Physioligico Anatomical features of the digestive system in children. Semiotics of digestive disoders. Acute appendicitis. Care of child
Embryogenesis
The digestive system develops from endoderm at 11-15 days since fertilization. Liver and pancreas appear as buds at 26-30 days since fertilization.
Physioligicoanatomical peculiarities of the digestive system
The main functions of the digestive system
1. To process and absorb nutrients.
2. The excretory function.
3. Detoxification.
4. Maintain fluid and electrolyte balance.
5. The mechanical function.
Morphology peculiarities of all parts of digestive system in infant
1. The mucous membrane is thin, soft, dry and easy to damage.
2. The submucosal layer is well vasculerised.
3. The submucosal layer consists of loose connective tissue.
4. Underdevelopment (immaturity) of muscular and elastic tissue.
Physiological peculiarities of digestive system in infant
1. The secretory function of digestive system is impaired.
2. Digestive system produces only small amounts of digestive juice.
3. Digestion is worsen when the food does not adequate of age of child.
Peculiarities of oral cavity in infant
1. It is relatively small.
2. Teeth are absent.
3. The palate is flat.
4. The tongue is relatively thick and wide.
5. The sucking fat in the cheeks fill the mouth and help maintaiegative pressure.
Peculiarities of pharynx in infant
1. It is relatively wide and short.
2. The oral part is on the same level as oral cavity.
3. The way which the food passage is lateral of larynx.
4. The baby can‘t breath and swallow the food at once.
Peculiarities of the oesophagus in infant
1. Average length of the oesophagus in newborn is 10 cm.
2. It is relatively narrow.
3. The entrance into the oesophagus is:
iewborn – between the III-IV cervical vertebra;
2 years old – IV-V cervical vertebra;
12 years old – VI-VII cervical vertebra;
4. The localization of lower oesophagus’ sphincter is the same in children of different age groups (X-XI thoracic vertebra).
5. Ratio between the length of the oesophagus and the length of the body is the same in children of different age groups (1:5).
Length of the oesophagus in children of different age groups
iewborn is 11-16 cm.
in 1.5-2 years – 22-24.5 cm.
in 15-17 years – 48-50 cm.
The constriction of the oesophagus
Anatomical
1. Upper constriction – in place of entrance into the oesophagus.
2. Middle constriction – in place of adjacent the trachea to oesophagus.
3. Lower constriction – in place of entrance through the diaphragm.
Physiological
1. Upper constriction – at the begining of the esophagus
2. Middle constriction – in place of adjacent the aorta to esophagus
3. Lower constriction – in place of entrance into the cardial part of the stomach.
Peculiarities of the stomach in infant
1. The stomach lying horizontally, is round until approximately 2 year of age.
2. In horizontally lying of baby the gastric fundus is lower as the antral part of the stomach.
3. Gastroesophageal reflux is frequent.
4. Cardial sphincter has a poor development of mucous membrane and muscular tunic.
5. Pyloric part is developed well.
6. The fundus of stomach is under the left dome of diaphragm.
7. The weight of the stomach is 6-7 g in newborn, in 1 year old 18-21 g.
The anatomical capacity of the stomach, cm3
Newborn – 30-35.
4 days – 45.
14 days – 90.
Iext months the anatomical capacity of the stomach increase for 25 cm3.
2 years – 500.
4 years – 700.
8 years – 1000.
An adult- 1200-160.
The physiological capacity of the stomach, cm3
Newborn – 7.
1 year – 250-350.
3 years – 400-600.
10 years – 1300-1500.
Peculiarities of the stomach in infant
1. The proteolytic function of the stomach juice in baby is 1/3 less than in adult.
2. Figures of common gastric acidity is in 2.5-3 times lower than in adult.
3. The fats of human’s milk is easy digestion by enzyme lipase of human’s milk, saliva and stomach juice.
4. Highly saturated fats is digestion only in a small intestine.
Peculiarities of the bowels in infant
1. The length is relatively longer then in adult.
2. Ratio of bowels length and body length are:
iewborn – 8.3:1;
1 year – 6.6:1;
16 years – 7.6 1;
an adult – 5.4:1.
3. The increasing of bowels length is slower than the increasing of length of the body.
4. The bowels are more mobile in infant.
Peculiarities of the small intestine in infant
1. The length is in two times less than in adult.
2. The length of small intestine mesentery is relatively longer.
3. The membrane is thin, is well vascularisied.
4. The intestinal glands are bigger then in adult.
5. The lymph cells are in each little parts of small intestine.
Peculiarities of the large intestine in infant
1. The large intestine is not completely developed.
2. The length of the large intestine is the same as the body length (in any age of a child).
3. Haustrumes appear after 6 month of life.
Peculiarities of the sigmoid colon in infant
1. It is longer.
2. It is mobile.
3. Increasing in size during the life.
4. The localization of sigmoid colon is something upper in children younger 5 years then in schoolchildren (in schoolchildren it is in the pelvic cavity).
Peculiarities of the rectum in infant
1. The localization is under the entrance into the small pelvis in preschoolchildren.
2. In schoolchildren the rectum is in the small pelvis.
3. It is longer.
3. It is mobile.
4. The ampulla of rectum is absent iewborn.
Peculiarities of the liver in infant
1. Before the birth the liver is the largest organ of the body.
2. It is in the upper quadrant of the abdomen and one part of the left and epigastrium.
3. The left lobe is very large before the birth.
Liver functions
1. Bile salts emulsify fats making them aviable to intestinal lipases.
2. Help make and products soluble and aviable for absorption by the intestinal mucosa, aid peristalis, fluid on enzyme, bile, sodium glucoholate sodium taurocholate, cholesterol, biliverdin, mucus, fat, lecitin, cells and cell debris.
3. Detoxification.
4. Glucose exchanges.
Hepatocytes functions
1. Synthesis of bile.
2. Storage (glycogen, fat, vitamins, copper, iron).
3. Biotransformation.
4. Synthesis of blood components.
General overview
The digestive system consists of the digestive tract, a tube extending from the mouth to the anus, and its associated accessory organs (primary glands), which secrete fluids into the digestive tract. The digestive tract is also called the alimentary canal. The term gastrointestinal tract technically only refers to the stomach and intestines.
The first section of the digestive tract is the mouth, or oral cavity. It is surrounded by the lips, cheeks, teeth,and palate, and it contains to the tongue.
The salivary glands and tonsils are accessory organs of the oral cavity. The oral cavity opens posteriorly into the pharynx, which in turn,continues inferiorly into the esophagus. The major accessory structures are single-celled or small, simple tubular mucous glands distributed the length of the pharynx and the esophagus. The esophagus opens inferiorly into the stomach. The stomach wall contains many tubelike glands from which acid and enzymes are released into the stomach and are mixed with ingested food. The stomach opens inferiorly into the small intestine. The first segment of the small intestine is the duodenum. The major accessory structures in the segment of the digestive tract are the liver,the gallbladder.and the pancreas. The next segment of the small intestine is the jejunum. Small glands exist along its length and it is the major site of absorption. The last segment of the small intestine is the ileum, which is similar to the jejunum except that fewer digestive enzymes and more mucus are secreted and less absorption occurs in the ileum. The last section of the digestive tract is the large intestine. Its major accessory glands secrete mucus. Its absorb water and salts and concentrates undigested food into feces. The first segment is the cecum, with the attached veriform appendix. The cecum is followed by the ascending, transverse, descending, and sigmoid colons and the rectum. The rectum joints the anal canal, which ends at the anus, the inferior termination of the digestive tract.
Disorders
Control signs:
1. Painful syndrome. Pain intensive, paroxysmal, after the meal, more often at night and on empty stomach. The pain is localized in epigastrium, umbilicus, right subcostal area, sometimes irradiates to waist or has spread character. Tenderness on palpation in pyloroduodenal area, muscular defence, and hyperesthesia of skin in tender zones (Zakhariev-Ged), positive sign of Mendel.
2. Dyspeptic syndrome: vomiting, nausea, heartburn, vomiting frequently causes relief, removing pain, decrease of appetite. Tendency to constipation (in patients with increased gastric acidity) or unstable stool (in patient with low gastric acidity).
3. Intoxication syndrome: weakness, lucidity, bad sleep, headaches, irritability, tearfulness, increased disposition to perspiration, blue shadows under the eyes.
Physical examination
Mouth and throat. The mouth is the beginning of the passageway to the digestive tract, but it also functions in the entry or exit of air. 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 mouth and throat are divided into three areas: (1) the oral cavity, which extends from the lips to the palatopharyngeal arches, (2) the oropharynx, which extends from the epiglottis to the lower edge of the adenoids, and (3) the nasopharynx, which extends from above the lower edge of the adenoids to the nasal cavity. The major structures that are visible on examination within the oral cavity and oropharynx are the mucosal lining of the lips and cheeks, gums or gingiva, teeth, tongue, palate, uvula, tonsils, and posterior oropharynx. Other pharyngeal structures that are not visible on examination are the epiglottis, lingual tonsils, and pharyngeal tonsils or adenoids.
With a cooperative child almost the entire examination can be done without the use of a tongue blade. The doctor asks the child 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 nurse can ask the child to use his fingers to move the outer lip and cheek to one side. Performing the examination in front of a mirror is a great aid in enlisting children’s cooperation. Another approach is using a puppet and letting the child examine its wide-open mouth.
Infants and toddlers, however, usually resist attempts to keep the mouth open. Because it is an upsetting part of the examination, it is reserved until last (with examination of the ears) or performed during episodes of crying. However, the use of a tongue blade to depress the tongue is necessary. The tongue blade is placed along the side of the tongue, not the center back area where the gag reflex is elicited. If the child resists in opening his mouth, pinching the nostrils closed forces the child to breathe by mouth and, therefore, open the mouth.
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. Koplik’s spots, indicative of measles during the prodromal stage, appear as grayish areas surrounded with a red, irregular areola. They first appear on the buccal mucosa opposite the lower molars. White curdy plaques or patches anywhere on the oral mucosa, but particularly on the surface of the tongue and hard palate, that bleed when scraped are signs of moniliasis or thrush.
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 nurse 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. The general rule for estimating the number of temporary teeth in children who are 2 years of age or younger is: the child’s age in months minus 6 months equals the number of teeth. 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. 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. Although parents frequently express concern regarding thumb-sucking and the development of orthodontic problems, thumb-sucking that ceases before the age of 6 years probably does little harm.
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 children 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.
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 child 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.
Examination of abdomen. Examination of the abdomen involves the usual four skills, except that the order is significantly changed. Inspection is followed by auscultation, percussion, and then palpation, which may distort the normal abdominal sounds. The nurse must have knowledge of the anatomic placement of the abdominal organs in order to differentiate normal, expected findings from abnormal ones.
The sequence of examining the abdomen changes according to the age and cooperativeness of the child. Frequently all four types of assessment are performed at different times. For example, the nurse may auscultate for bowel sounds following evaluation of heart and lung sounds at the beginning of the examination when the child is quiet. Inspection may occur at any time during the examination. Percussion usually follows lung percussion, and palpation may be done toward the end of the examination when the child is relaxed and more trusting of the nurse.
The abdominal cavity is the portion of the trunk from directly beneath the diaphragm and thoracic cavity to the region of the pelvic cavity. For descriptive purposes the abdominal cavity is divided into four quadrants by drawing a vertical line midway from the sternum to the pubic symphysis and a horizontal line across the abdomen through the umbilicus. This method of division actually includes the pelvic cavity. Each section is designated as follows: Right upper quadrant (RUQ) Right lower quadrant (RLQ) Left upper quadrant (LUQ) Left lower quadrant (LLQ)The abdominal cavity contains the major organs of digestion, and the pelvic cavity houses the internal reproductive organs, the lower parts of the digestive tract, and the urinary bladder. However, in infancy the bladder is an abdominal organ.
Inspection. The contour of the abdomen is inspected while the child is erect and supine. Normally the abdomen of infants and young children is quite cylindric and, in the erect position, fairly prominent because of the physiologic lordosis of the spine. In the supine position the abdomen appears flat. During adolescence the usual male and female contours of the pelvic cavity change the shape of the abdomen to form characteristic adult 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 children, whereas a concave abdomen is frequently suggestive of undernutrition. 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. In a healthy child a midline protrusion is usually a variation of normal muscular development. A tense, boardlike abdomen is a serious sign of paralytic ileus and intestinal obstruction.
The nurse 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. In infants and thin children peristaltic waves may be visible through the abdominal wall, and they always warrant careful evaluation. They are best observed by standing at eye level to and across from the abdomen. 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 children, the nurse should auscultate and palpate the aorta for any evidence of an aneurysm, a saclike enlargement of the vessel.
In children under 7 or 8 years of age, breathing is primarily abdominal. If the abdomen fails to move with respiration, even in older children, this may indicate serious abdominal problems. Conversely, if the thoracic muscles fail to move, so that breathing is confined to abdominal movement, pulmonary problems may be at fault. Normally chest and abdominal movements are synchronous.
The umbilicus is inspected for hemiation, fistulas, such as a patent urachus (an abnormal connection between the umbilicus and bladder), discharge, and hygiene. If a hemiation is present the sac is palpated for abdominal contents and the approximate size of the opening is estimated. Umbilical hernias are common in infants, especially in black children. Since “home remedies” for treatment such as taping coins over the umbilicus or using “belly binders” may be harmful to the skin and actually delay natural closure, a doctor should ask parents whether such procedures have been used. Umbilical hernias normally protrude and expand when the child coughs, cries, or strains.
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, which occurs more frequently in girls, 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 child’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.
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.
Palpation. Two types of palpation are performed, superficial and deep. In superficial palpation a doctor lightly places the hand against the skin and feels each quadrant, noting any areas of tenderness, muscle tone, and superficial lesions, such as cysts. Superficial palpation is often perceived as “tickling” by the child, which can interfere with its effectiveness. The nurse can avoid this problem by having the child “help” with the palpation by placing his hand over the doctor’s palpating hand or by distracting him with statements such as, “I am trying to feel what you had for lunch”. Admonishing the child to stop laughing only draws attention to the sensation and decreases cooperation. Positioning the child supine with the legs flexed at the hips and knees helps relax the abdominal muscles.
Tenderness anywhere in the abdomen during superficial palpation is always noted. There are two types of abdominal pain: (1) visceral, which arises from the viscera or internal organs such as the intestines, and (2) somatic, which arises from the walls or linings of the abdominal cavity such as the peritoneum. Visceral pain is usually dull, poorly localized, and difficult for the patient to describe. Somatic pain is generally sharp, well localized, and more easily described. When assessing abdominal pain, it is important to remember that the child will often respond with an “all-or-none” reaction – either there is no pain or great pain. Therefore all aspects of the examination must be carefully considered when ruling out conditions such as appendicitis.
A special phenomenon called rebound tenderness, or Blumberg’s sign, may be performed if the child complains of abdominal pain. It is produced by pressing firmly over part of the abdomen distal to the area of tenderness. When the pressure is suddenly released, the child feels pain in the original area of tenderness. This response is only found when the peritoneum overlying a diseased viscus or organ is inflamed, such as in appendicitis.
Deep palpation is used for palpating organs and large blood vessels and for detecting masses and tenderness that were not discovered during superficial palpation. If the child complains of abdominal pain, that area of the abdomen is palpated last. Normally palpation of the midepigastrium causes pain as pressure is exerted over the aorta, but this should not be confused with visceral or somatic tenderness.
The doctor palpates the abdominal organs by pressing them against the free hand, which is placed on the child’s back. Palpation begins in the lower quadrants and proceeds upward. In this way the edge of an enlarged liver or spleen is not missed. Except for palpating the liver, successful identification of other organs, such as the spleen, kidney, and part of the colon, requires considerable practice with tutored supervision.
The lower edge of the liver is sometimes palpable in infants and young children as a superficial mass 1 to 2 cm (1/2 to 3/4 inch) below the right costal margin (the distance is sometimes measured in fingerbreadths). If the liver is palpable 3 cm (l1/4 inches) or 2 fingerbreadths below the costal margin, it is considered enlarged and this finding is referred to a physician. Normally the liver descends during inspiration as the diaphragm moves downward. This downward displacement should not be mistaken for a sign of hepatomegaly. In older children the liver frequently is not palpable, although its lower edge can be estimated by percussing dullness at the costal margin.
The spleen is palpated by feeling it between the hand placed against the back and the one palpating the left upper quadrant. The spleen is much smaller than the liver and positioned behind the fundus of the stomach. The tip of the spleen is normally felt during inspiration as it descends within the abdominal cavity. It is sometimes palpable 1 to 2 cm below the left costal margin in infants and young children. A spleen that is readily palpated more than 2 cm below the right costal margin is enlarged and is always reported for further medical investigation.
Other anatomic structures that are sometimes palpable in children include the cecum, and sigmoid colon. The cecum is a soft, gas-filled mass in the right lower quadrant. The sigmoid colon is felt as a sausage-shaped mass that is freely movable over the pelvic brim in the left lower quadrant and is normally tender.
Although most of these structures are not routinely felt, one should be aware of their relative location and characteristics in order not to mistake them for abnormal masses. The most common palpable mass in children is feces. It may be associated with pain in the right lower quadrant because with constipation the left colon fills with stool and gas until the ileocecal valve is reached. Then the cecum becomes distended, causing pain, which may be erroneously associated with appendicitis.
Pylorostenosis
Pylorostenosis is a disease of infants of the first month of life due to a narrowing of the pyloric canal’s aperture because of muscular hypertrophy of the pylorus.
Clinical manifestation
– latent period,
– regurgitations up to abundant vomit without bile,
– dehydration,
– malnutrition,
– stomach peristalsis in a form of sand –glass,
– constipation.
Methods of Examination
Inquiry
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 the 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 myospasmolytic(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 coloration 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. Many chronic diseases are attended by general weakness, non-motivated fatigue, and decreased work capacity.
History of the present disease. When collecting anamnesis, it is necessary to find out if the patient had in his past history jaundice or acute diseases of the liver or the gall bladder(Botkin’s disease, acute cholecystitis, cholangitis), attacks of hepatic colics, enlargement of the liver or the spleen, which might be an early symptom of the present disease (chronic hepatitis, liver cirrhosis, chronic cholecystitis, cholangitis, cholelithiasis).
Life history of patient. When inquiring the patient it is necessary to establish factors that might be important for the aetiology of the present disease of the liver or bile ducts: liking for fat and meat foods, exposure to chemical and vegetable poisons (alcohol, carbon tetrachloride, compounds of phosphorus,copper,lead,arsenic;dichloroethane,etc.),poisoning with mushrooms containing strong hepatotropic poisons (e.g. helvellic acid, amanitotoxin, etc.), some infectious diseases (Botkin’s disease, lambliosis, typhoid fever, malaria, syphilis, etc.), diseases of the gastro-intestinal tract (gastritis, colitis), and diabetes mellitus. Familial predisposition’is also important in the development of some liver diseases (e.g. congenital benign hyperbilirubinaemia) and diseases of the gall bladder (cholelithiasis).
Physical Examination
INSPECTION
The general condition of the patient is first assessed. In the presence of marked functional hepatic insufficiency of various aetiology (liver cirrhosis, cancer, prolonged obstructive jaundice, etc.), the patients’s condition can be grave because of pronounced poisoning (hepatic coma). The patient’s condition may be grave in acute inflammatory diseases of the liver (abscess), gall bladder (acute cholecystitis), or bile ducts (acute cholangitis). But in many chronic diseases of the liver and the bile ducts, the general condition of the patient may remain satisfactory for long periods of time. Patients with hepatic colics are restless, they toss in bed, try to find (without success) a position in which the pain might be relieved. A hepatic coma is characterized by deranged consciousness in the form of pronounced euphoria or inhibition to complete loss of consciousness.
The general appearance (habitus) of the patient usually does not change. At the same time, a hypersthenic constitution with predisposition to obesity is often characteristic of patients with cholelithiasis. Quite the reverse, significant wasting (to cachexia) occurs in cirrhosis or malignant tumour of the liver or the bile ducts. If the disease of the liver begins in childhood or adolescence, the patient may look infantile.
An important diagnostic sign is jaundice of varying intensity. In order to assess correctly the colour of the skin, the patient should be inspected in daylight or in the light of the luminescent lamp. A subicteric symptom is jaundice of the sclera, the lower surface of the tongue, and the soft palate; next coloured are the palms, soles, and finally the entire skin. Inspection of the sclera helps differentiate between true (bilirubinogenic) and exogenic jaundice. Prolonged use of quinacrine, ethacridine lactate (rivanol), carotin (carrots), excess tangerines and oranges, exposure to trinitrotoluene and picric acid can cause slight jaundice of the skin (false jaundice) but the sclera is not coloured in such cases. Hepatic jaundice is usually attended by itching and scratching of the skin.
Icteric skin can be of various hues. The skin is orange-yellow (rubinicterus) due to accumulation of bilirubin in the skin; it is usually characteristic of the early stages of the disease. Lemon-yellow colour of the skin (flavinicterus) is characteristic of haemolytic jaundice. Greenish-yellow colour (verdinicterus) is due to accumulation of biliverdin (the product of gradual oxidation of bilirubin); it is mostly due to obstructive jaundice. In long-standing mechanical jaundice the skin becomes dark bronzy (melasicterus).
In certain cases the skin becomes pallid due to anaemization (haemorrhage from varicose oesophageal or haemorrhoidal veins in portal cirrhosis); the skin may be greyish (“dirty”) in patients with some hepatic diseases. Greyish-brown or brown skin is characteristic of haemochromatosis (bronzed diabetes or pigmentary cirrhosis of the liver), the disease associated with primary or secondary excessive absorption of iron in the intestine and accumulation of haemosiderin in various organs and tissues (in the first instance in the liver and the pancreas). Local hyperpigmentation of the skin in the right hypochondrium can be due to frequent application of a hot-water bottle, which indicates persistent pain in this region (in chronic diseases of the gall bladder).
Inspection of the skin (especially in obstructive and less frequently in parenchymatous jaundice) can reveal scratches due to severe itching. The scratches are often infected and purulent. Jaundice of this type can be attended by haemorrhagic diathesis—petechial eruption and haemorrhage into the skin (ecchymosis).
In patients with cirrhosis of the liver associated with disordered cholesterol metabolism, cholesterol is deposited intracutaneously in the form of yellow plaques (xanthomatosis) which are often located on the eyelids (xanthelasma) and less frequently on the hands, elbows and soles (xanthomas). Xanthomatosis occurs also in other diseases attended by cholesterol metabolic defect (atherosclerosis, diabetes mellitus, essential hyperlipaemia, etc.).
An important symptom for diagnosis of chronic diseases of the liver are spider angiomata . These are slightly elevated pulsating angiomata with fine vessels radiating from the centre. Their size varies from that of a pin head to 0.5-1 cm in diameter. The angiomata are often found on the neck, face, shoulders, hands, and the back; less frequently they are practically absent from the lower part of the body. The spider angiomata may disappear with improvement of the liver function. In addition to these angiomata, patients with chronic diseases of the liver may have specifically coloured palms and soles—liver palms; symmetrical reddening is especially characteristic in the thenar and hypothenar region. When pressed, the reddened site becomes pale but when the pressure is removed, the redness is quickly restored. The mechanism of development of the spider angiomata and liver palms is believed to be connected with the grave hepatic dysfunction of the liver during which oestrogens are destroyed incompletely and therefore act as a vasodilatory agent on the skin vessels.
Excess oestrogens in the blood are also associated with other symptoms that may be revealed on inspection. Patients with chronic diseases of the liver have a glassy crimson tongue (raspberry tongue). Uni- or bilateral enlargement of the mammary glands often occurs in men (gynaecomastia) along with defective growth of hair on the chin, chest, and the abdomen. Hair growth is decreased in the armpits and on the pubis in women. When the, hepatic condition improves, the hair growth is restored. Drum (Hippocratic) fingers, sometimes with white nails, occur in patients with chronic diseases of the liver. It is believed to depend on excess oestrogens and serotonin in the blood.
A greenish-brown Kayser-Fleischer ring round the outer edge of the cornea is characteristic of the Konovalov-Wilson disease (congenital disease characterized by decreased synthesis in the liver of ceruloplasmin, the copper transport protein, and its increased deposition in tissues).
Inspection of the mouth can reveal angular stomatitis (inflammation of the mucosa and skin in the mouth angles) characteristic of group B hypovitaminosis occurring amongst patients with chronic liver diseases. Inspection of the abdomen should be done with the patient in erect or lying position. Important diagnostic symptoms can often be found during inspection of the abdomen. The abdomen can be enlarged significantly due to accumulation of free fluid (ascites). This occurs in liver cirrhosis concurrent with portal hypertension. The abdomen may be enlarged due to pronounced hepato- or splenomegaly. When the patient with ascites stands erect, his abdomen becomes pendulous due to the downward flow of fluid ; in the lying position the abdomen is flattened (“frog belly”). The navel often becomes protruded in ascites when the patient stands erect. It is due to increased intra-abdominal pressure. This sign can be used to differentiate between enlargement of the abdomen in ascites (also large intra-abdominal tumours) and pronounced obesity (the navel is retracted).
Inspection of the abdomen can reveal another important symptom of portal hypertension, the presence of dilated venous network on the anterior abdominal wall. This network is formed by anastomoses of the portal and both vena cava systems. The superior vena cava and portal vein are anastomosed above the navel, while the portal and inferior vena cava are anastomosed below the navel; cavocaval anastomoses are located on the sides of the abdomen. Anastomoses may develop in obstructed blood flow in the inferior vena cava (thrombosis, compression, etc.). Dilated, swollen and twisted venous collaterals, found round the navel and radiating from it, form the so-called Medusa head. These symptoms are characteristic of the portal hypertension syndrome occurring in cirrhosis of the liver, thrombosis and compression of the portal vein. Establishing the direction of the blood flow in the collaterals helps determine the type of anastomosis and hence locate the vessel where the blood flow is obstructed in the system of the portal vein or the inferior vena cava. To that end a small area of the dilated venous branch is pressed between two fingers (with an attempt to empty this area from the blood). In a short lapse of time the pressure of the upper finger is released. If blood fills the vessel to the level of the other finger, the blood flows from the portal vein system to the inferior vena cava (i.e. in the downward direction). If the vessel remains empty, the blood flows upwards, i.e. from the vena cava inferior-system to the superior vena cava.
In patients with cachexia and pronounced enlargement of the liver, the right hypochondrium and epigastrium are protruded. If the abdominal wall is thin, the protruded surface is uneven and tuberous (in tumours or cysts of the liver). Only significantly enlarged gall bladder can be responsible for protrusion of the abdomen, especially in cachectic patients (in hydrops of the gall bladder, cancer of the common bile duct, or cancer of the pancreas head which compresses the common bile duct). The left hypochondrium is protruded in cases with considerably enlarged spleen attending cirrhosis of the liver (hepatolienal syndrome).
PERCUSSION
Percussion is used to determine the borders, size and configuration of the liver. The superior and inferior borders of the liver are outlined. Two superior borders of liver dullness are distinguished: relative dullness, which is the true upper border of the liver, and the absolute dullness, i.e. the upper border of that part of the anterior surface of the liver “which is directly adjacent to the chest and is not covered by the lungs. Practically, absolute dullness is only determined because the position of the superior border varies depending on the size and configuration of the chest, the height of the right diaphragm cupola, and also because the upper edge of the liver is deeply hidden behind the lungs. Finally, the liver usually becomes enlarged in the downward direction. This is determined by the position of its inferior edge.
Percussion of the liver is carried out with observation of the general rules of topographic percussion. Light percussion is used to determine the absolute liver dullness. The direction of percussion is from top to bottom, along the vertical lines, like in determining the borders of the right lung. The border is detected by contrast between the clear pulmonary resonance and liver dullness. The found border is marked on the skin by dots, by the upper edge of the pleximeter-finger, in each vertical line. Normally the superior border of absolute liver dullness is found in the right parasternal line at the superior edge of the 6th rib, in the right midclavicular line at the 6th rib, and in the right anterior axillary line at the 7th rib. In other words, the border of absolute dullness corresponds to the position of the lower edge of the right lung. The upper border of the liver can likewise be determined posteriorly, but normally the determination ends by percussion in the three mentioned lines.
Determination of the lower absolute dullness is difficult because of the presence of hollow organs in the vicinity of the liver. The stomach and the intestine give high tympany that masks the liver dullness. The lightest percussion should therefore be used. Direct percussion by one finger according to Obraztsov should better be used instead.
Determination of the lower border of absolute dullness (according to Obraztsov and Strazhesko) should be begun from the right part of the abdoimen along the right anterior axillary line with the patient in the horizontal position.
PALPATION
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.
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. The 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.
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 patient 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 by 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 onto the liver capsule; the liver is also tender when it is distended (e.g. in 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 of newgrowths in its wall, in overfilling with stones, in inflammation of the wall, etc.). An enlarged gall bladder is mobile during respiration (it performs lateral pendulum-like movements). The gall bladder loses its mobility in inflammation of the overlying peritoneum (pericholecystitis). In the presence of cholecystitis and cholelithiasis, the palpation is difficult because of sharp pain and reflectory rigidity of the muscles of the anterior abdominal wall.
Inquiry and survey of the patients with diseases of digestion system. A percussion of a stomach. Methods of definition of ascetics. A palpation of a stomach (surface rough and methodical penetrating, slipping after V. P. Obrazsov and N. D. Strazhesko).
The examination of the patient suffering by any disease of a gastrointestinal path begins, as it is usual, from inquiry.
At a history taking it is necessary to adhere to the plan and to begin from a passport part. Some of sectional of a passport part can have diagnostic value. For example, the diagnostic value of age of the patient consists that some illnesses (malignant tumors) more often are observed in elderly age. Series of illnesses more frequently meet at the persons of a particular sex (Bile stone illness is observed more often at the women and peptic ulcer at the men).
At collection of the basic complaints of the patient presence from the presence from presence from I pretences from detailed elaboration of the complaint, namely: localization of a pain, character, irradiation duration, time of their occurrence, communication (connection) with reception of nutrition, character of nutrition, communication (connection) with dyspeptically by the phenomena.
Visceral afferent nerves transmit the true visceral trans. abdominal pains. A visceral pain feature as blunt, stationary values on the character a pain with diffuse diffusion on a medial line of a stomach. The localization of feeling discomfort usually meets segmentation to a level innervation of the struck body.
The visceral pain at a digestive disturbance should be distinguished from an acute local pain arising at acute processes in abdominal cavity, affecting a peritoneum. Of stimulus to occurrence visceral be sick, coming from ïîëûõ of bodies, with a sleek musculation, in particular of stomach, are a spastic stricture, tension of a body, and also infringement of its motor function.
Localization of a pain
At disease of an esophagus or cardiac department of a stomach can arise chest pain, it is necessary for differentiating with diseases of heart (Pain arises, both at the act of a swallowing, and without it) and is a stationary value.
Pain in epigastria shine usually arises at defeats of a stomach, duodenum, bile duct, or pancreas. As the processes in colic trajectories or item (Ferri lactose become more intensive, the pain can be biased side ways and be localized in a typical place, for example pain caused by disease of colic trajectories – in the field of the right upper quadrate of a stomach and an apex of a scapula, and pain caused by disease of a pancreas, – in the left-hand upper quadrate of a stomach and in the left-hand part spins. The pain around of a belly button is usually bound (inter linked) to disease of a small bowel. The pain is lower than a belly button frequently is caused by appendicitis, diseases of a colon.
Whether it is important to establish is the pain of a stationary value (carcinoma of the stomach) it ceasing (acute gastric, colic).
Pain, which forces the patient to wake up from penetrating dream, more often it happens at an ulcer duodenum. At a reflex and esophagi’s the pain arises more often at the night in a position laying.
The important diagnostic attribute is the interrelation with reception of nutrition.
The occurrence soon after reception of nutrition speaks about disease of an esophagus, acute gastritis, carcinoma of the stomach. The occurrence of a pain in the remote terms from reception of nutrition can reflect inadequate empty of a stomach, at presence of an ulcer of a stomach effect of action of a hydrochloric acid on an ulcer). And on the contrary, disappearance of a pain after reception write or àíòàöèäíûõ of agents, is characteristic for an ulcer duodenum. At diseases of a stomach in a time dependence of occurrence be sick them part on early, incipient through 30-40 mines. After reception of nutrition, late, through 1 (2 -2 hours, night and hungry, which are abirritated after reception of nutrition.
Seasonal prevalence is sick, i.e. occurrence in the spring and autumn, is typical of a peptic ulcer, is especial at localization of process in îêîëî ïðèâðàòíèêîâîé of area.
To äèñïåïñè÷åñêèì to the complaints concern:
Appetite (is maintained, boosted, is dropped), the taste in a mouth (is not changed, poor taste), dryness in a mouth, off-flavor from a mouth, the thirst, heart burn, eructation (air, nutrition, rotten), nausea, vomiting connection with reception of nutrition, character of a vomiting), swallowing (free, labored, labored constantly or battle), feeling of gravity in the right hypochondria, sensation of completeness, levitation in an anticardium, inflation, gurgling, chair (frequency, flora, color, volume, impurities, smell).
Heart burn is a sensation of a burning sensation for thoracic or in top of epigastria area and èððàäèèðóþøåå in area of a neck. It is effect of infringement of a motor performance or tension of an esophagus, runaway of an acid or Bile in an esophagus (reflex) or borings of a mucous of an esophagus’s. At gastric-esophageal a reflex heart burn arises at a flexion of housing or laying on a spin. Can be accompanied by an acidic eructation, bitter eructation.
Aerophagia a meteorism ( )
Each act îòðûãèâàíèÿ precedes çàãëàòûâàíèå of air). Not îòðûãíóòàÿ the part gets in a stomach and in an intestine. Causing feeling of overflow. If air passes in an intestine causes an abdominal distention, or it appears in a splenic flexure of a colon (levitation in the left-hand quadrate of a stomach).
The meteorism – basic radiant production of intestinal gas is enzymatic activity of intestinal bacteria on carbohydrates and protein in a lumen of an intestine. Iorm they widespread in a thick intestine. The augmentation of an aerogenesis occurs after the use of particular foodstuff (leguminous, croup’s). The augmentation of an aerogenesis can occur and at infringement of an adsorption of carbohydrates at a deficit of an enzyme of lactose. Diaries, meteorism can arise at pathological development of bacteria in a thin intestine.
Anorexia
The loss of desire is. Can precede occurrence of an icterus at hepatitis, sign of a carcinoma of the stomach. At âíåêèàåèíûõ disease meets at a serious heart failure, pulmonary failure, uremia’s, psychogenic infringements. The distortion of appetite is sometimes scored which is expressed in predilection for inedible substances (coal, chalk, kerosene etc.). Is observed at the pregnant woman, and also at the persons with under secretor activity of a stomach.
The food faddish – is reduced to off-flavor in a mouth and obtrusion of gustatory sensations (carious teeth, adenoid disease, etc.).
Eructation –
This sudden and sonorous degeneration through a mouth of air which has accumulated in a stomach or an esophagus – an eructation by air, entering in a mouth of a small part of gastric contents – eructation by nutrition. The eructation is caused by cutting of a musculation of a stomach at an unclosed cardiac hole. At infringement of implement function of a stomach in a nem there are not proper to him iorm processes of fermentation and rotting with boosted ‘aerogenesis’. In first ” a case there is an eructation ïðîãîðêëè ” oil “, in another ” a case it is accompanied a smell ” rotten egg (hydrosulfuric). It specifies on far çàøåäøèé decay of protein containing sulfur. The acidic eructation is combined with a hyper secretion of a gastric juice and usually arises during an attack of a pain at a peptic ulcer. The eructation of bitter taste occurs at íàáðàñûâàíèè Bile in a stomach from duodenum. Ãíèëîñòíàÿ the eructation is characteristic for major gastrectasias, achelii with stagnation ” of contents (carcinoma of the stomach).
The nausea – reflector the act, bound about a boring ” of a vagus nerve, is shown by feeling of pressure in an anticardium. The giddiness “, diaphoresis, sialosis, ïîõîëîäàíèå ” of extremities is accompanied general by delicacy, the slope ” of arterial pressure Frequently precedes a vomiting, but ” can be and without it. The nausea arises at an initial boring of vomitive center. The conducting value belongs to nervous system, and also tons of a stomach ” duodenum, small bowels. From diseases of a stomach by nausea are accompanied acute gastric, the cancer etc. Arises after meal. Quite often arises at secretor failure of a stomach.
Vomiting: ( ) is caused exaltation ” of vomitive center, which is in an oblong brain, there is chemical receptors band. It gains signals from an intestine, from the kettle interior ear, composite reflector the act, during which occurs consensual ejaculation of contents of a stomach through an esophagus, pharynx, and mouth. Can be display of a protective reflex (reception of substandard nutrition (, or irritation, going from interior medium of an organism (disease of a gastrointestinal path, liver, kidneys).
The vomiting of a gastric parentage is caused by a boring of receptors of a mucous of a stomach, inflammatory process (gastric, a peptic ulcer) at hit in a stomach of proof acids and alkalis, and also substandard write, influencing on receptors of a stomach. At infringement ýâàêóàòîðíîé of function of a stomach (spastic stricture or stenosis, pyloric (the vomiting is bound to difficulty at empty of a stomach).
However vomiting can be caused and other factors: I) vomiting of a nervous parentage, the radiant it lays in main, spinal cord, peripheral nerves, 2) hemotogeno-toxic vomiting. Disease C.N.S., which result in rising intra-cranial, pressure result in a vomiting. A serious nausea and vomiting can arise at a myocardial infarction, is especial its localization’s in a back wall of a left ventricle. At endocrine diseases – diabetic acidosis and failure of paranephroses. A psychogenic vomiting. Frequently at the patients suffering by emotional frustration and a vomiting, the normal state of power supply is maintained, since at them not a vomiting, and regurgitation takes place faster. At presence of a vomiting it is necessary to inquire about time of its offensive, connection with ïðèåìîê write, pain, amount and character of vomitive masses, impurities to them. The vomiting incipient in the morning íàòîùàê with excretion of a plenty of slime, is observed at chronic gastritis, is especial at topers, the “acidic” morning vomiting testifies about night ãèïåðååêðåöèè of a stomach. A vomiting through 10-15 mines. After meal is observed at a ulcer and cancer of a cardiac department of a stomach and at acute gastritis. The vomiting in 2-3 hours, in height of digestion, is characteristic for a ulcer and cancer of a body of a stomach. At a ulcer pyloric or duodenum the vomiting is observed in 4-6 clocks after meal. The vomiting by nutrition, ñúåäåííîé on the eve, and even for 1-2 days, is characteristic for a pyloric stenosis. At the patients suffering by a peptic ulcer, the vomiting arises at height be sick also them takes out. The smell of vomitive masses to a cup acescent, but sometimes can be ãíèëîñòíûì (at processes of rotting in a stomach) and even êàëîâûì (at êàëîâîì a fistula between a stomach and traversal – colonic intestine (. The character of vomitive masses helps to put the diagnosis. From impurities meeting in vomitive masses, diagnostic value have a blood, slime in a plenty (at chronic gastritis bile in a plenty (at waist of a duodenal intestine, impurity of a blood (gastromenia and intestine).
Physical Research techniques
Survey
At blanket survey can pay on itself attention considerable, reaching up to a cachexia, ïîõóäàíèå, which meets at a carcinoma of the stomach, pyloric stenosis. The body height and mass of a body, dermal integument’s of a body their appendages, lymphatic clusters is paid attention to a state consciousness, bearing. The cyanotic coloring of a skin is observed after gastric bleedings. The skin dry with the changed appendages of a skin (dry fragile hair, ñëîÿùèåñÿ nails) can be observed at àõèëè÷åñêèõ gastricàõ, which result in poor salvaging Ferri lactas and occurrence of a sideropenia. The following stage is the survey of an oral cavity. Thus is paid attention to a state of teeth, tongue. The lack of considerable amount of teeth does not provide sufficient grinding right in a mouth, and presence retribution One teeth entail hit of microorganisms in a stomach. Tongue at series of diseases has the features: clean and wet at the not complicated peptic ulcer impose by gray – white scurf, badly smelling at acute gastritis, dry at abdominal to accident, atrophic tongue with rounded papilla’s at a carcinoma of the stomach, atrophic gastritis. At survey of a stomach it is necessary to pay attention to its shape, properties of an abdominal wall motion both abdominal wall, and bodies, visual through it, and pathological formations in abdominal cavity. At survey of area of a stomach the contours and peristalsis of a stomach can be visible at the exhausted people. At waist pyloric peristaltic motions are clearly visible as arbors uplifting an abdominal wall.
That it is better to be oriented in the topographical relation and as a matter of convenience descriptions of results of examination, abdominal cavity mentally carried out on a body of the patient by lines, part on particular areas and departments. By two horizontal lines: by one, bridging the tenth rib, another the upper bones of an ileac bone. By two verticals which have been carried out on periphery edges of direct muscles of a stomach, part abdominal cavity on 3 posed one above another in district of direct muscles of area, upper -, medial – 7, inferior – thus under is meant only that part, which meets to area of a stomach posed between coastal by an arc and the upper horizontal line. The departments abdominal cavity, restricted from above by diaphragm, and in front and from sides by last ribs wear the name sub coastal (). The departments, restricted in front by periphery edges of direct muscles, behind by backbone, from sides by a musculation of a prelim abdominal and lumbar area, from below by pelvic bones, wear the name Flank. ” Thus the upper departments between the carried out horizontal lines wear the name of ileac areas (), inferior departments, restricted from above by interosseous line and from below Lig. umbilical, it is accepted to term as inguinal areas (). The area posed between two verticals around of a belly button, wears the name umbilical (), and above a pubis – suprapubic (). The examination of a stomach will be carried out necessarily in two positions – vertical and horizontal. As many hernias, if they are insignificant, are not so appreciable in a horizontal position of the patient, and many tumors posed in the upper departments of abdominal cavity, sometimes are palpated only in a standing position. It is explained by manner in a horizontal position up diaphragms and smaller availability of a tumor at a palpation. At survey of the patient in a standing position the doctor sits, And the patient faces to the doctor by the person to it, completely having naked the stomach, At survey of a stomach first of all it is necessary to pay attention to a state of integument’s of a stomach, development of hypodermic veins, state of a belly-button, shape of a stomach visual pulsation’s, peristalsis of a stomach and intestine visual through an abdominal wall. The normal skin of a stomach at medial power supply of the patient is represented sleek, dim and ðîæàâøèõ of the women – rugosity with. At an edema or tension of a prelim abdominal becomes brilliant and intense. On a skin there can be devices of an eruption, venial of a network, hernia diverticulum, postoperative seams, pigmentation. The belly button iorm should be involved. The coordination of a belly button is observed at an obesity, meteorism. The diverticulum of a belly button is observed at accumulation of a fluid in abdominal cavity, the considerable diverticulum down to a head of the baby is observed at hernia of umbilical..
Is surveyed (stroma of a stomach, its conformity to a body build. It is necessary to note change of the shape of a stomach with conservation of its symmetry. (Total magnification or decrease of a stomach) or it by infringement it (diverticulum or sticking of its separate sites). The most often reasons of augmentation of a stomach is the meteorism, obesity, ascetics. Besides the reason of augmentation of a stomach can be served by (with) development of major cysts in abdominal cavity, tumors, ptosis of bodies abdominal cavity (snlanchoptosis ), swelling of an abdominal wall, clump of gas in abdominal cavity (pnemounirtonviz ). At survey of a stomach pay attention to various motions, which can be caused by respiratory excursions of a forward abdominal wall, peristalsis of a stomach or intestinal loops, ïîäëîæå÷íîé by a pulsation.
Palpation
Distinguish a surface (rough) and penetrating palpation. The surface palpation enables to spot restricted or blanket morbidity of an abdominal wall and degree of a strain of muscles it at pathological processes in abdominal cavity. Besides the surface palpation allows to reveal in an abdominal wall in aspiration, clusters, hernia, tumor, divarications of recti and to spot a sign Shetkin-Blumberga (intensifying of pain sensation at prompt putting taking out of an hand from a forward abdominal wall). The intensifying of pain sensation is caused by percussion inflamed a leaf of a peritoneum the patients with a poured or restricted peritonitis. The surface palpation of a stomach will be carried out in such a manner that the doctor, having occupied a position from the right leg from the patient, puts the right arm on a stomach of the patient floating and cautiously, not aspiring especially to penetrate deep into, begins pallpatory to explore all area of a stomach. Begin usually from the left-hand inguinal area (at absence of the complaints of the patient on a pain in this site of a stomach) gradually moves a palm from one place on another.
Consistently feel in the beginning didymium areas of a stomach ileac, lateral and subcoastal, and then unpaired epigastria, umbilical, and suprapubic. The morbid sites of a stomach feel in last turn. In avoidance reflectors of cutting of muscles of a prelim abdominal at the responsive subjects the attention of the patient by conversation is necessary to distract. Iorm an abdominal wall weak and painless. On a degree of an expressiveness blanket (diffuse) or the local stresses distinguish a resistance of an abdominal wall and muscle strain a rigidity of a musculation of a prelim abdominal. The resistance of an abdominal wall is observed at pathological changes in bodies abdominal cavity at absence of an inflammation of a peritoneum. Thus the resistance of an abdominal wall to palpating fingers decreases or passes at destruction of the patient. At a muscle strain there is more expressed and constant strain of a prelim abdominal in connection with involving in inflammatory process of a peritoneum. Thus the positive sign Shetkin-Blumberga is scored. The local stress of an abdominal wall is observed at a restricted peritonitis incipient at an acute cholecystitis, appendicitis, blanket strain at a poured peritonitis signaling about “accident” in abdominal a vacuity (a perforated ulcer of a stomach, intestine, perphortivania a cholecystitis, appendicitis. (. Then having asked the patient to uplift a head to inhale and to strain, the doctor puts along a forward median line tip close to and slightly bent fingers of the right arm and feels a white line of a stomach, from a xiphoid process up to a pubis. Iorm the strained platens of direct muscles of a stomach and umbilical a ring do not pass (miss) tip of fingers. At a discrepancy (diastase) of direct muscles of a stomach the fingers freely move apart muscle platens in the legs and will penetrate between them. With the purpose of revealing a hernia diverticulum will carry out also palpation of a white line of a stomach, umbilical of a ring in a position of the patient standing, having asked him to strain. If in any department of a stomach the morbidity is found out and in reply to it immediately during a palpation on the relevant site there is a moderate transient local resistance of muscles of an abdominal wall, speak about presence of a local resistance. Such response of muscles of an abdominal wall decreases or absolutely disappears at distraction of attention of the patient or after a long-lived stroking on a stomach. The local resistance of muscles of a stomach is caused by a pathology of interior bodies posed in a projection of a morbid site, less often by pathology of the abdominal wall more often. The pain at a local resistance, as a rule, blunt, tolerant, can be sometimes characterized as a hyper sensibility or discomfort. However at the sharply expressed spastic stricture of a sleek muscle. Rounds, for example of colic bubble or intestine, the pain happens acute (colic (. In case of involving in inflammatory process layers of a peritoneum (peritonitis (, pain at a palpation sharply expressed, intolerable. The considerable and proof strain of muscles of an abdominal wall retained irrespective of a palpation is simultaneously taped. The similar response of an abdominal wall is termed to a muscle strain, or muscle sewed up. At a poured peritonitis the muscle protection, as a rule, happens diffuse (“stiff” a stomach (, and at a local peritonitis – local. The palpation allows to reveal one more important sign of a boring of a peritoneum: the pain, îùóùàåìàÿéèüíûì at cautious submergence of an arm in abdominal cavity, is much more weak also more restricted, than that acute and poured pain, which arises if suddenly to stop pressure and promptly to take away a palpating arm from a stomach (sign Shetkin-Blumberga). At an acute appendicitis the sectional sign appears positive in a point a Poppy – Bernia posed on border of outside and medial thirds right umbilical of the line.
The surface palpation of a stomach quite often allows to spot the reason âçáóõàíèÿ or restricted diverticulum of a forward abdominal wall. In particular, at the liver, expressed augmentation, and lien sometimes it is possible them to feel already on this investigation phase. During a palpation hernia increase of umbilici, it is possible to find out containing loops of a small bowel, gurgling and sound of transfusion of a fluid. In series of cases contain of a hernia bag it is possible to set in abdominal cavity, however to do it is necessary with care, is especial at suspicion on a strangulated hernia. At êàíöåðîìàòîçå the peritoneum sometimes is so obtruded and gets thickened, that can be palpate as an original test under èñòîí÷åííûìè flaccid muscles of an abdominal wall.
Penetrating palpation and other auxiliary research techniques of bodies abdominal cavity
After carrying out of a surface palpation of a stomach research accessible at a penetrating palpation bodies abdominal cavity, determining their position, sizes, shape, consistence, state of a surface, presence of morbidity. Thus the padding pathological formations, in particular, tumors and cysts, Requirement of carrying out of examination same, as can be found out also at a surface palpation of a stomach. For decrease of a strain of muscles of a prelim abdominal it is necessary to ask the patient slightly to bend legs in êîëåíÿõ so that the soles completely stood on bed. In some cases a palpation follow-up will carry out at a vertical position of the patient. For improvement of boundaries of separate bodies alongside with palpation by a method will utilize a percussion and auscultation. Besides with the purpose of revealing morbidity in a projection of bodies penetrating laying in abdominal cavity and inaccessible forpalpation, apply a penetrating palpation. At the patients with an ascities for examination of bodies abdominal cavity will utilize a method of a balloting palpation. One of major requirements of carrying out of a penetrating palpation of bodies abdominal cavity is the knowledge of their projection on a forward abdominal wall: – left-hand subcoastal area: a cardiac department of a stomach, tail of a pancreas, lien, left-hand flexure of a colon intestine, upper pole of a left kidney; – epigastria area: a stomach, duodenum, body of a pancreas, left-hand share of a liver; the right subcoastal area: the right share of a liver, cholic bubble, right flexure of a colonic intestine, upper pole of a right kidney; the left-hand and right lateral areas (flank of a stomach (: accordingly descending and uprising departments of a colonic intestine, inferior poles of the left-hand and right kidneys, part of loops of a small bowel; – umbilical area: Loops of a small bowel, transversal colonic intestine, inferior horizontal part duodenum, major curvature of a stomach, head of a pancreas, – helices of kidneys, urethras; – left-hand ileac area: a sigmoid intestine, left urethra; – suprapubic area: loops of a small bowel, urinary bubble and uterus at their augmentation; – right ileac area: a caecum, terminal department of an ileac intestine, ÷åðâåîáðàçíûé a process, right urethra. Usually keeps the following sequence of a palpation of bodies abdominal cavity: a colon, stomach, pancreas, liver, cholic bubble, and lien. Examination of a body, in which projection at a surface palpation the morbidity is revealed, will carry out in last turn to avoid diffuse protective response of muscles of an abdominal wall. At a palpation of a colon, stomach and the pancreases will utilize a method in detail designed in. Item. Model and received .í The name of a method penetrating, slipping, methodical, topographical palpation.
The substance it is, that on an exhalation to penetrate by a brush into depth abdominal cavity and, slipping tip of fingers on a back wall of a stomach should to grope an explored body, then, to roll through it by fingers to spot its properties. At carrying out of examination the doctor puts a palm of the right arm on a forward abdominal wall in the field of a palpated body so that tip close to and slightly bent fingers were on one line and the long axes of an explored part of an intestine were aligned at edge of a palpated body. The major finger does not participate in a palpation. During examination the patient should breathe equally, penetrating, through a mouth, utilizing diafragmental a type of respiration. Thus the abdominal wall on an inspiration should rise, and on an exhalation – to fall. Having asked the patient to make an inspiration, the doctor moves together tip of fingers of a palpating arm a skin of a stomach forward, shaping before fingers a dermal crimp. The received thus reserve of a skin facilitates the further motion of an arm. After that on an exhalation, using lowering and relaxation of a forward abdominal wall, the fingers smoothly dip in depth of a stomach, overcoming resistance of muscles and trying to reach a back wall abdominal cavity. At some patients it manages to be carried out not at once, and during several respiratory motions. In such cases during an inspiration the palpating brush is necessary for retaining in a stomach on the achieved depth, that with the following exhalation to penetrate even more deeply. At the end of each exhalation tip of fingers of the south slip in a direction, perpendicular áëèííèêó of an intestine or edge of an explored body, before touch with palpated formation. Thus the fingers should move together with a skin, laying under them, instead of to slip on its surface. The found out body press to a back wall of a stomach to, to roll across it tip of fingers, will carry out a palpation. The enough complete representation about properties of a palpated body manages to be received during 3-5 respiratory cycles. At presence of a strain of muscles of a prelim abdominal it is necessary to try to cause their relaxation in a band of a palpation. With this purpose smoothly press by radial edge of the left-hand brush on a forward abdominal wall away from a palpated site. The colon is palpated in the following sequence: in the beginning sigmoid intestine, then blind, uprising, descending and transversal colonic. Iorm in overwhelming majority of cases it is possible palpated a sigmoid, blind and transversal colonic intestine, whereas uprising and descending the departments of a colon are palpated changeably. At a palpation of a colon determine its) diameter, density, character of a surface, mobility (is movable axes), presence of a peristalsis, óð÷àíèÿ and ïëåñêà, and also morbidity in reply to a palpation.
The sigmoid intestine is posed in the left-hand ileac area, has a skew course and almost perpendicularly intercrosses left-hand umbilical a line on boundary of outside and medial its thirds. A palpating brush have in the left-hand ileac area perpendicularly to course of an intestine so that the basis of a palm laid on a belly-button, and tip of fingers were guided to the leg ïåðå bottom upper axes of the left-hand ileac bone and were in a projection of a sigmoid intestine. A crimp of a skin displaces outside from an intestine. A palpation carries out ïèñàííûì by a method in a direction: outside both from below – inside and upward (rice).
It is possible to utilize and other method of a palpation of a sigmoid intestine. The right arm start from the left-hand leg) of a body and have so that the palm laid on before not upper axes of the left-hand ileac bone, and tip of fingers were in a projection of a sigmoid intestine. A dermal crimp in this case displace inside from an intestine and palpate in a direction: from within both from above – outside and downwards (rice).
Iorm the sigmoid intestine is palpated during 15 ñì as sleek, moderately dense streched by a diameter about a major finger of an arm. It is painless, does not hum, torpently and seldom peristalsis, is easily displaced at a palpation in limits 5 see. At elongation of a mesentery or most sigmoid intestine (colicho sigma) it can be palpated considerably medial, than usually.
The caecum is in the right ileac area and also has a skew course, intercrossing almost at right angle right umbilical a line on border of outside and medial its thirds.
Palpating brush have in right ileac area, that the palm laid on before not upper axes of the right ileac bone, and tip of fingers were guided to the leg of a belly-button and were in a projection of a caecum. At a palpation a dermal crimp move together inside from an intestine. Palpate in a direction: from within both from above – outside and downwards (rice).
Iorm the caecum has the shape of the sleek, softly elastic cylinder by a diameter in two transversal fingers. It a little dilated from top to bottom, where blindly comes to an end curved by bottom. The intestine is painless, is moderately mobile, and hums at pressing.
In the right ileac area a terminal department of an ileac intestine sometimes is possible pre pallpatory also which from below squint runs from the inside into a caecum. A palpation conduct along interior edge of a caecum in a direction from the top downward. If the ileac intestine is reduced and is accessible to a palpation, it is determined as sleek, dense, relative frame, painless streched in length 10-15 ñì
And diameter no more little finger. It is batchly relaxed, issuing loud gurgling , and thus as though disappears under an arm.
Uprising and descending the departments of a colon are posed is longitudinal, accordingly in the right and left-hand lateral areas (flank)
Stomach. They lay in abdominal cavity on the weak basis that impedes their palpation. Therefore it is necessary previously from below to frame
It is possible to press a dense bottom (basis), to which intestine at its palpation (conjoined manipulation). With this purpose at a palpation of a uprising colonic intestine the left-hand palm lay under the right lumbar area
Below than 12 ribs in a transversal trunk a direction so that tip
to closed and rectified fingers rested against a periphery edge lengthy
Muscles spins. A palpating right arm has in the right flank
Stomach is traversal to a course of an intestine so that the warrant(basis) of a palm was guided outside, and tip of fingers were on 2 ñì palpatory of a periphery edge of a direct muscle of a stomach. The dermal crimp is displaced by(with) medial intestines and palpate in a direction from within outside. Simultaneously by fingers of the left-hand arm press on lumbar area, trying to approach
Back abdominal wall to a palpating right arm (rice).. At
Palpation of a descending colonic intestine a palm of the left-hand arm advance
Further for a backbone also enclose(lay) in a transverse direction is mean
The left-hand lumbar area so that the fingers were outside from lengthy muscles spins. A palpating right arm start from the left-hand leg of a body and have in left-hand flank of a stomach traversally to course of an intestine so that the warrant(basis) of a palm was guided outside, and tip of fingers were on 2 ñì palpatory of a periphery edge of a direct muscle of a stomach. The crimp of a skin is displaced by(with) medial intestines and palpate in a direction from within outside, simultaneously pressing the left-hand arm on lumbar area (rice)..
Uprising and descending departments of a colon, if them it is possible
palpated, represent relative frame, moderately dense, painless cylinders by a diameter about 2 see.
The transversal colonic intestine is palpated in umbilical of area simultaneously by both arms(hand) a /bilateral palpation / immediately through lean direct muscles of a stomach. For this purpose the palms put is longitudinal on a forward abdominal wall from both legs(parties) from a median line so that tip of fingers settled down at a level of a belly button. A dermal crimp moves together in the leg of epigastria area and palpate in a direction from the top downward (rice).. If the intestine thus is not found out, a palpation retry, a little having biased initial position of fingers in the beginning is higher, and then is lower than a belly button.
Iorm the transversal colonic intestine has the shape traversally laying and arched from top to bottom, moderately of dense cylinder by a diameter about 2,5 see. It is painless, is easily displaced upwards and downwards. In case to grope a transversal colonic intestine it was not possible, it is necessary to iterate a palpation after a presence(finding) of major curvature of a stomach, which is posed on 2-3 ñì above than intestine. At the same time it is necessary to mean, that at the expressed visceroptosis the transversal colonic intestine quite often falls up to a level of a Basin.
At presence of pathological changes of a colon it is possible to reveal morbidity in its this or that department, and also series others ïðèìàêîâ, characteristic for particular diseases. For example, local expansion, inspissation and áóãðèñòaxes of a surface of a restricted site of a colon testify to more often its tumoral defeat, though can be sometimes caused by a considerable clump in an intestine solid êàëîâûõ of masses. Irregular ÷åòêîîáðàçíîå a thickening and inspissation of a wall of a colon or terminal department of an ileac intestine are observed at a granulomatosis of an intestine (illness of a Crown) and his(its) tubercular defeat. The alternating ñïàñòè÷åñêè by the reduced and swollen gas of sites, presence loud óð÷àíèÿ and capotement is characteristic for diseases of a colon inflammatory (colitis) or function parentage (irritable colon (.Ï At presence of a mechanical hindrance for advance êàëîâûõ àññ âûøåëåæàùèé the department of an intestine is enlarged in volume, frequently and strongly peristalsis. The parents(reasons) of a mechanical obstruction can be a cicatrical or tumoral stenosis of an intestine or about pressure her(it) from the outside, for example at ñïàå÷íîì process. Besides at presence of solderings and cancer of a colon the mobility of the struck department quite often considerably circumscribed. If in a stomach there is a local morbidity, but the palpation of a site, posed in this department, of an intestine does not cause a pain, it speaks about pathological process in the next bodies. At the patients with an ascites the presence even of small quantity (amount) of a free fluid in abdominal cavity essentially impedes a palpation of a colon. The small bowel usually is not accessible to a palpation, as lays penetrating in abdominal cavity and is extremely mobile, that does not allow pressing it to a back abdominal wall. However at an inflammatory defeat of a small bowel (enteritis) sometimes is possible palpated by its swollen gas and loops, issuing a capotement. Besides at the patients with a thin abdominal wall the penetrating palpation in umbilical of area enables to find out enlarged ìåçåíòåðàëüíûå (mesenteric) lymphatic clusters at their inflammation (mesadenitis) or defeat by metastasizes of a cancer. A stomach palpate also on a method Is model. Consistently feel major curvature and ïèëîðè÷åñêèé a department of a stomach. His(its) other departments iorm are not accessible to a palpation.
The major curvature of a stomach is posed in top umbilicalof area and is inverted by protuberance from top to bottom. Palpation’s that site of major curvature is accessible only which lays on a backbone. The right palm put is longitudinal on a stomach on a forward median line so that tip of fingers were guided to the leg of a xiphoid process and settled down on 2-4 ñì above than belly-button. A dermal crimp moves together before fingers. On an exhalation dip a brush in depth of a stomach, reach(achieve) a backbone and slip on it(him) tip of fingers in a direction from the top downward (rice).. To feel major curvature of a stomach it is possible approximately in half of cases. At a palpation the sensation ñîñêàëüçûâàíèÿ from the weak, sleek platen going traversally on a backbone to both legs(parties) from him(it) and representing äóïëèêàòóðó of walls of a stomach is framed.
The mobility of major curvature circumscribed, it is painless, quite often hums at a palpation. It is possible pre palpatory ïèëîðè÷åñêèé a department of a stomach much less often. It(he) is posed a little bit below xiphoid process, more to the right of a median line and has a skew direction: at the left both from below – to the right and upwards. A palpating palm put on right a direct muscle of a stomach a pain right costal of an arc so that tip of fingers settled down on à-4 ñì above than belly-button, were set in the leg left-hand coastal of an arc and laid in a projection ïèëîðè÷åñêîãî of a department of a stomach. Moving together before fingers a dermal crimp, will carry out(spend) a palpation in a direction at the left both from above – to the right and downwards (rice (.. Iorm ïèëîðè÷åñêèé the department of a stomach has the shape sleek, moderately dense, inactive painless stretched by a diameter no more little finger. The palpation it(him) is accompanied by a periodic(batch) relaxation, and sometimes original gurgling ì, reminding ìûøèíûé ïèñê. Similarly palpate major curvature and ïèëîðè÷åñêèé a department of a stomach in a position of the patient costing(standing). At presence a visceroptosis, is especial thin and at a weak abdominal wall, in a vertical position in series of cases it is possible palpated small curvature of a stomach as a thin muscle crimp laying of a below xiphoid process on a median line and a little bit(some) to the left from it(her). The palpation of a stomach sometimes allows to find out coming from it(him) pyloric, atony of walls of a stomach) or, less often, about considerable rising of secretor function of gastric Ferri lactase’s.
Examination of a stomach by methods of a percussion and aksyltation
Ïåðêó òîðíûé the method alongside with other described spheres of his(its) application at examination of bodies abdominal cavity has the important value for definition of the parent(reason) of augmentation of a stomach and, in particular, for revealing attributes of an ascetics. Above places of a clump of a free fluid in abdominal cavity at a percussion instead of a thympanitis the blunt sound is defined(determined), and at change of a position of a body the band of an obtrusion is promptly displaced. Therefore for detection of an ascetics will carry out(spend) a percussion of a stomach at various positions of the patient: laying on a spin and side, costing(standing), and also in a genucubital position. A percussion conduct from area of a tympanic sound. A finger – plessimeter thus align to guessed fluid level. Apply silent ïåðêó òîðíûå shocks. At a percussion of a stomach in a position of the patient laying on a spin a finger – plessimeter put is longitudinal on a forward median line so that the medial phalanx it(him) laid on a belly button. Percussea on umbilical of a line serially in a direction of the right and left-hand lateral departments (Frank) of a stomach before transferring a thympanitis in a blunt sound (rice (.. Iorm from both legs(parties) the boundary(border) of transferring of a tympanic sound in blunt passes on forward axillary lines. More medial locating of such boundary(border) testifies to a clump of a free fluid in abdominal cavity. In this case at carrying out of a percussion similarly in a position of the patient laying as on the right, and left-hand side (rice (., the boundary(border) ïðèòóïëåííîãî of a sound above a fluid in íèæåëåæàùåì flank of a stomach is biased in a medial direction, and the boundary(border) of a blunt sound in âûøåëåæàùåì flank will correspond(meet) to its normal position. At transferring the patient in a vertical position the fluid will move in bottom abdominal cavity. Therefore in lateral departments of a stomach the thympanitis will be taped, and the percussion on vertical identification lines in a direction from the top downward in the inferior half of stomach will reveal area of a blunt sound with horizontal high bound (rice (.. At transferring the patient in a genucubital position the site of a blunt sound will move in umblical area, whereas in other departments of a stomach the thympanitis will be defined(determined). A percussion thus will carry out(spend) in the direction of a belly-button, beginning her(it) it is consecutive from right and left-hand lateral Flank of a stomach, xiphoid process and pubis (rice (.. The method of a percussion in a genucubital position allows to reveal even small quantity(amount) of a free fluid in abdominal cavity. Applying the described method, it is necessary to mean the following. At the patients with the expressed ascetics sometimes in abdominal cavity such considerable quantity(amount) òðàíññóäàòà accumulates, that at any position of the patient above all departments of a stomach is taped blunt ïåðêó òîðíûé a sound. In these cases take into account sectional of survey: the sizes of a stomach, his(its) shape depending on a position of the patient, change of a skin of a forward abdominal wall and belly-button (with (.. At some pathological states in abdominal cavity the inflammatory exudate (ýêññóäàòèâíûé a peritonitis) or blood (salpingocuesis, tearing up of a lien or liver etc. (can collect. At such patients at change of a position of a body the fluid in abdominal cavity moves much more slowly, than at an ascetics. Moreover, at presence in abdominal cavity sacculated ýêññóäàòà, for example at the patients by a tubercular productive peritonitis, the boundary(border) of dullness above a fluid at change of a position will not change. At formation in abdominal cavity of a major cyst, as a rule, it is localized in median departments of a stomach, where an area of dullness irrespective of a position of a body of the patient is defined(determined), whereas in lateral departments of a stomach the thympanitis is maintained. Such cysts radiate from a pancreas or ovaries more often. Except for the specified reasons, meteorism and obesity can cause the augmentation of a stomach also. At presence of a meteorism above all departments of a stomach at a percussion the tympanic sound is defined(determined). At the patients with a gross obesity above all departments of a stomach the moderate obtrusion ïåðêó òîðíîãî of a sound not dependent from timely of a position is taped. However thus there is no such expressed augmentation of the sizes of a stomach, as at an ascetics with similar ïåðêó òîðíîé by a pattern.
Miss also diverticulum of a belly button and èñòî÷åíèå of a skin of an abdominal wall. Opposite(on the contrary), it is scored a considerable thickening of hypodermic fatty bed of a stomach and blanket attributes of an obesity. In doubtful cases alongside with a percussion for revealing an ascetics it is necessary follow-up to utilize a method çûáëåíèÿ (ôëþêòóàöèè (. Examination will carry out(spend) in a position of the patient laying on a spin. The doctor puts the left-hand palm on right flank of a stomach, and close by fingers of the right arm yields of a prompt jerk figurative motions on a symmetric site left-hand flank of a stomach. At presence in abdominal vacuities of a free fluid the left-hand arm feels oscillations of a fluid as waves çûáëåíèÿ, transiting from the left-hand half of stomach in right. To distinguish çûáëåíèÿ from gear oscillations of the intense abdominal wall, it is necessary to ask the assistant to press by ulnar edge of a palm on a stomach along a median line in the field of a belly button and to iterate examination (rice).. If çûáëåíèÿ was maintained, the exudate means, in abdominal cavity, and if the oscillations have disappeared, they were of gear character.
The mouth and throat
The examination of the mouth and throat is conducted with the patient sitting up either in bed, with the head resting comfortably back on pillows, or in a chair. A bright torch, a tongue depressor (spatula) and a pair of latex gloves are essential. The lips, teeth, gums, tongue, palate, fauces and oropharynx are then visualized systematically, and finally palpation of the sides of the tongue, floor of mouth and tonsillar regions is carried out.
Inspection
THE LIPS
Look closely at the philtrum (the shallow depression running from nose to upper lip) for the tell-tale scar of a repaired cleft lip. When present, particularly if associated with ‘nasal speech’, inspect the palate carefully for signs of a cleft. Next, look at the corners of the mouth for cracks or fissures (angular stomatitis). The cracks are reddish-brown, moist, superficial, linear ulcers radiating from the angles of the mouth. In children their origin is infective (perleche); they are common in the elderly when ill-fitting or deficient dentures result in overclosure of the mouth. Cheilosis is also seen in severe iron-deficiency anaemia; it also occurs in vitamin B2 (riboflavin) deficiency.
Observe any desquamation or inflammation of the lips (cheilitis). This is common and self-limiting in cold weather. Grouped vesicles on the lips on a red base with crusted lesions are seen in herpes simplex labialis commonly associated with coryza. This infection is usually of short duration and the lack of induration and ulceration serves to distinguish it from other more serious conditions. Recurrent actinic cheilitis with small blisters and exfoliation, however, is a premalignant condition found in people constantly exposed to the sun and wind, such as farmers and fishermen.
Look for any ulcer on the lips. Carcinoma (epithelioma) usually occurs on the lower lip away from the midline; the ulcer is indolent, flat and shallow, although in time the edge may become heaped up and induration may be felt. Epithelioma must be differentiated from keratoacanthoma, pyogenic granuloma and the chancre of primary syphilis. A keratoacanthoma (molluscum sebaceum) is a lesion due to overgrowth of the stratum granulosum of the skin. It usually presents as a firm, rounded nodule sometimes with ulceration; it is more common on the upper lip and heals spontaneously without treatment. Pyogenic granuloma is a soft red raspberry-like nodule on the upper lip, which often follows minor trauma. The upper lip is the commonest site of an extragenital chancre, which appears as a small, round lesion that is firm and indurated. A ‘snail-track ulcer’ in secondary syphilis has a serpiginous outline and greyish-white non-purulent exudate. In both epithelioma and chancre enlarged, painless cervical nodes are commonly felt. Rhagades, white scars at the angles of the mouth that extend into the mouth, due to cheilosis associated with congenital syphilis, are now only of historical interest. A crack in the middle of the lower lip in cold weather is a common, painful problem, but is of no sinister significance.
Very occasionally multiple small brown or black spots are seen on the skin around the mouth (circumoral pigmentation) which may also extend on to the lips and buccal mucosa. This pigmentation constitutes one of the triad of cardinal features of the Peutz-Jeghers syndrome and signifies underlying small bowel polyposis, a condition inherited as a Mendelian dominant. On the buccal mucosa the pigmentation may look very like that seen in Addison’s disease. Look carefully at the lips and tongue for telangiectasia. Their presence may signal the existence of others elsewhere in the intestine, which occasionally bleeds.
Now gently grasp the lower lip with the index finger and thumb of both hands and evert it fully, to display the mucous surface of the lip. Two lesions are commonly seen in this site: aphthous ulcers and retention cysts. Aphthous ulcers are small, superficial, painful ulcers with a white or yellow base and a narrow halo of hyperaemia. Such ulcers are also seen on the tongue, buccal mucosa and palate. Retention cysts of the mucous glands of the lips and buccal mucosa appear as round, translucent swellings, elevated from the surface with a characteristic white or bluish appearance. They are also found on the mucous surface of the lower lip.
THE TEETH
Ask the patient to grimace so as to show the teeth. If the patient wears dentures, ask him or her to remove them and open the mouth widely. Using a tongue depressor to retract first the lips and then the cheeks, note the number of teeth present and look for decay (caries). The tooth most commonly missing is an impacted unerupted third mandibular molar (wisdom tooth). Inspect both the buccal and lingual aspects of the teeth. It is said that lack of teeth may cause indigestion but many edentulous people suffer no indigestion whether they wear dentures or not. Look for any changes in the following.
Colour
Tartar deposition occurs mainly on the lingual aspect of the lower incisor and canine teeth and consists of precipitated calcium salts of saliva, which is stained brown in smokers. The chewing of betel nuts may also discolour the plaque of teeth a reddish-brown. Children up to the age of 8 treated with tetracycline (and children of expectant mothers so treated after the 14th week of pregnancy) are at risk of acquiring permanent staining of both the deciduous and permanent teeth. This takes the form of disfiguring horizontal bands, which may be yellow or grey and must not be mistaken for bands of hyperplasia on the enamel due to exanthematous fevers or any serious illness occurring during the development of the crowns. In endemic fluorosis, chalk-white patches appear on the teeth or the teeth present a dull, unglazed appearance, sometimes with pitting and brown staining (Maldon teeth).
Shape
Ill-formed hypoplastic teeth have a broad, concave biting edge, whilst some notching of the incisors is seen in those who persistently bite cotton or hold hairclips between their teeth. This must not be mistaken for Hutchinson’s teeth—a manifestation of congenital syphilis, but a very rare finding nowadays. In this condition the two central upper permanent incisors are rounded in section and notched at their biting edge. They may also be broader near the gum than at the crown, so as to be peg-shaped. The first permanent molars may be dome-shaped. The two central upper incisors are sometimes lost in leprosy. Patients who habitually induce vomiting, e.g. in anorexia nervosa, may show evidence of gastric acid-induced erosion of the inner surface of the incisors.
Ridging
Transverse ridging is sometimes seen in the permanent teeth of those who had vitamin C and D deficiency in infancy.
Enlargement of the lower jaw in acromegaly leads to alteration of the bite, so that the lower teeth may close outside the upper ones.
THE GUMS
Examine the gums at the same time as the teeth. Pink, healthy gums adhere closely to the necks of the teeth and have a sharp border. With increasing age gingival recession occurs, so making the teeth appear longer and exposing the cementum below the enamel. This makes it easier for infection to gain a hold.
In chronic marginal gingivitis, the gums are retracted, frequently bleed easily and lose their characteristic stippling. Sometimes pus can be squeezed from them (pyorrhoea alveolaris).
Acute herpetic gingivostomatitis due to the simplex virus occurs most commonly in infants and children. Many small vesicles appear on the gums, cheeks, palate, tongue and lips. The vesicles rupture to produce shallow ulcers with a yellowish floor and bright red margins. Vincent’s gingivostomatitis, an infection due to fusiform spirochaetes, characteristically destroys the interdental papillae. A thick, felted, greenish-grey sloughs is formed and halitosis is present. In patients exposed to lead compounds, a stippled blue line can often be observed running along the edge of the gum, especially opposite those teeth showing gingivitis. Similar lines may be produced by bismuth or mercury but these are uncommon signs. The gums in scurvy are swollen, irregular in outline, red, spongy and bleed easily. Hypertrophy of the gums may occur in pregnancy and in patients treated for long periods with phenytoin. Haemorrhages may be observed in the buccal mucous membrane in thrombocytopenic purpura and acute leukaemia.
Pus can form in a carious tooth to form an alveolar or dental abscess with throbbing pain, exacerbated by tapping the affected tooth. Localized swelling of the gum and swelling of the face (if pus has escaped through the lateral alveolar margin) are signs associated with this condition. Ill-fitting dentures can produce a granuloma or an ulcer on the gum at the point of pressure where the denture does not fit properly. Such a lesion has to be differentiated from a carcinomatous ulcer arising in the gum; the latter presents the same macroscopic features as malignant ulcers elsewhere in the mouth.
Epulis is a general term used to describe any swelling arising in the gum of the maxilla or mandible.
THE TONGUE
Ask the patient to protrude the tongue. Inability to do so fully (ankyloglossia) is seen, very rarely, in infants due to tongue-tie (a congenitally short frenulum linguae) or in advanced malignancy of the tongue involving the floor of the mouth. When carcinoma involves the side of the tongue (the commonest site) and the floor of the mouth, slight deviation towards the affected side may occur. Slight deviation is not uncommon and may be due to asymmetry of the jaws. In hemiplegia, deviation towards the paralysed side may be found. In lesions of the hypoglossal nerve or its nucleus there may be fasciculation of the affected side; later this side may be wasted and deeply grooved (lingual hemiatrophy). The tongue is large in acromegaly, cretinism, myxoedema, lymphangioma and amyloidosis. Tremor of the tongue may be due to nervousness, thyrotoxicosis, delirium tremens or Parkinsonism.
Next examine the dorsum of the tongue.
Colour
Is the tongue pale, red or discoloured? Pallor is seen in severe anaemia. Discoloration is most often due to the ingestion of coloured foods, e.g. red wine or coloured sweets.
Moistness
The state of the tongue gives some indication of the state of hydration of the body, provided the patient is not a mouth breather. A dry, brown tongue may be found in the later stages of any severe illness, but is found particularly in advanced uraemia and acute intestinal obstruction.
Fur
Furring of the tongue is of little value as an indication of disease. It is often found in heavy smokers. A brown fur, the ‘black hairy tongue’, is due to a fungus infection and is of no special significance, though frequently a source of great alarm to its possessor. The tongue of scarlet fever at first shows bright red papillae standing out of a thick white fur. Later the white coat disappears leaving enlarged papillae on a bright red surface — the ‘strawberry tongue’. Hairy leucoplakia is a common feature in patients with HIV infection. In chronic superficial glossitis, areas of leucoplakia (whitish opaque areas of thickened epithelium) are separated by intervening smooth and scarred areas; there are no normal papillae to be seen and the fissures run mainly in a longitudinal direction.
The papillae
Generalized atrophy of the papillae produces a smooth or bald tongue, which is characteristic of vitamin B12 deficiency but may also sometimes be found in iron-deficiency anaemia, coeliac disease and other gastrointestinal disorders and deficiency states, especially pellagra. In severe cases smoothness may be associated with wrinkling of the mucous membrane, which has then to be distinguished from fissuring of the tongue seen in chronic superficial glossitis due to syphilis, and congenital fissuring of the tongue or ‘scrotal tongue’, which is common and of no pathological significance. In congenital fissuring the papillae are normal but the surface is interrupted by numerous irregular but more or less symmetrical folds, which tend to run mainly horizontally. In median rhomboid glossitis a lozenge-shaped area of loss of papillae and fissuring is seen in the midline anterior to the foramen caecum. It feels nodular and may be mistaken for a carcinoma. It must also be distinguished from a lingual thyroid but this is situated posterior to the foramen caecum. Geographical tongue is another harmless anomaly characterized by localized irregular red areas of desquamated epithelium and filiform papillae surrounded by a whitish-yellow border; the papillae change in distribution and give the appearance of a map. The ‘false geographical tongue’ with a similar appearance occurs chiefly in children with fever.
The sides and undersurface
Ask the patient to open the mouth wide and protrude the tongue fully to one side. Then retract the cheek with a spatula. This displays the side and lateral undersurface well. Some patients find this impossible to do, so wrap a gauze swab around the tip of the tongue and with index finger and thumb gently pull the tongue out and to one side. Benign ulcers in this site are common and may be inflammatory or traumatic in origin, very often due to ill-fitting dentures or broken carious teeth; such ulcers tend to be painful, superficial and lack induration. However, in an elderly patient any ulcer at this site must be regarded as malignant until proved otherwise by biopsy; it is the most frequent site of carcinoma in the mouth and presents as a hard, indurated ulcer with everted raised edges.
Now ask the patient to retract the tongue fully and slightly elevate the tip with the mouth wide open. This displays the undersurface of the anterior tongue and floor of the mouth. Note the frenulum linguae and the orifice of the submandibular duct opening on either side of the base of the frenulum. The ampulla of each duct lies just proximal to the orifice and is a common site for calculi formed in the submandibular salivary gland to lodge. The calculus is seen as a white or yellow bleb distending an oedematous hyperaemic ampulla.
A small ulcer on the frenulum is sometimes seen in persistent coughing and particularly in whooping cough. Sublingual varicosities are common in the elderly. Two types of cyst may be found in the floor of the mouth:
• ranula, which forms a bluish-white translucent swelling of variable size and is due to blockage of the duct of a mucous gland; and
• sublingual dermoid cyst, a round opaque swelling lying beneath the mucosa either above or below the mylohyoid, which is due to sequestration of epidermal tissue beneath the skin along the embryological lines of fusion of the mouth.
THE BUCCAL MUCOSA
Inspect the buccal mucosa. Retract the cheek with a spatula. Note the opening of the parotid duct, which is seen as a tiny swelling opposite the upper second molar tooth. In the catarrhal stage of measles, before the appearance of the rash, small bluish-white spots, surrounded by a red areola, may be seen opposite the molar teeth. These are known as Koplik’s spots. In the same position irregular areas of dots of slate-grey or blue pigmentation are seen in Addison’s disease.
Aphthous ulcers, mucus retention cysts and papillomata present the same appearance on the buccal mucosa as elsewhere in the mouth. Mouth ulcerations —either aphthous or larger, more chronic lesions—are well-recognized manifestations of inflammatory bowel disease, particularly Crohn’s disease. Mouth ulcers in association with genital ulcers indicate Behcet’s syndrome. White opalescent patches (rather like white paint) of leucoplakia may also be seen on the inner aspect of the cheek; these should be differentiated from lichen planus, an oral manifestation of a skin disease, but in this case look elsewhere, especially on the arms and legs, for similar lesions. Thrush (monilial stomatitis), a fungal infection due to Candida albicans, presents as a different sort of white patch. It is seen as small white points raised somewhat above the surrounding surface, which is usually redder thaormal. As the infection gains hold so the lesions coalesce and may form extensive sheets throughout the mouth. Patches of thrush are apt to be mistaken for small milk curds, but curds can be easily detached, while thrush patches can be removed only with difficulty and then tend to leave behind a raw surface. Thrush is common in debilitated children, beneath unclean dentures and in patients on cytotoxic or immunosuppressive drugs. It is also seen frequently on surgical wards, especially in ill patients with sepsis in the postoperative period and those treated with broad-spectrum antibiotics, which destroy the normal bacterial flora of the mouth and thus allow the fungi to flourish. Oropharyngeal candidiasis is also a feature of cellular immunodeficiency states including AIDS.
THE PALATE, FAUCES, TONSILS AND PHARYNX
Ask the patient to put the head right back and keep the mouth wide open. Inspect the hard and soft palates and note the position of the uvula. Get the patient to say ‘ah’, which raises the soft palate and increases visibility of the fauces, tonsils and oropharynx.
If a good view of these structures has not been obtained, introduce a spatula to depress the base of the tongue and, if necessary, another spatula to retract the anterior pillar of the fauces to view the tonsils properly.
Again look for any ulcers, erythema or vesicles. Vesicles confined to one side of the hard palate which progress to painful oval ulcers are characteristic of herpes zoster of the maxillary division of the trigeminal nerve (fifth cranial); this disorder usually occurs in older patients and is accompanied by a characteristic skin rash in the corresponding dermatome on the face. Herpes zoster infection of the glossopharyngeal nerve (ninth cranial) produces similar lesions in the pharynx.
Malignant ulcers do occur on the hard palate but much less frequently than elsewhere in the mouth, and present the same appearances. Ectopic salivary gland tissue may be present in the mouth; the hard palate is the commonest site. Tumours of this tissue present as a smooth, hard swelling projecting from the surface of the hard palate, sometimes with central ulceration.
If a hole is seen in the hard palate it is usually due to one of the following:
• imperfect closure or breakdown after repair of a cleft palate;
• radionecrosis of bone following radiotherapy for treatment of local carcinoma; or
• tertiary syphilis with formation of a gumma.
Petechiae on the palate are common in glandular fever but they are also features of any form of thrombocytopenia, rubella and streptococcal tonsillitis. Oral lesions may be the presenting feature of glandular fever, enlarged tonsils are covered with a white exudate which tends to become confluent; there is oedema of the fauces and soft palate; and erythema of the oropharynx. This contrasts with the yellow punctate follicular exudate seen in streptococcal tonsillitis. Whenever a membranous exudate is seen, diphtheria should spring to mind and, as in all cases of mouth infection, a swab should be taken for bacteriological examination. The membrane in diphtheria varies in colour from white to green and often starts on the tonsil before spreading to the fauces and pharynx.
Finally, look at the pharynx. The presence on its surface of a number of small round or oval swellings, somewhat like sago grains, is so common as to be almost normal in appearance. In pharyngitis these are much increased.
Notice any vesicles or ulcers. In chickenpox (herpes varicella) oral lesions may be apparent before the characteristic rash appears. There is erythema of the pharyngeal and buccal mucosae, followed by vesicles, which progress to oval or round ulcers with a white slough. In herpangina (Coxsackie virus infection), which is also common in the young, similar lesions may be seen in the oropharynx, soft palate and uvula.
In the common cold (coryza), mucopus may be noticed on the posterior wall of the pharynx running down from the nasopharynx. Less commoowadays are a peritonsillar abscess (quinsy) and retropharyngeal abscess. The latter forms a smooth, tense, tender swelling which bulges forwards from the posterior wall of the oropharynx.
THE BREATH
Carious teeth, infection or ulceration of the gum, stomatitis, and retention and decomposition of secretion in the follicles of enlarged tonsils are the commonest sources of offensive breath. Characteristic odorous may be recognized:
• in ketosis, the breath smells of acetone;
• in uraemia, there is a fishy or ammoniacal odour;
• in hepatic failure, the odour is described as ‘mousy’;
• in suppurative conditions of the lung the breath may have a putrid smell;
• in bronchiectasis the odour has been compared to that of apple blossom with a hint of stale faeces.
• Paraldehyde and alcohol also impart their characteristic smells to the breath.
Palpation
Palpation forms an important, frequently neglected part of the examination of the mouth, particularly in patients who complain of oral symptoms or in whom unexplained cervical lymphadenopathy is found. Although not a routine part of physical examination, palpation in the mouth is imperative in anyone with a solitary or suspected ulcer in the oral cavity and bimanual palpation provides further information about such things as swellings in the floor of the mouth or cheek.
Impress on the patient that you will be as gentle as possible. Put on a disposable glove or finger cot, and ask the patient to remove any dentures and to open the mouth widely. With the tongue elevated and to one side, place the index finger of the right hand beneath the tongue on one side of the frenulum and run the finger back along the floor of the mouth. Even a small calculus can easily be felt in any part of the submandibular duct. Then come forwards, running the finger along the lingual side of the tongue to the midline and return on the buccal side of the gum towards the lower molar teeth. Now run the finger up the mucosa covering the ascending ramus of the mandible, and examine both palatal and buccal aspects of the gum of the upper jaw.
If an ulcer is present, try and decide whether any induration is present or not. To perform bimanual examination, with the index finger already inside the mouth, place the fingertips of the left hand flat beneath the mandible, or over the cheek, outside the mouth, and exert gentle pressure between your right index finger and the fingers of the left hand.
Now palpate the tongue and feel the dorsum and the lateral and undersurfaces with the index finger; it sometimes helps for the patient to protrude the tongue to one or other side to do this and, if necessary, the tongue can be held in a gauze swab between finger and thumb of the other hand.
Palpation of the posterior third of the tongue, fauces and tonsils is the least pleasant part for the patient as it usually causes gagging, and it is thus left until last. As before, the index finger is used and run over these structures as rapidly as possible. Feel for irregularity, ulceration and particularly induration, in order to detect a small or hidden carcinoma. Any abnormality felt in these sites in a patient with symptoms demands illuminated head lamp and laryngeal examination.
The abdomen
It is helpful when recording iotes or communicating information to colleagues to think of the abdomen as divided into regions. The two lateral vertical planes pass from the femoral artery below to cross the costal margin close to the tip of the ninth costal cartilage. The two horizontal planes, the subcostal and interiliac, pass across the abdomen to connect the lowest points on the costal margin, and the tubercles of the iliac crests respectively.
Remember that the area of each region will depend on the width of the subcostal angle and the proximity of costal margin to iliac crest, in addition to other features of bodily habitus which naturally vary greatly from one patient to the next.
Inspection
The patient should be lying supine with arms loosely by the patient’s sides, on a firm couch or mattress, the head and neck supported by enough pillows, normally one or two, sufficient for comfort. A sagging mattress makes examination, particularly palpation, difficult. Make sure there is a good light, that the room is warm and that your hands are warm. A shivering patient cannot relax and vital signs, especially on palpatiori, may be missed.
Stand on the patient’s right side and expose the abdomen by turning down all the bedclothes except the upper sheet. The clothing should then be drawn up to just above the xiphisternum and the sheet folded down across the upper thighs to expose the groins and genitalia. This point is important; many are the patients who present with intestinal obstruction due to a strangulated femoral or inguinal hernia where the diagnosis has been missed initially due to lack of proper exposure of the groins in an effort to save embarrassment. However, once full inspection has taken place the sheet may be pulled up to the level of the symphysis pubis to allay anxiety.
Inspection is an important and neglected part of abdominal examination. It is well worthwhile spending 30 seconds observing the abdomen from different positions to note the following features.
SHAPE
Is the abdomen of normal contour and fullness, or distended? Is it scaphoid (sunken)?
• Generalized fullness or distension may be due to fat, fluid, flatus, faeces or fetus.
• Localized distension may be symmetrical and centred around the umbilicus, as in the case of small bowel obstruction, or asymmetrical as in gross enlargement of the spleen, liver or ovary.
• Make a mental note of the site of any such swelling or distension; think of the anatomical structures in that region and note if there is any movement of the swelling, either with or independent of respiration.
• Remember that chronic urinary retention may cause palpable enlargement in the lower abdomen. A scaphoid abdomen is seen in advanced stages of starvation and malignant disease, particularly carcinoma of the oesophagus and stomach.
THE UMBILICUS
Normally the umbilicus is slightly retracted and inverted. As it is at the centre of the abdomen, one’s eyes inevitably come to rest on it at the same time as noting the general shape of the abdomen. If it is everted then an umbilical hernia may be present and this can be confirmed by feeling an expansile impulse on palpation of the swelling when the patient coughs. The hernial sac contains omentum, bowel or fluid. A frequent finding in the umbilicus of elderly obese women is a concentration of inspissated desquamated epithelium and other debris (omphalolith).
MOVEMENTS OF THE ABDOMINAL WALL
Normally there is a gentle rise in the abdominal wall during inspiration and a fall during expiration; the movement should be free and equal on both sides. In generalized peritonitis this movement is absent or markedly diminished, which helps to limit further spread of infection within the peritoneal cavity and the pain of peritoneal irritation (the ‘still, silent abdomen’). To aid the recognition of intra-abdominal movements shine a light across the patient’s abdomen. Even small movements of the intestine may then be detected by alterations in the pattern of shadows cast over the abdomen.
Visible pulsation of the abdominal aorta may be noticed in the epigastrium and is a frequent finding in nervous, thin patients. It must be distinguished from an aneurysm of the abdominal aorta, where pulsation is more obvious and a widened aorta is felt on palpation.
Visible peristahis of the stomach or small intestine may be observed in three situations:
• Obstruction at the pylorus. Visible peristalsis may occur where there is obstruction at the pylorus produced either by fibrosis following chronic duodenal ulceration or, less commonly, by carcinoma of the stomach in the pyloric antrum. Peristalsis will be seen as a slow wave either passing across the upper abdomen from left to right hypochondria or, if gross gastric dilatation is present, passing down to the suprapubic region and ascending to terminate in the right epigastrium. In pyloric obstruction, a diffuse swelling may be seen in the left upper abdomen but, where obstruction is long-standing with severe gastric distension, this swelling may occupy the left mid and lower quadrants. Such a stomach may contain up to 2 litres of fluid and, on shaking the abdomen, a splashing noise is usually heard (‘succussion splash’). This splash is frequently heard in healthy patients for up to 3 hours after a meal, so enquire when the patient last ate or drank.
In congenital pyloric stenosis of infancy not only may visible peristalsis be apparent but the grossly hypertrophied circular muscle of the antrum and pylorus may be felt as a ‘tumour’ to the right of the midline in the epigastrium. Both these signs may be elicited more easily after the infant has been given a feed.
• Obstruction in the distal small bowel. Peristalsis may be seen where there is intestinal obstruction in the distal small bowel or coexisting large and small bowel hold-up produced by distal colonic obstruction, with an incompetent ileocaecal valve allowing reflux of gas and liquid faeces into the ileum. Not only is the abdomen distended and tympanitic (hyperresonant) but the distended coils of small bowel may be visible in a thin patient and tend to stand out in the centre of the abdomen in a ‘ladder pattern’.
• As a normal finding in very thin, elderly patients with lax abdominal muscles or large, wide-necked incisional herniae seen through an abdominal scar.
SKIN AND SURFACE OF THE ABDOMEN
In marked abdominal distension the skin is smooth and shiny. Striae atrophied or gravidarum are white or pink wrinkled linear marks on the abdominal skin. They are produced by gross stretching of the skin with rupture of the elastic fibres and indicate a recent change in size of the abdomen, such as is found in pregnancy, ascites, wasting diseases and severe dieting. Wide purple striae are characteristic of Cushing’s syndrome and excessive steroid treatment.
Note any scars present, their site, whether they are old (white) or recent (red or pink), linear or stretched (and therefore likely to be weak and contain an incisional hernia).
Look for prominent superficial veins, which may be apparent in three situations : thin veins over the costal margin; occlusion of the inferior vena cava; and venous anastomoses in portal hypertension. However, small, thin veins over the subcostal margins are common and usually of no significance. Inferior vena caval obstruction not only causes oedema of the limbs, buttocks and groins, but in time distended veins on the abdominal wall and chest wall appear. These represent dilated anastomotic channels between the superficial epigastric and circumflex iliac veins below, and the lateral thoracic veins above, conveying the diverted blood from long saphenous vein to axillary vein; the direction of flow is therefore upwards. If the veins are prominenti enough, try to detect the direction in which thtj blood is flowing. Distended veins around the umbilicus (caput medusae) are uncommon but, if present, signify portal hypertension, other signs of which include splenomegaly and ascites. Distended veins represent the opening up of anastomoses between portal and systemic veins and are seen in other sites, such as oesophageal varices and piles.
Pigmentation of the abdominal wall may be seen in the midline below the umbilicus, where it forms the linea nigra and is a sign of pregnancy. Erythema ab igne is a brown mottled pigmentation produced by constant application of heat, usually a hot water bottle or heat pad, on the skin of the abdominal wall. It is a sign that the patient is experiencing severe pain.
Finally, inspect both groins, and the penis and
scrotum of a male, for any swelling and to ensure that both testes are in their normal position. Then bring the sheet up just to cover the symphysis pubis.
PALPATION
The stomach should be palpated in both the vertical and horizontal position of the patient because the lesser curvature of the stomach and its high standing tumors are impalpable in the lying position. First palpation should be superficial and tentative. Its aim is to establish tenderness of the epigastrium, irritation of the peritoneum (Shchetkin-Blumberg symptom), divarication of the abdominal muscles, the presence of hernia of the linea alba, tension in the abdominal wall in the region of the stomach, and the presence of muscular defence (defense musculaire). Deep palpation of the stomach should be carried out according to Obraztsov and Strazhesko. The examiner pulls up the skin on the abdomen and presses carefully the anterior wall of the abdomen to penetrate the depth until the examining fingers reach the posterior wall. When pressed against the posterior wall of the abdomen, the stomach slips from under the examining fingers. The shape of the stomach and the size of the examined part can thus be assessed. The greater curvature and the pylorus can best of all be examined by this method.
The greater curvature can be examined by deep sliding palpation in 50-60 per cent and the pylorus in 20-25 per cent of healthy subjects; the lesser curvature can be palpated in gastroptosis. The greater curvature is found to either side of the median line, 2—3 cm above the navel. It appears to palpating fingers as a ridge on the backbone and by its sides. In cases with gastroptosis, the greater curvature can descend below the navel. Correctness of determination can be confirmed if the position of the ridge coincides with that of the lower border of the stomach as determined by other techniques (by percussion, by the splashing sound or stethacoustic palpation). The pylorus is located in the triangle formed by the lower edge of the liver to the right of the median line, by the median line of the body, and the transverse line drawn 3-4 cm above the navel, in the region of the right rectus abdominis muslce. Since the position of the pylorus is oblique (upwards to the right) the palpating movements should be perpendicular to this direction, i.e. from left downwards to the right. The pylorus is identified by palpation as a band (tense or relaxed). When the pylorus is manipulated by the fingers, a soft rumbling sound can be heard. When contracted spastically (pylorospasm) the pylorus remains firm for a long time. Sometimes the pylorus is mistaken for cancer infiltration.
Palpation of the stomach can reveal tumors of the pylorus, of the greater curvature, and of the anterior wall. Tumors of the lesser curvature can be diagnosed with the patient in the upright position. Tumors of the cardial part of the stomach are inaccessible to palpation. Exact information on their location gives X-ray examination.
Palpation of the abdomen. Along with X-ray examination, palpation is the main method of physical examination in diagnosis of diseases of the addominal organs. This method was first appreciated by French physicians (G1enard). Later the Russian internists (Obraztsov, Strazhesko, and others) further developed this useful method.
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 tumors 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 sub-cutaneous 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 ppendicitis, 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 tumors, 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 of 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 organ is pressed against the posterior wall and the examining fingers continue moving over the examined intestine or the stomach 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. All 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. Palpations 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 extent 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 per cent of cases. The sigmoid is only impalpable 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 thickness 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). 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 terminale). 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 then slide laterally, perpendicularly to the axis of the intestine (Vasilenko).
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.
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 before the 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.
Main Clinical Syndromes.
Jaundice
Jaundice is an icteric colouration of the skin and mucosa by the increased content of bilirubin in the tissues and blood. The serum of blood taken from patients with true jaundice also becomes intense yellow. Jaundice is attended (often preceded) by changes in the colour of the urine, which becomes dark-yellow or brown; faeces can be very light or even colourless, or on the contrary, dark-brown.
Jaundice can develop very quickly, within 1-2 days, to become very intensive, or it can develop gradually and be not pronounced (subicteric). Patients themselves (or their relatives) notice yellow colour in their skin. They consult a doctor for this reason. Jaundice can develop with severe itching of the skin, skin haemorrhages and haemorrhages of the nose and the gastro-intestinal tract.
Jaundice occurs in many diseases of the liver, bile ducts, blood, and also diseases of other organs and systems, to which bilirubin metabolic disorders are secondary. Some clinical symptoms attending jaundice are to a certain degree suggestive of its type and origin. Accurate diagnosis of various types of jaundice is possible with special laboratory studies.
True jaundice can develop due to the following three main causes: (1) excessive decomposition of erythrocytes and increased secretion of bilirubin (haemolytic jaundice); (2) impaired capture of unbound bilirubin by the liver cells and its inadequate combination with glucuronic acid (parenchymatous jaundice); (3) obstacles to excretion of bilirubin with bile into the intestine and reabsorption of bound bilirubin in the blood (obstructive jaundice).
Haemolytic (haematogenous) jaundice develops as a result of excessive destruction of erythrocytes in the cells of the reticulohistiocytic system (spleen, liver, bone marrow). The amount of unbound bilirubin formed from haemoglobin is so great that it exceeds the excretory liver capacity to account for its accumulation in the blood and development of jaundice. Haemolytic jaundice is the main symptom of haemolytic anemia. It can also be a symptom of other diseases, such as B12 (folic) deficiency anemia, malaria, protracted septic endocarditis, and other diseases.
The skin of a patient with haemolytic jaundice is lemon-yellow. Skin itching is absent. The amount of unbound bilirubin in the blood is moderately increased (50-200 per cent); the van den Bergh test for bilirubin is indirect. Bilirubin is absent from the urine but the urine is still coloured rather intensely by the markedly increased (5-10 times) stercobilinogen and (partly) urobilinogen. Faeces are intense dark due to the presence of considerable amount of stercobilinogen.
Parenchymatous (hepatocellular) jaundice develops due to the damage of the parenchyma cells (hepatocytes). These cells can capture bilirubin of the blood and bind it with glucuronic acid (the natural detoxicating function of the liver). The natural process of bilirubin excretion in the bile in the form of bilirubin glucuronide (bound bilirubin) is thus impaired. The content of free and bound bilirubin in the blood serum thus increases 4-10 times. In rare cases the increase may be even greater: free bilirubin increases due to hepatocyte dysfunction and bound bilirubin content increases as a result of back diffusion of bilirubin glucuronide from biliary into blood capillaires in dystrophy of the liver cells. Bound bilirubin appears in the urine (bilirubin glucuronide is water soluble and easily passes via the capillary membranes as distinct from free bilirubin). Bile acids are also present in urine, but their content gradually increases. Excretion of stercobilinogen with faeces also decreases because the amount of bilirubin excreted by the liver into the intestine decreases, but faeces are rarely completely discoloured.
This type of jaundice is mainly determined by infection (virus hepatitis or Botkin’s disease, leptospirosis) and toxic affections of the liver (poisoning with mushrooms, phosphorus, arsenic and other chemical substances, medicinal preparations included). But parenchymatous jaundice can develop also in liver cirrhosis.
The skin of patients with this jaundice is typically yellow with a reddish tint. Skin itching is less frequent than in obstructive jaundice because the synthesis of bile acids by the affected liver cells is upset. Symptoms of pronounced hepatic insufficiency may develop in severe course of the disease.
There exists a group of congenital pigmentary hepatoses in which the liver is not affected pathologically, the functional tests are negative, while the process of bilirubin conjugation with glucuronic acid is upset at some of these stages (Gilbert syndrome). This condition is attended by a permanent or intermittent jaundice, which is sometimes pronounced and develops from infancy.
Obstructive (mechanical) jaundice develops due to partial or complete obstruction of the common bile duct. This occurs mostly due to compression of the duct from the outside, by a growing tumor (usually cancer of the head of the pancreas, cancer of the major duodenal papilla, etc.), or due to obstruction by a stone. Bile congestion above the point of obstruction develops and this elevates pressure inside bile passages in continuing bile excretion. As a result, the interlobular bile capillaries become distended and bile diffuses into the liver cells (where dystrophic processes develop) and passes into the lymph and the blood. Moreover, due to increased pressure inside fine bile capillaries, communications are formed at the periphery of the lobules between the capillaries and the lymph spaces, through which bile enters the blood vessels.
Skin and mucosa of patients with obstructive jaundice are yellow. Later, as bilirubin is oxidized to biliverdin, the skin and mucosa turn green and dark-olive. The bound bilirubin content in the blood with direct van der Bergh test is as high as 250-340 mmol/1 or 15-20 mg/100 ml, and more. In protracted jaundice associated with liver dysfunction, free bilirubin content increases as well. Bound bilirubin can be found in the urine (the presence of bile pigments is determined by urinalysis) to give it brown colour and bright-yellow foaming. Faeces are colourless either periodically (in incomplete obstruction, usually by a stone), or for lengthy periods of time (in compression of the bile duct by a tumor). Jaundice increases progressively in such cases; the skin and mucosa gradually turn greenish-brown; cachexia of the patient increases. In complete obstruction of the bile ducts, faeces become colourless (acholic); their colour is clayish and grey-white; stercobilin is absent from faeces.
Bound bilirubin and also bile acids produced by the hepatocytes in ample quantity (cholaemia) are delivered to the blood in this type of jaundice. Some symptoms associated with toxicosis develop: pronounced skin itching, which intensifies by night, and bradycardia (bile acids increase the tone of the vagus nerve by reflex). The nervous system is also affected: the patient develops rapid fatigue, general weakness, adynamia, irritability, headache, and insomnia. If it is impossible to remove the cause of impaten-cy of the common bile duct (stones or a tumor) the liver is gradually affected to add symptoms of hepatic insufficiency.
Portal Hypertension
Portal hypertension is characterized by a stable increase in the blood pressure in the portal vein. Portocaval anastomoses are dilated, ascites develops and the spleen increases in size.
Portal hypertension develops due to obstructed blood outflow from the portal vein as a result of its compression from the outside (by a tumor, enlarged lymph nodes of the porta hepatis in cancer metastases, etc.), or by obliteration of part of its intrahepatic branching in chronic affections of the liver parenchyma (in cirrhosis), or due to thrombosis of the portal vein or its branches. Growth and subsequent cicatrization of connective tissue at the site of degraded hepatic cells of a cirrhotic liver cause stenosis or complete obliteration of part of hepatic sinusoids and intrahepatic vessels. An obstacle is thus created to the blood flow, which increases portal pressure and interferes with blood outflow from the abdominal viscera. In these conditions, transudation of fluids from the vessels into the abdominal cavity is intensified to account for the development of ascites. Decreased oncotic pressure of plasma is an important factor in the development of ascites associated with liver cirrhosis. The pressure decreases because of upset synthesis of albumins in the liver. Sodium and water retention is also important. It occurs due to hypersecretion of aldosterone by the adrenal glands (secondary aldosteronism) and its inadequate inactivation in the liver. The time of the onset of ascites depends on the degree of development of collateral circulation, i.e. on portocaval anastomoses. For a long time the disturbed portal circulation can be compensated for by delivery of blood into the superior and inferior venae cavae from the portal vein via normally existing anastomoses. But in portal hypertension these anastomoses become highly developed.
There exist three groups of natural portocaval anastomoses: (1) in the zone of haemorrhoidal venous plexus; these are anastomoses between the inferior mesenteric vein (the portal vein system) and haemorrhoidal veins emptying into the inferior vena cava; haemorrhoidal nodes develop in portal hypertension which rupture to cause rectal haemorrhage; (2) anastomoses in the zone of the oesophagogastric plexus: this is a collateral leading through the left gastric vein, the oesophageal plexus, and hemiazygos vein into the superior vena cava. In pronounced portal hypertension, marked varicose nodes are formed in the lower portion of oesophagus whose injury (e.g. by hard food) is responsible for possible haemorrhage in the form of haematemesis (blood vomiting), which is the most serious complication of diseases attended by portal hypertension and which is a frequent cause of death; (3) anastomoses in the system of paraumbilical veins communicating with the veins of the abdominal wall and the diaphragm, carrying blood to the superior and inferior venae cavae. In portal hypertension, varicose veins radiate from the umbilicus to give a peculiar pattern known as the caput medusae.
The degree of increase in the pressure in the portal vein system can be determined by a special needle and a water pres’sure gauge. The pressure is measured in the spleen (splenometry) or in varicose veins of the oesophagus. In the latter case the needle is introduced through the oesophagoscope. It is believed that pressure in the spleen is the same as in the portal vein trunk. Normally it is 70-150 mm H2O, while in portal hypertension it rises to
400-600 mm H2O. Contrast techniques are used to reveal obstruction of the portal vein: these are splenoportography and in rare cases transumbilical portohepatography.
The spleen may be somewhat enlarged in venous congestion associated with portal hypertension.
Treatment. In order to remove portal hypertension, whose first danger are oesophagogastric and haemorrhoidal haemorrhages, the patients are operated on for placing anastomoses between the portal vein system and the inferior vena cava.
Hepatolienal Syndrome
The hepatolienal syndrome is characterized by concurrent enlargement of the liver and the spleen in primary affection of either of these organs. Involvement of both organs in a pathological process (diseases of the liver, blood, certain infections, poisoning) is explained by their richly developed reticulohistiocytic tissue. In certain cases, e.g. in thrombosis of the hepatic veins, simultaneous enlargement of the liver and the spleen is determined by venous congestion in them. In addition to palpation, scanning can be used to reveal the hepatolienal syndrome.
Considerable enlargement of the spleen is usually attended by its hyperfunction (hypersplenism), which is characterized by anaemia, leucopenia, and thrombocytopenia. The latter can cause haemorrhagic complications. These changes are explained by inhibition of the haemopoiesis in the bone marrow due to hyperactivity of the spleen as a result of which destruction of the blood cells in the spleen is intensified, and antierythrocytic, antileucocytic, and antithrombocytic autoantibodies are formed in the spleen.
Hepatic Insufficiency and Coma
Despite the considerable compensatory capacity of the liver, its grave acute and chronic diseases are attended by deep disorders in its numerous and very important functions due to the marked dystrophy and destruction of the hepatocytes. Clinicists define this condition as the hepatic insufficiency syndrome.
Depending on the character and acuity of the affection acute and chronic hepatic insufficiency are distinguished. The following three stages of the disease are also distinguished: (1) early compensated stage; (2) pronounced decompensated; and (3) terminal dystrophic stage that ends in a hepatic coma and death.
Acute hepatic insufficiency arises in grave forms of virus hematite (Botkin’s disease) and poisoning with hepatotropic substances (affecting the liver in the first instance). These may be chemical substances (e.g. phosphorus compounds, arsenic, large doses of alcohol) or vegetable poisons (inedible mushrooms containing amanitotoxin, helvellic acid, or muscarine extracted of male fern, etc.). Acute hepatic insufficiency develops rapidly, within several days or hours.
Chronic hepatic insufficiency develops in many chronic diseases of the liver, e.g. in cirrhosis and tumours. Its development is slow and gradual.
Development of hepatic insufficiency is underlain by marked dystrophy and necrobiosis of hepatocytes which is attended by a considerable impairment of all liver functions with formation of collaterals between the portal vein system and the venae cavae. Collaterals develop in cases when the blood flow from the portal vein into the liver is obstructed in any affection of this organ. Large amounts of blood containing toxic substances absorbable in the large intestine pass through the collaterals into the greater circulation system to bypass the liver. Hepatic insufficiency is explained by various complicated metabolic disorders in the liver, upset bile secretory and excretory function, and impaired detoxicating function of the liver.
The pathogenesis of hepatic coma is manifested by grave self-poisoning of the body due to almost complete dysfunction of the liver. The body is poisoned by the non-detoxicated products of intestinal (bacterial) protein decomposition, final products of metabolism, and especially ammonia. Normally, the major part of ammonia is captured by the hepatocytes and converted to urea (in the ornithine Kreb’s cycle), which is then excreted by the kidneys. Phenols, which are normally detoxicated in the liver by their combination with glucuronic and sulphuric acids, also have a toxic effect. Other toxic substances also accumulate in the blood in the presence of hepatic insufficiency. The electrolyte metabolism becomes upset, and in severe cases, hypokaliaemia and alkalosis develop.
Hepatic insufficiency may be aggravated and coma may be provoked by alcohol, barbiturates, some analgesics (morphine, promedol), protein-rich diet (which intensifies putrefactive processes in the intestine, production of toxic substances and their absorption in the blood), by profuse haemorrhage from the digestive tract (which often aggravates portal cirrhosis of the liver), by large doses of diuretics, instantaneous withdrawal of large amounts of ascitic fluid, severe diarrhoea, and the attending grave infectious diseases.
Clinical signs of hepatic insufficiency usually combine with symptoms of the liver disease that provoked hepatic insufficiency.
The intensification of the symptoms by stages is vividly illustrated by the progressive development of hepatic insufficiency (in patients with liver cirrhosis, tumour of the liver, and other diseases of this organ).
The clinical symptoms are absent during the early stage of hepatic insufficiency, but the body’s tolerance to alcohol and also to other toxic substances decreases, and the findings of laboratory load tests change.
During the second stage, clinical signs of hepatic insufficiency develop; first mild but later more pronounced non-motivated fatigue, poor appetite, increased weakness in usual physical exertion, frequent dyspepsia (poor tolerance of fat food, the presence of meteorism, rumbling and pain in the abdomen, changed stools), which are explained by disorders of bile secretion and digestive processes in the intestine. Upset assimilation of vitamins explains polyhypovitaminosis. Fever, which is not infrequent in hepatic insufficiency, can be due to both the main disease and impaired detoxication of some proteinous pyrogens by the liver. Jaundice and hyperbilirubinaemia with accumulation of free (indirect) bilirubin in the blood are frequent in hepatic insufficiency. Deranged structure of the liver and upset cholestasis can stimulate accumulation of bilirubin glucuronide (“direct” bilirubin) in the patient’s blood.
Deranged albumin synthesis in the liver and also pronounced hypoalbuminaemia can cause hypoproteinaemic oedema and intensify ascites, which often occurs in patients with chronic liver affections. Upset synthesis of some blood coagulating factors (fibrinogen, prothroinbin, proconvertin) and also decreased blood platelet content (due to hypersplenism that attends many chronic diseases of the liver) provoke the onset of haemorrhagic diathesis (skin haemorrhages, nasal bleeding, haemorrhage in the intestinal tract). Inadequate inactivation of oestrogens by the chronically affected liver provokes endocrine disorders (gynaecomastia in men, menstrual disorders in women, etc.).
Changes in laboratory tests (hepatic tests) are significant in the second stage of hepatic insufficiency. Characteristic is the decreased content of substances produced by the liver: albumin, cholesterol, fibrinogen, etc. Considerable changes in the liver function are also revealed by radioisotope hepatography.
The third, final stage of hepatic insufficiency is characterized by even deeper metabolic disorders and dystrophic changes, which are pronounced not only in the liver but also in other organs. Patients with chronic liver diseases develop cachexia. They also suffer from nervous and psychic disorders which are precursors of coma: decreased mental ability, slow thinking, slight euphoria, sometimes depression, and apathy. The patient becomes easily irritable, his moods are quickly changed, attacks of melancholy and frustration occur at times, and sleep is deranged. Derangement of consciousness and loss of orientation in time and space develop along with partial loss of memory, disordered speech, hallucinations, and somnolence. Specific tremor (slow and fast) of the upper and lower limbs is characteristic.
The precoma period may last from a few hours to several days and even weeks. The patient may recover from this state, but coma develops in most cases.
The clinical picture is characterized first by excitation and then by general inhibition (stupor) and progressive derangement of consciousness (sopor), to its complete loss (coma). The EEG curve is flattened. The reflexes are decreased, but hyperreflexia and pathological reflexes (sucking and grasping) develop. Motor anxiety, clonic convulsions due to hypokaliaemia, muscular twithching, and tremor of the extremities (arrhythmical and rhythmical twitching of the fingers and toes) are characteristic. Respiration rhythm becomes upset. Kussmaul respiration (less frequently Cheyne-Stokes respiration) develops. Incontinence of faeces and urine ensues. The patient’s breath (and also urine and sweat) smells “sweety hepatic” (fetor hepaticus) because of liberation of methyl mercaptan which is formed in deranged methionine metabolism. Inspection of the patient often reveals signs of haemorrhagic diathesis (bleeding gums, nasal and skin haemorrhage). The patient’s temperature in the ter minal period is subnormal. Jaundice is intensified. The liver may remain enlarged or its size may decrease. Laboratory tests show moderate anaemia, leucocytosis, increased ESR, low counts of platelets and fibrinogen; the prothrombin time increases, hepatic functional tests become sharply upset, and the bilirubin level increases. The content of residual nitrogen and ammonia in the blood serum increases to indicate secondary affections of the kidneys (the hepatorenal syndrome).Hyponatriaemia, hypokaliaemia, and metabolic acidosis develop. Hepatic coma usually terminates fatally. But the patient can in some cases be saved.
Clinical picture. Portal cirrhosis of the liver occurs mostly between the ages of 40 and 60. The incidence in men is twice higher than in women. Postnecrotic and biliary cirrhosis of the liver develop in younger patients, mostly in women.
Clinical manifestations of liver cirrhosis depend on the degree of affection of the liver cells and the associated hepatic dysfunction and portal hypertension, on the stage of the disease (compensated or decompensated), and also on the activity of the process. The following symptoms of the disease are most characteristic of the majority of patients with various forms of liver cirrhosis.
Pain in the region of the liver, in the epigastrium, or diffuse pain in the whole abdomen is usually dull and boring, intensifying after meals, especially after fatty food, ample drinking and physical exercise. Pain is usually associated with enlargement of the liver and distension of the capsule, or with necrotic foci located near the capsule, with perihepatic symptoms, and also concurrent inflammatory affections of the bile ducts.
Dyspepsia in the form of decreased appetite to complete anorexia, the feeling of heaviness in the epigastrium after meals, nausea, vomiting, meteorism and dyspeptic stools (especially after fatty meals) depend mainly on deranged secretion of bile and hence defective digestion. But they can also be associated with the attending dyskinesia of the bile ducts or alcoholic gastroenteritis.
Decreased work capacity, general weakness, fatigue and insomnia are often observed in cirrhosis of the liver. Fever is usually irregular and sometimes of the undulant type. It often attends postnecrotic cirrhosis of the liver and is explained by necrotic destruction of the liver cells. Marked fever is characteristic of the active period and infectious cirrhosis.
A haemorrhagic syndrome is observed in 50 per cent of patients with cirrhosis of the liver. Profuse bleeding from varicose veins of the oesophagus and the stomach can often be early signs of portal cirrhosis;they are caused by increased pressure in the veins of the oesophagus and the stomach. In other variants of cirrhosis nasal, gum, uterine and skin haemorrhages develop in marked decompensation. They depend on the decreased coagulability of blood due to liver dysfunction.
Signs of cirrhosis are as follows. Cachexia is especially characteristic of patients with portal cirrhosis of the liver. In long-standing disease the subcutaneous fat disappears along with atrophy of muscles, especially of the upper shoulder girdle. The appearance of such patients is quite specific: the face is very thin with grey or subicteric skin; the lips and the tongue are bright-red; the cheek bone region is affected by erythema; the extremities are thin and the abdomen is large (due to ascites, enlarged liver and spleen);the subcutaneous veins of the abdominal wall are dilated, the legs are oedematous. Malnutrition is usually associated with disordered digestion and assimilation of food, and impaired synthesis of proteins in the affected liver.
Jaundice (except the cases with biliary cirrhosis) is a sign of hepatocellular insufficiency associated with necrosis of the liver cells. The affected hepatocytes partly lose their capacity to capture bilirubin from blood and to bind it with glucuronic acid. Bilirubin excretion into bile is disordered as well. Free (indirect) and bound (direct) bilirubin of blood serum therefore also increases. Jaundice is usually characterized by partial decolouration of faeces and by the presence of bile in the duodenal contents. Jaundice is often attended by skin itching. Jaundice associated with biliary cirrhosis resembles obstructive jaundice; severe skin itching is observed. The intensity of jaundice varies from light subicteric to marked jaundice (depending on the degree of obstruction of the bile ducts). In prolonged obstruction of the extrahepatic duct the skin acquires a greenish tint which depends on oxidation of bilirubin to biliverdin. Moreover, brown pigmentation of the skin may also be observed. It depends on accumulation of melanin.
“Minor” signs of cirrhosis can also be revealed during examination of the patient. These signs are as follows: (1) spider angiomata (they may develop years before marked symptoms of the disease develop); their number increases and the colour intensifies during exacerbation of the disease; (2) erythema of the palms; (3) red lustrous lips, scarlet mucosa of the mouth, scarlet (lacquered) tongue; (4) gynaecomastia (increased mammary glands) and other female sex characters developing in men (decreasing growth of hair on the face, chest, abdomen, and the head); (5) xanthomatous plaques on the skin (observed in patients with biliary cirrhosis of the liver); (6) Hippocrates fingers with hyperaemic skin at the nail beds. Inspection of the abdominal skin can reveal dilation of the veins that can be seen through the thinned skin of the abdominal wall (caput medusae). Collateral venous system can be seen on the chest as well. Haemorrhoidal veins are often dilated.
Ascites is the most characteristic sign of portal cirrhosis. Ascites may develop slowly and the abdomen grow to huge size; the patient develops dyspnoea. Oedema may develop; hydrothorax may also occur in some cases. In other variants of cirrhosis, ascites develops at later stages of the disease.
Enlarged liver can be palpated in 50-75 per cent of patients with cirrhosis. The enlargement can be insignificant, only determinable by percussion, or considerable when the liver occupies the entire left part of the abdominal cavity. The liver is firm, the surface is sometimes irregular, and the lower edge sharp. Enlargement of the spleen is often attended by its increased activity (hypersplenism).
Laboratory findings. An active cirrhotic process is characterized by anaemia, leucopenia, thrombocytopenia, and increased ESR. Anaemia can be due to hypersplenism and gastro-intestinal haemorrhage, hepatocellular insufficiency, and often increased haemolysis, which is accompanied by reticulocytosis of the peripheral blood.
The blood serum bilirubin content becomes considerable only in the final stage of the disease. At the same time, the affection of the excretory function of the cirrhotic liver can be assessed by the presence of the conjugated fraction of bilirubin (bound bilirubin). Its content increases iormal and increased total bilirubin. The free bilirubin content increases in the blood serum as a result of upset conjugation of bilirubin in the liver cell and haemolysis. The blood serum bilirubin content varies in biliary cirrhosis of the liver from 26 to 340 mmol/l (1.5-20 mg/100 ml), mostly at the expense of bound bilirubin.
The presence of much urobilin in the urine indicates liver insufficiency. The amount of urobilin in the urine and stercobilin in the faeces decreases in the presence of pronounced jaundice when a small amount of bilirubin enters the intestine. Bilirubin is found in the urine of patients with jaundice.
The upset excretory function of the liver is manifested by retention of bromsulphthalein in the blood (during its intravenous administration) and also by radioisotopic hepatography and scanning of the liver.
Affection of liver cells is manifested by characteristic changes in the protein indices: decreased concentration of serum albumins and hypergammaglobulinaemia which in turn decreases the albumin-globulin coefficient. Activation of the inflammatory process in the liver involves an increase in the a2–globulins, while jaundice causes an increase in b-globulins. During remissions, all these changes become less pronounced. The blood level of lipids and cholesterol also increases considerably in the presence of biliary cirrhosis. A sensitive index of liver dysfunction is the decreased activity of cholinesterase. Transaminase activity increases in exacerbation of liver cirrhosis. Activity of alkaline phosphatase also increases in biliary cirrhosis.
The decreased prothrombin content (which is synthesized by the liver cells), increased antithrombin coagulative activity and decreased total coagulative activity of plasma are important in the aetiology of haemorrhagic diathesis in liver cirrhosis.
Laparoscopy and especially biopsy of the liver help reveal intravital morphological signs of each variant of liver cirrhosis. Varicose veins of the oesophagus are revealed by X-rays.
It is not always possible to differentiate between all variants of liver cirrhosis from the data of clinical and instrumental methods of examination, nevertheless, by comparing the mentioned signs, one caotice that the symptoms of portal hypertension in portal cirrhosis of the liver are often revealed long before the functional insufficiency develops. Hepatic insufficiency only develops at a later stage of the disease. But in the presence of postnecrotic cirrhosis of the liver, the symptoms of hepatic insufficiency develop early. They largely determine the entire clinical picture of the disease. Chronic jaundice (obstructive type) prevails in the clinical picture of biliary cirrhosis along with satisfactory general condition of the patient, who suffers from skin itching, sometimes fever (associated with chills); the blood alkaline phosphatase and cholesterol content increases. Transcutaneous cholangiography is used to determine the cause of cholestasis. The procedure is done when indicated.
Complaints of patients with compensated liver cirrhosis are not serious. : The disease is often revealed accidentally during examination (enlarged liver and spleen). Remissions may be long (measured by years). Decompensated active cirrhosis is characterized by marked symptoms of the disease and rapid progressive course.
Course. The course of the disease is usually progressive. The overall term of the disease is usually 3 to 5 years; in rare cases the disease may last 10 years and even longer (usually in biliary cirrhosis of the liver).
The terminal period of the disease, irrespective of the form of cirrhosis, is characterized by gastro-intestinal haemorrhage and progressive signs of functional insufficiency of the liver, with finally developing coma. These are two most frequent direct causes of death of patients with liver cirrhosis. Gastro-intestinal haemorrhage (blood vomiting and melaena) is caused by the rupture of varicose nodes in the lower third of the oesophagus or, less frequently, in the stomach. A direct cause of varicose haemorrhage is physical strain or local affection of the mucosa (e.g. by coarse food). Profuse haemorrhage (if it does not cause death) can cause anaemia with subsequent impairment of the function of the liver cells and accelerated development of hepatic coma.
Treatment. Cirrhosis of the liver in the compensation stage is treated by preventing its further affection with alcohol, toxic substances, etc., and also by rational organization of work regimen and nutrition (high-calorie diet rich in protein and vitamins). During decompensation stage, hospital treatment is required. Glucocorticosteroid hormones are given in the active process (except cases complicated by dilation of the oesophageal veins);syrepar (hydrolysate of cattle liver), essential (a complex preparation containing essential phospholipids), and vitamins are also prescribed. Patients with ascites are prescribed a diet restricted in salt and diuretics (periodically). If ascites cannot be cured by diuretics, the fluid is released by paracentesis.
In order to decrease the lipid content of the serum in primary biliary cirrhosis, lipoic acid preparations are prescribed. Skin itching is removed by cholestyramine (preparation binding fatty acids). Surgical treatment is indicated in cases with secondary biliary cirrhosis of the liver, e.g. in obstruction of the bile duct by a stone.
Acute gastritis is an acute inflammation of the stomach. From the point of view of pathological anatomy the following are distinguished: 1—simple, or catarrhal gastritis in which the gastric mucosa is inflamed; 2—corrosive gastritis, in which the submucous layer is also involved (with erosions, haemorrhages, and necrosis); and 3—phlegmonous gastritis characterized by purulent inflammation of all stomach layers.
Aetiology and pathogenesis. The food factor is the most important among all causes of gastritis. Rough, hot or cold food, food which is difficult to assimilate, and alcohol irritate the gastric mucosa causing gastritis. Some medicines (steroid hormones, salicylates, iodine preparations, etc.) can provoke acute gastritis. Acute or chronic infections (measles, scarlet fever, influenza, pneumonia) are often attended by acute gastritis. The nervous factor is also important. Acute gastritis is among the most important manifestations of food poisoning.
Symptoms. The manifestations of acute gastritis can vary from mild to very pronounced symptoms. Inflammation begins 2-4 hours after ingestion of the irritating factor, while the clinical symptoms develop in 6-8 hours. The patient complains of pain in the epigastrium, loss of appetite, nausea, and vomiting. The body temperature is often elevated and the pulse accelerated; the patient’s breath is foul, his tongue is coated with a dirty fur. Palpation of the abdomen is painful (epigastric pain); nausea intensifies. Changes in the blood include leucocytosis and increased ESR.
The onset of the disease is marked by hyperacidity which is followed by decreased gastric secretion. Gastroscopy reveals hyperaemic mucosa, the presence of mucus, and in some cases erosions and haemorrhage. The patient usually recovers in 2-4 days, while the stomach mucosa is completely restored in 10-15 days.
Course. The disease ends with recovery in most cases but acute gastritis may sometimes convert into a chronic process. Corrosive and phlegmonous gastritis runs a markedly more severe course. The stomach wall may be perforated and the prognosis in such cases is aggravated.
Treatment. The patient should abstain from food for 1-2 days. The stomach and the intestine should be emptied from food remains by irrigating it with water, isotonic sodium chloride solution or a0.5per cent sodium bicarbonate solution. If pain is severe, atropine and platyphylline should be administered subcutaneously; anaesthesine should be given for incoercible vomiting (0.3 g, 2-4 times daily). The patient should remain in bed and warmth should be applied to the epigastrium. Gastric lavage in acid poisoning should be done with warm water containing magnesium oxide, milk, and egg white; in alkali poisoning, the stomach should be irrigated with a weak acetic or citric acid solution. Gastric lavage is useful only if it is performed not later than 30 minutes after ingestion of poison. During the first and second days of acute gastritis the patient should be given a lot of liquid to drink (tea, rice water, citric juices). In severe cases up to \ litre of isotonic sodium chloride solution or a 5 per cent glucose solution should be infused subcutaneously during the first days of the disease. Yogurt, sour milk, thin porridge, soft-boiled eggs, and potato puree can be given in 3 or 4 days.
Chronic Gastritis
This is the affection of gastric mucosa with involvement of the secretory, motor, and other functions of the stomach. Chronic gastritis occurs in 50 per cent of all patients with gastroenterological pathology.
Aetiology and pathogenesis. Chronic gastritis is a polyaetiological disease. The aetiological factors are divided into exogenic and endogenic ones. The exogenic factors include inadequate diet, rough or spicy food, alcohol abuse, smoking tobacco, inhalation of acid or alkali vapours, etc. The endogenic factors causing chronic gastritis are diseases of the gall bladder, pancreas, thyroid or pituitary glands, upset metabolism (diabetes mellitus, podagra, obesity).
Pathological anatomy. Surface and atrophic (moderate and pronounced) gastritis are distinguished. Further subdivision includes hypertrophic and polypous gastrites. The morphological changes occurring in chronic gastritis are usually a combination of dystrophic changes in the glandular elements, hyperplastic and atrophic processes in the mucosa, inflammatory infiltration of the interstitial tissue, and a specific reconstruction of the glands.
Symptoms. Two forms of the disease are differentiated: 1—hypo-secretory gastritis; and 2—gastritis with normal or increased gastric secretion.
Gastritis with hyposecretion is marked by dyspepsia: eructation, nausea, and discomfort in the epigastrium. The patient often complains of an unpleasant taste in the mouth, vomiting on an empty stomach, and diarrhoea. Achylous diarrhoea occurs mainly in cases where external secretory pancreatic dysfunction accompanies gastric hyposecretion. Digestion is upset and putrefactive and fermentative processes develop in the intestine.
Diagnosis of chronic gastritis depends on the results of laboratory examination of gastric juice, gastroscopy, and on X-ray and biopsy findings. The study of histamine or pentagastrin stimulated secretion shows a markedly decreased output of hydrochloric acid. X-ray studies do not provide reliable information about the presence or absence of chronic gastritis. Only gastroscopy and biopsy of gastric mucosa can give reliable evidence. These methods supply full information concerning the size of the affected area and the character of chronic gastritis.
Course. The progress of the disease is slow. Exacerbations are followed by remissions. If the disease runs protracted course enteritis, colitis, cholecystitis, and anaemia may develop. The patients usually preserve their work capacity.
Chronic gastritis with normal or increased acidity occurs mostly in tobacco smokers and in alcohol abusers.
Symptoms. The patient complains of epigastric pain which usually occurs 2-3 hours after eating spicy food; night pain sometimes develops. The patient also complains of persistent heartburn, eructation, and sometimes vomiting. The tendency to spastic constipation develops. Gastrointestinal disorders often combine with symptoms of neurasthenia and vegetovascular dystonia (irritability, deranged sleep, rapid fatigue, hyperhidrosis, arterial hypotension, salivation, etc.).
Chronic gastritis with normal and increased acidity should be differentiated from peptic ulcer. X-ray and gastroscopy are decisive for diagnosis. X-ray examination reveals intensified peristalsis of the pylorus, chaotic relief of the gastric mucosa, and the presence of liquid in the stomach. A niche and deformities of the stomach and the duodenum can also be revealed in patients with peptic ulcer. Gastroscopy of patients with chronic gastritis with normal secretion reveals hyperaemic oedematous mucosa of the stomach. Morphological studies of gastric mucosa specimens reveal surface gastritis and sometimes moderately pronounced atrophic gastritis of the fundus.
Course. The course of chronic gastritis with normal gastric and increased gastric secretion is comparatively benign. The general condition of the patient is satisfactory and responds rapidly to therapy.
Treatment. The cause of the disease should first of all be eliminated, if possible. The patient must stop smoking and drinking alcohol and the diet should be normalized. Easily assimilated food (porridges, lean curds, soft-boiled eggs, potato puree, etc.) should be given during exacerbations of chronic gastritis with decreased secretion. Fatty meat, spices, or vegetables containing much cellular tissue should be excluded. Fruit and vegetable juices, vegetable and meat decoctions, boiled fish, and lean meat could be added to the diet later. Food should be taken at regular intervals and under comfortable conditions. Hydrochloric acid with pepsin or gastric juice should be prescribed for chronic gastritis with decreased acidity during the decompensation phase. Since absorption of vitamins is upset, vitamins C, PP, and B should be given supplementary.
The diet in chronic gastritis with normal and hypersecretion is the same as in peptic ulcer. Viscous soups, milk, jellies, omelette, and soft-boiled eggs should be preferred (diets No la and No 1b, see Ch. 27). Atropine, platyphylline, papaverine, belladonna preparations, and alkalis are given (like in peptic ulcer).
Chronic gastritis can be prevented by proper nutrition (regular and adequate meals under comfortable conditions). Smoking and drinking alcohol should be stopped, acute gastritis should be treated properly. Patients with chronic gastritis should receive appropriate treatment and follow all doctor’s orders concerning prophylaxis. Achylous gastritis is a predisposing factor of gastric cancer and the patients should, therefore, be regularly examined for early diagnosis of possible cancer.
Peptic Ulcer
Peptic ulcer is a chronic disease characterized by seasonal exacerbations with ulceration of the stomach wall or of the duodenum.
Aetiology and pathogenesis. Peptic ulcer is characterized by the development of defects in the walls of the stomach or the duodenum caused by the digestive action of gastric juice. Neurohumoral and local mechanisms of digestion, and also structural changes in the mucosa of the stomach and the duodenum are involved in the aetiology and development of the disease. Disorders in both the central and vegetative nervous systems attend gastroduodenal ulcer. Disorders in the central nervous system cause disturbances in the synthesis and secretion of hormones, primarily of the adrenal and pituitary
hormones. Hereditary traits are also important. The disease incidence is much higher among those whose parents suffer from peptic ulcer. Improper nutrition, excessive carbohydrate intake, rough food, alcohol, and tobacco provoke hypersecretion of gastric juice and formation of ulcer.
Pathological anatomy. The following types of peptic ulcer with its complications are distinguished: 1—a simple ulcer with no reactive changes around it; 2—callous ulcer characterized by infiltration and thickening of its edges; 3—penetrating ulcer with involvement of the adjacent organs, e.g. the pancreas, liver, transverse colon; 4—perforating ulcer opening into the abdominal cavity. The ulcer heals by cicatrization with formation of commissures, deformities of the stomach or the duodenum, and with contraction of the pylorus. The common location of ulcer is the lesser curvature; less frequently—the cardiac part of the stomach. The duodenum is usually affected in its bulb.
Clinical picture. The main symptom of the disease is abdominal pain which may be cutting, pressing, boring, etc. Pain is mostly localized below the stomach. In the presence of the duodenal ulcer the pain often radiates into the back, left hypochondrium, and left scapula. Depending on the time after meals, the pain can be classified as early (occurring 30-90 minutes after eating) and late (3-6 hours after eating). Early pain is more characteristic of gastric ulcer and late pain of duodenal ulcer. Pain may also occur when the patient is hungry. It is characteristic of the duodenal ulcer and is relieved after meals. Seasonal exacerbation of pain is characteristic of peptic ulcer: exacerbations usually develop in early spring or late autumn.
The dyspeptic symptoms are mainly heartburn and vomiting. Heartburn is caused by increased acidity of the gastric juice and regurgitation of the stomach contents into the oesophagus. Heartburn is more common after meals; less frequently it occurs at night or on a fasting stomach. Vomiting is more characteristic of ulcer in the distal portion of the stomach and the duodenum. Vomiting usually relieves the patient. Nausea and acid regurgitation are frequent in peptic ulcer. The appetite is usually normal but the patient often tries to abstain from eating for the fear of pain.
Palpation of the abdomen is important for the diagnosis of peptic ulcer. Palpation reveals muscular strain and tender spots in the epigastrium and right hypochondrium. The study of the gastric contents reveals its increased acidity, especially if the ulcer is located in the duodenum. Occult bleeding occurs in about 50 per cent of all cases.
X-ray examinations reveal the following: 1—a niche; 2—a stable deformity of the stomach and the duodenum; 3—regional spasm of the greater curvature; 4—spastic contraction of the stomach and the duodenum; 5—open pylorus. Gastroscopy and biopsy under visual control are very important diagnostically (especially in differential diagnosis of peptic ulcer and gastric cancer).
Common complications of peptic ulcer are haemorrhage, perforation, and penetration of the ulcer, stenosed pylorus, and cancerous degeneration of the ulcer. Gastric haemorrhage is manifested by haematemesis and tarry stools. Profuse haemorrhage manifests by anaemia, dizziness, weakness, tachycardia, and a fall of arterial pressure.
Perforating and penetrating ulcers are severe complications (perforation can cause acute peritonitis). Penetrating ulcer runs a less severe course. A perforating ulcer is manifested by a sudden severe pain which is first epigastric but later spreads over the entire abdomen. Percussion does not reveal liver dullness in the right hypochondrium. The abdomen is very painful to palpation during the first 2-3 hours; the abdominal muscles are strained. The pain lessens in 3-4 hours and the patient erroneously feels relieved. Signs of diffuse peritonitis appear in 7-8 hours: high body temperature, chills, accelerated pulse, falling arterial pressure. Palpation of the abdomen causes severe pain: symptoms of peritoneal irritation appear. Changes in the blood include: leucocytosis with the shift to the left and increased ESR.
Perforating ulcer of the stomach and the duodenum should be differentiated from intestinal obstruction, extrauterine pregnancy, perforating appendicitis, acute cholecystitis, and acute pancreatitis. X-ray examination reveals accumulation of gas in the abdomen in perforating ulcer. Extrauterine pregnancy with a rhexis of the oviduct has a special anamnesis, anaemia, and different localization of pain.
Stenosed pylorus is a stable narrowing of the pylorus in a protracted course of ulcer. The patient complains of severe pain at night, especially in the lying position. Vomiting is frequent and pain relieving. Anorexia and weight loss are characteristic. X-ray studies show distension of the stomach and retention of barium sulphate suspension.
It is difficult to detect the moment when an ulcer converts into cancer. Pain occurs irregularly and soon becomes permanent. The gastric secretion decreases and occult blood is constantly found in the faeces. Anaemia develops, the condition of the patient deteriorates, wasting is rapid, while medication is inefficient. Studying specimens taken from the ulcer bottom and ridges helps diagnose cancer.
The prognosis of peptic ulcer depends on the duration of the disease, its special features, and the presence of complications. The prognosis is worse if the relapses are frequent and difficult to manage. Duodenal ulcer converts into cancer in rare cases but it is more difficult to cure it than gastric ulcer.
Treatment of peptic ulcer may be either conservative or surgical. The following principles are important in conservative treatment: 1—early start of treatment; 2—physical and psychic rest; 3—appropriate diet; 4—medication and physiotherapy; 5—prohibition of alcohol and smoking; 6—observation of the regime and diet even when there are no exacerbations.
Exacerbations should be treated in the hospital. The patient may be discharged from the hospital only after 5-6 weeks of treatment.
The diet should be caloric and should decrease the secretory and, motor function of the stomach and the intestine. Smoked food, fats, spices and condiments (mustard, horse-radish, onions, vinegar, etc.) or food that stimulates gastric secretion (meat and fish soups, fried dishes, alcohol) should be excluded from the diet. During the first 1-2 weeks the patient should eat milk, viscous soups, soft-boiled eggs, jellies, and juices. Solid food should be crushed. The patient should eat 5-6 times daily. The temperature of cold dishes should not be below 15°C and of hot dishes, not above 50°C. The daily load should be about 2000 kcal. As the condition improves, the patient can eat milk porridges, steamed meat and fish (in addition to the previously given dishes). In 4-5 weeks the patient is allowed to eat wheat bread, lean meat and fish, sour milk, sour cream, curds, porridges, macaroni. As soon as the ulcer scars form, the diet is enlarged but the dietary principles should be observed for months and years after cicatrization of the ulcer.
Alkalis are given to neutralize the aggressive properties of gastric juice. Vicalin, vicair, roter, almagel, and other preparations are used. No-spa, papaverine, and halidor are administered for spasms. Cholinolytics are prescribed to inhibit the motor activity of the stomach and to decrease acidity (atropine, methacin, platyphylline). Trioxazine, chlordiazepoxide, and diazepam are given to relax the nervous system. Cimetidine, biogastrone, eglonyl, and some other preparations have been recently used in clinical practice.
Physical methods of treatment are also used: warming compresses, mud and paraffin packs, diathermia, and mineral waters. Warm procedures should be excluded in cases where haemorrhage or cancer is suspected. Operative treatment is indicated for complications, e.g. in perforating ulcer, in stenosed pylorus, and in conversion of ulcer into cancer.
A patient with haemorrhage should be ensured complete rest, cold on the epigastrium; peroral administration of medicines should be suspended; the patient should abstain from eating. A 1 per cent vikasol solution is injected subcutaneously, a 10 per cent calcium chloride solution and a 5 per cent e-aminocaproic acid should be injected intravenously. A transfusion of 100-200 ml of blood is also indicated. If the arterial pressure falls, caffeine or mesaton should be injected subcutaneously, or norepinephrine intravenously (dropwise).
Peptic ulcer can be prevented by a correct organization of the living and working conditions, a rational diet, abstention from alcohol and smoking, and by sports. A patient with peptic ulcer should be given a dispensary care in order to preclude possible exacerbations and to reveal early stages of cancerous degeneration.***
Stomach Cancer
Stomach cancer stands first on the list of the most common lethal malignancies.
Aetiology and pathogenesis. These are unknown. Hot and coarse food, smoking and drinking alcohol are among the predisposing factors. Chronic atrophic gastritis, peptic ulcer, polyps of the stomach, and pernicious anaemia can also promote the onset of stomach cancer.
Pathological anatomy. Stomach cancer is usually located in the pyloric part of the stomach and in its lesser curvature. Microscopically differentiated are adenocarcinoma, mucinous carcinoma, scirrhous carcinoma, solid carcinoma, medullary and non-differentiated carcinoma, and rare and mixed forms of cancer. Mucinous carcinoma spreads diffusely over the stomach wall spreading to the omentum and the peritoneum. Significant amounts of mucin can be determined histologically. Scirrhous carcinoma is a diffuse affection as well. Microscopy reveals formation of fibrous tissue in the submucous and muscular layers of the stomach. The lower the morphological differentiation of stomach cancer, the higher its malignancy.
Clinical picture. Symptoms of stomach cancer are quite varied and depend on the seat of cancer, the size of the affected area, and the morphological properties of the tumour. Two periods are distinguished during the course of cancer: early and progressive. The early period is latent. The symptoms of the previous disease (chronic gastritis, peptic ulcer, polyps) are observed. The disease is often symptomless. The test for occult blood is positive.
The gastric symptoms are often non-pronounced and the signs of metastases into the lymph nodes, the liver, the ovaries, and other organs are more prominent. If the tumour metastasizes into the liver, the patient develops jaundice and ascites, which frequently causes the erroneous diagnosis of primary cancer of the liver.
During the further progress of cancer, the patient loses weight with subsequent cachexia and anaemia. The patient often complains of epigastric pain and blood vomiting during this period. A firm tubercular tumour which moves during respiration can often be palpated.
Modern diagnosis of cancer is based on complex examinations of patients with suspected cancer. As a rule, cancer develops in patients aging over 40 and having various chronic diseases of the stomach {chronic atrophic gastritis with reconstruction of the mucous membrane, chronic peptic ulcers which do not undergo cicatrization for long periods of time, polyps, pernicious anaemia, etc.). X-ray gastroscopy, biopsy, and cytological methods of examination are the most informative in this respect. Complex examination is most effective for establishing a correct diagnosis of stomach cancer in about 95 per cent of all cases.
Course and complications. Stomach cancer can run a symptomless course for a protracted period of time. If the cardiac part is the seat of cancer, the passage of food in the terminal stage of the disease is difficult, eventually it becomes the cause of cachexia. The same picture is observed with cancer of the pyloric part of the stomach. The most dangerous complications of stomach cancer are haemorrhage, perforation, and penetration of the tumour. Profuse haemorrhage is more frequent with localization of cancer in the lesser curvature which is invested with large vessels. Perforated stomach is manifested by an acute abdomen.
Prognosis of stomach cancer, like that of all malignant tumours in general, is unfavourable. It is more benign if a radical operation is performed during the early stage of the disease. Chemotherapy and radiotherapy of stomach cancer are not effective enough.
Prophylaxis of stomach cancer consists primarily in revealing and treating precancer diseases, e.g. chronic atrophic gastritis, polyps, or callous ulcer. In the absence of contraindications, patients with gastric polyps and callous ulcer should be treated surgically.
Treatment. It has already been said that the only effective method is surgical. Total or partial resection should be done. Of medicinal preparations used to treat cancer 5-fluorouracyl is the most effective. The diet should be the same as in chronic gastritis. Food should be easily assimilated and rich in vitamins, fats, and proteins. Transfusion of blood or erythrocytic mass is indicated for haemorrhages and pronounced anaemia. In the presence of a marked pain syndrome, promedol and papaverine should be given. Morphine or pantopon, and also sedatives and vitamins should be given during the terminal stage of the disease.
Acute Enteritis
Enteritis is inflammation of the small intestine. Many factors are responsible for the onset of the disease. The most common of them are: 1—overeating, or eating spoiled food; 2—poisoning with mushrooms, medicines, arsenic, mercury, or other industrial poisons; 3—microorganisms (salmonellae, staphylococci, cholera vibrio, etc.) and their toxins; 4—allergy to some foods or medicines.
Clinical picture. Diarrhoea is the main clinical symptom of acute enteritis. Bowel movements are frequent (4-10; in severe cases to 20 daily). The patient complains of poor appetite, nausea, vomiting, abdominal pain, rumbling, and flatulence. The body temperature rises and the arterial pressure falls in severe cases. Because of the great loss of liquid and salts with stools, electrolyte disorders and dehydration develop. Faeces contain much mucus, muscular fibres, and fat.
Treatment. Bed-rest is recommended. Purgatives are given in acute food and industrial poisoning (1-2 tablespoonfuls of castor oil or 20-25 g of magnesium sulphate in half a glass of water). Water and tea are recommended during the first two days. A sparing diet is prescribed for the 3-5th days: ruskvs, mucinous soups, rice water, porridge, crushed vegetables, and lean meat. Rough or spicy food is contraindicated. The patient should eat 6-8 times daily in small portions. Belladonna preparations and papaverine (0.04 g, 3-4 times daily) are helpful. Inflammation in the intestine is treated with sulpha drugs: sulgin, phthalazole (1 g, 3-4 times daily) and antibiotics (laevomycetin, 0.5 g, 3-4 times daily). Dehydration is managed by infusing 1-1.5 litre daily of a 5 per cent glucose solution or isotonic sodium chloride solution (intravenously or subcutaneously). Since absorption of vitamins is impaired, ascorbic acid, nicotinic acid, and riboflavin are additionally prescribed.
Chronic Enteritis
The disease usually accompanies chronic gastritis (gastroenteritis) or colitis (enterocolitis).
Acute enteritis, deficiency of vitamins, proteins, or secretory insufficiency of the stomach and the pancreas may provoke chronic enteritis. Absorptions of nutrients is disordered in chronic enteritis, which eventually causes disorders in the motor and secretory functions of the small intestine.
Clinical picture. The patient complains of abdominal pain, distension of the abdomen, rumbling, and decreased appetite. Inspection of the patient reveals pallor, wasting and meteorism. Splashing sounds in the caecum can be heard during palpation; the umbilical region is tender. The patient defaecates from 2 to 8 times daily. The faeces are pasty, bubbling, and contain ample amounts of undigested starch grains, muscular fibres, fatty acids, and neutral fat.
The disease is characterized by periodic exacerbations. Hypovitaminosis, anaemia, and cachexia develop in severe and protracted cases.
Treatment. Food should be highly caloric and rich in proteins and vitamins. Vitamins C, PP, K, and B are prescribed as supplements. The diet should be the same as in acute enteritis (diet No. 4). Antibiotics and sulpha drugs, enteroseptol, viscous and astringent preparations are given in short courses.
Chronic Colitis
Chronic colitis is the inflammatory-degenerative disease of the large intestine causing its dysfunction. The disease may run an independent course or may occur along with enterocolitis.
The disease is commonly secondary to dysentery, intestinal lambliasis, and helminthiasis. Toxic colitis is more frequently secondary to poisoning with salts of heavy metals. Allergic and non-specific colitis are also distinguished. The former develops in patients hypersensitive to some foods.
The clinical picture of chronic colitis depends on the aetiology of the disease and the location of the process. The patient complains of abdominal pain and flatulence, tenesmus, diarrhoea with excretion of mucus alternating with constipation and weight loss. The patient also complains of nausea, vomiting, a bitter taste in the mouth, and decreased appetite. Symptoms of disorders of the central nervous system, e.g. irritability, headache, insomnia, are also present.
Examination reveals wasting, pallor, painful palpation and rumbling of the large intestine, and abdominal distension. Inflammation of the caecum manifests by pain during palpation of the right iliac region; the caecum is distended and tender. If the process is in the descending colon, the patient complains of pain in the region of the splenic flexure and abdominal distension. Inflammation of the rectum (proctitis) is manifested by a burning pain in the anus, painful defaecation, and tenesmus.
Non-specific ulcerative colitis is characterized by an ulcerative-inflammatory process combined with reparative processes and the growth of connective tissue. The onset of the disease is manifested by abdominal pain, frequent and liquid stools, presence of mucus and blood in faeces, painful palpation of the large intestine, and enlarged liver and spleen. The disease is progressive: it involves cachexia, anaemia, and trophic disorders.
Diagnosis of chronic colitis is based on clinical observations and findings of X-ray examinations, endoscopy, and examination of faeces. Mucus and blood are detected coprologically. Cultures of dysentery bacilli and positive serological tests confirm the diagnosis of chronic colitis of dysenteric aetiology. Spasms of the large intestine and deformities of the mucosal relief are visible in X-rays. Cicatricial changes develop ion-specific ulcerative colitis, which in turn cause contraction of the intestinal lumen. Hyperaemia of the mucosa and ulcers are revealed by rectoromanoscopy.
Treatment. Treatment depends on the cause of the disease. Diet therapy is especially important. Patients with chronic colitis are prescribed a diet including mucinous soups, weak] broth, soft porridge, curds, a small amount of meat, and fruit juices (not sweet). Food poorly tolerated by the patient should be excluded. If a patient
suffers from a chronic infection, antibiotics and sulpha drugs should be prescribed. Spasmolytics (atropine, papaverine, platyphylline, and belladonna preparations) are used to stop spasms of the intestine and relieve pain. Microenemas of camomile tea, potassium permanganate, silver nitrate (25-30 ml, 1 : 4000), and antipyrine are used for tenesmus. Oil enemas are also effective. Vegetable oil (50-100 ml) is warmed to 37-39°C and administered into the rectum. Patients with non-specific ulcerative colitis are treated with sulphasalazine preparations and corticosteroids (hydrocortisone). Vitamins (primarily, vitamins A, C, K, and B) are given in all cases.
Subwater baths, mud packs, novocaine electrophoresis, UHF, and inductothermy have a favourable effect on the function of the large intestine. Antihistaminic preparations (pipolphen, dimedrol), steroid hormones (prednisolone, dexamethasone, triamsinolone) are prescribed in allergic colitis.
The Basic Clinical Syndromes of Digestive Organs’ Diseases: the gastro-intestinal hemorrhage, the painful malabsorption, dyspepsia
The gastro-intestinal hemorrhage syndrome.
The digestive tube has many possibilities for hemorrhage. Its origin may be organic diseases (ulcer, carcinoma and others) and diseases of mucous membrane (due to local or common factors).
The peculiarities of hemorrhage from digestive tube are:
1. It occurs often.
2. It may be big, acute and life threatening.
3. Its origin is difficult to determine.
4. Patient often is the carrier of two or several ‘
aberrations.It is difficult to decide which one of themcauses hemorrhage.
5..Big hemorrhage from digestive tube has special consequences which aren’t met in other places.
There are the external and latent (occult) hemorrhages. There are such varieties of external hemorrhage: -the hemotemesis (black vomit), – the melena (defecation with digested blood), – the enterorrhagia (defecation with undigested blood). Hematemesis and melena often occur together. This testifies about external and big bleeding in upper part of digestive tube.
The pathologic physiology.
If it is the black vomit (the vomit with blood) then the origin of bleeding is located higher then duodenal flexure. Blood is accumulated in stomach, or flows from esophagus, or gets in due to reverse throwing from duodenum. Blood often is digested and influenced with gastric juice action before its discharging with vomit. Under hydrochloric acid action the hemoglobin transforms into hydrochloric hematin, therefore vomit masses are acidic, and have brown colour and look like coffee-grounds. But if the bleeding is quick, then blood from stomach discharges earlier than it mixes with gastric contents and has its natural look. But hemorrhage into stomach is not always accompanied with hematemesis (black vomit), often it is only melena. We don’t know yet why the blood discharges with vomit in some cases and doesn’t discharge in others. Perhaps, the hemorrhage speed and the stomach dilatation degree have influence on it. The melena may have origin of hemorrhage which is located higher (more oralic) than the ileum end. There is the enterorrhagia (the unchanged blood in stool) during hemorrhage from large intestine and rectum.
During melena blood is digested with proteolytic enzymes as protein food and its products of digestion dye stool into black colour, irritate intestine, cause the increasing movement of contents in it. Those feces will be chyme-like, a; sticky and black like tar. Only in exceptional cases the stool is formed, the intact fecal masses testify against melena.
On the base of experiments on the healthy volunteers it is known that for melena determination it is necessary to use 50-80 mL of blood (during milk diet) and 100 mL (during ordinary diet).
The clinical picture.
There are three stages of intensity:
1. If the total blood loss is lower than 350 mL then the expressed characters don’t appear. Patient without special prodromal signs has defecation and discharges tarry feces. Subjectivly he doesn’t feel anything or he has light disappearing nausea rigor and weakness. In many cases patient doesn’t pay attention at it. If the black vomit appears then patient becomes frightened and calls a doctor. The changes in blood quickly are equaled and during following examination we will not find considerable aberrations.
2. When big (360 mL and higher) hemorrhage appears, it is characterized by acute anemic syndrome: – nausea, – sweating, frickering in eyes, – sound in ears, – weakness, – syncopic state.Objectively patient is pale, covered with sweat, the rapid pulse is present, and the arterial pressure is decreased.
During following examinations of blood there are aberrations which have important meaning for diagnosis and prognosis. Right after hemorrhage the compensational mechanisms are turned on, due to them organism tries to keep the necessary circulating blood volume. In first of all it is the narrowing of vessels (it is the cause of pallor) and emptying of blood depository.
Then organism recovers its blood volume with taking away liquid from tissues. Due to this the blood plasma quickly (during few hours) renews. But the blood cells replacing continues longer (a few weeks) .
Because of watering of blood the anemia begins which is the index of hemorrhage value. This picture may feebly manifestate after bleeding due to absence of enough quantity of tissue fluid (the dehydratation). It leads to blood watering. The erythrocytes and hemoglobin quantity doesn’t correspond to hemorrhage, only after medical injection of liquid decreasing of these values occurs with delay.
3. The more painful manifestation of hemorrhage is the hemorrhagic shock. It develops when the compensatory mechanisms are not able to keep the blood volume at the sufficient level. It develops at right after hemorrhage or after several hours (the late or secondary shock).
The objective examination: Patient in shock state is very pale, with cold extremities, swallows air, manifestates the expressive anxiety and depression. Pulse is filiformis or isn’t found. The arterial pressure can’t determined, the consciousness is darkened.
Shock in higher stage is dangerous, if it continues few
hours, then unrecurrent changes of life important organs occur due to anoxia (of brain, heart, kidneys).
All these signs are characteristic for hemorrhage of any origin. The symptoms which are characteristic for gastro-intestinal hemorrhages are:
– the azotemia (resorption of blood protein),
– the often small hyperbilirubinemia,
– the often decreased prothrombin,
– the hypoalbuminemia (after big hemorrhages),
– the fever or moderative resorptional toxicoses (they may appear in 2-4 day after hemorrhage) .
The causes of black vomit and melena:
– ulcer of the stomach and the duodenal ulcer – 40-80%
– bleeding from mucose membrane of stomach or intestine (erosion) – 20-30%
– the varicosis of gullet and cardial part of stomach -5 – 30 %
– carcinoma of the stomach – 2-5%
– hiatal hernia – 10%
– hemorrhagic diathesis and other rare causes – 1-3%
The Painful Syndrome.
Pain is the spontaneous sensation. Painfulness is caused with examination (for example, palpation). The pain in abdomen region is somatic or visceral (internal).
The somatic (spinal) pain is caused during irritation of superficial tissues: skin, subcutaneous fat and parietal peritoneum which are provided with sensitive cerebrospinal nerves, pain is conducted with corresponding spinal nerve and spinothalamic fascicle to brain. This pain is acute and has certain localization without irradiation. The painfulness is in the pain localization region, the defance (tension of abdominal wall) is during peritoneum irritation (chemical, thermal, mechanic). This pain appears, for example durin ginjury of soft tissues of abdominal wall, abscess, irritation of neural abdominal radices during peritonitis, or epigastral hernia, the radicular pain during spondylosis. In many cases local painfulness during palpation is simultaneous to superficial sensitivity of skin during touching. During irritation of sensitive nerves in parietal peritoneum the abdominal wall strains without voluntar stimulation -“defance”.
The visceral (internal) pain appears during irritation of internal organs, and it is conducted with fibers of sympathetic system. Often impulse is the strain of muscular walls (in cavitary organs), the strain of capsule (of parenchymatous organs), pulling of mesentery, the vessels alterations.
REMEMBER! The radicular innervation of internal organs corresponds embrional state due to movement of different organs during development. Some of them appear out of region of corresponding dermal segments. Moreover, they always have sensitive fibers from several radices and the area of this crossing varies individually, basically all internal organs are innervated bilateralically (for example appendix).
Therefore, there are such characteristics of visceral pain: it is dull, without definite localization, it is felt on the middle abdomen line. It is lower than the aboral irritated region locates on digestive tube. It is never accompanied with tension of abdomen wall {“defance”). Its localization is specified with irradiation which is caused by transfer of pain into region of cerebrospinal nerves which appear from the same radices. That is the irradiation is typical depending on injuried organ. The painfulness during palpation is in the region of sore organ localization, the dermal hyperesthesia is in Head’s zone (examples: intestinal colic, uncomplicated ulcer).
If the impulse of visceral pain is very intensive or if there is anatomic injury of organ (movement of calculus, the incarceration of intestine), then typical phenomena begin to appear, they are such as irradiation or transfering pain. During irradiation the pain “is transfered” on the surface of body in those regions which are innervated with cerebrospinal incapsulated nerves from the same radices which innervate internal organ that is the pain origin.
The direction of irradiation is typical for certain organs and it is more useful for determination of its origin than when we know its localization. The irradiation compensates diffuse and unexact localization of visceral pain and gives possibility to use it in the diagnosis. During irradiative pain the increasing sensivity of skin of corresponding dermal segments (Head’s zones) appears.
The important criteria of ablominal pain:
1. Character. 5. Rhythm.
2. Localization. 6. Periodity.
3. Irradiation. 7. Impulse.
4. Duration.
1) The pure visceral syndrome appears in more superficial affection of organ, during unpenetrating ulcers. Therefore the less intensive biliary colic or appendicitis in beginning manifestates with pain in epigastral region and vomit just as during acute dyspepsia (therefore the mistakes are often). Here is the typical dependence on using drugs.
2) The visceral syndrom with irradiative pain (when the typical for this disease irradiation joins to described pain) . It talks about the more larger anatomic injury (.for example – the ulcer that penetrates into depth, the inflammation which affects the organ wall, the painful passaging of calculus with affection of mucous membrane or its sticking). The pain may be more durative, the dependence may be less expressed, the diagnosis may be easier.
localization. It is accompanied with palpative painfulness or with signs of peritoneum irritation. If it connects with 3) The somatic syndrome is the pain of acute character with exact preceding visceral syndrome, then thepathologic process occupies the peritoneum (the tissue which is provided with cerebrospinal nerves). For example:the deep penetration of ulcer (“the stroke with dagger”), the acute cholecystitis with pericholecystitis, the periappendicitis.
The Malabsorption syndrome.
(M.S.-french – disease + absorption; the synonyms -the absorption impairment syndrome, the intestinal absorption impairment syndrome) – this is the clinical syptomocomplex which is caused with impairment of absorption of one or several substances through the small intestine mucous membrane. The malabsorption syndrome may be initial (when it is caused with heredity) and secondary (acquired).
The pathogenic mechanisms of malabsorption syndrome vary. The following phases of digestion are affected:
1. The cavitary (pancreatic) phase of digestion – the deficiency of pancreatic enzymes.
2. The membranous phase – the intestinal enzymes deficiency.
3. The biliary phase (the intestinal dysbacterioses causes changes in structure of biliary acids and cholestasis).
4. The cellular phase (during atrophy of mucous membranes the process of absorption is affected).
5. The outflow phase (during breaches of intestinal lymph flow and mesenteric blood circulation).
THERE ARE SEVERAL CLASSIFICATIONS OF MALABSORPTION SYNDROME:
I. The initial malabsorption syndrome (hereditary):
intolerance of disaccharides (lactose, saccharose, isomaltose, trehalose) –
a) the disaccharide deficiency
b) the deficiency of peptidases (the gluteal deficiency, disease)
c) the deficiency of enterokinase
d) the intolerance of monosaccharides (glucose, galactose, fructose)
e) the breach of amino acids absorption (Hartnup’s disease, cystinuria, tryptophan malabsorption, methionin inalabsorption)
f) the breach of vitamin absorption (cyanocobalamin, folic acid etc.)
II. The secondary malabsorption syndrome (acquired)
a) gastrogenic one (gastrectomy, gastritis, Ca)
b) pancreatogenic one (diseases -pancreatitis, mucoviscedosis, Ca and others)
c) hepatogenic one (acute and chronic diseases of liver, the internal and external hepatic cholestasis)
d) enterogenic one (intestinal diseases such as enterocolitis, celiac disease, Crohn’s disease, diverticulitis, “blind loop” syndrome)
e) post-operative one (resection of small intestine)
f) endocrinic one (diabetes mellitus, during hyper- or hypothyrosis)
g) iatrogenic one (prolonged reception of anatibiotics, purgatives and others, radial therapy).
The clinical picture of malabsorption syndrome.
It is due to character of basic disease. The intensity of intestinal symptoms (stool disorder and others) depends on degree of involvement of large intestine into the pathological process.
Often the intestinal symptoms are absent. The common manifestation prevail, it is due to insufficiency of nutritional substances that enter into organs and tissues.
Patients complain of general weakness, increased fatiguability, decreased working ability, hyporexia and emaciation until cachexia.
The objective examination: xeroderma, hair shedding, brittleness of nails. There may be diarrhea, steatorrhea, creatorrhea; in blood there may be hypoproteineaia, dysproteinemia, changes in blood amino acid composition;
in urine there may be hyperaminoaciduria. Concentrations of cholesterol, common lipoids and their fractions are decreased in blood serum.
Often there are signs of deficiency of:
– thiamine (paresthesia in extremities, pains in legs, sleep disturbance)
– riboflavin (cheilitis, angular stomatitis)
– nicotinic acid (glossitis, pellagroid alterations of skin)
– ascorbic acid (stomatorrhagia) and other vitamins.
The clinical symptoms are due to such electrolitic breaches:
– hyponatremia (arterial hypotension, tachicardia, xeroderma, xeroglossia, thirst)
– hypokalemia (muscular debility, pain in muscules, weakness of tendinous reflexes, decreasing of intestinal motility, extrasystole)
– hypocalcemia (sense of numbness of lips and fingers;
increasing neuromuscular excitability, osteoporosis).
In hard cases there is osteomalacia with fractures of bones and tetany.
The clinical picture of M.S. depends on localization of the process in small intestine. For example, during affection of its proximal department the absorption of Ca, Fe, folic acid and vitamins of group B is impaired. If the middle department is affected, then absorption of amino and fatty acids is impaired. Absorption of monosaccharides is impaired if proximal and middle departments of small intestine are affected. If there is affection of distal department, then there is insufficient absorption of vitamin B-12 and biliary acids, often excretion of oxalates with urine is increased (it is called enteral oxalaturia).
THE DYSPEPSIA SYNDROME
Dyspepsias are disorders of digestion, or disorders that appear in result of impairment of digestive organs’ function (except pains and hemorrhages). The meaning of this term varies.
In English and American literature it is used as stomach upsets (epigastral ones) without paying attention at etiology (there are several types of dyspepsia, such as organic, reflex, systemic and functional ones).
In German literature this term is used for meaning of intestinal disturbances (fermentative and putrefactive dyspepsia).
Frenchmen call this way gastric or intestinal disturbances without definite cause.
Dyspepsia differs from other disturbances that don’t have relations to digestive organs. These differences are:
1. It depends on functional digestive organs activity (dependence on eating and defecation).
2. It is accompanied with expressive signs of disturbance of digestion (vomit, diarrhea, constipation etc.)
3. tt depends on type of food.
Depending on whether upper or lower part of digestive apparatus is affected, dyspeptic disturbances may be gastric dyspepsia or intestinal dyspepsia.
The symptoms of both dyspepsias combinate or change during systemic disturbances of digestion.
GASTRIC DYSPEPSIA includes following disturbances:
1. Sense of unpleasant weight in stomach.
2. Aerogastria and aerophagia.
3. Eructation.
4. Regurgition.
5. Heartburn.
6. Nausea (it may be with vomit).
7. Appetite disturbance.
8. Attack-like hypersalivation.
INTESTINAL DYSPEPSIA has following symptoms:
1. Sense of weight in stomach.
2. Grumbling and transfusion.
3. Flatulention.
4. As a rule, it combinates with dysfunction of movement in intestine (diarrhea or constipation) – the disturbances of defecation.
During FEKMENTATIVE DYSPEPSIA there are abdominal distension, a lot of gas bubbles; grueloidal stools with acidic reaction 2-3 times a day, they contain a lot of starch beans, cellulose, iodophilia, microbes. It occurs if there is diet with excessive amount of carbohydrates.
PUTREFACTIVE DYSPEPSIA is more common during
hyposecretion of stomach. Pepsin is absent, there is no bactericidal effect of gastric juice, quick movement of food causes disturbance of protein digestion. The stool is watery, it has black colour. It contains parts of undigested food, it has alkaline reaction and bad smell. During microscopic examination we can find a lot of fat, muscular fibers with preserved transversal and longitudinal striation. There is a lot of ammonia and organic compounds. lodophilic flora is absent.
Other unpleasant feelings that are connected with digestion are such as:
1. Unpleasant feelings in oral cavity (changes of teeth, diverticulum), bitter taste in mouth.
2. Heat in tongue (glossodynia) is during avitaminosis and anemia.
HICCUP(repeating hiccup) – the cental duediseases of brain such as sclerosis, encephalitis, meningitis; the peripherial due cold or hot food, irritation of phrenic nerve. If it is after operation on abdominal cavity, then it is peritonitis, carcinoma of intestine.
HICCUPPING is quick sudden involuntary inhalation with
simultaneous closing of vocal cords, therefore short acute piercing sound appears.
Jaundice
Jaundice is an icteric colouration of the skin and mucosa by the increased content of bilirubin in the tissues and blood. The serum of blood taken from patients with true jaundice also becomes intense yellow. Jaundice is attended (often preceded) by changes in the colour of the urine, which becomes dark-yellow or brown; faeces can be very light or even colourless, or on the contrary, dark-brown.
Jaundice can develop very quickly, within 1-2 days, to become very intensive, or it can develop gradually and be not pronounced (subicteric). Patients themselves (or their relatives) notice yellow colour in their skin. They consult a doctor for this reason. Jaundice can develop with severe itching of the skin, skin haemorrhages and haemorrhages of the nose and the gastro-intestinal tract.
Jaundice occurs in many diseases of the liver, bile ducts, blood, and also diseases of other organs and systems, to which bilirubin metabolic disorders are secondary. Some clinical symptoms attending jaundice are to a certain degree suggestive of its type and origin. Accurate diagnosis of various types of jaundice is possible with special laboratory studies.
True jaundice can develop due to the following three main causes: (1) excessive decomposition of erythrocytes and increased secretion of bilirubin (haemolytic jaundice); (2) impaired capture of unbound bilirubin by the liver cells and its inadequate combination with glucuronic acid (parenchymatous jaundice); (3) obstacles to excretion of bilirubin with bile into the intestine and reabsorption of bound bilirubin in the blood (obstructive jaundice).
Haemolytic (haematogenous) jaundice develops as a result of excessive destruction of erythrocytes in the cells of the reticulohistiocytic system (spleen, liver, bone marrow). The amount of unbound bilirubin formed from haemoglobin is so great that it exceeds the excretory liver capacity to account for its accumulation in the blood and development of jaundice. Haemolytic jaundice is the main symptom of haemolytic anemia. It can also be a symptom of other diseases, such as B12 (folic) deficiency anemia, malaria, protracted septic endocarditis, and other diseases.
The skin of a patient with haemolytic jaundice is lemon-yellow. Skin itching is absent. The amount of unbound bilirubin in the blood is moderately increased (50-200 per cent); the van den Bergh test for bilirubin is indirect. Bilirubin is absent from the urine but the urine is still coloured rather intensely by the markedly increased (5-10 times) stercobilinogen and (partly) urobilinogen. Faeces are intense dark due to the presence of considerable amount of stercobilinogen.
Parenchymatous (hepatocellular) jaundice develops due to the damage of the parenchyma cells (hepatocytes). These cells can capture bilirubin of the blood and bind it with glucuronic acid (the natural detoxicating function of the liver). The natural process of bilirubin excretion in the bile in the form of bilirubin glucuronide (bound bilirubin) is thus impaired. The content of free and bound bilirubin in the blood serum thus increases 4-10 times. In rare cases the increase may be even greater: free bilirubin increases due to hepatocyte dysfunction and bound bilirubin content increases as a result of back diffusion of bilirubin glucuronide from biliary into blood capillaires in dystrophy of the liver cells. Bound bilirubin appears in the urine (bilirubin glucuronide is water soluble and easily passes via the capillary membranes as distinct from free bilirubin). Bile acids are also present in urine, but their content gradually increases. Excretion of stercobilinogen with faeces also decreases because the amount of bilirubin excreted by the liver into the intestine decreases, but faeces are rarely completely discoloured.
This type of jaundice is mainly determined by infection (virus hepatitis or Botkin’s disease, leptospirosis) and toxic affections of the liver (poisoning with mushrooms, phosphorus, arsenic and other chemical substances, medicinal preparations included). But parenchymatous jaundice can develop also in liver cirrhosis.
The skin of patients with this jaundice is typically yellow with a reddish tint. Skin itching is less frequent than in obstructive jaundice because the synthesis of bile acids by the affected liver cells is upset. Symptoms of pronounced hepatic insufficiency may develop in severe course of the disease.
There exists a group of congenital pigmentary hepatoses in which the liver is not affected pathologically, the functional tests are negative, while the process of bilirubin conjugation with glucuronic acid is upset at some of these stages (Gilbert syndrome). This condition is attended by a permanent or intermittent jaundice, which is sometimes pronounced and develops from infancy.
Obstructive (mechanical) jaundice develops due to partial or complete obstruction of the common bile duct. This occurs mostly due to compression of the duct from the outside, by a growing tumor (usually cancer of the head of the pancreas, cancer of the major duodenal papilla, etc.), or due to obstruction by a stone. Bile congestion above the point of obstruction develops and this elevates pressure inside bile passages in continuing bile excretion. As a result, the interlobular bile capillaries become distended and bile diffuses into the liver cells (where dystrophic processes develop) and passes into the lymph and the blood. Moreover, due to increased pressure inside fine bile capillaries, communications are formed at the periphery of the lobules between the capillaries and the lymph spaces, through which bile enters the blood vessels.
Skin and mucosa of patients with obstructive jaundice are yellow. Later, as bilirubin is oxidized to biliverdin, the skin and mucosa turn green and dark-olive. The bound bilirubin content in the blood with direct van der Bergh test is as high as 250-340 mmol/1 or 15-20 mg/100 ml, and more. In protracted jaundice associated with liver dysfunction, free bilirubin content increases as well. Bound bilirubin can be found in the urine (the presence of bile pigments is determined by urinalysis) to give it brown colour and bright-yellow foaming. Faeces are colourless either periodically (in incomplete obstruction, usually by a stone), or for lengthy periods of time (in compression of the bile duct by a tumor). Jaundice increases progressively in such cases; the skin and mucosa gradually turn greenish-brown; cachexia of the patient increases. In complete obstruction of the bile ducts, faeces become colourless (acholic); their colour is clayish and grey-white; stercobilin is absent from faeces.
Bound bilirubin and also bile acids produced by the hepatocytes in ample quantity (cholaemia) are delivered to the blood in this type of jaundice. Some symptoms associated with toxicosis develop: pronounced skin itching, which intensifies by night, and bradycardia (bile acids increase the tone of the vagus nerve by reflex). The nervous system is also affected: the patient develops rapid fatigue, general weakness, adynamia, irritability, headache, and insomnia. If it is impossible to remove the cause of impaten-cy of the common bile duct (stones or a tumor) the liver is gradually affected to add symptoms of hepatic insufficiency.
Portal Hypertension
Portal hypertension is characterized by a stable increase in the blood pressure in the portal vein. Portocaval anastomoses are dilated, ascites develops and the spleen increases in size.
Portal hypertension develops due to obstructed blood outflow from the portal vein as a result of its compression from the outside (by a tumor, enlarged lymph nodes of the porta hepatis in cancer metastases, etc.), or by obliteration of part of its intrahepatic branching in chronic affections of the liver parenchyma (in cirrhosis), or due to thrombosis of the portal vein or its branches. Growth and subsequent cicatrization of connective tissue at the site of degraded hepatic cells of a cirrhotic liver cause stenosis or complete obliteration of part of hepatic sinusoids and intrahepatic vessels. An obstacle is thus created to the blood flow, which increases portal pressure and interferes with blood outflow from the abdominal viscera. In these conditions, transudation of fluids from the vessels into the abdominal cavity is intensified to account for the development of ascites. Decreased oncotic pressure of plasma is an important factor in the development of ascites associated with liver cirrhosis. The pressure decreases because of upset synthesis of albumins in the liver. Sodium and water retention is also important. It occurs due to hypersecretion of aldosterone by the adrenal glands (secondary aldosteronism) and its inadequate inactivation in the liver. The time of the onset of ascites depends on the degree of development of collateral circulation, i.e. on portocaval anastomoses. For a long time the disturbed portal circulation can be compensated for by delivery of blood into the superior and inferior venae cavae from the portal vein via normally existing anastomoses. But in portal hypertension these anastomoses become highly developed.
There exist three groups of natural portocaval anastomoses: (1) in the zone of haemorrhoidal venous plexus; these are anastomoses between the inferior mesenteric vein (the portal vein system) and haemorrhoidal veins emptying into the inferior vena cava; haemorrhoidal nodes develop in portal hypertension which rupture to cause rectal haemorrhage; (2) anastomoses in the zone of the oesophagogastric plexus: this is a collateral leading through the left gastric vein, the oesophageal plexus, and hemiazygos vein into the superior vena cava. In pronounced portal hypertension, marked varicose nodes are formed in the lower portion of oesophagus whose injury (e.g. by hard food) is responsible for possible haemorrhage in the form of haematemesis (blood vomiting), which is the most serious complication of diseases attended by portal hypertension and which is a frequent cause of death; (3) anastomoses in the system of paraumbilical veins communicating with the veins of the abdominal wall and the diaphragm, carrying blood to the superior and inferior venae cavae. In portal hypertension, varicose veins radiate from the umbilicus to give a peculiar pattern known as the caput medusae.
The degree of increase in the pressure in the portal vein system can be determined by a special needle and a water pres’sure gauge. The pressure is measured in the spleen (splenometry) or in varicose veins of the oesophagus. In the latter case the needle is introduced through the oesophagoscope. It is believed that pressure in the spleen is the same as in the portal vein trunk. Normally it is 70-150 mm H2O, while in portal hypertension it rises to
400-600 mm H2O. Contrast techniques are used to reveal obstruction of the portal vein: these are splenoportography and in rare cases transumbilical portohepatography.
The spleen may be somewhat enlarged in venous congestion associated with portal hypertension.
Treatment. In order to remove portal hypertension, whose first danger are oesophagogastric and haemorrhoidal haemorrhages, the patients are operated on for placing anastomoses between the portal vein system and the inferior vena cava.
Hepatolienal Syndrome
The hepatolienal syndrome is characterized by concurrent enlargement of the liver and the spleen in primary affection of either of these organs. Involvement of both organs in a pathological process (diseases of the liver, blood, certain infections, poisoning) is explained by their richly developed reticulohistiocytic tissue. In certain cases, e.g. in thrombosis of the hepatic veins, simultaneous enlargement of the liver and the spleen is determined by venous congestion in them. In addition to palpation, scanning can be used to reveal the hepatolienal syndrome.
Considerable enlargement of the spleen is usually attended by its hyperfunction (hypersplenism), which is characterized by anaemia, leucopenia, and thrombocytopenia. The latter can cause haemorrhagic complications. These changes are explained by inhibition of the haemopoiesis in the bone marrow due to hyperactivity of the spleen as a result of which destruction of the blood cells in the spleen is intensified, and antierythrocytic, antileucocytic, and antithrombocytic autoantibodies are formed in the spleen.
Cirrhosis of the Liver
Cirrhosis of the liver is a chronic progressive disease characterized by increasing hepatic insufficiency in connection with dystrophy of the liver cells, cicatricial cirrhosis, and structural reconstruction of the liver.
Aetiology. Cirrhosis of the liver is a polyaetiological disease. It may develop due to (1) infection (virus of epidemic hepatitis); (2) alcoholism; (3) protein and vitamin-deficient diet; (4) toxico-allergic factor; (5) cholestasis. Of the mentioned aetiological factors, the leading role in this country belongs to the virus of epidemic hepatitis. Cirrhosis caused by the virus is probably explained by its long persistence in the liver cells.
Chronic alcoholic poisoning is also a very important aetiological factor. It affects absorption of vitamins and proteins in the intestine to provoke cirrhosis of the liver. It also acts directly and specifically on metabolism of the liver cells. The alimentary factor (malnutrition, mainly protein and vitamin deficit) is a frequent cause of liver cirrhosis in some developing countries. In this country the alimentary factor (malnutrition) is only of endogenous origin: deranged absorption of proteins and vitamins (in grave chronic diseases of the gastrointestinal tract, in patients with total resection of the stomach, resection of the intestine, chronic pancreatitis, and in some other cases). Toxic cirrhosis of the liver arises in repeated and chronic exposure to carbon tetrachloride, compounds of phosphorus or arsenic, in food poisoning (inedible mushrooms, seeds of heliotrope). Toxico-allergic cirrhosis of the liver includes also affections connected with hypersensitivity (autoallergy) to various drugs (aminazine, chloroform, some antibiotics, sulpha preparations, etc); hypersensitivity can cause dystrophy and necrosis of the liver parenchyma.
Obturation of intra and extrahepatic bile ducts and their inflammation cause congestion of bile and cholestasis, and are important factors in the development of biliary cirrhosis.
The aetiological factor does not always determine the way of development of liver cirrhosis. One and the same factor can cause various morphological variants of cirrhosis (portal, postnecrotic, and biliary); at the same time various aetiological factors can cause similar morphological changes.
Pathogenesis. The pathogenesis of liver cirrhosis is closely connected with morphogenesis. The greatest importance in the developmental mechanism of liver cirrhosis belongs to recurrent necrosis of the liver cells which is provoked by aetiological factors and cause collapse of the reticulin framework of the liver, formation of cicatrices, and derangement of circulation in the adjacent portions of the preserved liver parenchyma. Intact hepatocytes or lobe fragments begin their intense regeneration under the effect of growth stimulants supplied from the necrotic focus. The formed large nodes of regenerated tissue compress the surrounding tissue with the invested vessels; the hepatic veins are compressed especially strongly. The blood outflow becomes upset to provoke portal hypertension and formation of anastomoses between the branches of the portal and hepatic veins that facilitate intrahepatic circulation. Blood now bypasses the liver parenchyma to impair drastically its blood supply, to cause new ischaemic necroses, and to stimulate the progress of cirrhosis even in the absence of the primary aetiological factor. Collagenous connective tissue grows intensively: connective tissue partitions (septa) grow into the parenchyma from the periportal fields to cause fragmentation of the liver lobules. These false lobules can later become the source of nodular regeneration. Chronic direct exposure to certain toxic hepatotropic substances, and also autoimmune and some other mechanisms are important in the pathogenesis of certain forms of cirrhosis.
Clinical picture. Portal cirrhosis of the liver occurs mostly between the ages of 40 and 60. The incidence in men is twice higher than in women. Postnecrotic and biliary cirrhosis of the liver develop in younger patients, mostly in women.
Clinical manifestations of liver cirrhosis depend on the degree of affection of the liver cells and the associated hepatic dysfunction and portal hypertension, on the stage of the disease (compensated or decompensated), and also on the activity of the process. The following symptoms of the disease are most characteristic of the majority of patients with various forms of liver cirrhosis.
Pain in the region of the liver, in the epigastrium, or diffuse pain in the whole abdomen is usually dull and boring, intensifying after meals, especially after fatty food, ample drinking and physical exercise. Pain is usually associated with enlargement of the liver and distension of the capsule, or with necrotic foci located near the capsule, with perihepatic symptoms, and also concurrent inflammatory affections of the bile ducts.
Dyspepsia in the form of decreased appetite to complete anorexia, the feeling of heaviness in the epigastrium after meals, nausea, vomiting, meteorism and dyspeptic stools (especially after fatty meals) depend mainly on deranged secretion of bile and hence defective digestion. But they can also be associated with the attending dyskinesia of the bile ducts or alcoholic gastroenteritis.
Decreased work capacity, general weakness, fatigue and insomnia are often observed in cirrhosis of the liver. Fever is usually irregular and sometimes of the undulant type. It often attends postnecrotic cirrhosis of the liver and is explained by necrotic destruction of the liver cells. Marked fever is characteristic of the active period and infectious cirrhosis.
A haemorrhagic syndrome is observed in 50 per cent of patients with cirrhosis of the liver. Profuse bleeding from varicose veins of the oesophagus and the stomach can often be early signs of portal cirrhosis;they are caused by increased pressure in the veins of the oesophagus and the stomach. In other variants of cirrhosis nasal, gum, uterine and skin haemorrhages develop in marked decompensation. They depend on the decreased coagulability of blood due to liver dysfunction.
Signs of cirrhosis are as follows. Cachexia is especially characteristic of patients with portal cirrhosis of the liver. In long-standing disease the subcutaneous fat disappears along with atrophy of muscles, especially of the upper shoulder girdle. The appearance of such patients is quite specific: the face is very thin with grey or subicteric skin; the lips and the tongue are bright-red; the cheek bone region is affected by erythema; the extremities are thin and the abdomen is large (due to ascites, enlarged liver and spleen);the subcutaneous veins of the abdominal wall are dilated, the legs are oedematous. Malnutrition is usually associated with disordered digestion and assimilation of food, and impaired synthesis of proteins in the affected liver.
Jaundice (except the cases with biliary cirrhosis) is a sign of hepatocellular insufficiency associated with necrosis of the liver cells. The affected hepatocytes partly lose their capacity to capture bilirubin from blood and to bind it with glucuronic acid. Bilirubin excretion into bile is disordered as well. Free (indirect) and bound (direct) bilirubin of blood serum therefore also increases. Jaundice is usually characterized by partial decolouration of faeces and by the presence of bile in the duodenal contents. Jaundice is often attended by skin itching. Jaundice associated with biliary cirrhosis resembles obstructive jaundice; severe skin itching is observed. The intensity of jaundice varies from light subicteric to marked jaundice (depending on the degree of obstruction of the bile ducts). In prolonged obstruction of the extrahepatic duct the skin acquires a greenish tint which depends on oxidation of bilirubin to biliverdin. Moreover, brown pigmentation of the skin may also be observed. It depends on accumulation of melanin.
“Minor” signs of cirrhosis can also be revealed during examination of the patient. These signs are as follows: (1) spider angiomata (they may develop years before marked symptoms of the disease develop); their number increases and the colour intensifies during exacerbation of the disease; (2) erythema of the palms; (3) red lustrous lips, scarlet mucosa of the mouth, scarlet (lacquered) tongue; (4) gynaecomastia (increased mammary glands) and other female sex characters developing in men (decreasing growth of hair on the face, chest, abdomen, and the head); (5) xanthomatous plaques on the skin (observed in patients with biliary cirrhosis of the liver); (6) Hippocrates fingers with hyperaemic skin at the nail beds. Inspection of the abdominal skin can reveal dilation of the veins that can be seen through the thinned skin of the abdominal wall (caput medusae). Collateral venous system can be seen on the chest as well. Haemorrhoidal veins are often dilated.
Ascites is the most characteristic sign of portal cirrhosis. Ascites may develop slowly and the abdomen grow to huge size; the patient develops dyspnoea. Oedema may develop; hydrothorax may also occur in some cases. In other variants of cirrhosis, ascites develops at later stages of the disease.
Enlarged liver can be palpated in 50-75 per cent of patients with cirrhosis. The enlargement can be insignificant, only determinable by percussion, or considerable when the liver occupies the entire left part of the abdominal cavity. The liver is firm, the surface is sometimes irregular, and the lower edge sharp. Enlargement of the spleen is often attended by its increased activity (hypersplenism).
Laboratory findings. An active cirrhotic process is characterized by anaemia, leucopenia, thrombocytopenia, and increased ESR. Anaemia can be due to hypersplenism and gastro-intestinal haemorrhage, hepatocellular insufficiency, and often increased haemolysis, which is accompanied by reticulocytosis of the peripheral blood.
The blood serum bilirubin content becomes considerable only in the final stage of the disease. At the same time, the affection of the excretory function of the cirrhotic liver can be assessed by the presence of the conjugated fraction of bilirubin (bound bilirubin). Its content increases iormal and increased total bilirubin. The free bilirubin content increases in the blood serum as a result of upset conjugation of bilirubin in the liver cell and haemolysis. The blood serum bilirubin content varies in biliary cirrhosis of the liver from 26 to 340 mmol/l (1.5-20 mg/100 ml), mostly at the expense of bound bilirubin.
The presence of much urobilin in the urine indicates liver insufficiency. The amount of urobilin in the urine and stercobilin in the faeces decreases in the presence of pronounced jaundice when a small amount of bilirubin enters the intestine. Bilirubin is found in the urine of patients with jaundice.
The upset excretory function of the liver is manifested by retention of bromsulphthalein in the blood (during its intravenous administration) and also by radioisotopic hepatography and scanning of the liver.
Affection of liver cells is manifested by characteristic changes in the protein indices: decreased concentration of serum albumins and hypergammaglobulinaemia which in turn decreases the albumin-globulin coefficient. Activation of the inflammatory process in the liver involves an increase in the a2–globulins, while jaundice causes an increase in b-globulins. During remissions, all these changes become less pronounced. The blood level of lipids and cholesterol also increases considerably in the presence of biliary cirrhosis. A sensitive index of liver dysfunction is the decreased activity of cholinesterase. Transaminase activity increases in exacerbation of liver cirrhosis. Activity of alkaline phosphatase also increases in biliary cirrhosis.
The decreased prothrombin content (which is synthesized by the liver cells), increased antithrombin coagulative activity and decreased total coagulative activity of plasma are important in the aetiology of haemorrhagic diathesis in liver cirrhosis.
Laparoscopy and especially biopsy of the liver help reveal intravital morphological signs of each variant of liver cirrhosis. Varicose veins of the oesophagus are revealed by X-rays.
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.
Table 10.1
Normal laboratory values of biochemical analysis of blood
glucose 3.33-5.55 mmol/L
bilirubin total 8.5-20.5 mkmol/L
unconjugated 2/3 of total
conjugated 1/3 of total
protein total 60.0-80.0 g/L
ALT 0.1-0.75 mkmol/g/L
AST 0.1-0.45 mkmol/g/L
Amylase 16-32 dye units/l
A number of gastrointestinal disorders are caused by disturbance in motor function. Some, such as Hirschsprung’s disease, produce typical signs of obstruction and are alternately classified as obstructive disorders.
