The major symptom of peptic ulcer is chronic recurrent painful upper abdominal disorder. The cause of ulcer pain may be due to: (1) increased acidity at the ulcer site and the relief of pain to a decrease in luminal acidity. Pain threshold to the stimulation of acid is decreased; (2) hypertension of mero-muscle; (3)stimulation of acid to ulcer surface.
Upper abdominal pain has some characters as follows:
location: The most common location of ulcer pain is left and epigastrium in gastric ulcer, and right and epigastrium in duodenal ulcer.
Property: The property of ulcer pain is usually persistent, dull, burning, distending, or hungry sensation lasting for 1-2 hours or 3-4 hours.
Periodic and seasonal change: In gastric ulcer episodes of ulcer pain usually occur 1/2-2 hours after meals and disappear before next meal. On the contrary, in duodenal ulcer the episodes of ulcer pain usually occur 3-4 hours after meals and can be relieved by ingestion of food. Thus, the duodenal ulcer pain is also termed empty pain.
The comose seasons of gastroduodenal ulcer are times between fall and winter, or winter and spring, strongly associated with cold climate.
chronic and recurrent episodes: The episodes of annual recurrences during particular seasons may last weeks to months.
other accompanied symptoms
Acid regurgitation, belching, nausea, vomiting, anorexia, constipation, and weight loss are often accompanied with ulcer pain.
The physical examination is usually not helpful in uncomplicated peptic ulcer disease. Epigastric tenderness is an insensitive and nonspecific finding and correlates poorly with the presence of an active ulcer crater. Rarely, peptic ulcer is associated with multisystem syndromes that may produce physical findings.
bleeding: Bleeding is the most common complication of peptic ulcer disease, and peptic ulcer is the most common source of acute upper gastrointestinal bleeding. Risk of bleeding is unrelated to duration of ulcer disease. Hemorrhage results from erosion of the ulcer into a blood vessel. The most common sign of acute bleeding is melena, with or without hematemesis. Major blood loss (1500ml) can result in circular failure. The ulcer pain may be relieved after bleeding.
Perforation: An ulcer may penetrate the wall of the duodenal or stomach, resulting in sudden, severe, constant abdominal pain that reaches maximal intensity rapidly. The pain may quickly becomes generalized. Marked abdominal tenderness to palpation and diffuse, boardlike rigidty of the abdominal wall musculature are present. Hypotension and tachycardia usually occur owing to intraperitoneal fluid loss. Patients with penetration into solid organs usually present with intractable ulcer pain.
Obstruction: Gastric outlet obstruction is caused by edema, smooth muscle spasm, fibrosis, or a combination of these processes. Obstruction delays gastric emptying and commonly causes nausea, vomiting, epigastric fullness or bloating, anorexia, early satiety, and a fear of eating. Epigastric pain is frequent and may be relieved temporarily by vomiting. Vomiting is often copious and may contain undigested food but usually no bile. Physical examination may reveal visible peristalsis in the epigastrium, or a succussion splash over the stomach.
Cancer transformation: Cancer foci may be present in association with an ulcer, especially gastric ulcer. Thus, all gastric ulcers must be suspected of having small areas of malignancy even when the ulcer appears benign by radiography or endoscopy. Biopsy and cytologic examination reveal the true nature of the lesion.
2.. Acute Peritonitis
Bacterial peritonitis most commonly results from perforation of an abdominal viscus caused by trauma, obstruction, infarction, neoplasm, foreign bodies, or primary inflammatory disease. It can be classified as:
generalized and localized peritonitis, based on the inflammation range.
Primary and secondary peritonitis, based on the source of disease.
Nonbacterial and infected peritonitis, base on the character of first stage of inflammation.
Regardless of etiology, abdominal pain, nausea, vomiting, tachycardia, and fever are usually present. The severity of these symptoms is related to the extent of contamination: in generalized peritonitis, shock is often present and may be profund, whereas signs and symptoms may be minimal if infection is localized.
In severe cases, there may be exquisite, diffuse, direct, and rebound tenderness and rigidity of the abdomen; bowel sounds are usually diminished or absent, and distention may be present. Tachycardia or unexplained hypotension may herald peritonitis in elderly patients or those receiving corticosteroids in whom the clinical manifestations are masked or suppressed.
Cirrhosis is an irreversible alteration of the liver architecture, consisting of hepatic fibrosis and areas of nodular regeneration. So it is a pathological diagnosis. Identified causes include viral hepatitis, alcoholic hepatitis, schistosomiasis, malnutrition, chronic severe heart failure, and a fen drugs and toxins. Based on pathological characters, it can be classified into several types as micronodular, macronodular, mixed, and nodular undistinct.
Compensatory cirrhosis may remain clinically silent for many years and frequently is discovered unexpectedly, often during the evaluation of an unrelated condition. When the disease becomes clinically manifest, its symptoms are usually nonspecific (malaise, lethergy) or related to portal hypertension and include ascites, splenomegaly, hypersplenism, or bleeding esophageal varices. Fever, jundice, testicular atrophy and gynnecomastia(men), menstrual irregularities (women), and muscle wasting are found frequently.
The liver may be large or small and usually has a firm consistency. Spider angiomas, palmar erythema, parotid enlargement, splenomegaly, and edema are found frequently.
In discompensatory stage, presentation due to portal hypertension are very common as follows:
ascites: It is the most notable clinical manifestation of liver cirrhosis.
Portal collateral circulation: The portal-systemic collaterals may be formed as: (1)The veins that lie in the mucosa of the gastric fundus and esophagus are of greatest clinical interest because, when dilated, they form gastric and esophageal varices. (2)The remnant of the umbilical vein may also dilate. If flow through this vessel becomes great enough, a loud venous hum may be audible over the path of the umbilical vein. Dilated abdominal wall veins are common and are especially prominent when the patient stands. (3) The hemorrhoidal veins may also act as collaterals.
Splenomegaly and hypersplenism: Hypersplenism may lead to thrombocytopenia, leukopenia, and/or anemia.
Acute appendicitis is termed as acute bacterial infection of appendix. It is the most common disease in acute abdomen.
Typically, the illness begins with vague abdominal discomfort followed by slight nausea, anorexia, and indigestion. The pain is persistent and continuous but not severe. Within several hours the pain shifts to the right lower quadrant, becoming localized and causing discomfort on moving, walking, or coughing. The patient often has a sense of being constipated.
Examination will show cough tenderness localized to the right lower quadrant. There will be well-localized tenderness to one-finger palpation and possibly very slight muscular rigidity. Rebound tenderness is classically referred to the same area. Peristalsis is normal or slightly reduced. The temperature is only slightly elevated in the absence of perforation. Poorly localized epigastric pain heralds the onset of appendicitis in a retrocecal or retroileal appendix. At this point, the psoas sign may be positive.
Perforation is a accompanied by more severe pain and higher fever than in appendicitis. It is one of the complications of acute appendicitis, unusual for the acutely inflamed appendix to perforate within the first 12 hours.
Intestinal Obstruction is a common acute abdomen. It can be classified into 3 types according to the causes:
mechanical obstruction: Clinically this condition is most common. The cause of it may be adhesion, intussusception, strangulated hernia, et al.
dynamic obstruction: It can be further classified into paralytic and spastic obstruction. The former is more common, as seen in acute generalized peritonitis or after surgery.
Vascular obstruction: The cause usually is thrombosis in mesenteric vein, resulting in intestinal ischemia.
Furthermore, intestinal obstruction can be classified into simple and strangulated obstruction, complete and incomplete obstruction, or acute and chronic obstruction.
Deep, visceral, cramping pain is usually referred to the gastrium. Severe, continuous abdominal pain suggests intestinal ischemia or peritonitis. The degree of pain is much more severe in small intestinal obstruction than in large intestinal obstruction. In the latter, vomiting is a late finding and may not occur at all if the ileocecal valve prevents reflux. The onset and character of vomiting may indicate the level of the lesion. Recurrent vomiting of bile-stained fluid is typical early sign of proximal small bowel obstruction. Feculent vomiting is a late manifestation. Constipation or obstipation is a universal feature of complete obstruction, although the colon distal to obstruction may empty after the initial symptoms begin. Constipation itself is hardly an absolute indicator of intestinal obstruction. However, obstipation (the absence of passage of both stool and flatus) strongly suggests mechanical bowel obstruction if there is progressive painful abdominal distention or repeated vomiting.
Painful aspects, breathless, tachycardia, and even shock may be present in patients with bowel obstruction. The abdomen should be carefully inspected before palpation. Signs may include tensely distended abdomen, visible peristalsis occurring in advanced bowel obstruction, soft doughy fullness in early paralytic ileus or mesenteric thrombosis, peristaltic rushes synchronous with colic, infrequent tinkly or squeaky sounds, muscular tautness and rigidity, and tenderness.
Case and Problem Based Larning Approach Ascites
A 57-year-old female patient was admitted on Jan. 20th 2003 because of “fatigue and anorexia for 2 months, abdominal swelling and oliguria for half a month”. Two months ago, the patient began to feel fatigue, decreased tolerance of physical activities and anorexia without any identifiable causes. She used to eat 100g rice every meal, but now she could only eat 50g. She also had low fever and felt better after taking anti-cold medications.
Half a month ago, the patient began to feel abdominal swelling. Her pants’ waist belt became tight for her. Urine volume decreased to 500 ml everyday and its color was dark. Then the patient went to the nearby district hospital and took the abdominal ultrasound examination. The result showed she had liver cirrhosis, splenomegaly, and large volume of ascites. The patient had acute hepatitis B 20 years ago. During the years after the acute infection, her liver function was abnormal intermittently.
She had no habit of smoking or drinking alcohol. She was married and had one son and one daughter. Her daughter and husband were both healthy. Her son had hepatitis B infection. Her father died of primary hepatic cancer. Her mother is still alive.
Physical Examination: T: 37.5°C, BP:16/10KPa, R:18/min, HR: 100/min. Consciousness, hepatic face, mild jaundice of sclera, liver palm(+), spider angioma on left neck, no palpation of lymph nodes, lung auscultation negative, heart (-). Abdominal findings: obvious abdominal bulge (marked protuberance of the abdomen), no distention of abdominal wall veins, soft, no pain, shifting dullness(+), normal active intestinal sound, moderate edema of the lower limbs, NS(-).
CLINICAL THINKING (Questions and Answers)
(1) According to the patient’s symptoms, physical signs and the findings of the abdominal ultrasonography, we confirmed the diagnosis of ascites.
(2) Among the causes of ascites, liver cirrhosis accounts for 80% while other causes such as cancer, heart failure, tuberculosis, renal disease and pancreatic disease account for 20%. Because the patient had the history of hepatitis B infection and the abdominal ultrasonography also suggested liver cirrhosis, the cause for this patient’s ascites was most likely secondary to liver cirrhosis.
(3) To ascertain the cause of ascites is very important for the diagnosis and treatment of ascites. Before we start the treatment, diagnostic paracentesis is necessary. According to the analysis of ascites, including routine tests, biochemical tests, and etiological tests, we could further verify the cause of ascites and make differential diagnosis of simple ascites of liver cirrhosis and ascites of cirrhosis.
Blood test showed WBC 2.3×109/L, RBC 3.5×1012/L,Hb95g/L, BPL45×109/L. Liver function test showed TB/CB 21/37μmol/L, A/G 32/49g/L, ALT 75U/L, AST 94U/L. Serologic tests for hepatitis B showed HBsAg(+), anti-HBe(+), anti- HBc(+), others(-). A diagnostic paracentesis was performed on the day of admission and the analysis of the ascitic fluid was as follows.
Routine tests showed the fluid was clear in appearance, an absolute RBC count of 10/μL and a WBC count of 25/μL. Biochemical tests of the fluid showed protein concentration of 5g/L，albumin concentration of 2g/L and specific gravity of 1.010. Culture for bacteria showed negative result. Cytology study of the fluid was also negative.
CLINICAL THINKING (Questions and Answers)
(4) The patient’s blood test showed that the blood counts were low. This is consistent with the diagnosis of liver cirrhosis and hypersplenism. The patient’s liver function test showed a reversed ratio of albumin to globulin, mild hyperbilinemia and elevated transaminases. This is also consistent with the decompensated stage of liver cirrhosis. Serologic tests in hepatitis B suggested that the cause of liver cirrhosis was chronic hepatitis B infection. All the laboratory tests further confirmed the diagnosis of liver cirrhosis.
(5) For this patient with ascites, the most valuable examination is paracentesis. Let’s go over the standard in the differential diagnosis of ascites. According to the traditional standard, ascitic fluid can be divided into exudate or transudate. Transudate is characterized by clear appearance, protein concentration <25g/L, gravity <1.018, cell count <100/μL and negative bacteria culture, whereas exudate is characterized by cloudy appearance, protein concentration >25g/L, gravity >1.018, cell count >500/μL and often with positive bacterial culture. Transudate is often caused by liver cirrhosis, heart failure and renal disease. Exudate is more often caused by tumor, tuberculosis and pancreatic disease. The transudate ascitic fluid could become exudate when spontaneous bacterial peritonitis occurs. It is obvious that the analysis of this patient’s ascitic fluid confirms its classification as transudate.
(6) Serum ascites albumin gradient [(SAAG) = (32-2)g/L =30g/L(>11g/L)] in this patient indicated that the ascites was due to portal hypertension. Therefore, the diagnosis of liver cirrhosis with ascites could be confirmed.
Chapter 6 Genitalia, Anus, and Rectum Inspection of the genitalia, anus, and rectum is one of the important parts of the systemic physical examination, which should not be ignored. The correct inspection can result in a high degree of accuracy in the diagnosis of abnormalities. However, because of wide variation in the appearance of normal genitalia, the examiner must rely on a careful history, inspection, and palpation to distinguish healthy, normal structures from those that are malformed of diseased.