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Duodenal perforations can either be free or contained. Free perforation arises when bowel contents leak freely into the abdominal cavity and cause diffuse peritonitis. Contained perforation occurs when the ulcer creates a full-thickness hole, but free leakage is prevented by contiguous organs such as the pancreas wall off the area. This activity reviews the evaluation and management of duodenal perforation and explains the healthcare team's role in evaluating and treating patients with this condition. Objectives: Assess the presentation of duodenal perforation. Identify the risk factors for developing duodenal perforation. Evaluate the treatment for duodenal perforation. Examine the significance of enhancing care coordination among interprofessional team members to optimize patient outcomes in cases of duodenal perforation. Access free multiple choice questions on this topic.

Anatomically, the duodenum is part of the gastrointestinal tract between the stomach and small intestine. It includes 4 segments: The proximal segment is a duodenal bulb, which connects to the liver via the hepatoduodenal ligament containing the hepatic artery, the portal vein, and the common bile duct. The second or descending segment is surrounding the pancreatic head. The third segment is the horizontal part. The superior mesenteric vessels are ventral to this segment. The fourth segment follows the jejunum. Duodenal perforation is a rare but lethal condition.[1] The mortality rate ranges from 8% to 25% in the literature.[2][3][4] In 1688, the perforated duodenal ulcer was described by Muralto and reported by Lenepneau.[5] Subsequently, in 1894, Dean reported the first case, which successfully underwent surgical closing of a perforated duodenal ulcer.[6] In 1929, Cellan-Jones described a technique for repairing perforations by using an omental, and later, in 1937, Graham modified that technique.[7][5] Duodenal perforation can either be free or contained. Free perforation arises when bowel contents leak freely into the abdominal cavity and cause diffuse peritonitis. Contained perforation occurs when the ulcer creates a full-thickness hole, but contiguous organs, such as the pancreas, that wall off the area prevent free leakage.[5] Peptic ulcer disease is a significant cause of duodenal perforation.[8] Typically, patients with duodenal ulcers have nocturnal abdominal pain or feel hungry. If perforation occurs, it usually can cause a sudden onset of severe pain in the upper abdomen.[9] However, in immunocompromised or elderly patients, the clinical signs can be undetectable and delay diagnosis. Imaging has an essential role in diagnosis and, subsequently, for early resuscitation. Appropriate selection of therapeutic alternatives and risk assessment can decrease the risk of morbidity and mortality.[10]

Underlying Duodenal Pathology Peptic ulcer disease (PUD): H. pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs) are 2 major causes of PUD and, subsequently, duodenal perforation.[8] Although the incidence of PUD has decreased in recent years, it is still the main cause of duodenal perforation.[11] Smoking, physiological stress, previous history of PUD, and corticosteroids are other risk factors for a perforated peptic ulcer (PPU).[12] Alcohol consumption is known to cause an increase in gastrin secretion and damage gastric mucosa. However, studies did not show that alcohol can cause PUD.[13] Duodenal diverticula [14] Infectious disease (tuberculosis, rotavirus, norovirus, Ascaris lumbricoides) [15][16][17] Autoimmune conditions, including scleroderma, Crohn disease, and abdominal polyarteritis nodosa.[18][19][20] Duodenal ischemia [21] Impacted gallstones in the duodenum [22] Chemotherapy [23][24] Tumors [25] Iatrogenic: Due to the widespread use of endoscopic procedures, it is becoming more common.[26] Endoscopic perforations: These include diagnostic and therapeutic procedures. However, the incidence of perforation is higher in therapeutic procedures. Operative injury: Surgical instruments can cause duodenal perforation. Laparoscopic cholecystectomy can perforate the duodenum (0.015%) during thermal burns by electrocautery or blunt or sharp dissection.[27][28] Trauma: Isolated duodenal injuries are uncommon and usually occur with other organ injuries.[29] Foreign bodies: Thin and sharp foreign bodies correlate with higher perforation risk.[30] Spontaneous perforations: Spontaneous perforations occur in neonates with unknown underlying causes.[31]

Although the incidence of PUD has decreased in recent years, it is still the prominent cause of duodenal perforation.[11] Annually, peptic ulcer disease (PUD) affects 4 million people worldwide, with an incidence rate of 1.5% to 3%.[32][33] About 5% of patients with PUD experience perforation in their lifetime.[34] Decreased PUD rates are explained by eradication treatment for Helicobacter pylori and using proton pump inhibitors (PPIs). However, the perforation of peptic ulcers is still concerning. The aging population, overuse of non-steroidal anti-inflammatory drugs (NSAIDs), and NSAIDs' interaction with selective serotonin reuptake inhibitors and steroids are possible reasons that can explain the high incidence of perforation.[4][35] Furthermore, studies show that H. pylori prevalence ranges from 50% to 80% in patients with perforated duodenal ulcers.[36] Studies show more ulcer perforation occurs in the morning, and the mechanism is explainable by circadian variation in acid secretion.[10] Post-endoscopic retrograde cholangiopancreatography (ERCP)  duodenal perforations reported with rate ranges from 0.09% to 1.67%.[37][38] Sphincter of Oddi dysfunction, old age, precut, anatomical abnormalities, and injection of contrast medium are the factors that cause an increased risk of post-ERCP duodenal perforations.[39][40] Less than 2% of traumatic abdominal injuries involve the duodenum.[41] Less than 1% of ingested foreign bodies can cause gastrointestinal perforations.[42]

Underlying Duodenal Pathology The leading causes of perforated peptic ulcers remain NSAID use and H. pylori.[11] NSAIDs can reduce prostaglandin secretion by inhibiting COX-1 in the gastrointestinal tract, leading to a gastroduodenal mucosal injury. NSAID use in specific patients, such as co-prescription of antiplatelets, corticosteroids, anticoagulants, age over 65 years, heart disease, and peptic ulcer disease history, can increase the risk of gastroduodenal mucosal injury.[43] Prolonged and high-dose NSAID use are additional risk factors for gastroduodenal mucosal injury. Furthermore, studies revealed that piroxicam and ketorolac have the highest mucosal injury effect in the NSAID family.[44] H. pylori infection is another contributory factor for duodenal ulcers. Possibly, H. pylori, by inducing gastric metaplasia, stimulating Immune response and gastric acid secretion, and reducing mucosal defense, can cause duodenal injury and, subsequently, duodenal perforation.[45] Iatrogenic The Stapfer classification categorizes post-ERCP duodenal perforations into 4 types. The endoscope causes type I perforations (lateral or medial duodenal wall perforations). Type II perforations or peri-Vaterian injuries occur during sphincterotomy. Type III perforations or distal bile duct injuries are caused by basket or wire instrumentation, and type IV perforations are diagnosed by retroperitoneal air on imaging and are usually asymptomatic.[46] Duodenal perforation can be either free or contained. Free perforation arises when bowel contents leak freely into the abdominal cavity, causing diffuse peritonitis. Contained perforation occurs when the ulcer creates a full-thickness hole, but free leakage is prevented by contiguous organs such as the pancreas wall off the area.[5] In duodenal perforation, gastric acid juice initially leaks into the peritoneal cavity, leading to profound chemical peritonitis. In this phase, the patients can appear free of symptoms. If the leakage is not closed, food particles can reach the peritoneal cavity and gradually develop into bacterial peritonitis, leading to abdominal symptoms.[5]

To obtain a thorough history, clinicians should query patients regarding perforated peptic ulcer risk factors. However, if the PPU occurred, the patient's history does not change the treatment plan.[9] Typical symptoms for a PPU are defined by sudden onset of abdominal pain, which never completely subsides, even with premedical remedies. The classic triad in PPU patients is tachycardia, sudden onset of abdominal pain, and abdominal rigidity. Abdominal tenderness with rigidity and tachycardia are common clinical signs.[9] Three phases define the clinical manifestations of PPU. Within 2 hours of onset (initial phase), tachycardia, epigastric pain, and cold extremities are characteristic. Within 2 to 12 hours (second phase), pain becomes generalized and increases with movement. Fluid moving along the right paracolic gutter can lead to typical signs such as right lower quadrant tenderness and abdominal rigidity. Over 12 hours (third phase) can manifest as abdominal distension, fever, and hypotension.[13] Patients with retroperitoneal perforation present more indolently without peritoneal signs.[5]

Laboratory Tests Laboratory tests commonly used to rule out differential diagnoses items: Increased serum amylase levels less than 4 times normal can be associated with PPU.[47] Serum gastrin levels are useful in diagnosing Zollinger-Ellison syndrome in patients with a history of recurrent ulcers.[13] Leukocytosis and high C-reactive protein levels indicate existing of inflammation or infection.[48] Blood cultures are necessary before starting antibiotics.[49] An arterial blood gas measures the level of metabolic compromise in septic patients.[10] Radiography In acute upper abdominal pain, an urgent upright chest radiograph (CXR) is a basic essential test for duodenal perforation. Upright CXR shows free air below the diaphragm in 75% of patients. However, it can be normal, especially in patients who present early after symptom initiation.[50] Existing of free air on upright CXR in patients with abdominal symptoms establishes the diagnosis of PPU. In some patients with the abdomen, an X-ray may reveal the Rigler sign (air in the intestinal lumen and outside of the bowel wall), a football sign (a large volume of free gas appears in a large round black area), and gas surrounding the soft tissue structures such falciform ligament or liver edge.[51][52] Normal upright X-rays do not rule out duodenal perforation, and in stable patients who are clinically suspicious of duodenal perforation, it is essential to evaluate by computed tomography scan.[5] A non-contrast computed tomography scan is suitable to see free air below the anterior abdominal wall in patients with acute kidney injury. The diagnostic accuracy of PPU detection by computed tomography scan is about 98%.[53] Oral diatrizoate can help diagnose PPU when the computed tomography scan is unavailable and upright CXR does not show free air. However, the absence of leakage does not exclude PPU, as the perforation can seal off spontaneously.[54] A double-contrast computed tomography scan is the most valuable method for diagnosing duodenal perforation.[55] Computed tomography perforation features include duodenal wall thickening, extravasated oral contrast, extraluminal air, fat stranding, and periduodenal fluid collection.[55]

Management of duodenal perforations depends on the type of perforation. Two kinds of perforation are defined as contained or non-contained perforation. Non-contained perforation is divided into 2 subgroups: minor or major. Contained perforations are when free leakage is prevented by contiguous organs such as the pancreas wall off the area. It is feasible to do conservative management in this type of perforation. Before starting conservative management, it is essential to evaluate patients using a diatrizoate study to confirm the absence of leakage. Conservative management includes intravenous fluid therapy, nil per os, intravenous proton pump inhibitors (PPIs), broad-spectrum antibiotics, H. pylori eradication, and repeated clinical assessment.[5] The data shows that somatostatin can be useful for enterocutaneous fistula closure.[56] In contained perforation patients, studies reported the mortality rate with conservative management was 3% versus 6.2% with surgical management.[57] The essential components of conservative management of duodenal perforation are gatherable as “R”s: (1) Repeated clinical examination; (2) Radiologically undetected leak; (3) Repeated blood investigations; (4) Resources for monitoring; (5) Respiratory and renal support; and (6) Readiness to operate.[13] Non-contained perforations are when bowel contents leak freely into the abdominal cavity. Minor and major perforations are 2 subtypes of this group.[5] Minor non-contained perforations: Endoscopic or simple surgical repair are 2 primary management strategies for this group. Endoscopic management includes through-the-scope clips, over-the-scope clips, detachable snare loops with clips, and self-expandable metal stents.[5] Through-the-scope clip management is favorable for linear perforations less than 1 cm, while in perforations with a range from 1 to 3 cm, over-the-scope clips, detachable snare loops with clips, and self-expandable metal stents are suitable management options.[58] Simple surgical treatment is another option for the management of minor non-contained perforation. The surgeon can perform it with or without an omental patch. Alternatively, a free omental plug (Graham patch) or a pedicled omental flap, known as a Cellan–Jones repair, can be sutured into the perforation.[5][7] Studies did not show any benefit for drain placement after surgical repair.[59]

Minor non-contained perforations: Endoscopic or simple surgical repair are 2 primary management strategies for this group. Endoscopic management includes through-the-scope clips, over-the-scope clips, detachable snare loops with clips, and self-expandable metal stents.[5] Through-the-scope clip management is favorable for linear perforations less than 1 cm, while in perforations with a range from 1 to 3 cm, over-the-scope clips, detachable snare loops with clips, and self-expandable metal stents are suitable management options.[58] Simple surgical treatment is another option for the management of minor non-contained perforation. The surgeon can perform it with or without an omental patch. Alternatively, a free omental plug (Graham patch) or a pedicled omental flap, known as a Cellan–Jones repair, can be sutured into the perforation.[5][7] Studies did not show any benefit for drain placement after surgical repair.[59] Major non-contained perforations: These types of perforations usually need reconstructive surgery, which includes duodenoduodenostomy (first option), Roux-en-Y duodenojejunostomy (second option), and Billroth II operation.[41] Perforation in the first or proximal second portion requires management by the Billroth II operation.[60]

Before imaging, the differential diagnosis for epigastric abdominal pain remains large and includes: Abdominal aortic aneurysm Acute coronary syndrome Aortic dissection Pancreatitis Appendicitis Boerhaave syndrome Cholecystitis Cholelithiasis Diverticulitis Duodenitis Esophagitis Gastroesophageal reflux disease Foreign body ingestion Gastritis Hepatitis Ventral hernia Mesenteric ischemia Small bowel obstruction Volvulus Pneumonia

Mortality rate in PPU patients reported ranging from 1.3% to 20%.[61][62][63] Other studies have reported 30 days mortality rate reaching 20%.[35] The primary prognostic factor is the duodenal perforation and treatment time interval. The interval time greater than 24 hours increases mortality.[5] The American Society of Anesthesiologists (ASA) and Boey scores are the most commonly validated scoring systems to predict outcomes in duodenal perforation.[13] Boey score factors include concomitant severe medical illness, preoperative shock, and the duration of perforation over 24 hours. When all these factors are positive, the total score count is 3, which predicts mortality as 38% and morbidity as 77%.[64] The American Society of Anesthesiologists (ASA) score uses the present systemic disease and degree of comorbidity as parameters to predict the outcome of PPU.[64] Significant risk factors that increase the mortality rate are co-morbidities, resection surgery, presence of shock at admission, female, elderly patients, metabolic acidosis, a delayed presentation of more than 24 hours, acute renal failure, hypoalbuminemia, smokers, and being underweight.[65][66] Studies show the mortality rate is higher in patients older than 65 compared to younger patients.[65] The postoperative mortality rate in patients with PPU is estimated to be 6% to 10%.[67] Delays in treatment greater than 24 hours, age over 60 years old, concomitant diseases, and systolic blood pressure less than 100 mmHg are the main risk factors that increase the mortality rate.[68]

Sepsis is common and accounts for 40% to 50% of fatalities in patients with PPU. On arrival in the operating room, about 30% to 35% of patients with PPU have sepsis. More than 25% of the patients Within the first month of surgery develop septic shock, which causes a mortality rate of 50% to 60%.[10] Postoperative complications were reported in 30% of patients.[69] Age greater than 40 years, a history of shock, and a larger size of perforation are reported as risk factors that cause an increase in the rate of postoperative complications.[70] Common surgical complications include pneumonia, wound dehiscence, peritonitis, incisional hernia, enterocutaneous fistula,intra-abdominal collection/abscess, surgical site infection, and ileus. Surgical site infection (32%) has been reported as the most common complication after surgery.[70]

Patients should be aware of the possible risk factors for duodenal perforation and try to avoid them. Peptic ulcers are still the leading cause, so prevention of duodenal perforation is the same as peptic ulcer disease. Patients need to avoid using NSAIDs. If patients need to take NSAIDs for any reason, they should try to take them at a low dose and for the shortest duration. Consider prophylaxis (such as PPI or H2 blockers) if patients require NSAIDs for a long time. Patients with peptic ulcer disease should follow gastroenterologist recommendations. Quit smoking

PUD is treatable with medications. However, PUD may perforate and lead to high mortality risk. The classic triad for PPU is the sudden onset of abdominal pain, abdominal rigidity, and tachycardia. Physicians should know that a normal upright chest X-ray does not rule out duodenal perforation. Early diagnosis, quick resuscitation, and urgent surgical intervention are crucial to improving outcomes. Experienced teams should direct conservative management. The gold standard treatment is still exploratory laparotomy and omental patch repair. During the hospital stay, nurses monitor the patient's vital signs and educate the patients and their families. Once the patients have been discharged, they should receive education from the medical care team regarding lifestyle modification, including quitting smoking and avoiding NSAIDs as much as possible. Patients with positive H. pylori should take medication to eradicate the infection; data shows this can decrease the mortality rate. Gastroenterology nurses should follow up with patients, educate them, and update the team regarding their condition. The pharmacist should discuss with patients the importance of medication compliance (such as PPI, H2 blocker, or H. pylori treatment) to decrease the mortality rate and limit NSAID use. Only through an interprofessional team approach can clinicians reduce the mortality and morbidity of duodenal perforation. Older age, shock, delayed surgery, definitive surgery, and ASA risk can lead to poor patient outcomes with PPU undergoing emergency surgery. Hence, improving overall outcomes requires proper resuscitation from shock, decreasing delayed surgery grade, reserving definitive surgery for selected patients, and improving ASA scores.[66][65]