Clinical Characteristics of the Acute Abdomen Since pain is the most prominent presenting complaint in a patient with an acute abdomen, it is important to know the origin, location, radiation and character of abdominal pain in order to understand its significance. The perception of abdominal pain is first visceral and then becomes somatic. The abdominal viscera and the visceral peritoneum receive sensory fibers via the sympathetic chain from T5 through L3. The sensory supply to the viscera is sparse and visceral pain is vague and poorly localized. The alimentary tract from the esophagus to the anal canal is insensitive to many stimuli which produce intense pain in other structures. The gut can be biopsied, crushed or cauterized without pain. If the bowel or any other hollow viscus is distended or if its muscle coat goes into spasm, however, pain is felt. The cause of visceral pain is tension in the muscle fibers produced by stretching of the wall, spasm of the muscle or stretching of the capsule of the organ. Violent peristaltic contractions occur in an attempt to force luminal contents through an obstruction. Pain associated with obstruction is severe and cramping in nature, but intermittent, with pain-free intervals and is called colic. Ischemia of visceral muscle gives rise to pain because the gut loses motility and becomes distended. Visceral pain of ischemic origin is caused most often by strangulation of the bowel in hernia or volvulus. A less frequent cause is acute mesenteric thrombosis. The parietal peritoneum which lines the abdominal cavity and the interior surfaces of the diaphragm derives sensory fibers from the somatic nerves T6 through L1. When the parietal peritoneum is irritated, somatic pain results. Somatic pain is with localized tenderness and spasm of the muscle groups supplied by the dermatome of origin of the pain stimulus. For example, the right lower quadrant (RLQ) pain, tenderness and muscle spasm associated with appendicitis is caused by inflammation of the contiguous RLQ parietal peritoneum. The abdominal signs in perforated peptic ulcer, on the other hand, are generalized because diffusion of highly acid fluid throughout the peritoneal cavity causes intense irritation of all the parietal peritoneal surfaces. Pain experienced at a site other than that stimulated but in somatic zones supplied by the same or adjacent segments of the spinal cord is called referred pain. Visceral pain is referred to three zones located in the midline of the abdomen. The localization of abdominal pain indicates which organs may be involved. Epigastric pain is associated with structures innervated by T6-T8, the stomach, duodenum, pancreas, liver, biliary tree and associated parietal peritoneum. Periumbilical pain is related to innervation from T9 to T10 and includes the small intestine, appendix, and upper ureters. Hypogastric pain has its origin in structures innervated by Tll and T12, the colon, bladder, lower ureters and uterus. The pattern of radiation of pain may provide important clues as to its origin. For example, pain which initially is located in the periumbilical area and then moves to the RLQ occurs with appendicitis, whereas pain in the epigastrium which radiates to the tip of the right scapula is frequently found with acute cholecystitis. Such shifting or radiation of pain to a localized site with local tenderness and muscle spasm denotes local inflammation of the parietal peritoneum and suggests a circumscribed inflammatory process. The pain of renal colic usually is felt in the flank and radiates towards the groin on the same side. Pain that involves the entire abdomen almost immediately after onset is usually due to flooding of the peritoneal cavity with an irritating fluid from a perforated ulcer, or from blood and chorionic tissue in a ruptured ectopic pregnancy. A general rule to follow is that the majority of severe abdominal pain occurs in patients who have enjoyed fairly good health and which persists as long as six hours is caused by diseases requiring surgical intervention. Obviously, there are always exceptions to any rule. View attachment 16485 Other features of pain and associated GI symptoms which may provide important clues as to cause are listed below in tabular form with some examples of each. Type of onset sudden - rupture of viscus, mesenteric thrombosis gradual - cholecystitis, appendicitis Quality dull - initial epigastric pain of appendicitis sharp - renal or biliary colic or obstruction of gut aching - pelvic inflammatory disease pleuritic - intensified by breathing lancinating - acute pancreatitis tearing - dissecting aneurysm Intensity severe - rupture of viscus or blood in the peritoneal cavity moderate - RLQ appendiceal mild peptic ulcer, without perforation Temporal features continuous - acute pancreatitis pulsatile - abdominal aneurysm colicky - lumen obstruction, intermittent severe pain with pain-free intervals frequency & duration transient pain of short duration which does not recur is usually insignificant. The longer the duration the more likely a surgical condition. Factors which intensify or relieve pain relation to meals - peptic ulcer pain relieved by food, cholecystitis pain aggravated by fatty meal posture jack-knifing - leg drawn up to decrease peritoneal irritation in suppurative appendicitis motion - any movement causes intense pain in generalized peritonitis and the patient lies motionless Associated nausea and vomiting nausea & vomiting - reflex, or irritative non-specific vomiting occurs in many conditions. In surgical disease such as acute appendicitis, anorexia always occurs and vomiting, if it occurs, usually follows abdominal pain rather than preceding it, as in gastroenteritis. Repeated vomiting of large amounts occurs in gut obstruction, is often bile stained and may become fecal. Protracted vomiting time - early in high GI obstruction; late in low GI obstruction character of vomitus - blood - bleeding ulcer bile stained - obstruction below ampulla of Vater fecal - intestinal obstruction, mechanical or with paralytic ileus; copious amount Diarrhea most common with acute gastroenteritis or food poisoning, but it may occur with appendicitis or other focal inflammatory lesions of the gut Constipation or obstipation With complete small bowel obstruction - unrelenting constipation (obstipation) after fecal material below obstruction has been passed. Progressive constipation with carcinoma of the large bowel. Gas stoppage with decreased or absent bowel sounds - paralytic ileus All of the patient's symptoms must be carefully considered and analyzed, especially with regard to organs most likely to give rise to acute conditions. Extraabdominal conditions which simulate the acute abdomen arise most often in the heart, lungs, urinary tract and female reproductive organs. The age and sex of the patient will provide helpful leads as to which conditions responsible for a "hot belly" are most likely, outlined below: Age - newborn - congenital anomalies, gut atresia, imperforate anus, malrota2ion, diaphragmatic hernia Neonatal - hypertrophic pyloric stenosis (males), megacolon, hernia Later infancy - intussusception Childhood and young adults - hernia, appendicitis - most common but can occur at any age Young adolescent females - "mittelschmerz" - rupture of graafian follicle with LLQ or RLQ abdominal pain occurring in the middle of the menstrual cycle. Females - gallbladder - female, fair, fat, forty ectopic pregnancy pelvic inflammatory disease Males - peptic ulcer Advancing age - mesenteric thrombosis or embolus often after myocardial infarction, large bowel neoplasms, diverticulitis Past history of disease or abdominal operation abdominal scars, adhesions - intestinal obstruction peptic ulcer - possible perforation chronic cholecystitis or biliary colic - acute cholecystitis Physical Examination Careful and complete data collection by history and physical exam is the prime diagnostic aid to avoid errors of omission and to separate those conditions which require immediate surgery from those which require watchful expectancy, or those which require medical rather than surgical management. Often the patient's condition is such that extensive laboratory investigation requiring many hours would compromise the patient's life and thus the outcome often depends on a precise and detailed history and physical examination. A complete general physical examination provides essential data for making the diagnosis, determining the urgency of the condition, assessing the patient as an operative risk, and making a sound management plan. First, the patient is surveyed rapidly for fever and/or evidence of shock, hemorrhage, anemia, dehydration or cardiac decompensation. When necessary, if the patient is severely ill and/ or shocked, resuscitative treatment should be started immediately and a detailed history and examination deferred temporarily. On observation of the patient, the severity and character of the pain may be apparent. Temperature, pulse, respiration and blood pressure are recorded, providing a base line for later observation. Complete and systemic examination of all organ systems is done next, usually deferring abdominal rectal and pelvic examination until last. It is important that the heart and lungs be carefully examined, not only to determine if an extraabdominal cause for abdominal pain is present, but to determine whether the patient is in satisfactory condition for surgery if this is indicated. The abdominal examination, including pelvic and rectal, provides information which indicates the type and degree of the intraabdominal process on which the diagnosis can be based and the recommendation for or against surgical intervention determined. The abdomen must be exposed completely for examination. The patient should be in a comfortable supine position with the knees slightly flexed to relax the abdominal musculature, and the examiners hand should be warm. A calm sympathetic approach and gentleness in examination on the part of the practitioner are very helpful. The patient is asked to point with one finger to the area of greatest pain, and the examiner should be especially gentle when studying these areas. Inspection of the abdomen may reveal significant surgical scars. Auscultation of the abdomen is performed next. The intestine is quite sensitive to touch, and peristaltic bowel sounds can be best evaluated by listening to the abdomen before palpating it. Auscultation is most helpful in determining functional activity of the bowel. When alterations in bowel sounds occur in association with other changes, they have clinical significance. Decrease in gastrointestinal motility and function is part of the reaction to local and general stress. For example, an acute fracture of the femur will cause a paralytic ileus and a silent abdomen, as will generalized peritonitis. The inhibition generally does not persist and, after several hours or days, sounds will be heard again as bowel function resumes following appropriate treatment. Bowel sounds in established mechanical obstruction may be striking. The sounds are loud, booming, rhythmical, and synchronous with colicky pain. As the bowel becomes distended, the sounds become more high pitched and take on a tinkling quality. Borborygmi is the term applied to the very hyperactive bowel sounds associated with mechanical obstruction. Early in bowel obstruction peristaltic activity can be very vigorous. In time, however, the obstructed bowel fatigues and bowel motility decreases, resulting in hypoactive or absent bowel sounds as distention-inhibition and vascular impairment of the intestine develop. The next step is systematic palpation of the abdomen with light pressure (to a depth of about 1 cm) beginning at a distance from the area of maximal tenderness and alternately testing and comparing each side with the opposite side, while observing the patient closely for wincing or other evidence of pain. The entire abdomen is palpated systematically for areas of tenderness, muscle spasm, or presence of masses. Any specific areas which may appear abnormal should be retested and re-evaluated. Deep palpation, again done gently, gives more information about deep tenderness or the nature, size, and consistency of any lesion or mass. On deeper palpation the examiner advances the probing fingers deeper into the patient's abdomen when the patient inspires, as this maneuver tends to relax the musculature of the abdominal wall. When muscle spasm and tenderness are very marked, deep palpation is quite painful, uninformative and unnecessary. Persistent localized tenderness, point tenderness , is the most important sign of peritoneal inflammation. In acute appendicitis, when point tenderness is definite, it is an indication for surgery. Rebound tenderness may be demonstrated when pain is experienced on sudden release of deep pressure. Information concerning a localized area of peritoneal irritation may also be obtained by having the patient rise on his toes and come down suddenly on his heels, identifying where pain is felt. This is the so-called "jarring test" and it is said to be more objective than the rebound test. Percussion of the abdomen is helpful in demonstrating gas or fluid in hollow organs or in the free peritoneal cavity. When the abdomen is enlarged and hyperresonant, intestinal distention or pneumo-peritoneum should be considered. Free fluid within the peritoneal spaces is demonstrated by testing for a fluid wave and shifting dullness. In ascites, bulging in the flanks may be observed. Dullness to percussion can be helpful in determining the size of an enlarged spleen or liver or a solid tumor mass. The physical examination must include rectal palpation in the male and pelvic and rectal examination in the female. Fecal impaction, pelvic abscess, and neoplasms may produce signs of intestinal obstruction. When an inflamed appendix lies low in the pelvis, there may be rectal tenderness or a palpable pelvic mass in the absence of abdominal signs. Disease of the female pelvic organs may produce acute abdominal conditions. Bimanual pelvic examination may reveal a tubal or ovarian mass, exquisite tenderness on movement of the cervix, or bloody or purulent cervical discharge, suggestive of acute pelvic complications. If physical findings are equivocal, the patient should be reexamined at frequent intervals until a diagnosis can be made and/or proper management of the patient determined. Laboratory Tests Urgency of acute abdominal conditions usually precludes prolonged investigation. There are only a few specific tests or examinations which may be relied upon to give clear cut answers to the exact cause of the acute condition. Urine and blood should be examined routinely. Pus or blood in the urine suggest disease of the urinary tract and can also result from an inflamed appendix lying in proximity to the ureter or bladder. In dehydration the specific gravity of the urine may be increased, and the red cell and hemoglobin values increased as a result of hemoconcentration. The total leukocyte count and percentage of polymorphonuclear cells are usually elevated in acute inflammatory conditions, whereas early in the course of intestinal obstruction there may be no significant alterations. Conditions in which tissue necrosis occurs, as in a strangulated intestinal obstruction, are generally associated with a marked polymononuclear leukocytosis. With acute appendicitis, the leukocytosis isn't great unless you already have a perforated appendix. The serum amylase test is essential when the possibility of acute pancreatitis exists. This possibility should be kept in mind in all patients with acute severe upper abdominal pain. Serum amylase values in excess of 500 units are significant and levels of 1500-2000 units or more are not unusual in the early stages of severe acute pancreatitis. Certain tests are indicated when extraabdominal conditions are suspected as the cause of an acute abdomen. These include blood and urine sugar determinations in diabetic keto- acidosis, hemoglobin electrophoresis in possible sickle cell crisis, chest x-ray in pneumonia, EKG in coronary artery disease, and lead levels in children with pica and anemia with an eye to chronic lead poisoning. Serum electrolytes to determine the degree of dehydration and electrolyte imbalance should be done when fluid loss has been significant.
X-ray Examination Plain x-ray films of the abdomen in the supine and upright positions can often provide immediate information which helps to confirm a diagnosis or exclude certain diagnoses which have been considered. Gas below the diaphragm in the upright film is almost pathognomonic or perforation of a hollow viscus, usually a ruptured peptic ulcer or a traumatic perforation. In mechanical small bowel obstruction, plain films in the upright position reveal dilated distended loops of gut with fluid levels above the obstruction, and absence of gas below the obstruction, i.e., terminal ileum and colon. Generalized distention of large and small bowel occurs in paralytic ileus. Plain films may reveal the presence of radiopaque gall stones or kidney stones. Usually upper GI barium studies are contraindicated because of the possibility of barium leakage into the peritoneal cavity when perforation is impending or perforation exists. Barium enema is an important diagnostic aid in intussusception of infants and children, and sometimes is used therapeutically under low pressure to reduce the intussusception. Barium enema may also be helpful in diverticulosis of the colon and in large bowel neoplasms, where sigmoidoscopy and biopsy may be helpful. When acute cholecystitis is suspected, intravenous cholangiography is useful for differential diagnosis. When the patient is acutely ill, investigation and supportive treatment should proceed concurrently, if a specific diagnosis is not immediately apparent. Supportive treatment includes nasogastric suction to relieve distention, intravenous fluids to correct fluid and electrolyte imbalance and to provide maintenance during periods of no oral intake, and typing and cross- matching of blood for possible transfusion. Except in a case of severe prostrating pain, narcotics should not be used until diagnosis is established because they may mask important clinical features of the pain. In acute infectious conditions antibiotics are usually begun after cultures have been obtained and a diagnosis fairly well established because they may alter early characteristic clinical features which may be important in diagnosis. Choice of antibiotics will be determined by sensitivity results on cultures. Now for brief clinical pictures of the diseases listed in Objective 2, a through e. Table I and II summarize salient clinical features of the more common conditions which cause or mimic the acute abdomen. a. Acute Appendicitis In acute appendicitis pain is typically the first symptom. The initial pain is diffuse and not well localized, with a dull pain in the epigastrium or periumbilical region. After a period of a few hours, the pain shifts to the right lower quadrant (RLQ) of the abdomen and becomes more localized and severe. Anorexia is an important symptom in patients with appendicitis. Nausea and vomiting are variable in frequency and intensity, and when they do occur, they usually follow the abdominal pain. However, the majority of patients lose the desire to eat or drink and may actually have an aversion to food. Temperature, pulse, and respiratory rate are within normal limits early in the disease. Later the temperature may be elevated, but seldom exceeds 101 degrees unless perforation has occurred. At the onset, the patient with colicky pain (due to a fecalith in the lumen) may be somewhat restless. However when the pain becomes localized in the RLQ, the patient usually prefers to lie on the right side with the thigh flexed. Localized tenderness in the RLQ is the single most important finding in acute appendicitis. The degree of muscle guarding varies considerably and rebound tenderness may be demonstrable. Rectal examination is essential in the examination of patients suspected of having appendicitis. When the appendicitis is in the retrocecal position, rectal examination elicits marked tenderness which may be minimal or absent on abdominal examination. Laboratory determinations are of limited value. The white cell count may be normal or slightly elevated in the range of 10-12,000 with some increase in the number of neutrophils. With perforation of the appendix, the white count and percentage of neutrophils increase markedly. The chief complication of acute appendicitis is perforation with abscess formation or diffuse peritonitis. Often the severe right lower quadrant pain subsides promptly at the time of perforation and the patient is relieved of acute symptoms for a brief period. Steady pain, however, then develops that may spread to involve the remainder of the abdomen as the clinical picture associated with diffuse peritonitis develops. When the clinical picture of appendicitis is equivocal, a short period of observation of two to four hours may be helpful as the patient is carefully observed for progression of symptoms. No narcotics should be given. Repeated examination and determination of temperature, pulse, respiratory rate and white cell and differential counts should be done at frequent intervals, until the diagnosis is established or disproven. A wide variety of problems may mimic acute appendicitis. Rupture of a graafian follicle in the right ovary (mittelschmerz) may simulate appendicitis. This is a common cause of lower quadrant pain of ovarian origin and typically occurs in the midportion of the menstrual cycle. Other conditions which may simulate acute appendicitis include pelvic inflammatory disease, mesenteric adenitis in young children, and diverticulitis. Obviously the specific treatment of appendicitis is appendectomy. The prognosis is excellent when the operation is performed before perforation occurs. Perforation of the acutely inflamed appendix is a serious complication which still results in significant morbidity and mortality. b. Acute Small Intestinal Obstruction Acute obstruction of the small bowel in adults is caused most commonly either by incarcerated hernia or by post-operative adhesions within the peritoneal cavities. Age has a significant influence upon the cause of small bowel obstruction. In newborns, congenital problems such as atresia and meconium ileus are important causes of obstruction. In young children, intussusception is encountered with frequency. In general, the higher the site of the obstruction within the intestinal tract, the more severe the symptoms. Pain is usually sudden in onset, severe, and spasmodic in nature because it results from vigorous peristaltic activity of the bowel as it attempts to propel the intestinal contents through the site of obstruction. The patient will often double up with pain during cramping distress and then have a brief period of freedom from distress. Vomiting occurs early in high intestinal obstruction and is copious in amount. Initially the vomitus contains gastric contents, followed by small intestinal contents later, usually bile colored. If persistent vomiting occurs, and if the obstruction is in the lower part of the small bowel, the vomitus becomes fecal in character. Usually with established intestinal obstruction the patient is unable to pass flatus or stools spontaneously. Bowel contents beyond the obstruction may be passed, however, and in children with intussusception, this material contains bloody mucus which gives it the characteristic "currant jelly" appearance. In the early stages, temperature, pulse rate and respiratory rate are normal, as is the white count. Increased temperature with elevated white count suggest that strangulation- obstruction is developing. On examination, inspection will reveal the presence or absence of surgical scars or evidence of inguinal or femoral hernia. Palpation is usually not revealing but with intussusception, a sausage-shaped mass may be felt in the right abdomen. This mass is the invaginated segment of the small intestine. Progressive distention occurs. Tenderness and muscle rigidity in the presence of intestinal obstruction are suggestive of peritoneal inflammation and strangulation-obstruction. Auscultation will reveal increased bowel sounds. During episodes of pain, loud high pitched peristaltic rushes occur. As distention progresses, interference with neurogenic and vascular elements of the bowel develops, motility is reduced and bowel sounds are decreased. Vomiting with high intestinal obstruction is associated with significant loss of fluid and electrolytes, and dehydration and electrolyte imbalance ensue rapidly unless the obstruction is relieved. Circulatory impairment leads to ischemia and necrosis of the gut wall and progressive reduction in all bowel functions. Plain x-ray films are often diagnostic. The bowel loops above the obstruction are distended with gas and fluid with absence of gas seen below the level of obstruction. In the upright film fluid levels are found in the dilated loops. The conditions most likely to be confused with bowel obstruction are those in which colicky pain in a smooth muscle organ is the outstanding symptom; thus diseases of the gall bladder, the urinary tract, and the female pelvic organs may resemble an intestinal obstruction. Paralytic ileus or functional intestinal obstruction must also be considered. Surgery is not indicated for paralytic ileus and may adversely affect its course. Examination of the abdomen with a stethoscope is most helpful. Bowel sounds in paralytic ileus are hypoactive to absent, in contrast to the hyperactive sounds associated with mechanical obstruction. Treatment of mechanical obstruction consists in relieving the obstruction surgically at the earliest time consistent with safety of the patient. The distention must be corrected by suction-decompression and fluid-electrolyte-blood deficits repaired, but the operation should be done as soon as possible when the patient is in satisfactory condition and before ischemic necrosis develops. Strangulation of the bowel is a dangerous complication which is the cause of most deaths from obstruction. When blood supply is compromised, the involved segments become necrotic, perforate easily with diffuse soiling of the peritoneal cavity, and resection of the gangrenous bowel will be required. c. Acute Mesenteric Vascular Occlusions Mesenteric artery occlusion can result from thrombosis or embolism which usually arises from a recent myocardial infarction or atrial fibrillation. This is a rare but serious cause of an acute abdomen, characterized by sudden onset of severe diffuse abdominal pain associated with nausea, vomiting, progressive distention, and sometimes bloody diarrhea. Typically, the pain is out of proportion to the physical findings which are minimal at the onset. Initially peristalsis is hyperactive, then gradually diminishes. When peristalsis is absent, the bowel wall is usually not viable. Signs of peritonitis develop rapidly with distinctly elevated white cell count and elevated temperature. X-ray films of the abdomen may reveal wide-spread gas and fluid filled loops of bowel but negative x-ray findings do not exclude this diagnosis. It can be suspected in a patient who has a cardiac lesion capable of embolization and sudden onset of diffuse severe pain, blood in the stools and the rapid development of signs of peritonitis. d. Perforated Duodenal Ulcer Perforation of a duodenal ulcer is one of the important causes of the development of sudden severe abdominal pain. Typical history involves a male usually between 20 and 40 years of age who has a history of episodes of epigastric distress relieved by milk and antacids. The episode of perforation is usually dramatic, with sudden, severe, midepigastric pain which spreads rapidly to involve the entire abdomen. The patient lies very still and resists any movement, which is very painful. After the appearance of pain, the patient may vomit once or twice but vomiting is not a common feature of perforated ulcer. The pain is so severe and prostrating that the patient may faint. On examination, the patient appears very ill, in great distress, with moderate tachycardia. Blood pressure is usually normal for the first several hours. Palpation demonstrates diffuse abdominal tenderness and rigidity of the muscle wall which has been described appropriately as "board like." Auscultation reveals the bowel sounds to be absent or markedly diminished. The white blood cell count increases quickly and may rise to 15,000 within a few hours. An upright film of the chest and abdomen will reveal air under the diaphragm in about 85Z of the cases. This is pathognomonic of a perforated ulcer, in conjunction with the characteristic history and physical findings already described. Acute pancreatitis may be difficult to distinguish from a perforated ulcer. Many patients with pancreatitis have either a history of alcoholism or gallstone disease. The onset of pancreatitis is more gradual and is often associated with prodromal episodes of epigastric distress 2-3 weeks before the onset of the severe pain which is constant, epigastric in location and radiates through to the back. Muscle tenderness and spasm may be limited to or more marked in the upper abdomen and the rigidity is less marked than with a perforated ulcer. The serum amylase level is markedly elevated in inflammatory disease of the pancreas and free air under the diaphragm is not found on x-ray examination. Lobar pneumonia involving the right lower lobe may lead to a mistaken diagnosis of subdiaphragmatic disease. A careful history and examination of the patient should provide a clue to the pulmonary disease. Rapid respiration, cyanosis, dyspnea, cough, and fever are helpful signs. X-ray will confirm the RLL consolidation and absence of free air under the diaphragm. Rupture of the abdominal aneurysm may produce sudden severe prostrating pain, but the picture of blood loss and shock predominates quickly, suggesting the true nature of the catastrophe which may be rapidly fatal. e. Peritonitis Causes of peritonitis have already been discussed. It is obvious that the onset of peritonitis varies widely depending in large part upon the organ involved and the nature of the primary process. Perforation of a duodenal ulcer occurs suddenly and dramatically and the initial insult is primarily a chemical peritonitis due to the acid gastric juice. Bacterial invasion occurs later. Perforation of the acutely inflamed gall bladder is more insidious and may occur with few, if any, changes in the clinical picture in a patient with acute cholecystitis. When the origin of the peritonitis lies in the pelvis, as with pelvic inflammatory disease, the patient may report that the pain began in the hypogastrium and spread upward. Physical findings may vary widely. Temperature and pulse rate are elevated in most patients. Pain is the most important symptom and is usually very severe and most pronounced in the area of origin of the peritoneal contamination. At first it is often a localized peritonitis in the right upper abdomen when the gall bladder perforates, or in the left lower quadrant following perforation of sigmoid diverticulitis. Spreading of the pain to involve more of the abdomen is a strong evidence that generalized peritonitis is developing. Pain in the shoulders indicates involvement of the diaphragmatic surfaces by the inflammatory process but does not assist materially in localizing the site or origin. Vomiting is a commonly associated symptom which is usually reflex at first, but becomes more pronounced as paralytic ileus develops with progression of peritoneal inflammation. On examination, the patient appears pale, in great pain, with beads of sweat on the forehead. Any motion is painful and the patient usually lies very still with thighs flexed to relax abdominal musculature. Respirations are splinted and shallow. Auscultation reveals decreased to absent bowel sounds. On palpation there is generalized tenderness and rigidity of the abdominal walls. Rectal examination and pelvic examinations in women are important for diagnosis of rectocecal appendix, PID, tubal pregnancy and neoplasm. The diagnosis of acute peritonitis is usually not difficult. It is of great importance, however, to determine the cause of the peritonitis in order to institute appropriate treatment promptly. The most commonly encountered diseases that lead to peritonitis when not treated are acute appendicitis, acute cholecystitis, perforated peptic ulcer, and acute diverticulitis. Early removal or closure of the source of peritoneal contamination is a fundamental rule of treatment when possible. For example, a perforated appendix must be removed, a ruptured ulcer must be closed, and a necrotic segment of gut must be resected. An exception to this rule would be the nonsurgical antibiotic treatment of acute pelvic inflammatory disease which has caused leakage into the abdominal cavity. Careful attention must be given to the patient's preoperative state and all necessary measures taken to improve his condition. This usually requires the correction of fluid and electrolyte imbalance, blood deficits, suction-decompression of the gastrointestinal tract and institution of vigorous antibiotic therapy. Early operation is indicated as soon as the patient's condition permits. Source
