepatocellular and cholestatic conditions and therefore is not necessarily helpful in differentiating between the two.

         In addition to the enzyme tests, all jaundiced patients should have additional blood tests, specifically an albumin and a prothrombin time, to assess liver function. A low albumin suggests a chronic process such as cirrhosis or cancer. A normal albumin is suggestive of a more acute process such as viral hepatitis or choledocholithiasis. An elevated prothrombin time indicates either vitamin K deficiency due to prolonged jaundice and malabsorption of vitamin K or significant hepatocellular dysfunction. The failure of the prothrombin time to correct with parenteral administration of vitamin K indicates severe hepatocellular injury.

The results of the bilirubin, enzyme, albumin, and prothrombin time tests will usually indicate whether a jaundiced patient has a hepatocellular or a cholestatic disease. The causes and evaluation of each of these is quite different.

         Hepatocellular diseases that can cause jaundice include viral hepatitis, drug or environmental toxicity, alcohol, and end-stage cirrhosis from any cause. Cholestatic Conditions.  When the pattern of the liver tests suggests a cholestatic disorder, the next step is to determine whether it is intra- or extrahepatic cholestasis. Distinguishing intrahepatic from extrahepatic cholestasis may be difficult. History, physical examination, and laboratory tests are ofteot helpful. The next appropriate test is an ultrasound. The ultrasound is inexpensive, does not expose the patient to ionizing radiation, and can detect dilation of the intra- and extrahepatic biliary tree with a high degree of sensitivity and specificity. The absence of biliary dilatation suggests intrahepatic cholestasis, while the presence of biliary dilatation indicates extrahepatic cholestasis. False-negative results occur in patients with partial obstruction of the common bile duct or in patients with cirrhosis or primary sclerosing cholangitis (PSC) where scarring prevents the intrahepatic ducts from dilating.

         In patients with apparent intrahepatic cholestasis, the diagnosis is often made by serologic testing in combination with percutaneous liver biopsy.  The list of possible causes of intrahepatic cholestasis is long and varied. A number of conditions that typically cause a hepatocellular pattern of injury can also present as a cholestatic variant. Both hepatitis B and C can cause a cholestatic hepatitis (fibrosing cholestatic hepatitis) that has histologic features that mimic large duct obstruction. This disease variant has been reported in patients who have undergone solid organ transplantation. Hepatitis A, alcoholic hepatitis, EBV, and CMV may also present as cholestatic liver disease. 

TESTS THAT MEASURE BIOSYNTHETIC FUNCTION

OF THE LIVER

         Serum Albumin  Serum albumin is synthesized exclusively by hepatocytes. Serum albumin has a long half-life: 15 to 20 days, with approximately 4% degraded per day. Because of this slow turnover, the serum albumin is not a good indicator of acute or mild hepatic dysfunction; only minimal changes in the serum albumin are seen in acute liver conditions such as viral hepatitis, drug-related hepatoxicity, and obstructive jaundice. In hepatitis, albumin levels below 3 g/dL should raise the possibility of chronic liver disease. Hypoalbuminemia is more common in chronic liver disorders such as cirrhosis and usually reflects severe liver damage and decreased albumin synthesis. One exception is the patient with ascites in whom synthesis may be normal or even increased, but levels are low because of the increased volume of distribution. However, hypoalbuminemia is not specific for liver disease and may occur in protein malnutrition of any cause, as well as protein-losing enteropathies, nephrotic syndrome, and chronic infections that are associated with prolonged increases in serum interleukin-1 and/or tumor necrosis factor levels that inhibit albumin synthesis. Serum albumin should not be measured for screening in patients in whom there is no suspicion of liver disease. Serum Globulins.  Serum globulins are a group of proteins made up of gamma globulins (immunoglobulins) produced by B lymphocytes and alpha and beta globulins produced primarily in hepatocytes. Gamma globulins are increased in chronic liver disease, such as chronic hepatitis and cirrhosis. In cirrhosis, the increased serum gamma globulin concentration is due to the increased synthesis of antibodies, some of which are directed against intestinal bacteria. This occurs because the cirrhotic liver fails to clear bacterial antigens that normally reach the liver through the hepatic circulation.

         Increases in the concentration of specific isotypes of gamma globulins are often helpful in the recognition of certain chronic liver diseases. Diffuse polyclonal increases in IgG levels are common in autoimmune hepatitis; increases greater than 100% should alert the clinician to this possibility. Increases in the IgM levels are common in primary biliary cirrhosis, while increases in the IgA levels occur in alcoholic liver disease.

         Coagulation Factors.  With the exception of factor VIII, the blood clotting factors are made exclusively in hepatocytes. Their serum half-lives are much shorter than albumin, ranging from 6 hours for factor VII to 5 days for fibrinogen. Because of their rapid turnover, measurement of the clotting factors is the single best acute measure of hepatic synthetic function and helpful in both the diagnosis and assessing the prognosis of acute parenchymal liver disease. Useful for this purpose is the serum prothrombin time, which collectively measures factors II, V, VII, and X. Biosynthesis of factors II, VII, IX, and X depends on vitamin K. The prothrombin time may be elevated in hepatitis and cirrhosis as well as in disorders that lead to vitamin K deficiency such as obstructive jaundice or fat malabsorption of any kind. Marked prolongation of the prothrombin time, >5 s above control and not corrected by parenteral vitamin K administration, is a poor prognostic sign in acute viral hepatitis and other acute and chronic liver diseases.

Microscopic examination of a stool.

 Microscopic examination of a stool specimen stained with Sudan is a simple screening test for steatorrhea. Chemical analysis of 3-day stool collection for fat, with the patient on a standard diet, is used to establish the diagnosis of steatorrhea. The D-xylose absorption test is about 90% accurate in distinguishing mucosal disease from pancreatic insufficiency. Leakage of protein into the intestinal lumen may cause hypoproteinemia and can be demonstrated by the recovery in stools of the serum protein a1-antitrypsin or intravenously administrated markers such as iodine- or chromium-labeled isotopes.

         Diarrhea as a symptom may be either a decrease in stool consistency, an increase in stool volume, an increase iumber of bowel movements, or any combination of these three changes. In contrast, diarrhea as a sign is a quantitative increase in stool water or weight of >200 to 225 mL, or g per 24 h, when a western-type diet is consumed. Individuals consuming a diet with a higher fiber content may normally have a stool weight of up to 400 g/24 h. Thus, it is essential that the clinician clarify what an individual patient means by diarrhea, especially since 10% of patients referred to gastroenterologists for further evaluation of unexplained diarrhea do not have an increase in stool water when it is determined quantitatively. Such patients may have small, frequent, somewhat loose bowel movements with stool urgency that is indicative of proctitis but do not have an increase in stool weight or volume.

         Measurement of stool electrolytes and osmolality requires the comparison of stool Na+ and K+ concentrations determined in liquid stool to the stool osmolality to determine the presence or absence of a so-called stool osmotic gap.

The cation concentrations are doubled to estimate stool anion concentrations. The presence of a significant osmotic gap suggests the presence in stool water of a substance(s) other than Na/K/anions that presumably is responsible for the patient’s diarrhea. Originally, stool osmolality was measured, but it is almost invariably greater than the required 290 to 300 mosmol/kg H2O, reflecting bacterial degradation of nonabsorbed carbohydrate either immediately before defecation or in the stool jar while awaiting chemical analysis, even when the stool is refrigerated. As a result, the stool osmolality should be assumed to be 300 mosmol/kg H2O. When the calculated difference is >50, an osmotic gap is present, suggesting that the diarrhea is due to a nonabsorbed dietary nutrient, e.g., a fatty acid and/or carbohydrate. When this difference is <25 to 50, it is presumed that a dietary nutrient is not responsible for the diarrhea. Since elements of both osmotic (i.e., malabsorption of a dietary nutrient) and secretory diarrhea may be present simultaneously, this separation at times is less clear-cut at the bedside than when used as a teaching example. Ideally, the presence of an osmotic gap will be associated with a marked decrease in stool output during a prolonged fast, while the absence of an osmotic gap will likely be present in an individual whose stool output had not been reduced substantially during a period of fasting.

         At times, however, a timed (72-h) quantitative stool collection, preferably on a defined diet, must be obtained to determine stool fat content and establish the presence of steatorrhea. The presence of steatorrhea then requires further assessment to establish the pathophysiologic process(es) responsible for the defect in dietary lipid digestion-absorption.

Diagnostic and management possibilities of endoscopy with biopsy in gastroenterology.

         Gastrointestinal endoscopy has been attempted for over 200 years, but the introduction of semi-rigid gastroscopes in the middle of the twentieth century marked the dawn of the modern endoscopic era. Since then, rapid advances in endoscopic technology have led to dramatic changes in the diagnosis and treatment of many digestive diseases. Innovative endoscopic devices and new endoscopic treatment modalities continue to expand the use of endoscopy in patient care.

Flexible endoscopes provide either an optical image (transmitted over fiberoptic bundles) or an electronic video image. Operator controls permit deflection of the endoscope tip; fiberoptic bundles bring light to the tip of the endoscope; and working channels allow washing, suctioning, and the passage of instruments. Progressive changes in the diameter and stiffness of endoscopes have improved the ease and patient tolerance of endoscopy.

         Upper Endoscopy. Upper endoscopy, also referred to as esophagogastroduodenoscopy (EGD), is performed by passing a flexible endoscope through the mouth into the esophagus, stomach, bulb, and second duodenum.

 

         The procedure is the best method of examining the upper gastrointestinal mucosa. While the upper gastrointestinal radiographic series has similar accuracy for diagnosis of duodenal ulcer, EGD is superior for detection of gastric ulcers and permits directed biopsy and endoscopic therapy, if needed. Topical pharyngeal anesthesia is used, and intravenous conscious sedation is given to most patients in the United States to ease the anxiety and discomfort of the procedure, although in many countries EGD is routinely performed without sedation. The recent development of ultrathin, 5-mm diameter endoscopes for transnasal, unsedated EGD may decrease the use of sedation for EGD in the United States, also decreasing the costs and risks of the procedure.

         Colonoscopy  Colonoscopy is performed by passing a flexible colonoscope through the anal canal into the rectum and colon. The cecum is reached in over 95% of cases, and the terminal ileum can often be examined. Colonoscopy is the “gold standard” for diagnosis of colonic mucosal disease. Barium enema is more accurate for evaluation of diverticula and for accurate measurement of colonic strictures, but colonoscopy has greater sensitivity for polyps and cancers. Colonoscopy is more uncomfortable than EGD for most patients, and conscious sedation is usually given before colonoscopy in the United States, although a willing patient and a skilled examiner can complete the procedure without sedation in many cases.

 

            Flexible Sigmoidoscopy  Flexible sigmoidoscopy is similar to colonoscopy but visualizes only the rectum and a variable portion of the left colon, typically to 60 cm from the anal verge. This procedure causes abdominal cramping, but it is brief and is almost always performed without sedation. Flexible sigmoidoscopy is primarily used to screen asymptomatic, average-risk patients for colonic polyps and may also be used for evaluation of diarrhea and hematochezia.

Enteroscopy  Enteroscopy is the relatively new field of small-bowel endoscopy. Two techniques are currently used. “Push” enteroscopy is performed with a long endoscope similar in design to an upper endoscope. The enteroscope is pushed down the small bowel with the help of a stiffening overtube that extends from the mouth to the duodenum. The mid-jejunum can often be reached; an instrument channel is present for biopsies or endoscopic therapy. “Sonde” enteroscopy uses a very thin, long, flexible endoscope with a weighted tip and no biopsy capability. The sonde enteroscope is passed through the nose, dragged to the duodenum by a standard endoscope, then slowly propelled forward by intestinal peristalsis for several hours. The cecum or distal ileum is reached in most cases. The small-bowel mucosa is examined during sonde enteroscope withdrawal, although parts of the mucosa may be missed when the endoscope is pulled back around turns. The major indication for these procedures is unexplained small-bowel bleeding.

         Endoscopic Retrograde Cholangiopancreatography (ERCP)  During ERCP, a side-viewing endoscope is passed through the mouth to the duodenum, the ampulla of Vater is identified and cannulated with a thin plastic catheter, and radiographic contrast material is injected into the bile duct and pancreatic duct under fluoroscopic guidance. When indicated, the sphincter of Oddi can be opened using the technique of endoscopic sphincterotomy. Stones can be retrieved from the ducts, and strictures of the ducts can be biopsied, dilated, and stented. ERCP is often performed for therapy but remains an important diagnostic tool, especially for bile duct stones. Endoscopic retrograde cholangiopancreatography (ERCP) is an imaging technique used to diagnose diseases of the pancreas, liver, gallbladder, and bile ducts. It combines endoscopy and x-ray imaging.

Choledocholithiasis

 

         Fluoroscopic image of multiple common bile duct stones seen at the time of ERCP and duodenoscope assisted cholangiopancreatography (DACP). The stone was impacted in the distal common bile duct and was crushed with intracorporeal lithotripsy.

            ERCP is used in the management of diseases that affect the gastrointestinal tract, specifically the pancreas, liver, gall bladder, and bile ducts. The pancreas is an organ that secretes pancreatic juice into the upper part of the intestine. Pancreatic juice is composed of specialized proteins that help to digest fats, proteins, and carbohydrates. Bile is a substance that helps to digest fats; it is produced by the liver, secreted through the bile ducts, and stored in the gallbladder. Bile is released into the small intestine after a person has eaten a meal containing fat.

         A doctor may recommend ERCP if a patient is experiencing abdominal pain of unknown origin, weight loss, or jaundice. These may be symptoms of biliary disease. For instance, gallstones that form in the gallbladder or bile ducts may become stuck there, causing cramping or dull pain in the upper right area of the abdomen, fever, and/or jaundice. Other causes of biliary obstruction include tumors, injury from gallbladder surgery, or inflammation. The bile ducts may also become narrowed (called a biliary stricture) as a result of cancer, blunt trauma to the abdomen, pancreatitis (inflammation of the pancreas), or primary biliary cirrhosis (PBC). PBC may be caused by a condition called primary sclerosing cholangitis, an inflammation of the bile ducts that may cause pain, jaundice, itching, or other symptoms. These symptoms may also be experienced by a patient with cholangitis, or with infection of the bile ducts caused by bacteria or parasites.

 

         In endoscopic retrograde cholangiopancreatography, an endoscope is introduced into the patient’s mouth and fed through the esophagus, stomach, and duodenum (small intestine) (A). A dye is released into the ducts (B). A series of x rays is taken, and a tumor may be visible with the endoscope (C). (Illustration by GGS Inc.)

         Endoscopic Ultrasound (EUS)  EUS utilizes high-frequency ultrasound transducers incorporated into the tip of a flexible endoscope. Ultrasound images are obtained of the gut wall and adjacent organs, vessels, and lymph nodes. By sacrificing depth of ultrasound penetration and bringing the ultrasound transducer close to the area of interest via endoscopy, very high resolution images are obtained. EUS provides the most accurate preoperative local staging of esophageal, pancreatic, and rectal malignancies, although it does not detect most distant metastases. EUS is also highly sensitive for diagnosis of bile duct stones, gallbladder disease, submucosal gastrointestinal lesions, and chronic pancreatitis. Fine-needle aspiration of masses and lymph nodes in the posterior mediastinum, abdomen, and pelvis can be performed under EUS guidance.

 

         Oral, intravenous and percutaneous transhepatic  cholecystocholangiography.

Oral cholecystography (OCG) is a useful procedure for the diagnosis of gallstones but has been largely replaced by ultrasound. However, OCG is still useful for the selection of patients for nonsurgical therapy of gallstone disease such as lithotripsy or bile acid dissolution therapy. In both these settings, OCG is used to assess the patency of the cystic duct and gallbladder emptying function. Further, OCG can also delineate the size and number of gallstones and determine whether they are calcified.

Combined Biliary-Duct Obstruction and Pancreatic-Duct Obstruction Due to a Small Mass in the Pancreatic Head. 

Cholangiographic Images in a Patient with Both Choledocholithiasis and an Ampullary Tumor.

Comparing characteristic of ultrasonography, computed tomography, magnetic resonance imaging in the diagnosis of the diseases of the alimentary tract, liver, biliary system and pancres.

Ultrasonography of the gallbladder is very accurate in the identification of cholelithiasis and has several advantages over oral cholecystography. The gallbladder is easily visualized with the technique, and in fact, failure to image the gallbladder successfully in a fasting patient correlates well with the presence of underlying gallbladder disease. Stones as small as 2 mm in diameter may be confidently identified provided that firm criteria are used [e.g., acoustic “shadowing” of opacities that are within the gallbladder lumen and that change with the patient’s position (by gravity)]. In major medical centers, the false-negative and false-positive rates for ultrasound in gallstone patients are about 2 to 4%. Biliary sludge is material of low echogenic activity that typically forms a layer in the most dependent position of the gallbladder. This layer shifts with postural changes but fails to produce acoustic shadowing; these two characteristics distinguish sludges from gallstones. Ultrasound can also be used to assess the emptying function of the gallbladder.

 

         Ultrasonography can provide important information in patients with acute pancreatitis, chronic pancreatitis, pancreatic calcification, pseudocyst, and pancreatic carcinoma. Echographic appearances can indicate the presence of edema, inflammation, and calcification (not obvious on plain films of the abdomen), as well as pseudocysts, mass lesions, and gallstones. In acute pancreatitis, the pancreas is characteristically enlarged. In pancreatic pseudocyst, the usual appearance is that of an echo-free, smooth, round fluid collection. Pancreatic carcinoma distorts the usual landmarks, and mass lesions greater than 3.0 cm are usually detected as localized, echo-free solid lesions. Ultrasound is often the initial investigation for most patients with suspected pancreatic disease. However, obesity, excess small- and large-bowel gas, and recently performed barium contrast examinations can interfere with ultrasound studies.

         CT is the best imaging study for initial evaluation of a suspected chronic pancreatic disorder and for the complications of acute and chronic pancreatitis. It is especially useful in the detection of pancreatic tumors, fluid-containing lesions such as pseudocysts and abscesses, and calcium deposits. Most lesions are characterized by (1) enlargement of the pancreatic outline, (2) distortion of the pancreatic contour, and/or (3) a fluid filling that has a different attenuation coefficient thaormal pancreas. However, it is occasionally difficult to distinguish between inflammatory and neoplastic lesions. Oral water-soluble contrast agents may be used to opacify the stomach and duodenum during CT scans; this strategy permits more precise delineation of various organs as well as mass lesions. Dynamic CT (using rapid intravenous administration of contrast) is useful in estimating the degree of pancreatic necrosis and in predicting morbidity and mortality. Spiral (helical) CT provides clear images much more rapidly and essentially negates artifact caused by patient movement.

         Endoscopic ultrasonography (EUS) produces high-resolution images of the pancreatic parenchyma and pancreatic duct with a transducer fixed to an endoscope that can be directed onto the surface of the pancreas through the stomach or duodenum. Although criteria for abnormalities on EUS in severe pancreatic disease have been developed, the true sensitivity and specificity of this procedure has yet to be determined. In particular, it is not clear whether EUS can detect early pancreatic disease before abnormalities appear on more conventional radiograph tests such as ultrasonography or CT. The exact role of EUS versus ERCP and CT has yet to be defined.

         Magnetic resonance cholangiopancreatography (MRCP) is now being used to view both the bile duct and the pancreatic duct. Nonbreath-hold and 3D turbo spin-echo techniques are being utilized to produce superb MRCP images. The main pancreatic duct and common bile duct can be seen well, but there is still a question as to whether changes can be detected consistently in the secondary ducts. MRCP may be particularly useful to evaluate the pancreatic duct in high-risk patients such as the elderly because this is a noninvasive procedure.

Normal Results of Magnetic Resonance Cholangiopancreatography in a Patient after Cholecystectomy.

 

Normal MRCP image showing the common bile duct (curved arrow) and the pancreatic duct (arrow). Note the fluid filled duodenum.

 

         Both EUS and MRCP may replace ERCP in some patients. As these techniques become more refined, they may well be the diagnostic tests of choice to evaluate the pancreatic duct. ERCP is still needed to perform therapy of bile duct and pancreatic duct lesions.

         Selective catheterization of the celiac and superior mesenteric arteries combined with superselective catheterization of others arteries, such as the hepatic, splenic, and gastroduodenal arteries permits visualization of the pancreas and detection of pancreatic neoplasms and pseudocysts. Pancreatic neoplasms can be identified by the sheathing of blood vessels by a mass lesion. Hormone-producing pancreatic tumors are especially likely to exhibit increased vascularity and tumor staining. Angiographic abnormalities are noted in many patients with pancreatic carcinoma but are uncommon in patients without pancreatic disease. Angiography complements ultrasonography and ERCP in the study of patients with a suspected pancreatic lesion and may be carried out if ERCP is either unsuccessful or nondiagnostic.

         ERCP may provide useful information on the status of the pancreatic ductal system and thus aid in the differential diagnosis of pancreatic disease. Pancreatic carcinoma is characterized by stenosis or obstruction of either the pancreatic duct or the common bile duct; both ductal systems are often abnormal. In chronic pancreatitis, ERCP abnormalities include (1) luminal narrowing, (2) irregularities in the ductal system with stenosis, dilation, sacculation, and ectasia, and (3) blockage of the pancreatic duct by calcium deposits. The presence of ductal stenosis and irregularity can make it difficult to distinguish chronic pancreatitis from carcinoma. It is important to be aware that ERCP changes interpreted as indicating chronic pancreatitis actually may be due to the effects of aging on the pancreatic duct or to the fact that the procedure was performed within several weeks of an attack of acute pancreatitis. Although aging may cause impressive ductal alterations, it does not affect the results of pancreatic function tests (i.e., the secretin test). Elevated serum and/or urine amylase levels after ERCP have been reported in 25 to 75% of patients, but clinical pancreatitis is uncommon. In a series of 300 patients, pancreatitis occurred in only 5 patients after ERCP. If no lesion is found in the biliary and/or pancreatic ducts in a patient with repeated attacks of acute pancreatitis, manometric studies of the sphincter of Oddi may be indicated. Such studies, however, do increase the risk of post-ERCP/manometry acute pancreatitis. Such pancreatitis appears to be more common in patients with a nondilated pancreatic duct.

         Although one or more radiologic abnormalities are found in over 50% of patients, the findings are inconstant and nonspecific. The chief value of conventional x-rays [chest films; kidney, ureter, and bladder (KUB) studies] in acute pancreatitis is to help exclude other diagnoses, especially a perforated viscus. Upper gastrointestinal tract x-rays have been superseded by ultrasonography and computed tomography (CT). A CT scan may confirm the clinical impression of acute pancreatitis even in the face of normal serum amylase levels. Importantly, CT is quite helpful in indicating the severity of acute pancreatitis and the risk of morbidity and mortality. Sonography and radionuclide scanning [N-p-isopropylacetanilide-iminodiacetic acid (PIPIDA) scan; hepatic 2,6-dimethyliminodiacetic acid (HIDA) scan] are useful in acute pancreatitis to evaluate the gallbladder and biliary tree.