Perforation Emed

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History of the Procedure

Lau and Leow have indicated that perforated peptic ulcer was clinically recognized by 1799, but

the first successful surgical management of gastric ulcer was by Ludwig Heusner in Germany in1892. In 1894, Henry Percy Dean from London was the first surgeon to report successful repair

of a perforated duodenal ulcer.[1]

Partial gastrectomy, although performed for perforated gastric ulcer as early as 1892, did not

become a popular treatment until the 1940s. This was carried out as a result of the perceived high

recurrence rate of ulcer symptoms after simple repair. The physiologic effects of truncalvagotomy on acid secretion had been known since the early 19th century, and this approach was

introduced to the treatment of chronic duodenal ulcer in the 1940s. The next development in the

management of peptic ulcer disease was the introduction of high selective vagotomy in the late

1960s. However, neither of these approaches proved to be useful, and several postoperativecomplications, including high rates of ulcer recurrence, have limited their use. Currently, in

patients with gastric perforation, simple closure of perforated ulcers is more commonly

performed than is gastric resection.[2]

During World War I, the mortality rate following isolated injuries of the small intestine and

colon was approximately 66% and 59%, respectively. The possible reasons for the high mortalityand morbidity rates at that time may have been related to the following factors:

Knowledge in the area of bowel injuries and the pathophysiologic changes triggered bysuch injuries was inadequate.

Clinical skills and diagnostic techniques that allow early detection of such injuries werelacking.

Intravenous saline solutions or blood transfusions were not used in the management ofhypovolemia and hemodynamic changes of these patients.

No antibiotics were available. Laparotomy was not recommended in abdominal injuries. The technical maneuvers to assess bowel injuries and to mobilize ascending and

descending colon were generally not recommended.

During the early years of World War II, Ogilvie, a leading surgeon in the British Army,

recommended colostomy for management of all colonic injuries. This notion was supported by apublication from the office of the Surgeon General of the United States. However, the data

presented in Ogilvie's series were not convincing. He reported a mortality rate of 53% for

colonic injuries treated with colostomy, a rate similar to that observed during World War I.

According to Ogilvie, colostomy apparently failed to improve the mortality rate in World War II

because primary repairs were used to treat less-severe injuries during World War I. Many

patients in World War I were treated expectantly and were not included in the mortality data. Onthe other hand, Ogilvie's data included all patients with bowel injuries. These apparent

differences in the methodology used convinced surgeons to continue using colostomies in such

injuries after World War II.


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Several reports clearly indicated that surgeons used colostomy during the Korean and Vietnam

wars, particularly in the management of left colonic injuries. However, in civilian injuries, it has

been reported that primary repair can be successfully used. By the end of 1980s, primary repairwas considered to the management strategy of choice, and it has replaced the use of colostomies

in the treatment of civilian patients in most hospitals in the United States, the United Kingdom,

Europe, and Australia. At present, primary repairs are widely used for such bowel injuries.

Problem

Upper bowel perforation can be described as either free or contained. Free perforation occurswhen bowel contents spill freely into the abdominal cavity, causing diffuse peritonitis (eg,

duodenal or gastric perforation). Contained perforation occurs when a full-thickness hole is

created by an ulcer, but free spillage is prevented because contiguous organs wall off the area (as

occurs, for example, when a duodenal ulcer penetrates into the pancreas).

Lower bowel perforation (eg, in patients with acute diverticulitis or acute appendicitis) results in

free intraperitoneal contamination.

Epidemiology

Frequency

In children, small bowel injuries following blunt abdominal trauma are infrequent, with an

incidence of 1-7%. Evidence shows, however, that the incidence of these injuries is increasing.

In adults, perforations of peptic ulcer disease were a common cause of morbidity and mortality

with acute abdomen until the latter half of the 20th century. The rate has fallen in parallel withthe general decline in the prevalence of peptic ulcer disease. Duodenal ulcer perforations are 2-3

times more common than are gastric ulcer perforations. About a third of gastric perforations are

due to gastric carcinoma.

Approximately 10-15% of patients with acute diverticulitis develop free perforation. Although

most episodes of perforated diverticulum are confined to the peridiverticular region or pelvis,patients occasionally present with signs of generalized peritonitis. The overall mortality rate is

relatively high (~20-40%), largely because of complications, such as septic shock and multiorgan

failure.

In elderly patients, acute appendicitis has a mortality rate of 35% and a morbidity rate of 50%. Amajor contributing factor to morbidity and mortality in these patients is the presence of 1 or moresevere medical conditions coexisting with, but predating, the appendicitis.

Endoscopy-associated bowel injuries are not a common cause of perforation. For example,perforations related to endoscopic retrograde cholangiopancreatography (ERCP) occur in about

1% of patients.[3]


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Etiology

Penetrating injury to the lower chest or abdomen (eg, knife injuries) - In cases ofpenetrating trauma, the small bowel is the most commonly injured intra-abdominalviscus, because it is coiled in the abdomen and occupies most of the area of the peritoneal

cavity. In addition, the small bowel is attached to a mesentery and is highly mobile. Blunt abdominal trauma to the stomach - Such injuries are more common in children than

they are in adults and include vehicle-related trauma, bicycle handlebar injuries, and

seatbelt syndrome.

Ingestion of aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs),[4] and steroids -Intestinal perforation from such causes is particularly observed in elderly patients.Prescribing NSAIDs to patients with diverticular disease carries an increased risk of

colonic perforation.

Presence of a predisposing condition - Predisposing conditions include peptic ulcerdisease, acute appendicitis, acute diverticulitis, and inflamed Meckel diverticulum.Indeed, acute appendicitis is still one of the common causes of bowel perforation in

elderly patients and is associated with relatively poor outcomes.[5] Bowel injuries associated with endoscopy - Injuries can occur with ERCP and

colonoscopy.[3, 6, 7, 8]

Endoscopic biliary stent - Dislocation and migration of biliary stents to the intestine maycause bowel perforation.

[9]

Intestinal puncture as a complication of laparoscopy - Factors that may predisposepatients to this complication are obesity, pregnancy, acute and chronic bowel

inflammation, and bowel obstruction.

Bacterial infections - Bacterial infections (eg, typhoid fever) may be complicated byintestinal perforation in about 5% of patients. Perforation in these patients may

unexpectedly occur after their condition has started to improve.

Inflammatory bowel disease - Bowel perforation may occur in patients with acuteulcerative colitis, and perforation of the terminal ileum may occur in patients with

Crohn's disease.

Perforation secondary to intestinal ischemia (eg, ischemic colitis) Bowel perforation by intra-abdominal malignancy, lymphoma, or metastatic renal

carcinoma - Even benign tumours, such as desmoid tumours (eg, those originating from

the fibrous tissues of the mesentery), may cause bowel perforation.

Radiotherapy of cervical carcinoma and other intra-abdominal malignancies - This maybe associated with late complications, including bowel obstruction and bowel

perforation.[10]

Necrotizing vasculitis - Wegeners granulomatosis affecting the viscera, althoughuncommon, may cause bowel ulcerations and perforations.

[11]

Kidney transplantation - Following kidney transplantation, gastrointestinal perforationsmay occur as a complication. In these cases, the perforation is usually related to the use

of high doses of immunosuppressive medications, a treatment employed in the earlypostoperative period and in the management of acute rejection episodes.

[12]

Ingestion of caustic substances - Accidental or intentional ingestion of caustic substancesmay result in acute intestinal perforation and peritonitis. Delayed perforation may occurup to 4 days after acid exposure.
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Foreign bodies (eg, toothpicks) - These may cause perforation of the esophagus, stomach,or small intestine, with intra-abdominal infection, peritonitis, and sepsis.

Pathophysiology

Normally, the stomach is relatively free of bacteria and other microorganisms because of its highintraluminal acidity. Most persons who experience abdominal trauma have normal gastric

functions and are not at risk of bacterial contamination following gastric perforation. However,

those who have a preexisting gastric problem are at risk of peritoneal contamination with gastric

perforation. Leakage of acidic gastric juice into the peritoneal cavity often results in profoundchemical peritonitis. If the leakage is not closed and food particles reach the peritoneal cavity,

chemical peritonitis is succeeded by gradual development of bacterial peritonitis. Patients may

be free of symptoms for several hours between the initial chemical peritonitis and the later

occurrence of bacterial peritonitis.

The microbiology of the small bowel changes from its proximal to its distal part. Few bacteria

populate the proximal part of the small bowel, whereas the distal part of the small bowel (thejejunum and ileum) contains aerobic organisms (eg,Escherichia coli) and a higher percentage of

anaerobic organisms (eg,Bacteroides fragilis). Thus, the likelihood of intra-abdominal or wound

infection is increased with perforation of the distal bowel.

The presence of bacteria in the peritoneal cavity stimulates an influx of acute inflammatory cells.

The omentum and viscera tend to localize the site of inflammation, producing a phlegmon. (Thisusually occurs in perforation of the large bowel.) The resulting hypoxia in the area facilitates

growth of anaerobes and produces impairment of bactericidal activity of granulocytes, which

leads to increased phagocytic activity of granulocytes, degradation of cells, hypertonicity of fluidforming the abscess, osmotic effects, shift of more fluids into the abscess area, and enlargement

of the abdominal abscess. If untreated, bacteremia, generalized sepsis, multiorgan failure, andshock may occur.

Presentation

History

A careful medical history often suggests the source of the problem, which is subsequently

confirmed by clinical examination and radiologic study findings. Possible etiologies include the

following:

Penetrating injury or blunt trauma to the lower chest or abdomen Aspirin, NSAIDs, or steroid intake, particularly in elderly patients Treatment for peptic ulcer disease or ulcerative colitis; perforation due to acute ulcerative

colitis (usually identified by the history of the primary disease and the results of past

investigations)

Abdominal pain


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o Ask patients about the time of onset of pain, the duration and location of pain, thecharacteristics of pain, relieving and aggravating factors, and other symptoms

associated with abdominal pain. A history of similar attacks may also suggest theetiology.

o Sharp, severe, sudden-onset epigastric pain that awakens the patient from sleepoften suggests perforated peptic ulcer. Differentiate this from conditions such ascholecystitis and pancreatitis. Painless perforation of a peptic ulcer can occur withsteroid use. The presence of shoulder pain suggests involvement of the parietal

peritoneum of the diaphragm.

o In elderly patients, consider the possibility of perforated diverticulitis or rupturedacute appendicitis if the pain is located in the lower abdomen. Approximately 30-

40% of elderly patients with acute appendicitis present more than 48 hours after

the onset of abdominal pain. (Delayed presentation is usually associated with

increased risk of perforation.) Elderly patients may have minimal pain.

o In young adults with pain in the lower abdominal quadrant, consider perforatedappendicitis as a possible diagnosis. Acute appendicitis with sudden perforation is

usually associated with illness of several hours. The pain is typically localized inthe right lower quadrant of the abdomen, unless the disease process has

progressed to generalized peritonitis. In young women, also consider ruptured

ovarian cyst and ruptured tuboovarian abscess in the differential diagnosis.

Vomiting - This occurs, albeit uncommonly, in patients with a perforated ulcer. Vomitingis, however, frequently noted in patients with acute cholecystitis. In patients with

appendicitis, pain almost always precedes vomiting by 3-4 hours. The converse is true in

gastroenteritis.

Hiccup - This is a common late symptom in patients with a perforated peptic ulcer. History of travel to or of residing in tropical areas, with symptoms suggestive of typhoid

fever (eg, fever, abdominal pain, abdominal distension, constipation, bilious vomiting)

History of endoscopic procedures, such ascolonoscopy[3, 6, 7, 8] History of chronic disease, such as ulcerative colitis

Physical

General appearance and vital signs - Take vital signs and assess for any hemodynamicchanges. (Take pulse and blood pressure measurements with the patient lying in bed andsitting, and note any postural changes.)

Abdominal examinationo Examine the abdomen for any external signs of injury, abrasion, and/or

ecchymosis. Observe patients' breathing patterns and abdominal movements with

breathing, and note any abdominal distension or discoloration. (In perforatedpeptic ulcer disease, patients lie immobile, occasionally with knees flexed, and the

abdomen is described as boardlike.)

o Carefully palpate the entire abdomen, noting any masses or tenderness.Tachycardia, fever, and generalized abdominal tenderness may suggest

peritonitis. Abdominal fullness and doughy consistency may indicate intra-

abdominal hemorrhage.

o Tenderness on percussion may suggest peritoneal inflammation.
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o Bowel sounds are usually absent in generalized peritonitis. Rectal and bimanual vaginal and pelvic examination - These examinations may help in

assessing conditions such as acute appendicitis, ruptured tuboovarian abscess, andperforated acute diverticulitis.

Differential diagnosis

Peptic ulcer disease Gastritis Acute pancreatitis Cholecystitis, biliary colic Endometriosis Acute gastroenteritis Ovarian torsion Pelvic inflammatory disease Acute salpingitis Diverticular disease Acute appendicitis Meckel diverticulum Typhoid fever Ischemic colitis Crohn's disease Inflammatory bowel disease Colitis Constipation

Relevant Anatomy

The peritoneal cavity is lined with a single layer of mesothelial cells, connective tissue

(including collagen), elastic tissues, macrophages, and fat cells. The parietal peritoneum covers

the abdominal cavity (ie, abdominal wall, diaphragm, pelvis); the visceral peritoneum covers allof the intra-abdominal viscera, forming a cavity that is completely enclosed except at the open

ends of the fallopian tubes.

The peritoneal cavity is divided by the transverse mesocolon. The greater omentum extends from

the transverse mesocolon and from the lower pole of the stomach to line the lower peritoneal

cavity. Abdominal organs, such as the pancreas, duodenum, and ascending and descendingcolon, are located in the anterior retroperitoneal space; the kidneys, ureters, and adrenal glands

are found in the posterior retroperitoneal space. Other abdominal organs, the liver, stomach,gallbladder, spleen, jejunum, ileum, transverse colon, sigmoid colon, cecum, and appendix are

found within the peritoneal cavity.

A small amount of fluid sufficient to allow movement of organs is usually present in theperitoneal space. This fluid is normally serous (protein content of < 30 g/L, < 300 WBCs/L). Inthe presence of infection, the amount of this fluid increases, its protein content climbs to more


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than 30 g/L, and the white blood cell (WBC) count increases to more than 500 WBCs/L; in

other words, the fluid becomes an exudate.

Contraindications

Surgery is contraindicated in the presence of general contraindications to anesthesia andmajor surgery, such as severe heart failure, respiratory failure, or multiorgan failure.

Surgery is contraindicated if the patient refuses the operation and no evidence ofgeneralized peritonitis exists.

Surgery is contraindicated if a contrast meal confirms spontaneous sealing of theperforation (eg, perforated duodenal ulcer) and the patient prefers a nonsurgical

approach.

Laboratory Studies

Complete blood cell (CBC) count

o Parameters suggestive of infection (eg, leukocytosis) - Leukocytosis may beabsent in elderly patients.

o Elevated packed blood cell volume - This suggests a shift of intravascular fluid. Blood culture for aerobic and anaerobic organisms Liver function and renal function tests - Findings may be within reference ranges (or

nearly so) if no preexisting disorder is present.

Imaging Studies

Erect radiographs of the chest are recognized as the most appropriate first-lineinvestigation when a perforated peptic ulcer is considered likely.[13] However, inapproximately 30% of patients, no free gas can be identified. Thus, an erect

posteroanterior chest radiograph is not sufficiently sensitive to rule out

pneumoperitoneum in patients presenting with upper abdominal pain.

Plain supine and erect radiographs of the abdomen are the most common first steps in thediagnostic imaging evaluation of patients presenting with medical history and/or clinical

signs suggestive of bowel perforation. Findings suggestive of perforation include the

following:

o Free air trapped in the subdiaphragmatic locations - If the quantity of free air isgreat enough, its presence can be visualized on the supine radiograph of the

abdomen, allowing clear definition of the inner and outer surface of the wall of

the bowel.o Visible falciform ligament - The ligament may appear as an oblique structure

extending from the right upper quadrant toward the umbilicus, particularly when

large quantities of gas are present on either side of the ligament.

o Air-fluid level - This is indicated by the presence of hydropneumoperitoneum orpyopneumoperitoneum on erect radiographs of the abdomen.


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Water-soluble radiologic contrast media administered orally or through anasogastric tube can be used as an adjunct diagnostic tool to detect any

intraperitoneal leak.

The perforation has sealed at presentation in approximately 50% ofpatients. For those who favor a nonoperative approach, contrast radiology

is routine in the management of these patients. Ultrasonograms of the abdomen

o Localized gas collection related to bowel perforation may be detectable,particularly if it is associated with other ultrasonographic abnormalities (eg,

thickened bowel loop).

o The site of bowel perforation can be detected by ultrasonography (eg, gastric vsduodenal perforation, perforated appendicitis vs perforated diverticulitis).

o Ultrasonograms of the abdomen can also provide rapid evaluation of the liver,spleen, pancreas, kidneys, ovaries, adrenals, and uterus.

Computed tomography (CT) scans of the abdomen - This modality can be a valuableinvestigative tool, providing differential morphologic information not obtainable with

plain radiography or ultrasonography.o CT scans may provide evidence of localized perforation (eg, perforated duodenal

ulcer) with leakage in the area of the gallbladder and right flank with or without

free air being apparent.

o CT scans may show inflammatory changes in the pericolonic soft tissues andfocal abscess due to diverticulitis (may mimic perforated colonic carcinoma).

o CT scans may not provide definitive radiographic evidence of perforated Meckeldiverticulitis.

Other Tests

Laparoscopy may significantly improve surgical decision making in patients with acuteabdominal pain, particularly when the need for operation is uncertain.

Diagnostic Procedures

Peritoneal diagnostic tap may be useful in determining the presence of intra-abdominalblood, fluid, and pus.

Peritoneal lavage is more valuable in the presence of a history of blunt abdominal trauma.o The presence of blood or purulent material or the detection of bacteria on Gram

stain suggests the need for early surgical exploration.

o Alkaline phosphatase concentration in the peritoneal lavage is a helpful andsensitive test that may be used to detect occult blunt intestinal injuries. A

concentration greater than 10 IU/L has been shown to be a sensitive and reliable

test in the detection of occult small bowel injuries.

Fine-catheter peritoneal cytologyo This procedure involves the insertion of a venous cannula into the peritoneal

cavity, through which a fine umbilical catheter is inserted while the patient is

under local anesthesia.


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o Peritoneal fluid is aspirated, placed on a slide, and stained for examination undera light microscope for percentage of polymorphonuclear cells.

o A value greater than 50% suggests a significant underlying inflammatory process.o This test, however, provides no clue as to the exact cause of inflammation.

Medical Therapy

The mainstay of treatment for intestinal perforation is surgery.[14]

Emergency medical care

includes the following steps:

Establish intravenous access, and initiate crystalloid therapy in patients with clinical signsof dehydration or septicemia.

Do not give anything by mouth. Start intravenous administration of antibiotics to patients with signs of septicemia.

Antibiotics should cover aerobic and anaerobic organisms. The goals of antibiotic

treatment are to eradicate infection and to minimize related postoperative complications.

However, if symptoms and signs of generalized peritonitis are absent, a nonoperative policy may

be used with antibiotic therapy directed against gram-negative and anaerobic bacteria.[15, 16]

Antibiotics

Antibiotics have proven effective in decreasing the rate of postoperative wound infection and in

improving outcome in patients with intraperitoneal infection and septicemia.

Metronidazole (Flagyl) is typically used in combination with an aminoglycoside to provide broadgram-negative and anaerobic coverage. It is reduced to a product that interacts with

deoxyribonucleic acid (DNA) to cause a loss of helical DNA structure and strand breakage,resulting in inhibition of protein synthesis and cell death in susceptible organisms. Adult dosingis 7.5 mg/kg IV before surgery. Pediatric dosing is 15-30 mg/kg/d IV divided bid/tid for 7 d. It is

a pregnancy category B drug.

Gentamicin (Garamycin, Genoptic, Gentacidin) is an aminoglycoside antibiotic with gram-

negative coverage. It is used in combination with both an agent against gram-positive organisms

and one that covers anaerobes. Although it is not the DOC, consider gentamicin if penicillins orother less-toxic drugs are contraindicated, when clinically indicated, and in mixed infections

caused by susceptible staphylococci and gram-negative organisms. Dosing regimens are

numerous; adjust dose based on CrCl and changes in volume of distribution. It may be given

IV/IM. In adults, the loading dose before surgery is 2 mg/kg IV; thereafter, dosing is 3-5mg/kg/d divided tid/qid. In infants, dosing is 7.5 mg/kg/d IV divided tid. In children, dosing is 6-

7.5 mg/kg/d IV divided tid. It is a pregnancy category C drug.

Cefotetan (Cefotan) is a second-generation cephalosporin that inhibits bacterial cell wall

synthesis by binding to 1 or more of the penicillin-binding proteins. It inhibits the final

transpeptidation step of peptidoglycan synthesis, resulting in cell wall death. Adult dosing is 2 g


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IV once before surgery. In children < 3 months, dosing is not established. In those >3 months,

dosing is 30-40 mg/kg IV once before surgery. It is a pregnancy category B drug.

Cefoxitin (Mefoxin) is also a second-generation cephalosporin that inhibits bacterial cell wall

synthesis by binding to 1 or more of the penicillin-binding proteins. It inhibits the final

transpeptidation step of peptidoglycan synthesis, resulting in cell wall death. Adult dosing is 2 gIV once before surgery, followed by 4 doses of 2 g IV q4-6h. In children < 3 months, dosing is

not established. In those >3 months, dosing is 30-40 mg/kg IV before surgery, followed by 3

doses of 2 g IV q4-6h for 24 h. It is a pregnancy category B drug.

Cefoperazone sodium (Cefobid) is a third-generation cephalosporin that inhibits bacterial cell

wall synthesis by binding to 1 or more of the penicillin-binding proteins. It inhibits the finaltranspeptidation step of peptidoglycan synthesis, resulting in cell wall death. Adult dosing is 2-4

g/d IV divided q12h. Pediatric dosing is 100-150 mg/kg/d IV divided q8-12h, not to exceed 12

g/d. It is a pregnancy category B drug.

Surgical Therapy

The goals of surgical therapy are as follows:

To correct the underlying anatomical problem To correct the cause of peritonitis To remove any foreign material in the peritoneal cavity that might inhibit WBC function

and promote bacterial growth (eg, feces, food, bile, gastric or intestinal secretions, blood)

Preoperative Details

Correct any fluid or electrolyte imbalance. Replace extracellular fluid losses byadministering Hartmann solution or a similar solution that has an electrolyte compositionsimilar to plasma.

Central venous pressure (CVP) monitoring is essential in critically ill and/or elderlypatients, in whom cardiac impairment may be exacerbated by large fluid loss.

Administer systemic antibiotics (eg, ampicillin, gentamicin, metronidazole), making abest estimation regarding the likely organisms.

Nasogastric suction is required to empty the stomach and reduce the risk of furthervomiting.

Urinary catheterization is used to assess urinary flow and fluid replacement. Administer analgesics, such as morphine, in small intravenous doses, preferably as a

continuous infusion.

Intraoperative Details

Operative management depends on the cause of perforation. Perform urgent surgery either onpatients not responding to resuscitation or following stabilization and maintenance of adequate

urine output. All necrotic material and contaminated fluid should be removed and accompanied


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by lavage with antibiotics (tetracycline 1 mg/mL). Decompress distended bowel via a nasogastric

tube.

Laparoscopic or laparoscopic-assisted (minilaparotomy) surgery is also being increasingly used

with outcomes comparable with conventional laparotomy. Experience and the advancement in

accessories have enabled endoscopic repair of a significant number of intestinal perforations,such as iatrogenic perforation. Management of such cases needs to be individualized to the

patient.

In a study involving 934 patients with sigmoid diverticulitis, Ritz et al found that the risk of free

perforation in acute sigmoid diverticulitis decreases with the increases in the number of previous

episodes of sigmoid diverticulitis. They concluded that the first episode has the highest risk for afree perforation. Therefore, the indication for colectomy should not be made based on the

potential risk of free perforation.[17]

Postoperative Details

Intravenous replacement therapy: The aim of intravenous replacement therapy is tomaintain intravascular volume and hydrate the patient. Monitor by CVP measurementand urinary output.

Nasogastric drainage: Perform nasogastric drainage continuously until drainage becomesminimal. At that stage, the nasogastric tube may be removed.

Antibiotics: Continue administration of the antibiotics commenced preoperatively unlessthe results of cultures taken at the time of the operation reveal that the causative

organisms are resistant to them.

o The goal of antibiotic therapy is to achieve levels of antibiotics at the site ofinfection that exceed the minimum inhibitory concentrations for the pathogens

present.o In the presence of intra-abdominal infections, gastrointestinal function is often

impaired; therefore, oral antibiotics are not efficacious, and intravenousantibiotics are recommended.

o If no obvious improvement in the patient's condition occurs within 2-3 days,consider the following possibilities:

The initial operative procedure was inadequate. Complications have occurred. A superinfection has occurred at a new site. The dose of antibiotic is inadequate. The antibiotics used do not provide adequate coverage for anaerobes and

gram-negative organisms. Analgesics: Analgesics, such as intravenous morphine, should be given continuously or

in small doses at frequent intervals.

Follow-up

For patients treated with a nonsurgical approach, follow-up care consists of the following:
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o Gram-negative infections are associated with a much worse prognosis than gram-positive infections, possibly because of associated endotoxemia.

Renal failure and fluid, electrolyte, and pH imbalance Gastrointestinal mucosal hemorrhage: This complication is usually associated with

failure of multiple organ systems and is probably related to a defect in the protective

gastric mucosa. Mechanical intestinal obstruction: Mechanical obstruction of the intestine is most often

caused by postoperative adhesions.

Postoperative delirium: The following factors may cause a predisposition to postoperativedelirium:

o Advanced ageo Drug dependencyo Dementiao Metabolic abnormalitieso Infectionso Previous history of deliriumo

Hypoxiao Intraoperative/postoperative hypotension

Outcome and Prognosis

Outcome is improved with early diagnosis and treatment. The following factors increase the risk

of death:

Advanced age Presence of preexisting underlying disease Malnutrition The nature of the primary cause of bowel perforation Appearance of complications

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