There are few situations in clinical medicine which demand prompt and decisive action as frequently as does acute abdominal pain. Acute conditions of the abdomen are produced by inflammatory, obstructive, or vascular
mechanisms and are manifested by sudden onset of abdominal pain, gastrointestinal symptoms and varying degrees of local and systemic reaction. They require urgent treatment, often including emergency operation. Their urgency usually precludes prolonged investigation and there are few specific tests or examinations which may be relied upon to give clear-cut answers as to the exact cause of the acute condition.
If surgery carried no risk and did not adversely affect the course of some diseases, it would be safe to say "if in doubt, operate." Unfortunately, laparotomy itself carries risks and the course of some disorders such as acute pancreatitis and paralytic ileus is adversely influenced by anesthesia and surgery .
The diagnosis of acute conditions, therefore, frequently resolves itself into arriving at a fairly immediate judgement derived from an accurate and detailed history, a careful physical examination and a few selected lab tests and x-ray studies. While gathering the evidence, changes should be evaluated in terms of pathophysiologic alterations rather than specific diagnoses, and attention must be given to the need for supportive measures while investigation is underway.
On completion of this minicourse you will be able to:
The acute abdomen may be defined generally as an intraabdominal process causing severe pain and often requiring surgical intervention. It is a condition that requires a fairly immediate judgement or decision as to management. General causes of the acute abdomen may be divided into six large categories:
Each of these categories has many typical examples, of which only a few of the more common conditions will be discussed in this minicourse.
The inflammatory category of causes may be divided into two subgroups: 1) bacterial, and 2) chemical. Some common examples of the bacterial causes would include acute appendicitis, diverticulitis, and some cases of pelvic inflammatory disease. An example of a chemical cause would be a perforation of a peptic ulcer, where spillage of acid gastric contents causes an intense peritoneal reaction.
Mechanical causes of an acute abdomen include such obstructive conditions as incarcerated hernia, post-operative adhesions, intussusception, malrotation of the gut with volvulus, congenital atresia or stenosis of the gut. The most common cause of large bowel mechanical obstruction is carcinoma of the colon.
Vascular entities producing an acute abdomen include mesenteric arterial thrombosis or embolism. When the blood supply is cut off, necrosis of tissue results, with gangrene of the bowel.
Congenital defects can produce an acute abdominal surgical emergency any time from the minute of birth (with conditions such as duodenal atresia, omphalocele or diaphragmatic hernia) to years afterward in conditions such as chronic malrotation of the intestine.
Traumatic causes of an acute abdomen range from stab and gunshot wounds to blunt abdominal injuries producing such conditions as splenic rupture. History or evidence of trauma should make this diagnosis fairly obvious.
1. What is meant by the term "acute abdomen?"
2. Give an example of an acute abdomen due to each of the following mechanisms:
1. The term refers to acute conditions arising within the abdomen associated with severe abdominal pain, requiring fairly immediate management and often requiring surgery.
2. One example of each is:
OBJ. 2. Describe the cause and pathophysiology of the following acute abdominal diseases:
Inflammation in the appendix has the same features and follows the same course as inflammation elsewhere in the gut. Its importance is a function of its frequency as a serious surgical condition with significant complications.
Obstruction of the appendiceal lumen by fecaliths with interference of the vascular supply are important features in its pathogenesis. The essential element causing inflammation of the wall of the appendix is invasion by bacteria. The usual organisms in the inflamed appendix are colon bacilli and streptococci, organisms commonly found in the intestinal tract. Obstruction of the lumen and vascular occlusion probably contribute by breaking down the resistance of the wall of the appendix to invasion by potential pathogens in the gut.
The earliest lesion is a superficial ulceration of the mucosa. Spread then occurs from the mucosa to the muscle layers and the serosa and the lumen may become filled with pus. Interference with circulation leads to areas of necrosis and perforation of the appendix, with spread of infection to the peritoneal cavity. If the infection becomes walled off around the appendix a localized abscess may result. Otherwise a generalized peritonitis results.
The same sort of inflammatory process may occur in acute diverticulitis which usually involves the descending and sigmoid colon. This is promoted by the lodging of fecal material in a diverticulum with spread of inflammation to surrounding tissue, and is accompanied by left lower quadrant pain.
In acute cholecystis there is inflammation of the wall of the gall bladder due so chemical damage from the action of concentrated bile, promoted by an obstruction of the cystic duct, usually by stones. Bacterial infection with streptococci or colon bacilli may supervene. In acute cholecystis the gall bladder is large and has a thick edematous wall. The mucosa shows areas of ulceration and necrosis and leukocytes are present in the wall. Pus may fill the cavity, with an empyema of the gall bladder. Necrosis and rupture may occur.
Complete obstruction to the passage of intestinal content is caused either by mechanical obstruction of the lumen or by paralysis of the intestinal muscles (paralytic ileus) and may cause death in a relatively short period of time unless relieved. Acute mechanical obstruction of the small bowel is caused most commonly either by strangulated hernia or by adhesions and bands, usually post-operative, with the peritoneal cavity.
Age has a significant influence on the cause of small bowel obstruction. In newborns, congenital problems such as atresia of the gut are important causes of obstruction and in small children intussusception is encountered with frequency. The obstruction may be an entirely mechanical occlusion of the lumen, which is the case with an incarcerated hernia, congenital atresia of the lumen of the gut, and kinking and external compression of the gut by peritoneal adhesions, usually post-operative in origin.
There may, however, be an associated interference with the blood and nerve supply for the intestines, in which case the bowel is said to be strangulated. Obstruction such as an incarcerated hernia, if not promptly reduced, causes increasing edema of the gut with impairment of the blood supply. Volvulus with twisting of the mesentery and intussusception (where one segment of the small bowel invaginates into another) also cause interference with nerve and blood supply. Ischemic necrosis or infarction of the bowel wall occurs unless the blood supply is promptly restored. The involved portion of the intestine becomes in turn congested, edematous, necrotic and finally gangrenous. In general, the higher the site of an obstruction within the intestinal tract, the more severe are the associated symptoms of excessive vomiting with dehydration and chemical disturbances occurring because of a great loss of water and electrolytes.
The most common cause of lower intestinal obstruction is carcinoma of the distal portion of the colon. The development of the clinical picture is slower than in small bowel obstruction and patients do not appear as ill in comparable stages. Usually the acute episode of large bowel obstruction is superimposed on progressive change of bowel habits, with decreasing caliber of the stools and increasing constipation.
Functional intestinal obstruction due to neurogenic factors which cause paralysis of the intestinal muscle and failure of peristalsis is fairly common. It is termed adynamic or paralytic ileus and it occurs to some extent in most patients who have undergone abdominal surgery, and may be associated with shock or any severe trauma, such as hip fracture. Ischemia of the intestine also rapidly inhibits motility and paralytic ileus results. Paralytic ileus is commonly a concomitant of generalized peritonitis. Paralytic ileus is treated nonoperatively by suction and decompression of the intestine, and is adversely affected by anesthesia and surgery. It is important to differentiate a functional from a mechanical obstruction, where surgery is imperative.
Paralytic ileus is the end-result in a mechanical obstruction, unless the compromised blood supply is promptly restored. Otherwise there may be inexorable progression, terminating in gangrene.
Interference with the blood supply to a segment of the intestine, as in thrombosis or embolism of the superior mesenteric vessels, results in a paralytic obstruction without any mechanical blockage. The majority of patients with embolism involving the superior mesenteric artery have a cardiac lesion that is capable of thrombus formation and emboli. Recent myocardial infarction and atrial fibrillation are the two cardiac problems that give rise most often to mesenteric emboli. The segment of intestine which is deprived of its blood supply rapidly becomes congested, edematous and finally necrotic.
While all the factors responsible for the development and persistence of chronic peptic ulcers are not thoroughly understood, the one factor of established importance is the action of acidpepsin gastric content on the duodenal mucosa with ulcer formation. In some individuals there seems to be too much gastric acid secretion with respect to the degree of protection provided for the mucosa. Peptic ulcers are constant in location, being found in the pyloric portion of the stomach near the lesser curvature and the first portion of the duodenum proximal to the ampulla. These chronic ulcers appear as deep, punched-out, funnel-shaped craters whose base is covered with grayish necrotic material. The base of the ulcer is composed of fibrous scar tissue which may cause deformity of the duodenal bulb, demonstrable by x-ray.
Hemorrhage may result from erosion of large vessels in the base of the ulcer. Perforation may result when the ulcer continues to penetrate deeply and erodes through the wall of the duodenum into a remarkable series of dramatic changes. Spillage of acidpeptic gastric juice, bile, and pancreatic juice causes a marked chemical inflammation of the peritoneum comparable to a burn. Bacterial invasion may soon follow. Within a short time massive amounts of extracellular fluid may be extravasated into the area of peritoneal injury and this loss of fluid may bring about hypovolemic shock.
Acute pancreatitis may closely simulate a perforated duodenal ulcer. The effects are caused by the escape of lytic pancreatic enzymes into the gland itself. These act on the parenchyma of the gland, blood vessels and fatty tissue causing edema, necrosis, hemorrhage, and suppuration of varying degree. It appears to be due to increased pancreatic secretion with partial or complete obstruction of outflow and raised intraductal pressure. It may occur suddenly with severe abdominal pain, peripheral vascular collapse or shock, and may be fatal.
The peritoneal cavity, lined by serous peritoneal membranes which cover the viscera and the parietal walls, is a closed sac except for the openings of the fallopian tubes in the female. General inflammation of the peritoneal cavity is usually caused by bacterial invasion, which may result by spread: 1) from a ruptured viscus such as a perforated peptic ulcer or gangrenous appendix; 2) through an ischemic and necrotic but unruptured bowel wall, as in strangulated hernia, mesenteric occlusion, or volvulus; or 3) as a result of extension of infection from abdominal organs such as occurs with a liver abscess or a pelvic inflammatory disease.
The majority of cases of peritonitis involve organisms found in the normal flora of the gastrointestinal tract. Perforation of a hollow viscus is most frequently the source of entry of these organisms. The peritoneal infection may become walled off and limited to a localized area as in an appendiceal abscess, or there may be generalized peritonitis, which may be a serious complication of any of the diseases described above in a-d.
1. Outline the sequence of events in the pathogenesis of acute perforated appendicitis.
2. The two most common causes of acute mechanical small bowel obstruction in adults are:
3. What is the sequence of changes which occur when a loop of bowel becomes strangulated?
4. What is the underlying mechanism of the rapid development of generalized peritonitis, hypovolemic shock and perforated duodenal ulcer?
5. How do necrosis and gangrene differ?
1. Obstruction of appendiceal lumen by a fecalith is followed by edema and interference with blood supply, ulceration of mucosa and bacterial invasion of the appendiceal wall. Extension of infection to muscle layers and serosa (viscera] peritoneum) is followed by increasing impairment of blood supply, ischemia, necrosis and perforation. Spillage of infected materials results in localized or generalized peritonitis.
2. Incarcerated hernia. Post-operative adhesions.
3. Mechanical obstruction, as in an incarcerated hernia, causes increasing distention of the bowel, edema of the gut wall and interference with nerve and blood supply. The segment of gut which has an impaired blood supply is said to be strangulated. Unless the obstruction is relieved and blood supply promptly restored, the involved portion rapidly becomes in turn more congested, edematous, ischemic, necrotic, and finally gangrenous. The nonviable wall is friable and perforated easily or may allow passage of infected material into the peritoneal cavity without gross perforation.
4. With acute perforation of duodenal ulcer, there is immediate spillage of highly irritating acid-pepsin gastric contents into the peritoneal cavity, causing an intense peritoneal reaction with a generalized chemical peritonitis. The peritoneal injury is comparable to an extensive chemical burn, and large amounts of extracellular fluid may be extravasated into the area of peritoneal injury, causing hypovolemic shock.
OBJ. 3. Identify and describe the symptoms, signs, clinical course, and laboratory and x-ray findings for the acute abdominal diseases listed under Objective 2.
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.
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.
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.
most common with acute gastroenteritis or food poisoning, but it may occur with appendicitis or other focal inflammatory lesions of the gut
With complete small bowel obstruction - unrelenting constipation (obstipation) after fecal material below obstruction has been passed. Progressive constipation with carcinoma of the large bowel.
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:
abdominal scars, adhesions - intestinal obstruction peptic ulcer - possible perforation chronic cholecystitis or biliary colic - acute cholecystitis
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.
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.
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.
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.
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.
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.
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.
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.
1. What are the differences between visceral and somatic pain?
2. Visceral pain from these organs would be experienced in what zone of the abdomen?
3. Identify the usual pattern of radiation of pain which suggests a diagnosis of:
4. a. Describe the pain which occurs with acute small bowel
b. Describe the early bowel sounds in acute small bowel obstruction.
5. On physical examination, what is the most important and dependable early signs of peritoneal inflammation?
6. On an upright film of the abdomen, demonstration of free air beneath the diaphragm is practically pathognomonic of?
7. What is the most likely diagnosis with the following data?
a. Peristaltic pain - colicky in nature. Copious vomiting of bile stained material. Failure to pass stool, previous abdominal operation or presence of hernia.
b. History of alcoholism or gallstones. Diffuse epigastric tenderness and severe pain which radiates to the back. Elevation of serum amylase levels.
1. Visceral pain results from gut distention and stretching or spasm of the muscle fibers. It is carried by sympathetic nerve fibers, and is experienced as dull, vague, poorly localized pain in the mid zones of the abdomen.
Somatic pain results when the parietal peritoneum is inflamed or irritated. It is carried by sensory fibers in somatic nerves. It is better defined, more localized, greater in intensity, and is associated with localized tenderness and spasm of the muscle groups supplied by the same dermatome of the cord.
2. a. epigastrium b. periumbilical area c. hypogastrium d. hypogastrium
4. a. intermittent severe, cramping, colicky pain, with pain-free intervals b. the bowel sounds are loud, booming, rhythmical and synchronous with the colicky pain
5. localized point tenderness
6. ruptured hollow viscus
7. a. mechanical small bowel obstruction, due to post-operative
adhesions or an incarcerated hernia
b. acute pancreatitis
OBJ. 4. Identify the clinical features that help to distinguish the surgical from the nonsurgical acute abdomen.
In Tables I and II are summarized characteristic features for differential diagnosis of common conditions which may either cause or mimic an acute abdomen. Table IV divides these diseases into surgical and nonsurgical groups. Although it is not always possible to make an exact diagnosis preoperatively, it is obvious that certain clinical features of intraabdominal disease are highly suggestive or practically pathognomonic of an acute abdomen which may require prompt surgical intervention. These features which may occur singly or in combination are listed below:
The character, location and radiation of the pain along with other associated symptoms and signs as summarized in Tables I and II will be helpful in establishing a diagnosis and deciding whether surgery is indicated.
When significant abdominal pain occurs in association with extraabdominal disease, diagnosis can fairly readily be established by careful history, physical exam and appropriate laboratory or x-ray studies. For example, chest x-ray will confirm RLL pneumonia suggested by the respiratory symptoms and signs associated with RUQ pain and tenderness. Similarly, in acutely ill patients with coronary occlusion with severe pain, radiating to neck, shoulder and left arm, the EKG is very helpful.
In addition, there is a miscellaneous group of diseases which have been mentioned earlier where severe abdominal pain is a prominent symptom. The diagnosis may be missed and the patient subjected to needless and hazardous surgery if these are not considered and diagnosed or excluded by careful evaluation and appropriate tests, when suspected. These include: "Mittelschmerz," mesenteric adenitis, bite of a black widow spider (bay be followed by abdominal cramps and board-like rigidity of the abdomen which are relieved by intravenous injection of calcium gluconate).
TABLE I - Differential Diagnosis of Diseases Causing Upper Abdominal Pain *Acute *Acute *Perforated Acute Pleurisy Coronary Appendicitis Cholecystitis Peptic Ulcer Pancreatitis and Occlusion Pneumonia Age Usually under 40 Over 40 30-50 30-50 Any Age Over 40 Sex Both Female, fat Rare in females Females pre- Both Male dominate Pain Epigastric; Severe; radiates History of ulcer Sudden onset In upper ab- Lancinating; shifts to RLQ; to back and in 60-75%; sud- after large domen, not lo- radiates to constant with shoulder; re- den onset, in- meal; severe calized; relieved left exacerbations quires morphine; tense, constant constant; ra- by splinting shoulder and relieved by anti- pain; requires diates to back respiratory arm spasmodic morphine requires muscles morphine Vomiting Exception, but Reflex; may be Not prominent Always Exception Reflex always anorexia much retching Appear- Not acutely ill Worn because of Acutely ill; Acutely ill; Restless; may Dyspneic; ance until periton- pain keeps abdomen shock-like if have grunting cyanotic; itis immobile; shock- necrosis respirations very rest- like less; sweat- ing; BP sub- normal Temp. 99-1OOF; higher 99-102 F Subnormal Subnormal at 100-103 F Normal to after perfora- onset; later subnormal tion variable Tender- Localized RLQ Localized in RUQ Diffuse, more in Epigastric; re- Epigastric; in- Upper abdo- ness rebound upper abdomen; bound; bowel consistent; men, but board-like ri- sounds de- no restriction changeable gidity; absent creased of abdominal and incon- bowel sounds respiratory sistent movement Labora- Leukocytosis Leukocytosis Leukocytosis Serum amylase High leukocy- Leukocytosis tory elevated tosis ECG very helpful X-ray No help May show stones Free air in 85% "Sentinel loop" Chest x-ray No help or nonvisualiza- 4 hr. after onset of small bowel diagnostic tion of gall-bladder TABLE II - Differential Diagnosis of Diseases Causing Lower Abdominal Pain *Acute Ureteral Acute *Ectopic Appendicitis Obstruction Salpingitis Pregnancy Diverticulitis Age Usually under 40 Under 40 Under 40 Under 40 Over 40 Sex Both Both Female Female Male Pain Epigastric; shifts Severe, knife- Dull, constant Sharp, knife- Dull cramping; to RLQ; constant like; begins in both LQ; recurrent like (usually not LLP pain; diarrhea with exacerbations lumbar area; ra- attacks; jarring diagnosable until diates to groin, is painful; back- rupture occurs) scrotum, thigh, ache; dysuria dysuria; frequency Menses -- -- No change or men- Missed or scanty -- orhagia period; 15-25% have no irregularity Temp. 90-100 F before Normal 99-102 F Normal 99-101 F perforation Tenderness Localized RlQ; Costovertebral; Bilateral LQ; Unilateral LQ; LLQ; rebound, mass+- rebound none in abdomen suprapubic; re- rebound mild distention +- bound *Surgical TABLE II (continued) *Acute Ureteral Acute *Ectopic Appendicitis Obstruction Salpingitis Pregnancy Diverticulitis Pelvic Tenderness high --- Exquisite tender- Cervix moderately -- Exam on right ness on movement tender to movement; Rectal of cervix; profuse bloody discharge purulent discharge (dirty brown) Labs Normal sed. Hematuria; no Vaginal or cervi- Aschheim-Zondek Leukocytosis rate; leukocytosis leukocytosis cal culture pos. may or may not be for gonococcus; positive; cul-de sedimentation sac puncture-blood rate elevated X-ray No help See stone on No help No help No help unless flat 85%; IV barium x-ray pre- pyelogram helps viously showed diverticulosis *Surgical
1. Just for fun, as an index of the complexity of the problem, see if you can come up with a dozen causes of right lower quadrant pain in a teen-age girl.
2. Identify 2 or 3 clinical features of each of the above on which a reasonable presumptive diagnosis can be based.
3. Which of the above require immediate or fairly immediate surgery? Explain the clinical features which led you to decide that surgery is indicated in each of the conditions you selected.
OBJECTIVE 4 Answers
3. Acute appendicitis, obviously. RLQ point tenderness is indicative of localized inflammation of contiguous parietal peritoneum, resulting from extension of the appendiceal infection through the serosa.
Rupture of an ectopic pregnancy. The sudden severe onset of pain suggests a ruptured viscus and the rapid development of shock suggests massive hemorrhage which may flood the peritoneal cavity and cause generalized peritoneal irritation.
Twisted ovarian cyst. Although this has not been discussed, when torsion of the pedicle occurs, there is sudden interference with blood supply (as in the cause of volvulus of the mesentery). This causes sudden onset of severe pain and the patient appears ill and shocky. Unless blood supply is promptly restored, ischemic necrosis of the cyst wall and perforation with spillage will ensue.
OBJ. 5. Construct an approach to evaluation and management of the acute abdomen.
Table III categorizes conditions which cause or simulate an acute abdomen according to the type of onset, the pathogenesis, the presenting clinical picture, and the urgency of need for medical and/or surgical treatment. Table IV divides the disease into surgical or nonsurgical groups. These tables provide the schema for evaluation and management of acute abdominal conditions.
Priority I indicates catastrophic events, such as perforation of a viscus, massive hemorrhage, sudden arterial occlusion with extensive tissue necrosis, all of which are characterized by sudden onset of severe prostating continuous pain, moderate to extreme abdominal tenderness and muscle spasm, and rapid development of shock. There is marked tissue damage and fluid loss from traumatic chemical or vascular insult. Immediate institution of supportive and resuscitative measures (i.e., intravenous correction of fluid and electrolyte imbalance, blood replacement, gastric suction, vasopressor agents, oxygen, narcotics) is imperative. Emergency operation as soon as the patient's condition permits must be done to repair a perforated viscus, to restore blood supply by relief of strangulation- obstruction, or to control hemorrhage in a ruptured ectopic pregnancy, ruptured spleen and (hopefully when conditions permit) a dissecting aneurysm.
Acute pancreatitis, which may have a sudden catastrophic onset, is treated nonoperatively with supportive and resuscitative measures, as outlined above, with nasogastric suction to control or prevent paralytic ileus, and with antibiotics to control or prevent infection. The pathophysiology of acute pancreatitis involves intrapancreatic activation of digestive enzymes and autodigestion of the pancreas with edema, hemorrhage and necrosis of the gland. Surgical treatment for acute pancreatitis is no longer strictly taboo due to better fluid and electrolyte management.
It may be difficult to differentiate acute pancreatitis from other catastrophic conditions. The clinical picture and markedly elevated serum amylase will be helpful. Differentiation of an acute myocardial infarction is ordinarily not a difficult diagnostic problem and the EKG will be helpful. An acute dissecting aneurysm may progress with such rapidity that there may be little or no time for diagnosis or surgical treatment.
In this catastrophic group, emergency treatment is imperative. Without treatment, rapid and progressive deterioration of the patient occurs, and the prognosis is very guarded.
Priority II includes conditions associated with vigorous smooth muscle contractions in an attempt to propel luminal contents past an obstruction. This is the so-called colic group, which is characterized by severe intermittent recurrent cramping pain and serious disturbance in gastrointestinal function when the obstruction is in the small bowel.
Marked systemic reactions are not generally encountered in the early stages of gut obstruction, but become severe as the process advances. In bowel obstruction the need for surgical treatment is urgent to prevent ischemic necrosis of the gut, but not as critical as in the catastrophe category. There is more time for studies and preparation of the patient. Diagnosis can usually be established by careful clinical evaluation of the patient, characteristic hyperactive bowel sounds, and demonstration by x- ray of distended loops of gut above the level of obstruction. Fluid and electrolyte imbalance must be corrected and distention relieved by nasogastric suction before operation. The prognosis is good in cases seen early but much more serious when ischemic necrosis of gut occurs and resection of gangrenous bowel is required.
Biliary and renal colic are treated conservatively with use of meperidine (Demerol) for relief of pain and relaxation of smooth muscle spasm to facilitate passage of the calculus. Both renal and biliary colic are treated medically with diet, fluids and narcotics, and surgery is usually not required, at least for the acute episode of colic.
At times a marked gastroenteritis or a fecal impaction may cause severe colicky pain, but history, physical exam, and the benign course will obviate any serious consideration of ill-advised surgery.
Priority III, the lowest category of urgency, includes inflammatory conditions associated with abdominal pain and a possible acute abdomen. The progression of inflammatory changes occurs over a period of several hours to a few days. Initially the systemic and abdominal manifestations are not severe and there is considerably more time to observe and evaluate the patient. With progression of inflammation and infection, pain and tenderness increase, become more localized, and fever and leukocytosis increase. Without treatment, there is further tissue damage, and perforation and peritonitis may ensue. Clinical diagnosis is usually possible on the basis of clinical feature and tests (see Tables I and II).
Until a diagnosis or a decision to operate is made, narcotic analgesics should not be used lest they mask the pain which is such an important diagnostic feature of the disease. Similarly, antibiotics may alter the course and they should be deferred until diagnosis is established. Operative and nonoperative measures should be instituted, according to the diagnosis and indications, and the prognosis is generally favorable.
Acute appendicitis is prototypic of the acute inflammatory group. Diagnosis is clinical and early operation is indicated before suppuration and perforation occur.
Diverticulitis is an inflammatory process occurring in diverticulosis of the colon in older adults. It is usually treated medically with antispasmodics, intestinal antibiotics and diet. Colostomy or colectomy may become necessary for patients with repeated attacks who fail to respond to medical therapy. When the lumen of a diverticulum becomes obstructed, inflammation occurs within the diverticulum and spreads to adjacent bowel wall. The most common complication is perforation with localized peritoneal inflammation. This causes the so-called LLQ appendicitis for which surgery is required.
Acute cholecystitis is generally a complication of chronic cholecystitis and occurs when the gall bladder outlet is suddenly and completely occluded, usually by a stone. Plain film of the abdomen may reveal radiopaque stones and gall bladder studies with contrast media show a nonfunctioning gall bladder. When the patient is in good condition and the acute attack is of short duration, cholescystectomy is the treatment of choice. In more seriously ill patients with more chronic infection, operation may be deferred 6 weeks, until the acute process has subsided due to medical treatment. The important nonoperative measures include gastrointestinal decompression, parenteral fluids, antibiotics and close observation of the patient for evidence of progression of disease or impending rupture.
Nonsurgical diseases in the inflammatory category (listed in Table IV) include the following:
A child who has moderately high fever 102 or more, with abdominal pain, and RLQ tenderness (although it may be LLQ or bilateral) will have acute mesenteric adenitis 80% of the time, rather than appendicitis. Mesenteric adenitis is associated with an acute pharyngitis, often with a leukocytosis of 15-20,000 and surgical intervention is not required. Sometimes the diagnosis cannot be made with certainty except at operation. When the danger of laparotomy is considerably less than that of a possible perforated appendix, operation is justified, and 4 out of 5 is a pretty good batting average.
Regional enteritis is a chronic granulomatous inflammation of the terminal ileum, characterized by chronicity, weight loss and bouts of infection, diarrhea, and cramping abdominal pain. Occasionally acute exacerbations may mimic an acute abdomen. Barium study of the small intestine gives a characteristic "string" appearance in the involved segment. Medical treatment is symptomatic and supportive.
Acute pelvic inflammatory disease can be readily diagnosed by its clinical features and by culture of cervical discharge. Treatment is medical and includes vigorous appropriate antibiotic therapy along with general supportive measures.
Finally, there is a miscellaneous group of conditions (see Table IV) in which abdominal pain is a prominent feature. To avoid mistakes in diagnosis and unnecessary and harmful surgery, it is important that these conditions be kept in mind and tested for when indicated, as discussed in Section 4.
TABLE III - Management of Acute Conditions of the Abdomen According to Urgency and Clinical Patterns PRIORITY PATTERN MECHANISM CLINICAL PICTURE MANAGEMENT I Pain, collapse, shock Perforation, hemor- Sudden severe pain; shock Immediate resuscitative (catastrophic), e.g., rhage, thrombosis, or shocklike state; abdo- and supportive measures; perforated ulcer, rup- necrosis minal tenderness; rigidity; diagnostic studies; early tured ectopic pregnancy, silent abdomen; severe operation if indicated acute pancreatitis, systemic reaction mesenteric thrombosis, ruptured aneurysm, etc. II Pain (intermittent), Obstruction of hol- Recurrent cramping pains; Establish diagnosis if colic, e.g., acute intes- low muscular organ vomiting; distention; noisy possible; correct systemic tinal obstruction, biliary (smooth muscle); abdomen; systemic reaction imbalances; early operation colic, ureteral colic strangulation may be slight to moderate; x-ray if indicated impending or existent may be diagnostic III Pain, tenderness, inflam- Irritation due to bac- Pain variable, usually in- Clinical iagnosis usually matron, e.g., acute ap- terial, chemical, creasing, tenderness-local- possible; early operation pedicitis, acute chole- ischemic factors ized, then diffuse with in appendicitis, proper cystitis, acute diver- rupture; muscle spasm, timing of all therapy ticulitis, acute salpin- often a mass; systemic (fluids, antibiotics, gitis reaction moderate to operation) severe TABLE IV - Specific Diseases Causing or Simulating an Acute Abdomen According to Categories of Urgency and Need Surgical Nonsurgical Catastrophe Rupture of a hollow organ - Acute pancreatitis (Priority I) spontaneous or traumatic Coronary thrombosis (peptic ulcer, ectopic preg- Dissecting aneurysm - nancy) with massive hemorrhage (with immediate diagnosis Rupture of a solid organ - and appropriate condi- usually traumatic (spleen, tions - surgical). liver, kidney) Acute vascular occlusion (mesenteric accident, strangulating obstruction) Massive hemorrhage, peptic ulcer, esophageal varices. Colic Acute intestinal obstruction Biliary colic, renal (Priority II) small and large bowel colic, gastroenteritis, Acute appendicitis (colic fecal impaction from fecalith in lumen) Inflammation Acute appendicitis Mesenteric adenitis (Priority III) Acute cholecystitis Regional enteritis Acute diverticulitis Pelvic inflammatory disease Ruptured ovarian follicle (Mittelschmerz) Urinary tract infection Pneumonia and pleuritis Miscellaneous Diabetic acidosis Lead poisoning Sickle cell crisis Black widow spider bite
OBJECTIVE 5 - Questions
2. In acute inflammatory conditions of the abdomen with a more gradual onset and less rapidly progressive course, what clinical features and tests are most helpful in arriving at a diagnosis and/ or management plan?
4. A 6-year old male child enters your office with pain in the right lower quadrant. He looks flushed and feverish and his temperature is 102.8. He has enlarged tender anterior cervical lymph nodes and his pharynx is beefy red in color. His WBC and differential is 18,000 with 80X polys. He has tenderness in his abdomen, somewhat more marked in the right lower quadrant. He has been anorexic for the last two meals and has vomited twice. How would you manage this patient?
5. If in doubt, why not always operate?
6. A 40-year old patient has a three-year history of epigastric distress relieved by mild and antacids. During the past 3 months, she has had a severe, cramping, colicky epigastric pain, radiating to RUQ and right scapula and requiring Demerol for relief. She has also noticed that for several months fatty foods cause indigestion and epigastric distress, which is not relieved by mild and antacids. ROS reveals that the patient has consumed abut 1/2 pint gin daily for the past two years. She is seen because of sudden onset of severe prostating epigastric pain 2 hours earlier which has now become very severe and generalized, with diffuse abdominal tenderness and rigidity. She appears acutely ill and shocked. She is obviously in severe pain which is aggravated by any movement.
OBJECTIVE 5 - Answers
2. 1) complete history and physical to exclude extraabdominal causes of abdominal pain; 2) location and radiation of pain; 3) localized tenderness and muscle spasm; 4) base line recording of T. R. P. WBC, and differential; 5) repeat determinations for increasing evidence of infection - increased temperature, increased WBC, increased % neutrophils; 6) frequent reevaluation of patient for progression of physical signs.
4. This is a common problem in children. It may be difficult or impossible to distinguish between acute appendicitis and acute mesenteric adenitis without operating. Most surgeons are considered correct in this decision with a batting average of 80% - that is to say, operating on at least 20% of children who ultimately do not have appendicitis but in fact do have mesenteric adenitis. If the body temperature is significantly elevated, 102 or above, 80% of the time the abdominal pain is not due to acute appendicitis. This patient should be treated with antipyretics and clear liquids and a throat culture taken, with reexamination of the patient 2-3 hours later for point tenderness if the pain persists. Antibiotics should be withheld until a more definitive diagnosis is made - e.g., throat culture positive for Group A beta hemolytic streptococci. On reexamination several hours later, if more localized RLQ tenderness is present, there is no choice except to operate. The mesenteric nodes may be found to be inflamed and enlarged and the appendix normal. The appendix is removed, however, to prevent a similar problem in the future. If on the other hand, after an interval of several hours, pain and tenderness have decreased, syptomatic treatment is continued until culture reports are back. If positive for beta strep, penicillin is given for ten days.
5. Surgery and anesthesia create trauma and additional stress in an already ill patient. Two conditions especially which cannot be relieved by surgery, seem to be definitely adversely affected by anesthesia and laparotomy, i.e., acute pancreatitis and paralytic ileus. Paralytic ileus often occurs temporarily following any type of abdominal surgery, apparently from disturbed gut function from handling. Post operative adhesions may result from surgery and cause obstruction later. Sound judgement is required. Any time the possibility of serious complications such as perforation or gangrene is present, the danger of not operating outweighs that of surgery.
The recent episodes of RUQ colicky pain with radiation to the right scapular area severe enough to require Demerol for relief are typical of biliary colic. Gallstones and indigestion aggravated by fatty foods add up to cholecystitis, which can become acute when obstruction to the flow of bile occurs. Onset of acute cholecystitis is usually not so sudden or prostrating as that described, although it can be superimposed on biliary colic. The pain, tenderness and muscle guarding remain localized in the RUQ, with pain radiating to back and right shoulder, rather than quickly becoming generalized, as it does when spillage of acid-pepsin gastric contents occurs.
Acute pancreatitis may have a sudden onset of severe prostrating epigastric pain as described. It is often associated with alcoholism and gallstones, and is more common in women. The pain, tenderness, and muscle spasm usually is limited to the upper abdomen with radiation to the back, and the rigidity is less diffuse and marked than with perforated ulcer.
So, while the history and findings are most suggestive of a perforated duodenal ulcer, both acute pancreatitis and acute cholecystitis have to be considered very seriously. The rapid development of generalized pain, tenderness and rigidity are not typical of either. Acute cholecystitis usually has a more gradual onset, but the clinical manifestations and course of acute abdominal conditions do not always accommodate us by being entirely typical.
The diagnosis then would be: 1) acute perforated duodenal ulcer, 2) cholelithiasis (gallstones).
If acute cholecystitis had been most likely on the basis of demonstration of gall stones and a nonfunctioning gallbladder by cholangiography, with no free air in peritoneal cavity and normal serum amylase, more time for evaluation -and preparation of the patient would have been available, and for a considered judgement as to whether surgery should be done now or after the acute process has subsided.
If, on the other hand, acute pancreatitis had seemed most likely on the basis of no free air under the diaphragm and a markedly elevated serum amylase, surgery is not only not indicated, but is definitely contraindicated because it has an adverse effect on an already critically ill patient. Resuscitative and supportive measures are indicated in all urgent and catastrophic acute abdominal conditions.