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Duodenal Perforation


Duodenal Perforation

Article Author:
Afshin Amini
Article Editor:
Richard Lopez
Updated:
4/14/2020 12:20:02 PM
For CME on this topic:
Duodenal Perforation CME
PubMed Link:
Duodenal Perforation

Introduction

Anatomically the duodenum is part of the gastrointestinal tract between the stomach and small intestine. It includes four segments:

1) The proximal segment is known as a duodenal bulb, which connects to the liver via hepatoduodenal ligament containing the hepatic artery, the portal vein, and the common bile duct.

2) The second or descending segment is surrounding the pancreases head.

3) The third segment is the horizontal part. The superior mesenteric vessels are ventral to this segment.

4) The fourth segment follows the jejunum.

Duodenal perforation is a rare but lethal condition.[1] The mortality rate ranges reported 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 has 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 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 that wall off the area.[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 sudden onset of severe pain in the upper abdomen.[9] However, in immunocompromised or elderly patients, the clinical signs can be undetectable and lead to 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]

Etiology

Underlying duodenal pathology

1) Peptic ulcer disease (PUD): H. pylori infection and non-steroidal anti-inflammatory drugs (NSAIDs) are two major causes for 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 to increase gastrin secretion and damage gastric mucosa. However, studies did not show that alcohol can cause PUD.[13]

2) Duodenal diverticula [14]

3) Infectious disease (TB, rotavirus, norovirus, Ascaris lumbricoides)[15][16][17]

4) Autoimmune conditions, including scleroderma, Crohn disease, and abdominal polyarteritis nodosa.[18][19][20]

5) Duodenal ischemia [21]

6) Impacted gallstones in the duodenum [22]

7) Chemotherapy [23][24]

8) Tumors [25]

Iatrogenic: Due to the widespread use of endoscopic procedures, it is becoming more common.[26]

1) Endoscopic perforations: It includes diagnostic and therapeutic procedures. However, the incidence of perforation is higher in therapeutic procedures.  

2) 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 correlations with higher perforation risk.[30]

Spontaneous perforations: It occurs in neonates with the unknown underlying causes.[31]

Epidemiology

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 rates of PUD are explainable by eradication treatment for Helicobacter pylori and the use of proton pump inhibitors (PPIs). However, perforation of peptic ulcers is still concerning. The aging population, overuse of non-steroidal anti-inflammatory drugs (NSAIDs), NSAIDs interaction with selective serotonin reuptake inhibitors, and steroids are possible reasons which can explain the high incidence of perforation.[4][35] Furthermore, studies show that H. pylori prevalence ranges are 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 involves the duodenum.[41]

Less than 1% of ingested foreign bodies can cause gastrointestinal perforations.[42]

Pathophysiology

Underlying duodenal pathology: The leading causes of perforated peptic ulcers remain NSAIDs use and H. pylori.[11] NSAIDs can reduce prostaglandin secretion by inhibition of COX-1 in the gastrointestinal tract, which leads to a gastroduodenal mucosal injury. NSAID use in specific patients such as co-prescription of antiplatelets, corticosteroids and anticoagulants, age over 65 years, heart disease, and history of peptic ulcer disease 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 reduce mucosal defense can cause duodenal injury and subsequently duodenal perforation.[45]

Iatrogenic: The Stapfer classification categorizes post-ERCP duodenal perforations in four types. The endoscope itself 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 caused by basket or wire instrumentation and type IV perforations diagnosed by retroperitoneal air on imaging and usually are 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, initially, gastric acid juice leaks into the peritoneal cavity, which leads to profound chemical peritonitis. In this phase, the patients can appear free of symptoms. If the leakage is not closed, then food particles can reach the peritoneal cavity and gradually develop to bacterial peritonitis leading to abdominal symptoms.[5]

History and Physical

If possible, to obtain a thorough history, clinicians should query patients regarding perforated peptic ulcer risk factors. However, if the PPU occurred, patient history does not change the treatment plan.[9] Typical symptoms for a perforated peptic ulcer (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 two 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. More than 12 hours (third phase), can manifest as abdominal distension, fever, and hypotension.[13]

Patients with retroperitoneal perforation present more indolently without peritoneal signs.[5]

Evaluation

Laboratory tests: Usually used to rule out differential diagnoses.

Raising in serum amylase less than four times than normal levels can be associated with PPU.[47]

Serum gastrin levels are useful in patients who have a history of recurrent ulcers to establish the diagnosis of Zollinger Ellison syndrome.[13]

Leukocytosis and high C-reactive protein level 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 symptoms initiation.[50] Existing of free air on upright CXR in patients with abdominal symptoms establishes the diagnoses of PPU. In some patients with the abdomen, X-ray may reveal Rigler’s sign (air in the intestinal lumen and outside of bowel wall), football sign (a large volume of free gas appears a large round black area) and gas surrounding the soft tissue structures such falciform ligament or liver edge.[51][52] Normal upright x-ray does not rule out duodenal perforation, and in stable patients who are clinically suspicious for duodenal perforation is essential to evaluate by computed tomography (CT) scan.[5] A non-contrast CT scan is suitable to see free air just below the anterior abdominal wall in patients with acute kidney injury. The diagnostic accuracy of PPU detection by CT scan is about 98%.[53] Oral diatrizoate can help to diagnose PPU when the CT scan is not available, 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 (CT) scan is the most valuable method for diagnosing duodenal perforation.[55]

CT features of perforation include duodenal wall thickening, extravasated oral contrast, the presence of extraluminal air, fat stranding, and periduodenal fluid collection.[55]

Treatment / Management

Management of duodenal perforations depends on the type of perforation. Two kinds of perforation defined as contained or non-contained perforation. Non-contained perforation divide into two subgroups as minor or major perforation.

1) 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 by diatrizoate study to confirm the absence of leakage. Conservative management consists of intravenous fluid therapy, nil per os (NPO), 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% as opposed to 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]

2) Non-contained perforations are defined when bowel contents leak freely into the abdominal cavity. Minor and major perforations are two subtypes of this group.[5]

A)Minor non-contained perforations: Endoscopic or simple surgical repair are two primary management strategies for this group. Endoscopic management includes through-the-scope clips (TTSC), over-the-scope clips (OTSC), detachable snare loops with clips, and self-expandable metal stents (SEMS).[5] TTSC management is favorable for linear perforations less than 1 cm while in perforation with a range from 1 to 3 cm OTSC, detachable snare loop with clips, and SEMS 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, which is known as a Cellan–Jones repair, can be sutured into the perforation.[5][7] Studies did not show any benefit for the placement of drain after surgical repair.[59]

B) 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]

Differential Diagnosis

   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

Prognosis

Mortality rate in perforation peptic ulcer (PPU) patients reported with ranging from 1.3% to 20%.[61][62][63] Other studies have reported 30 days mortality rate reaching 20%.[35] The main prognostic factor is the time interval between the duodenal perforation and treatment. The interval time greater than 24 hours increases mortality.[5] The American Society of Anesthesiologists (ASA) score and Boey score are the most common 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 the 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 delay 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-year-old 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 more than 60 years old, concomitant diseases, and systolic blood pressure less than 100 mmHg are the main risk factors that increase the mortality rate.[68]

Complications

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 reported in 30% of patients.[69] Age greater than 40 years, a history of shock, and a larger size of perforation 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. From these, surgical site infection (32%) has reported as a most common complication after surgery.[70]

Postoperative and Rehabilitation Care

 In a non-randomized study reported that using the management protocol from admission to 3 days after laparoscopic repair reduced the 30-days mortality rate from 27% to 17%. Management protocol in this study includes the minimization of surgical delay, preventing, detecting, and treating sepsis.[10] In small randomized clinical trials in turkey concluded in patients with ASA score I or II, early removal of tubes and early start of oral intake reduce patients' hospital stay by about three days.[71] A meta-analysis by wong et al. reported in duodenal ulcer perforation patients eradication of H. pylori has a significant effect of reducing recurrent ulcer incidence at eight weeks and one year in post-surgical patients.[72] Despite in gastric ulcer perforation patients, endoscopy follows up is not recommended in patients with duodenal ulcer perforation due to low risk of malignancy in such patients.[10]

Consultations

Following a diagnosis of duodenal perforation, consult with a gastroenterologist and gastrointestinal surgeon.

 

 

Deterrence and Patient Education

Patients should be aware of the possible risk factors for duodenal perforation and try to avoid them. Peptic ulcer is still the leading cause, so prevention of duodenal perforation is the same as for peptic ulcer disease.

  • Patients need to avoid using NSAIDs
  • If for any reason patients need to take NSAIDs, they should try to take it at a low dose and the shortest duration
  • Consider prophylaxis (such as PPI or H2 blockers) if patients need to take NSAIDs for a long time
  • Patients with peptic ulcer disease should follow gastroenterologist recommendations
  • Quit smoking

Enhancing Healthcare Team Outcomes

PUD can be treated 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 be aware that 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 have a vital role in the monitoring of the patients' vital signs and educate the patients and families. Once the patients discharge, they should receive education from the medical care team to change their lifestyles, which includes quitting smoking and avoiding the consumption of NSAIDs as much as possible. Patients with positive H. pylori should take medication to eradicate the infection, which data shows can decrease the mortality rate. Gastroenterology nurses should follow with patients, educate them, and update the team regarding the patient's 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. Only through an interprofessional team approach can clinicians reduce the mortality and morbidity of duodenal perforation. [Level 5]

Older age, presence of shock, delayed surgery, definitive surgery, and ASA risk are factors that cause poor outcomes in patients with PPU undergoing emergency surgery. Hence, to improve overall outcomes is needed proper resuscitation from shock, decreasing delay surgery grade, reserving definitive surgery for selected patients, and improving ASA score.[66][65] [Level 4]


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