Gastrointestinal perforation medical therapy: Difference between revisions

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{{CMG}}; {{AE}} {{MAD}}
{{CMG}}; {{AE}} {{MAD}}
{{Gastrointestinal perforation}}
==Overview==
==Overview==
Initial management of the patient with gastrointestinal perforation includes intravenous fluid therapy and broad-spectrum [[antibiotics]]. Patients with intestinal perforation can have severe volume depletion. The administration of intravenous [[proton pump inhibitors]]. [[Electrolyte disturbance|Electrolyte abnormalities]] correction especially [[metabolic alkalosis]] if [[fistula]] developed. The severity of any [[Electrolyte disturbance|electrolyte abnormalities]] depends upon the nature and volume of material leaking from the [[gastrointestinal tract]]. Intravenous [[vasopressors]] are useful in patients who remain hypotensive despite adequate fluid resuscitation or who develop cardiogenic [[pulmonary edema]]. [[Norepinephrine]] is the first-line single agent in septic shock. The addition of a second or third agent to [[norepinephrine]] may be required.
== Gastrointestinal perforation medical therapy ==
* Initial management of the patient with gastrointestinal perforation includes:
* Initial management of the patient with gastrointestinal perforation includes:
* Intravenous fluid therapy and broad-spectrum antibiotics.
* Intravenous fluid therapy and broad-spectrum [[antibiotics]]. Patients with intestinal perforation can have severe volume depletion.
* The administration of intravenous proton pump inhibitors is appropriate for those suspected to have an upper gastrointestinal perforation.
* The administration of intravenous [[proton pump inhibitors]]
* Patients with intestinal perforation can have severe volume depletion.
* [[Electrolyte disturbance|Electrolyte abnormalities]] correction especially [[metabolic alkalosis]] if [[fistula]] developed. The severity of any [[Electrolyte disturbance|electrolyte abnormalities]] depends upon the nature and volume of material leaking from the [[gastrointestinal tract]].
* Electrolyte abnormalities correction especially metabolic alkalosis if fistula developed. The severity of any electrolyte abnormalities depends upon the nature and volume of material leaking from the gastrointestinal tract.


==== '''Antibiotics''' ====
==== '''Antibiotics''' ====
Broad-spectrum antibiotic therapy is initiated if the level of perforation is unknown. The following tabel shows the regimens of choice in these cases:
[[Broad-spectrum antibiotic]] therapy is initiated if the level of perforation is unknown. The following tabel shows the regimens of choice in these cases:<ref name="pmid10893372">{{cite journal| author=Ibrahim EH, Sherman G, Ward S, Fraser VJ, Kollef MH| title=The influence of inadequate antimicrobial treatment of bloodstream infections on patient outcomes in the ICU setting. | journal=Chest | year= 2000 | volume= 118 | issue= 1 | pages= 146-55 | pmid=10893372 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10893372  }}</ref>
{| class="wikitable"
{| class="wikitable"
|'''Regimen'''
|'''Regimen'''
Line 17: Line 21:
| colspan="2" |'''First choice regimens'''
| colspan="2" |'''First choice regimens'''
|-
|-
|Ampicillin-sulbactam
|[[Ampicillin-Sulbactam|Ampicillin-sulbactam]]
|3 g IV every six hours
|3 g IV every six hours
|-
|-
|Piperacillin-tazobactam
|[[Piperacillin-tazobactam]]
|3.375 or 4.5 g IV every six hours
|3.375 or 4.5 g IV every six hours
|-
|-
|Ticarcillin-clavulanate
|[[Ticarcillin-Clavulanate|Ticarcillin-clavulanate]]
|3.1 g IV every four hours
|3.1 g IV every four hours
|-
|-
|Ceftriaxone
|[[Ceftriaxone]]
|1 g IV every 24 hours (or 2 g IV  every 12 hours for CNS infections)
|1 g IV every 24 hours
|-
|-
|Metronidazole
|[[Metronidazole]]
|500 mg IV every eight hours
|500 mg IV every eight hours
|-
|-
| colspan="2" |'''Alternative regimens'''
| colspan="2" |'''Alternative regimens'''
|-
|-
|Ciprofloxacin '''or'''
|[[Ciprofloxacin]]
|400 mg IV every 12 hours
|400 mg IV every 12 hours
|-
|-
|Levofloxacin
|[[Levofloxacin]]
|500 or 750 mg IV once daily
|500 or 750 mg IV once daily
|-
|-
|Metronidazole
|[[Metronidazole]]
|500 mg IV every eight hours
|500 mg IV every eight hours
|-
|-
|Imipenem-cilastatin
|[[Imipenem-Cilastatin|Imipenem-cilastatin]]
|500 mg IV every six hours
|500 mg IV every six hours
|-
|-
|Meropenem
|[[Meropenem]]
|1 g IV every eight hours
|1 g IV every eight hours
|-
|-
|Doripenem
|[[Doripenem]]
|500 mg IV every eight hours
|500 mg IV every eight hours
|-
|-
|Ertapenem
|[[Ertapenem]]
|1 g IV once daily
|1 g IV once daily
|}
|}


==== Intravenous fluid therapy ====
==== Intravenous fluid therapy ====
* Tissue perfusion is predominantly achieved by the aggressive administration of intravenous fluids, given at 30 mL/kg within the first '''three '''hours following presentation.[7-12].  
* Tissue perfusion is achieved by the aggressive administration of intravenous fluids, given at '''30 mL/kg''' within the first '''three '''hours following presentation.<ref name="pmid24635773">{{cite journal| author=ProCESS Investigators. Yealy DM, Kellum JA, Huang DT, Barnato AE, Weissfeld LA et al.| title=A randomized trial of protocol-based care for early septic shock. | journal=N Engl J Med | year= 2014 | volume= 370 | issue= 18 | pages= 1683-93 | pmid=24635773 | doi=10.1056/NEJMoa1401602 | pmc=4101700 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24635773  }}  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24935515 Review in: Ann Intern Med. 2014 Jun 17;160(12):JC9]</ref>
* using the following targets to measure the response:  
* Using the following targets to measure the response:<ref name="pmid25272316">{{cite journal| author=ARISE Investigators. ANZICS Clinical Trials Group. Peake SL, Delaney A, Bailey M, Bellomo R et al.| title=Goal-directed resuscitation for patients with early septic shock. | journal=N Engl J Med | year= 2014 | volume= 371 | issue= 16 | pages= 1496-506 | pmid=25272316 | doi=10.1056/NEJMoa1404380 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25272316  }}  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25775347 Review in: Ann Intern Med. 2015 Mar 17;162(6):JC4]</ref><ref name="pmid25776532">{{cite journal| author=Mouncey PR, Osborn TM, Power GS, Harrison DA, Sadique MZ, Grieve RD et al.| title=Trial of early, goal-directed resuscitation for septic shock. | journal=N Engl J Med | year= 2015 | volume= 372 | issue= 14 | pages= 1301-11 | pmid=25776532 | doi=10.1056/NEJMoa1500896 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25776532  }}  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26280432 Review in: Ann Intern Med. 2015 Aug 18;163(4):JC10]</ref>
* central venous oxyhemoglobin saturation (ScvO<sub>2</sub>) ≥70 percent
* Central venous oxyhemoglobin saturation (ScvO<sub>2</sub>) ≥70 percent
* central venous pressure (CVP) 8 to 12 mmHg, mean arterial pressure (MAP) ≥65 mmHg
* [[Central venous pressure]] (CVP) 8 to 12 mmHg
* urine output ≥0.5 mL/kg/hour [8-10]
* [[Mean arterial pressure]] (MAP) ≥65 mmHg. A [[central venous catheter]] and an [[arterial catheter]] are placed, although they are not always necessary.
* A lack of benefit of resuscitation protocols has also been reported in low income settings. As an example, in a randomized trial of 212 patients with sepsis (defined as suspected infection plus two systemic inflammatory response syndrome criteria) and hypotension (systolic blood pressure ≤90 mmHg or mean arterial pressure <65 mmHg) in Zambia, a protocolized approach of aggressive fluid resuscitation, monitoring, blood, and vasopressor transfusion within the first six hours of presentation resulted in a higher rate of death (48 versus 33 percent) when compared with usual care [16]. However, several flaws including crude measurements of monitoring, lower than usual rates of lactate elevation, larger than typical volumes of fluid resuscitation, and use of dopamine (as opposed to norepinephrine) in a population with a high percentage of patients with human immune deficiency virus may have biased the results.
* [[Urine output]] ≥0.5 mL/kg/hour
* The importance of timely treatment, particularly with antibiotics, was illustrated in a database study of nearly 50,000 patients with sepsis and septic shock who were treated with various types of protocolized treatment bundles (that included fluids and antibiotics, blood cultures, and serum lactate measurements) [17]. Compared with those in whom a three-hour bundle (blood cultures before broad spectrum antibiotics, serum lactate level) was completed within the three-hour time frame, a higher in-hospital mortality was reported when a three-hour bundle was completed later than three hours (odds ratio [OR] 1.04 per hour). Increased mortality was associated with the delayed administration of antibiotics but not with a longer time to completion of a fluid bolus (as part of a six hour bundle) (OR 1.04 per hour versus 1.10 per hour).
* The clinical and hemodynamic response and the presence or absence of [[pulmonary edema]] must be assessed before and after each bolus.
* The clinical and hemodynamic response and the presence or absence of pulmonary edema must be assessed before and after each bolus.  
* Crystalloid solutions ([[Saline (medicine)|saline]], [[Lactated Ringer's solution|Ringer's lactate]]) is the fluid of choice in treatment of [[sepsis]] or [[septic shock]].
* Evidence from randomized trials and meta-analyses have found no convincing difference between using albumin solutions and crystalloid solutions (eg, normal saline, Ringer's lactate) in the treatment of sepsis or septic shock, but they have identified potential harm from using pentastarch or hydroxyethyl starch [18-27]. There is no role for hypertonic saline [28].
* [[Pentastarch]] or [[hydroxyethyl starch]] have been identified harmful. Use of [[HES]] resulted in increased mortality.<ref name="pmid24635772">{{cite journal| author=Caironi P, Tognoni G, Masson S, Fumagalli R, Pesenti A, Romero M et al.| title=Albumin replacement in patients with severe sepsis or septic shock. | journal=N Engl J Med | year= 2014 | volume= 370 | issue= 15 | pages= 1412-21 | pmid=24635772 | doi=10.1056/NEJMoa1305727 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24635772  }}  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25023272 Review in: Ann Intern Med. 2014 Jul 15;161(2):JC6]</ref>
* Use of HES resulted in increased mortality and renal replacement therapy. [20]
* There is no role for [[Hypertonic|hypertonic saline]].<ref name="pmid28219612">{{cite journal| author=Asfar P, Schortgen F, Boisramé-Helms J, Charpentier J, Guérot E, Megarbane B et al.| title=Hyperoxia and hypertonic saline in patients with septic shock (HYPERS2S): a two-by-two factorial, multicentre, randomised, clinical trial. | journal=Lancet Respir Med | year= 2017 | volume= 5 | issue= 3 | pages= 180-190 | pmid=28219612 | doi=10.1016/S2213-2600(17)30046-2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28219612  }}</ref>
* a central venous catheter and an arterial catheter are placed, although they are not always necessary. For example, an arterial catheter may be inserted if blood pressure is labile, sphygmomanometer readings are unreliable, restoration of perfusion is expected to be protracted (especially when vasopressors are administered), or dynamic measures of fluid responsiveness are selected to follow the hemodynamic response.
* An [[arterial catheter]] may be inserted if blood pressure is labile, [[sphygmomanometer]] readings are unreliable, restoration of perfusion is expected to be protracted, or dynamic measures of fluid responsiveness are selected to follow the hemodynamic response.
* One trial that randomized patients to a target MAP of 65 to 70 mmHg (low target MAP) or 80 to 85 mmHg. [72][73]
* '''Static'''
 
* Traditionally, in addition to MAP, the following static CVC measurements were used to determine adequate fluid management:
* CVP at a target of 8 to 12 mmHg
* ScvO<sub>2</sub> ≥70 percent (≥65 percent if sample is drawn off a PAC)
* '''Dynamic'''
Respiratory changes in the vena caval diameter, radial artery pulse pressure, aortic blood flow peak velocity, left ventricular outflow tract velocity-time integral, and brachial artery blood flow velocity are considered dynamic measures of fluid responsiveness. There is increasing evidence that dynamic measures are more accurate predictors of fluid responsiveness than static measures, as long as the patients are in sinus rhythm and passively ventilated with a sufficient tidal volume. For actively breathing patients or those with irregular cardiac rhythms, an increase in the cardiac output in response to a passive leg-raising maneuver (measured by echocardiography, arterial pulse waveform analysis, or pulmonary artery catheterization) also predicts fluid responsiveness. Choosing among these is dependent upon availability and technical expertise, but a passive leg raising maneuver may be the most accurate and broadly available. Future studies that report improved outcomes (eg, mortality, ventilator free days) in association with their use are needed. Further details are provided separately.
 
Although the optimal frequency is unknown, we follow serum lactate in patients with sepsis until the lactate value has clearly fallen. While guidelines promote normalization of lactate [3], only lactate-guided resuscitation has not been convincingly associated with improved outcomes.
 
Patients having persistent hypoperfusion despite adequate fluid resuscitation and antimicrobial treatment should be reassessed for fluid responsiveness (see 'Hemodynamic' above) adequacy of the antimicrobial regimen and septic focus control (see 'Septic focus identification and source control' above) as well as the accuracy of the diagnosis and the possibility that unexpected complications or coexisting problems have occurred (eg, pneumothorax following CVC insertion) (see "Evaluation of and initial approach to the adult patient with undifferentiated hypotension and shock"). Other options including vasopressors, glucocorticoids, inotropic therapy, and blood transfusion are discussed in this section.
 
'''Vasopressors'''
* Intravenous vasopressors are useful in patients who remain hypotensive despite adequate fluid resuscitation or who develop cardiogenic pulmonary edema.  
* Guidelines state a preference for central venous and arterial access especially when vasopressor administration is prolonged or high dose, or multiple vasopressors are administered through the same catheter [3]; while this is appropriate, waiting for placement should not delay their administration and the risks of catheter placement should also be taken into account.
* Data that support norepinephrine as the first-line single agent in septic shock are derived from numerous trials that have compared one vasopressor to another [86-92].
* The addition of a second or third agent to norepinephrine may be required (eg, epinephrine, dobutamine, or vasopressin) with little data to support agent selection. For patients with refractory septic shock associated with a low cardiac output, an inotropic agent may be added.
'''Indications for abdominal exploration''' 
* Many patients will require urgent surgical intervention to limit ongoing abdominal contamination and manage the perforated site. Immediate surgical consultation is appropriate whenever perforation is confirmed or even strongly suspected to determine if immediate surgical intervention is needed and the interval of time to surgery.
* Patients with evidence of perforation and the following clinical signs benefit from immediate surgery:
* Abdominal sepsis or worsening or continuing abdominal pain and/or signs of diffuse or extensive peritonitis.
* Complete or closed-loop bowel obstruction
* Bowel ischemia: Main initial management is recommended except vasoconstricting agents and digitalis should be avoided, since they can exacerbate mesenteric ischemia. If vasopressors are needed, dobutamine, low-dose dopamine, or milrinone are preferred since they have less of an effect on mesenteric perfusion as compared with other vasopressors. '''Pain control''' and systemic anticoagulation are recommended to prevent thrombus formation and propagation, unless patients are actively bleeding.
 
=== Specific organs management ===
'''Esophagus''' 
 
covered stents are increasingly being used to manage some patients with esophageal perforation.
 
Placed endoscopically, the stent covers the perforation while healing occurs.
 
Complications associated with stents include bleeding, fistula and injury to adjacent structures, kinking, erosion, and reflux. Stents also have a tendency to migrate, which occurred in 33 percent of patients in one series [119].
 
However, stenting provides a window of time that may allow initial stabilization and healing, and conversion to open repair is always an option should the stent fail [120].
 
Notwithstanding innovations in conservative care for esophageal perforation, open surgery remains the mainstay of treatment. Surgical options for esophageal perforation include primary repair, repair over a drain, and, in the case of severe stricture or tumor, esophagectomy and esophageal exclusion [51,117]. The approach to open surgical repair depends upon the level of the perforation and may involve a neck incision and/or thoracotomy and, for lower esophageal perforation, potentially an upper abdominal incision as well. Specific management is reviewed in detail elsewhere.
 
'''PRINCIPLES OF SURGICAL MANAGEMENT''' — Primary repair of the perforation site is the optimal procedure, even if the diagnosis is delayed greater than 24 hours. The exceptions to performing a primary repair include a cervical perforation that cannot be accessed but can be drained, diffuse mediastinal necrosis, a perforation too large for the esophagus to be re-approximated, an esophageal malignancy, preexisting end-stage benign esophageal disease (eg, achalasia), or if the patient is clinically unstable [12-14]. Surgical alternatives to primary repair in these settings are discussed below (see 'Alternatives to primary surgical repair'below).
 
'''Primary surgical repair''' — A primary repair is performed when, in the judgement of an experienced surgeon, the closure can heal.
 
'''General principles for esophageal repair''' — The following general principles are used to perform a repair of a perforation of the cervical, thoracic, or abdominal esophagus (figure 4):
 
●First, devitalized tissue is debrided from the perforation site.
 
●Second, the muscular layer is incised longitudinally along the muscle fibers superior and inferior to the perforation to expose the entire extent of the mucosal injury. Failure to visualize the proximal and distal extent of the mucosal disruption is the most common reason for a persistent leak.
 
●Third, the mucosa is closed with absorbable interrupted sutures and the muscularis layer is closed with interrupted nonabsorbable sutures. Narrowing of the esophageal lumen should be avoided using precise reapproximation.
 
When there has been a delay in diagnosis greater than 24 hours, and/or substantial extraluminal contamination from the leakage of fluid and debris has occurred, the integrity of the repair can be enhanced with the use of a vascularized pedicle flap. The most common flap used is the intercostal muscle flap (figure 5 and figure 6). Other options for a flap include serratus muscle, latissimus dorsi muscle, diaphragm, parietal pleura, omentum, and gastric fundus.
 
If the gastric fundus is used to buttress a lower esophageal repair, the gastroesophageal junction should be placed in the normal intra-abdominal location to avoid severe and debilitating gastroesophageal reflux. A Dor fundoplication (partial anterior wrap) is an excellent alternative for an intra-abdominal perforation.
 
'''Cervical perforation''' — Cervical perforations are typically more easily treated than perforations of the thoracic or intra-abdominal esophagus [2]. A primary repair of a cervical perforation is performed if the perforation can be clearly visualized and there is no distal obstruction. Otherwise, drainage of the perforation is adequate to control the leak since the anatomic structures of the neck typically confine extraluminal contamination to a limited space and thereby enhance spontaneous healing (figure 7). (See 'Drainage only' below.)
 
The surgical approach to control a perforation in the cervical esophagus begins with an incision in the left neck along the lower third of the sternocleidomastoid (SCM) muscle (figure 8), unless the perforation is documented or visualized from the right neck [15]. The surgical dissection proceeds with identification of the anatomic structures such as the carotid sheath, trachea, spine, and recurrent laryngeal nerve, which should be preserved. Soft retractors, including the fingers of the surgeon and first assistant, are used to retract the esophagus and trachea in order to avoid recurrent laryngeal nerve injury.
 
The following surgical techniques are used to expose and manage the perforated cervical esophagus (figure 9) [1,15]:
 
●The SCM muscle and carotid sheath are retracted laterally
 
●The middle thyroid vein and the omohyoid muscle are divided
 
●The trachea and esophagus are bluntly retracted medially
 
●The esophagus is carefully and bluntly dissected posteriorly along the retropharyngeal plane
 
●All devitalized tissue is debrided
 
Blunt dissection should be carried into the mediastinum posterior to the esophagus and anterior to the prevertebral fascia to assure adequate drainage of the infection. The perforation should be primarily repaired when clearly visualized, as described above. However, if the perforation is not clearly visualized, then the perforation site is drained. (See 'General principles for esophageal repair' above.)
 
The wound is irrigated, widely drained with Jackson-Pratt drains that are brought out through the bottom of the incision or through a separate dependent site, and loosely closed in layers with interrupted absorbable sutures. Alternatively, when heavy contamination is present, the wound may be left open and packed with wet to dry dressings or a wound vac (see "Negative pressure wound therapy"). The authors do not routinely use a nasogastric tube. A feeding tube is only considered in patients presenting with significant malnutrition.
 
'''Thoracic perforation''' — A thorough knowledge of the relationship of the esophagus to the adjacent vital structures is necessary when planning the surgical approach to a thoracic perforation (figure 1 and figure 10). The level of the perforation of the thoracic esophagus determines the surgical approach to controlling the leak and repairing the perforation. As an example, a mid-esophageal perforation is approached through a right thoracotomy at the sixth or seventh intercostal space while a distal esophageal perforation is approached through a left thoracotomy at the seventh or eighth intercostal space (figure 11).
 
The following surgical techniques are used to expose the thoracic esophagus (figure 12):
 
●Prior to entering the thoracic cavity, a posteriorly based intercostal muscle flap is harvested as a potential buttress of a primary repair (figure 5).
 
●The thoracotomy is performed, the lung is retracted anteriorly, which can be facilitated by the mobilization of the pleural reflection and inferior pulmonary ligament (figure 12).
 
●The pleural space is evacuated of debris and the devitalized tissue in the mediastinum is debrided.
 
●The esophagus is encircled with a Penrose drain proximal to the perforation to facilitate dissection (figure 13).
 
●The perforation is localized and the repair is planned based on the size of the perforation, the friability of the esophagus, the degree of surrounding contamination, and the clinical status of the patient.
 
●The repair is then buttressed with a pedicled flap (eg, intercostal muscle flap) utilizing interrupted absorbable sutures. An alternative to the intercostal muscle flap (figure 6) is the parietal pleura flap if the intercostal muscle is not available or the intercostal blood supply has been compromised (figure 14).
 
●The wound is copiously irrigated and drained utilizing two 28 to 32 French chest tubes. One chest tube is positioned in proximity to the site of injury to ensure adequate drainage if the repair breaks down and the second posterior to the repair.
 
●Pulmonary decortication is performed if exudate and debris are present to facilitate adequate lung expansion.
 
●A nasogastric tube is guided past the site of repair and into the stomach, taking care to avoid damaging the repair site.
 
●A jejunostomy feeding tube can be inserted by a mini-laparotomy procedure at the time of the esophageal repair. The authors prefer to place feeding tubes on clinically stable patients with significant extraluminal contamination when a prolonged intensive care unit admission is anticipated or on patients who present with significant malnutrition.
 
'''Abdominal perforation''' — The general principles for the management of an intra-abdominal esophageal perforation are the same as those described for perforations of the cervical and thoracic esophagus (figure 15). These surgical principles include a careful dissection to isolate the esophagus without damaging vital structures, removal of debris and devitalized tissues, and debridement of the area of perforation.
 
A laparotomy is the preferred approach to repair a perforation of an intra-abdominal esophagus. The left triangular ligament (peritoneal attachment of the liver to the diaphragm [16]) of the liver is divided and the liver is retracted laterally (figure 16). This maneuver provides access to the esophageal hiatus, which is proximal to the perforation. Division of the short gastric vessels will help mobilize the gastroesophageal junction for improved exposure and access to the perforation (figure 17).
 
Following the primary suture repair, the hiatus is closed posteriorly with interrupted silk sutures to create an opening that accommodates only the esophagus and a fingertip. A Dor (partial 180° anterior wrap) or a Nissen (complete 360° posterior wrap) fundoplication is used to buttress the site of repair depending on the site of perforation and patients' preoperative history of swallowing dysfunction. The peritoneum is then copiously irrigated with isotonic saline, Jackson-Pratt drains are placed near the site of repair, and a feeding jejunostomy tube is placed for postoperative alimentation.
 
'''Postoperative management''' — This approach is used to manage patients with an esophageal perforation at any site:
 
●Nutritional support is necessary until oral feedings can be initiated and effectively sustained. The patient remains NPO for approximately seven days. Jejunal tube feedings are started on postoperative day two or three in stable patients without evidence of an ileus.
 
●If a jejunostomy feeding tube was not inserted at the time of the repair of the perforation, a central line can be inserted for administration of parenteral nutrition when a prolonged period of delay of enteral feedings is anticipated. Generally, this is not indicated in previously well-nourished patients with iatrogenic injuries and minimal contamination.
 
●The patient is maintained on intravenous broad spectrum antibiotics typically for 7 to 10 days, depending on the clinical status.
 
●A contrast esophagram is obtained on postoperative day seven if the patient is clinically stable. If there is no evidence of an esophageal leak or postoperative ileus, the nasogastric tube is removed and oral feedings are initiated.
 
●Drains remain in place until patients are tolerating oral feedings and without clinical evidence of a leak.
 
'''Stomach and duodenum''' 
 
Most perforations of the stomach and duodenum require surgical repair (open or laparoscopic) [123-131]. The most common surgery for perforated peptic ulcer disease is oversewing the ulcer or the use of a Graham patch, which is used because suturing an inflamed ulcer can be difficult or impossible. The advent of natural orifice transluminal endoscopic surgery (NOTES) has led to the development of several methods of endoscopic gastric closure [132-134]. Regardless of whether an open, laparoscopic, or NOTES approach is used to provide local control or perform a definitive ulcer operation, it is important to obtain a biopsy of the ulcer margins in all patients with a gastric perforation to rule out gastric carcinoma.
 
Treatment for perforated duodenal diverticulum is usually diverticulectomy with closure of the duodenum. Omental fat can be used to buttress the repair with drainage tubes to permit egress of residual infected fluid. A subtotal gastrectomy with a Billroth II procedure or Roux-en-Y is sometimes used when extensive inflammation is present in the region.
 
'''Perforated peptic ulcer'''
 
 A major decision when treating patients with ulcer perforation is whether and when to operate. After resuscitation, emergent operation and closure with a piece of omentum is the standard of care for patients with an acute perforation and a rigid abdomen with free intraperitoneal air. If the patient is stable or improving, especially if spontaneous sealing of the perforation has been demonstrated, nonoperative management with close monitoring is a reasonable option. With any free perforation, regardless of the presence or size of the leak, if the patient's status is deteriorating, urgent surgery is indicated. Prolonged efforts to establish a diagnosis or pursue nonoperative care despite worsening status can be counterproductive, since a needed operation will be delayed. In addition, surgery is indicated in circumstances where the cause of an acute abdomen has not been established or the patient's status cannot be closely monitored. (See "Surgical management of peptic ulcer disease", section on 'Perforated peptic ulcer'.)
 
The management of patients with small to moderate leaks who are clinically stable is less clear. Currently, the standard of care for such patients is surgery, but some studies suggest that these patients can be managed nonoperatively:
 
●The efficacy of initial conservative therapy with a nasogastric tube, antibiotics, and H2 blockers was compared with immediate laparoscopic surgical repair in a randomized trial of 83 patients with a perforated peptic ulcer [84]. Surgery was required in 11 of 40 patients (28 percent) in the conservative therapy group because of failure to improve clinically after 12 hours. The other 29 patients in the conservative therapy arm were successfully managed without surgery. The two groups did not differ significantly in terms of morbidity or mortality. However, the hospital stay was 35 percent longer in the group treated conservatively. Also, patients over 70 years old were less likely to respond to conservative treatment. The authors concluded that an initial period of nonoperative treatment with careful observation was safe in patients under age 70 years.
 
●A prospective study of 82 patients with perforated peptic ulcers treated patients with nasogastric suction and intravenous H2 receptor antagonists [85]. If patients did not show clinical improvement after 24 hours, surgery was performed. With this approach, surgery was avoided in 44 patients (54 percent). Factors associated with surgery included the size of the pneumoperitoneum, abdominal distension, heart rate >94 beats per minute, pain on digital rectal examination, and age >59 years. Overall mortality in the study was 1 percent.
 
Data also suggest that if spontaneous sealing occurs, patients do well without surgery. A study of 152 patients whose perforations sealed spontaneously found re-leakage in only two patients, comparing favorably with postoperative re-leak rates [77]. The probability of sealing with nonoperative care and intravenous PPIs or H2 receptor antagonists has not been studied; however, over 50 percent of patients with perforated duodenal ulcers have sealed spontaneously when first examined.
 
Some patients require nonoperative management because severe comorbid illnesses preclude surgery [86,87]. In a retrospective series of 30 high-risk patients treated nonoperatively, 11 patients were treated with H2 receptor antagonists (prior to 1996) and 19 were treated with omeprazole 40 mg daily (1996 and later) [86]. Mortality was 64 percent in the early period and 11 percent in the later period. Hypotension upon presentation was a major risk factor for a poor outcome. These data raise the hypothesis that PPI treatment promotes sealing of perforations. However, a low mortality rate (3.5 percent) was also seen in a series of 84 high-risk patients treated with percutaneous drainage and H2 receptor antagonists [87].
 
Nonoperative management may also be considered for patients with delayed presentations. If the patient has a persistent leak across the perforation, surgery may be indicated, but can be complicated by peritoneal contamination. Other options in this setting include nonoperative care with percutaneous peritoneal drainage, especially for patients who are not good surgical candidates [87].
 
Patients with perforated ulcers should have an upper endoscopy to look for evidence of malignancy, to biopsy for H. pylori, and to assess for ulcer healing. To allow the perforation to heal, we suggest waiting at least two weeks prior to performing an upper endoscopy. If the procedure does not need to be done urgently, we prefer to wait six to eight weeks to allow for ulcer healing. At that time, biopsies can be obtained to look for infection with H. pylori and to rule out malignancy (particularly in the case of a nonhealing gastric ulcer). (See "Peptic ulcer disease: Management", section on 'Endoscopy after initial therapy'.)
 
'''Surgical approach''' — For patients who require surgery for a perforated ulcer, the surgical approach depends upon the location of the ulcer. This topic is discussed in detail elsewhere. (See "Surgical management of peptic ulcer disease", section on 'General principles of ulcer surgery'.)
 
'''PENETRATION''' — Ulcer penetration refers to penetration of the ulcer through the bowel wall without free perforation or leakage of luminal contents into the peritoneal cavity. A longstanding ulcer history is common, but not invariable, in patients who develop penetration. Penetration often comes to attention because of a change in symptoms or involvement of adjacent structures. The change in symptom pattern may be gradual or sudden; it usually involves a loss of cyclicity of the pain with meals, and loss of food and antacid relief. The pain typically becomes more intense, of longer duration, and is frequently referred to the lower thoracic or upper lumbar region.
 
Surgical series suggest that penetration occurs in 20 percent of ulcers, but only a small proportion of penetrating ulcers become clinically evident [88]. Penetration occurs in descending order of frequency into the pancreas, lesser omentum, biliary tract, liver, greater omentum, mesocolon, colon, and vascular structures. Antral and duodenal ulcers can penetrate into the pancreas. Pyloric or prepyloric ulcers can penetrate the duodenum, eventually leading to a gastroduodenal fistula evident as a "double" pylorus.
 
Penetration can be associated with a wide array of uncommon complications including perivisceral abscess (evident on computed tomography or ultrasonography) [89], erosion into vascular structures leading to exsanguinating hemorrhage (aortoenteric fistula) [90], or erosion into the cystic artery [91]. Rare biliary tract complications include erosion into the biliary tree with choledochoduodenal fistula, extrahepatic obstruction, or hemobilia [92]. Fistulization into the pancreatic duct has also been reported with penetrating duodenal ulcers [93].
 
Gastrocolic fistulae are seen with greater curvature gastric ulcers, particularly marginal ulcers [72,94]. Typical features of this complication include pain, weight loss, and diarrhea; feculent vomiting is an uncommon, but diagnostic, symptom. A duodenocolic fistula can also occur.
 
A penetrating ulcer is suspected clinically when an ulcer in the proper region is found (image 4) [68]. Mild hyperamylasemia can develop with posterior penetration of either a gastric or duodenal ulcer, but clinical pancreatitis is uncommon.
 
No rigorous studies are available to guide the management of penetrating ulcers. Management should follow the intensive measures outlined for refractory ulcers. (See "Approach to refractory or recurrent peptic ulcer disease".)
 
'''Small intestine''' 
 
Treatment of small intestinal perforation is performed by closing the perforation in one or two layers. If an injury has devitalized the small intestine or if it has been long-standing, producing indurated tissue, a small bowel resection is performed.
 
'''Appendix''' 
 
Approximately 30 percent of those with acute appendicitis present with perforation. Younger children often have atypical or vague symptoms and are more likely to present after perforation has occurred [137]. The management of perforated appendicitis is discussed in detail separately.
 
'''''PERFORATED APPENDICITIS''''' 
 
 Patients with perforated appendicitis may appear acutely ill and have significant dehydration and electrolyte abnormalities, particularly if fever and vomiting have been present for a long time. The pain usually localizes to the right lower quadrant if the perforation has been walled off by surrounding intra-abdominal structures such as the omentum but can be diffuse if generalized peritonitis ensues. On imaging studies, appendicitis can present with a contained perforation (an inflammatory mass often referred to as a "phlegmon," or an intra-abdominal or pelvic abscess) or, rarely, a free perforation.
 
Other unusual presentations of appendiceal perforation can occur, such as retroperitoneal abscess formation due to perforation of a retrocecal appendix or liver abscess formation due to hematogenous spread of infection through the portal venous system. An enterocutaneous fistula can result from an intraperitoneal abscess that fistulizes to the skin. Appendiceal perforation can result in a small bowel obstruction, manifested by bilious vomiting and obstipation. High fevers and jaundice can be seen with pylephlebitis (septic portal vein thrombosis) and can be confused with cholangitis.
 
Perforation is found in 13 to 20 percent of patients who present with acute appendicitis [68]. Perforation rate is higher among men (18 percent men versus 13 percent women) and older adults [21,68]. Although perforation is a major concern when evaluating a patient with symptoms that have lasted more than 24 hours, the time course of progression of appendicitis to necrosis and perforation varies among patients, and perforation can develop more rapidly and should always be considered. Approximately 20 percent of patients with perforated appendicitis present within 24 hours of the onset of symptoms [69].
 
The management of perforated appendicitis depends on the condition of the patient (stable versus unstable), the nature of the perforation (contained versus free perforation), and whether an abscess or phlegmon is present on imaging studies (algorithm 1):
 
'''Unstable patients or patients with free perforation''' — A free perforation of the appendix can cause intraperitoneal dissemination of pus and fecal material and generalized peritonitis. These patients are typically quite ill and may be septic or hemodynamically unstable, thus requiring preoperative resuscitation. The diagnosis is not always appreciated before exploration.
 
For patients who are septic or unstable, and for those who have a free perforation of the appendix or generalized peritonitis, emergency appendectomy is required, as well as drainage and irrigation of the peritoneal cavity. Emergency appendectomy in this setting can be accomplished open or laparoscopically; the choice is determined by surgeon preference with consideration of patient condition and local resources. (See 'Appendectomy for perforated appendicitis' below.)
 
'''Stable patients''' — Stable patients with perforated appendicitis who have symptoms localized to the right lower quadrant can be treated with immediate appendectomy or initial nonoperative management. Both approaches are safe. A 2017 Cochrane review of two randomized trials concluded that the quality of the evidence was too low to make a recommendation [70]. Thus, the decision ultimately rests with the treating surgeon. We suggest the following initial approach based on imaging findings on presentation (algorithm 1):
 
●Patients with an appendiceal abscess should be treated with intravenous antibiotics and percutaneous, image-guided drainage of the abscess. Immediate appendectomy is an alternative option for these patients, especially if the abscess is not amenable to percutaneous drainage. (See 'Appendectomy for perforated appendicitis' below.)
 
●Patients with a phlegmon of the right lower quadrant should be treated with intravenous antibiotics. Repeat imaging is often performed to follow the resolution (or progression) of the phlegmon, and to exclude other complications that could evolve over time (eg, abscess formation). The authors of this topic do not perform immediate appendectomy in patients with a phlegmon associated with perforated appendicitis.
 
Patients who fail initial antibiotic therapy clinically or radiographically require rescue appendectomy, whereas those who respond to initial antibiotic therapy can be discharged with oral antibiotics to complete a 7- to 10-day course (in total) and return for follow-up in six to eight weeks. (See 'Initial nonoperative management' below.)
 
'''Colon and rectum''' 
 
Several options exist for treating perforated diverticulitis. Most cases of diverticulitis with contained perforation or small abscess can be treated nonoperatively with antibiotics with or without percutaneous drainage. Resection is usually required for more severe diverticular complications [139].
 
The incidence of perforation during colonoscopy increases as the complexity of the procedure increases and is estimated at 1:1000 for therapeutic colonoscopy and 1:1400 for overall colonoscopies. The presence of collagenous colitis appears to predispose to perforation during colonoscopy [140]. In one series, the rectosigmoid area was most commonly perforated (53 percent), followed by the cecum (24 percent) [141]. In this series, most perforations were due to blunt injury, 27 percent of perforations occurred with polypectomy, and 18 percent of perforations were produced by thermal injury. Almost 25 percent of patients presented in a delayed fashion (after 24 hours). Polypectomy patients, in contrast to screening patients, were more likely to present in a delayed fashion. Most of the postprocedural perforations occurred in patients who had undergone bowel preparation, making primary anastomosis feasible. A poorly prepared bowel was a predictor of feculent peritonitis.
 
A myriad of other etiologies can lead to colonic or rectal perforation. NSAID use has been associated with serious diverticular perforation, with diclofenac and ibuprofen being the most commonly implicated drugs [43]. Glucocorticoids are also associated with diverticular perforation. Stercoral perforation, caused by ischemic necrosis of the intestinal wall by stool, is also possible, particularly in older individuals [142,143]. Perforation after barium enema or colonoscopy has been reported in patients with collagenous colitis [140]. Foreign bodies, either ingested or inserted, can cause colorectal perforation [144]. Colon perforation can also be related to collagen-vascular diseases such as Ehlers-Danlos syndrome type IV [145,146], Behcet's syndrome [147], and eosinophilic granulomatosis with polyangiitis (Churg-Strauss) [148]. Perforation has been reported with anorectal manometry in the setting of a rectal anastomosis [149]. Perforation is also associated with invasive amebiasis of the colon [150]. In pediatric populations, bacterial colitis, particularly with nontyphoid Salmonella, can lead to perforation [151].
 
Colon perforations can be treated by simple suture if the perforation is small, often using a laparoscopic approach [152]. If the perforation is larger and devascularizing the colonic wall, colon resection will be necessary [153]. Patients with a perforated colon due to neoplasm also require resection [154]. Laparoscopic treatment of complicated disease is feasible but has a higher rate of conversion to open operation compared with uncomplicated disease [155]. A primary anastomosis is preferred, whenever feasible [139,156]. Primary anastomosis may be combined with proximal "protective" ostomy in those with complicated diverticulitis or malignancy. Colonic perforation due to Ehlers-Danlos syndrome is best treated with resection or exteriorization, or subtotal colectomy.
 
'''''Acute colonic diverticulitis'''''
 
Since most patients with diverticulitis are treated medically, surgery is only indicated when diverticular disease is either not amenable or refractory to medical therapy (algorithm 1) [5,7-9].
 
'''Indication for emergency surgery''' — Acute diverticulitis with frank (free) perforation is a life-threatening condition that mandates emergency surgery [5,9-11]. (See 'Resection' below.)
 
'''Indications for urgent surgery''' — Urgent surgery (in which an operation is generally required during the same hospitalization) should be performed in patients with one of the indications discussed below.
 
'''Failure of medical treatment''' — Patients who deteriorate or fail to improve after three to five days of inpatient intravenous antibiotics may require urgent surgery, as further medical therapy is unlikely to resolve their diverticulitis. (See "Acute colonic diverticulitis: Medical management", section on 'Failure of inpatient medical treatment'.)
 
'''Obstruction''' — Patients who present with colonic obstruction attributable to acute diverticulitis should undergo surgical resection of the involved colonic segment. Because acute diverticulitis and colon cancer can both cause colonic obstruction and are difficult to distinguish by abdominopelvic computed tomography (image 1), surgery in this setting is required to rule out cancer and also to relieve symptoms of obstruction. (See "Acute colonic diverticulitis: Medical management", section on 'Obstruction' and "Overview of mechanical colorectal obstruction", section on 'Surgical management'.)
 
Colonic obstruction due to diverticular disease is rarely complete, which allows bowel preparation to be attempted. Alternatively, on-table lavage can be used to clean out the fecal load, which may also permit a primary anastomosis.
 
Endoluminal stenting may not be helpful for colonic obstruction caused by diverticulitis. In a systematic review, treating benign colorectal obstructions (most due to diverticulitis) with self-expanding stents resulted in more cases of perforation (12 versus 4 percent), stent migration (20 versus 10 percent), and recurrent obstruction (14 versus 7 percent) than stenting malignant colorectal obstructions [12]. When stenting was used as a bridging therapy to surgery, only 43 percent of patients with diverticulitis successfully avoided a stoma. (See "Enteral stents for the management of malignant colorectal obstruction".)
 
'''Abscess failing nonoperative intervention''' — In contemporary practice, diverticular abscesses are typically treated with percutaneous image-guided drainage or with intravenous antibiotics if the abscess is too small or inaccessible to percutaneous drainage. Surgery may be indicated for patients who deteriorate or fail to improve within two to three days of percutaneous intervention or antibiotic therapy, as a persistent intraabdominal abscess is unlikely to respond to further nonoperative management. (See "Acute colonic diverticulitis: Medical management", section on 'Abscess'.)
 
'''Indications for elective surgery''' — Patients may require elective colon surgery because of persistent symptoms from conditions such as diverticular fistula or chronic smoldering diverticulitis. In addition, asymptomatic patients with a history of acute diverticulitis may be offered elective surgery based upon their risk of developing serious complications or dying from a recurrent diverticulitis attack.
 
'''Fistula''' — As a result of diverticulitis, a fistula can develop between the colon and another pelvic organ, such as the bladder, vagina, uterus, small bowel, or the abdominal wall. Diverticular fistulas rarely close spontaneously, and therefore require surgical correction. The management of diverticular fistula is discussed separately. (See "Acute diverticulitis complicated by fistula formation".)
 
'''Chronic smoldering diverticulitis''' — Patients with acute diverticulitis who initially respond to medical treatment but subsequently develop recurrent symptoms, such as left lower quadrant abdominal pain, alteration in bowel movements, and/orrectal bleeding, are described as having chronic smoldering diverticulitis. If the symptoms persist for longer than six weeks, patients should be referred for surgical evaluation. However, since patients with irritable bowel syndrome or other functional gastrointestinal disorders may present similarly, patients with chronic symptoms after an acute diverticulitis attack must be evaluated carefully before being offered surgery. (See "Acute colonic diverticulitis: Medical management", section on 'Symptomatic patients after initial attack'.)
 
'''Asymptomatic but high-risk patients''' — We offer elective surgery to patients who had a prior episode of complicated diverticulitis and those who are immunosuppressed because such patients could develop serious complications or die from recurrent attacks of diverticulitis.
 
'''Patients with prior complicated attack''' — Elective surgery is indicated for patients with one prior episode of '''complicated'''diverticulitis, such as a microperforation that was treated with antibiotics, or an abscess that was treated with percutaneous drainage and/or antibiotics. Studies show that such patients are at a greater risk of developing complications or dying from a recurrent attack, and therefore would benefit from early elective surgery [13,14]. (See "Acute colonic diverticulitis: Medical management", section on 'Complicated first attack'.)
 
'''Patients who are immunocompromised''' — Most surgeons would offer elective surgery to immunocompromised patients after a single attack of diverticulitis because they often require emergency surgery due to an atypical and delayed presentation. Elective surgery is associated with lower morbidity and mortality rates compared with emergency surgery in these and other patients. (See "Acute colonic diverticulitis: Medical management", section on 'Immunosuppression'.)
 
'''CHOOSING A SURGICAL TECHNIQUE''' — For patients who require surgery for diverticulitis, the choice of technique depends upon the patient's hemodynamic stability, extent of peritoneal contamination, and surgeon experience [15].
 
'''Resection''' — The primary goal of surgery is to remove the diseased colonic segment, the feasibility of which is predicated upon a patient's hemodynamic stability.
 
'''Hemodynamically unstable patients''' — Patients who require emergency surgery for perforated diverticulitis may be too ill to tolerate a definitive colon resection and reconstruction. For such patients, a damage control laparotomy with limited resection of the diseased colonic segment with or without reconstruction should be performed expeditiously [16]. (See "Overview of damage control surgery and resuscitation in patients sustaining severe injury" and 'Drainage procedures' below.)
 
'''Hemodynamically stable patients''' — Patients undergoing emergency surgery who are hemodynamically stable and all other patients undergoing urgent or elective surgery should be able to tolerate a definitive resection of the involved colonic segment [17-21] (figure 1). (See 'Colonic resection with end colostomy (ie, Hartmann's procedure)' below.)
 
'''Reconstruction''' — The secondary goal of surgery is to restore intestinal continuity if possible. The choice of reconstructive techniques largely depends upon the extent of peritoneal contamination as assessed by the Hinchey classification system [22]:
 
●Stage I – Pericolic or mesenteric abscess
 
●Stage II – Walled-off pelvic abscess
 
●Stage III – Generalized purulent peritonitis
 
●Stage IV – Generalized fecal peritonitis
 
'''Diffuse contamination (Hinchey III or IV)''' — Hinchey III or IV diverticulitis is characterized by generalized purulent or fecal peritonitis, for which a primary anastomosis is contraindicated. The preferred surgical treatment is a Hartmann's procedure with end colostomy. (See 'Colonic resection with end colostomy (ie, Hartmann's procedure)' below.)
 
'''Localized contamination (Hinchey I or II)''' — Hinchey I or II diverticulitis is characterized by one or more localized abscesses in the pericolonic, mesenteric, or pelvic locations. Patients with Hinchey I or II diverticulitis can usually tolerate a preoperative bowel preparation. Thus, if the abscess can be resected with the colonic segment, a primary anastomosis can be performed in these patients. (See 'One-stage procedures' below.)
 
If there are concerns about either contamination or inflammation involving the surrounding tissue (eg, with a large pelvic abscess), a primary anastomosis can be performed while protected by a diverting ostomy (eg, loop ileostomy or colostomy). Compared with an end colostomy, a protective loop ostomy is easier to reverse at a later time. (See 'Colonic resection with primary anastomosis and protective ostomy' below.)
 
'''Minimal contamination (elective surgery)''' — Elective surgery is typically performed six or more weeks after an episode of acute diverticulitis when all infection and inflammation have resolved. Thus, a primary anastomosis without protective ostomy (ie, a one-stage procedure) is standard. (See 'One-stage procedures' below.)
 
'''SURGICAL TECHNIQUES'''
 
'''One-stage procedures''' — A one-stage procedure (ie, colon resection with primary anastomosis) is typically performed during elective surgery or during urgent surgery in patients with Hinchey I or II diverticulitis who have an abscess that can be resected along with the involved colonic segment. (See 'Localized contamination (Hinchey I or II)' above and 'Minimal contamination (elective surgery)' above.)
 
A primary anastomosis is contraindicated for patients who have Hinchey III or IV diverticulitis, and relatively contraindicated for patients with significant medical comorbidities, poor nutritional status, immunosuppression, or other factors that could lead to anastomotic complications [23].
 
To qualify for a one-stage resection, the bowel must be well-vascularized, non-edematous, and the anastomosis should be tension-free and well-prepared. The distal resection margin is typically placed in the upper third of the rectum, where the taenia coli converge. The proximal margin is placed where the colon becomes soft and non-edematous. It is not necessary to resect all diverticula-bearing colon proximal to the intended anastomosis to prevent recurrence since diverticula in the transverse or descending colon rarely cause further symptoms [24].
 
'''Open versus laparoscopic approach''' — A one-stage colon resection for diverticulitis can be performed open or laparoscopically. The laparoscopic approach is preferred when feasible. Growing evidence suggests that laparoscopic surgery in this setting can be performed safely with superior short-term outcomes and comparable long-term outcomes [25-35]. As examples:
 
●In a meta-analysis of 19 studies comparing 1014 patients undergoing elective laparoscopic surgery with 1369 patients undergoing open surgery, open surgery was associated with significantly higher rates of wound infection (relative risk [RR] 1.85, 95% CI 1.25-2.78), blood transfusion (RR 4.0, 95% CI 1.67-10.0), postoperative ileus (RR 2.70, 95% CI 1.52-5.0), and incisional hernia (RR 3.70, 95% CI 1.56-8.33) [36]. The rates of serious complications (eg, anastomotic leak or stricture, inadvertent enterotomy, small bowel obstruction, intraabdominal bleeding, or abscess formation) were comparable between the groups.
 
●A randomized trial performed after the meta-analysis found that laparoscopic surgery resulted in a significantly shorter duration of postoperative ileus (76 versus 106 hours) and length of hospital stay (5 versus 7 days), as well as a trend towards less postoperative pain (4 versus 5 on a visual analog pain scale), when compared with open surgery [37].
 
●Another randomized trial found that patients who underwent laparoscopic versus open surgery had similar complication rates and reported similar quality of life during the early postoperative period and at 12 months [38].
 
Laparoscopic surgery for diverticular disease can be performed with the standard multiport technique or with a technique called single-incision laparoscopic colectomy (SILC). Studies showed that SILC is feasible and safe when performed by experienced surgeons [39,40]. In a prospective study of 330 patients with diverticular disease, patients who underwent SILC had lower peak pain scores compared with patients who underwent a standard laparoscopic procedure (4.9 versus 5.6) [39]. The techniques of single-incision laparoscopic surgery are discussed elsewhere. (See "Abdominal access techniques used in laparoscopic surgery", section on 'Single-incision ports and placement'.)
 
'''Two-stage procedures''' — A two-stage procedure is primarily used for patients with Hinchey III or IV diverticulitis, and for those with Hinchey I or II diverticulitis who have excessive contamination or inflammation of the surrounding tissues or other risk factors for anastomotic leakage. (See 'Diffuse contamination (Hinchey III or IV)' above and 'Localized contamination (Hinchey I or II)'above.)
 
'''Colonic resection with end colostomy (ie, Hartmann's procedure)''' — Hartmann's procedure is the most commonly performed two-stage procedure and the preferred approach for patients with Hinchey III or IV diverticulitis. (See 'Diffuse contamination (Hinchey III or IV)' above.)
 
A Hartmann's procedure involves resecting the diseased colonic segment, creating an end colostomy and a rectal stump, followed by reversal of the colostomy three months later [18] (figure 1).
 
Because creating a mucous fistula by bringing the distal end of the transected bowel through the abdominal wall is often not possible after resecting the entire sigmoid colon, many surgeons mark the rectal stump with a long nonabsorbable suture and tack it to the anterior abdominal wall or sacral promontory to help identify the rectal stump at the second-stage operation.
 
Subsequent closure of the colostomy is a technically difficult operation associated with high morbidity and mortality rates [41,42]. As a result, colostomy closure is only performed in approximately 50 to 60 percent of all patients after a Hartmann's procedure [43,44].
 
'''Colonic resection with primary anastomosis and protective ostomy''' — Another two-stage approach resects the colonic segment and creates a primary anastomosis protected by a proximal diverting stoma (colostomy or ileostomy) at the first operation (figure 2), and closes the stoma at the second operation.
 
This approach is most commonly used in Hinchey I or II diverticulitis when there are relative contraindications to primary anastomosis (eg, excessive contamination/inflammation of surrounding tissue) but the bowel is not edematous. It is the preferred approach in this setting because a protective stoma is easier to close than an end colostomy with a rectal stump [45,46]. (See 'Localized contamination (Hinchey I or II)' above.)
 
Although a primary anastomosis is generally not performed for perforated (Hinchey III or IV) diverticulitis, a primary anastomosis protected by a diverting ileostomy has been attempted in such patients. In a randomized trial of 62 patients with left-sided colonic perforation due to Hinchey III or IV diverticulitis, patients treated with a primary anastomosis with diverting ileostomy, compared with patients treated with a Hartmann's procedure, had similar mortality (9 versus 13 percent) and morbidity rates (75 versus 67 percent) after the first operation [47]. However, a greater percentage of patients treated with a primary anastomosis with diverting ileostomy underwent stoma reversal (90 versus 57 percent); and reversal of the diverting ileostomy in those patients required less operative time (73 versus 183 minutes), length of hospital stay (6 versus 9 days), and resulted in fewer serious complications (0 versus 20 percent), compared with colostomy reversals in patients treated with a Hartmann's procedure. Further studies are required before this approach can be recommended for general use in all patients with Hinchey III or IV diverticulitis.
 
'''Drainage procedures''' — Drainage procedures include laparoscopic lavage and a classic three-stage procedure. Drainage procedures are rarely performed because they do not definitively address the underlying diverticular disease. However, they may be useful in treating septic patients who are too ill to tolerate a resectional procedure. (See 'Hemodynamically unstable patients'above.)
 
'''Laparoscopic lavage''' — Laparoscopic lavage and drainage were introduced as an approach to avoid laparotomy and fecal diversion in patients with complicated diverticulitis [48-51]. Based upon the best available data, we do not use laparoscopic lavage in stable patients with Hinchey III or IV diverticulitis. Instead, we perform sigmoidectomy with or without a colostomy depending upon each patient's clinical condition. (See 'Diffuse contamination (Hinchey III or IV)' above.)
 
Although a 2010 systematic review of retrospective studies found a low mortality rate of 2 percent and avoidance of a permanent stoma in the majority of patients who underwent laparoscopic lavage [52], subsequent randomized trials reported conflicting results:
 
●In one trial (SCANDIV), 199 patients suspected of having perforated diverticulitis based upon detection of free air by abdominal computed tomography scan were randomly assigned to undergo emergency surgery with laparoscopic lavage or sigmoidectomy [53]. Compared with sigmoidectomy, laparoscopic lavage achieved similar mortality (13.9 versus 11.5 percent) and severe morbidity rates (30.7 versus 26 percent) at 90 days. However, patients who were treated with laparoscopic lavage were more likely to require reoperation (20.3 versus 5.7 percent) for complications such as secondary peritonitis (6 versus 0 patients) or missed sigmoid cancer (4 versus 0 patients).
 
●Another randomized trial (LOLA) including 90 patients with purulent perforated diverticulitis showed that laparoscopic lavage produced a higher combined major morbidity and mortality rate within 30 days compared with sigmoidectomy (39 versus 19 percent) [54]. At 12 months, the rates were comparable between the two groups (65 percent for lavage versus 63 percent for sigmoidectomy).
 
●Another trial (DILALA) randomly assigned 83 patients to laparoscopic lavage or Hartmann's procedure after a laparoscopic diagnosis of purulent perforated diverticulitis [55,56]. The mortality rates were similar at both 90 days (8 versus 11 percent) and one year (14 versus 15 percent); the major morbidity rates were similar at 30 (13 versus 18 percent) and 90 days (21 versus 25 percent). The reoperation rates were similar at 30 days (13 versus 17 percent). At one year, however, fewer patients required reoperation after laparoscopic lavage (28 versus 63 percent). In addition, laparoscopic lavage resulted in shorter operative time (1 versus 2.5 hours) and hospital stay (6 versus 9 days for index admission; 8 versus 14 days at one year).
 
In all three trials, the major morbidity and mortality rates were similar between the two groups. The trials, however, reported different reoperation rates, which affected their conclusions (table 1). DILALA was the only trial that favored laparoscopic lavage, largely due to lower reoperation rates.
 
However, reoperation rates can be affected by how they are calculated (table 1). All patients in DILALA assigned to sigmoidectomy underwent colostomy, and colostomy reversals were counted as reoperations. Thus, the reoperation rate in this trial of 63 percent at one year after sigmoidectomy was almost entirely accounted for by colostomy reversals. In contrast, only approximately one-half of patients assigned to sigmoidectomy in LOLA underwent initial colostomy, and colostomy reversals were '''not''' counted as reoperations, resulting in a reoperation rate of just 19 percent. SCANDIV only reported 90-day reoperation rates, which would not have been affected by colostomy reversals, as reversals typically occur three to six months after the initial surgery.
 
Short-term (30- or 90-day) reoperation rates, which by definition excluded colostomy reversals, are more comparable among the three trials (table 1). After laparoscopic lavage, the short-term reoperation rates were lower in DILALA (13 percent at 30 days) than in SCANDIV (20 percent at 90 days) and LOLA (48 percent at 30 days). The lower reoperation rate after laparoscopic lavage in DILALA may be attributed to better pre-enrollment identification and exclusion of patients with fecal perforation and sigmoid carcinoma, which were the major reasons for reoperations in all three trials. In SCANDIV, patients did not undergo a diagnostic laparoscopy before randomization. In LOLA, although patients did undergo a diagnostic laparoscopy, the authors argued that patients with perforated diverticulitis often developed a phlegmon that obscured visualization of the deep pelvis.
 
In common practice, it is unclear how conclusively fecal perforation and/or sigmoid carcinoma can be excluded during the initial evaluation. Thus, sigmoidectomy remains our standard treatment for perforated diverticulitis. We only use laparoscopic lavage in select patients after excluding fecal perforation (Hinchey class IV) by diagnostic laparoscopy, and after excluding either colon cancer or ongoing colonic air leak (from perforation) by intraoperative sigmoidoscopy.


Patients who are candidates for laparoscopic lavage should be advised that a reoperation (usually sigmoidectomy) may be necessary if laparoscopic lavage fails to control the sepsis or a sigmoid carcinoma is later found. The reoperation rate is likely to increase further with longer follow-up; LOLA reported that 20 percent of patients treated with laparoscopic lavage developed recurrent diverticulitis within just the first year [54].
==== Dynamic measures for circulation ====
* There is an evidence that dynamic measures are more accurate predictors of fluid responsiveness than static measures. These measures include:<ref name="pmid28101605">{{cite journal| author=Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R et al.| title=Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016. | journal=Intensive Care Med | year= 2017 | volume= 43 | issue= 3 | pages= 304-377 | pmid=28101605 | doi=10.1007/s00134-017-4683-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28101605  }}</ref>
* Respiratory changes in the [[Vena cavae|vena cava]]
* [[Radial artery]] pulse pressure
* Aortic blood flow peak velocity
* Left ventricular outflow tract velocity-time integral
* Brachial artery blood flow velocity are considered dynamic measures of fluid responsiveness
* Serum [[Lactic acid|lactate]] in patients with sepsis should be assessed until the lactate value has clearly fallen.


'''Drainage and diversion''' — A classic procedure for colonic perforation includes three stages: the first stage involves drainage but not resection of the diseased segment and construction of a proximal diverting stoma; the second stage involves resection of the diseased segment with a primary anastomosis under the protection of the proximal stoma; the third stage closes the proximal stoma.
==== '''Vasopressors''' ====
* Intravenous [[vasopressors]] are useful in patients who remain hypotensive despite adequate fluid resuscitation or who develop cardiogenic [[pulmonary edema]].<ref name="pmid20200382">{{cite journal| author=De Backer D, Biston P, Devriendt J, Madl C, Chochrad D, Aldecoa C et al.| title=Comparison of dopamine and norepinephrine in the treatment of shock. | journal=N Engl J Med | year= 2010 | volume= 362 | issue= 9 | pages= 779-89 | pmid=20200382 | doi=10.1056/NEJMoa0907118 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20200382  }}</ref>
* [[Norepinephrine]] is the first-line single agent in septic shock.<ref name="pmid7933396">{{cite journal| author=Marik PE, Mohedin M| title=The contrasting effects of dopamine and norepinephrine on systemic and splanchnic oxygen utilization in hyperdynamic sepsis. | journal=JAMA | year= 1994 | volume= 272 | issue= 17 | pages= 1354-7 | pmid=7933396 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7933396  }}</ref>
* The addition of a second or third agent to [[norepinephrine]] may be required ([[epinephrine]], [[dobutamine]], or [[vasopressin]]).
* [[Central venous catheter|Central venous]] and [[Arterial catheter|arterial access]] especially when [[vasopressor]] administration is prolonged or high dose, or multiple vasopressors are administered through the same catheter.


This classic procedure has been largely replaced by other procedures (eg, the Hartmann's procedure) because of a higher postoperative mortality rate with the three-stage procedure (26 versus 7 percent) [57,58]. In contemporary practice, the three-stage procedure is only performed when inflammation precludes safe pelvic dissection of the colon from critical sidewall structures (eg, iliac vessels and ureters), or when the patient is unstable. Drainage and fecal diversion in these situations can serve as a temporizing measure to allow treatment of infection and inflammation before further surgery or transfer to a more experienced center. (See "Overview of mechanical colorectal obstruction", section on 'Three-stage'.)
== References ==
{{Reflist|2}}

Latest revision as of 04:05, 4 February 2018


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohammed Abdelwahed M.D[2]

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Overview

Initial management of the patient with gastrointestinal perforation includes intravenous fluid therapy and broad-spectrum antibiotics. Patients with intestinal perforation can have severe volume depletion. The administration of intravenous proton pump inhibitors. Electrolyte abnormalities correction especially metabolic alkalosis if fistula developed. The severity of any electrolyte abnormalities depends upon the nature and volume of material leaking from the gastrointestinal tract. Intravenous vasopressors are useful in patients who remain hypotensive despite adequate fluid resuscitation or who develop cardiogenic pulmonary edema. Norepinephrine is the first-line single agent in septic shock. The addition of a second or third agent to norepinephrine may be required.

Gastrointestinal perforation medical therapy

Antibiotics 

Broad-spectrum antibiotic therapy is initiated if the level of perforation is unknown. The following tabel shows the regimens of choice in these cases:[1]

Regimen Dose
First choice regimens
Ampicillin-sulbactam 3 g IV every six hours
Piperacillin-tazobactam 3.375 or 4.5 g IV every six hours
Ticarcillin-clavulanate 3.1 g IV every four hours
Ceftriaxone 1 g IV every 24 hours
Metronidazole 500 mg IV every eight hours
Alternative regimens
Ciprofloxacin 400 mg IV every 12 hours
Levofloxacin 500 or 750 mg IV once daily
Metronidazole 500 mg IV every eight hours
Imipenem-cilastatin 500 mg IV every six hours
Meropenem 1 g IV every eight hours
Doripenem 500 mg IV every eight hours
Ertapenem 1 g IV once daily

Intravenous fluid therapy

Dynamic measures for circulation

  • There is an evidence that dynamic measures are more accurate predictors of fluid responsiveness than static measures. These measures include:[7]
  • Respiratory changes in the vena cava
  • Radial artery pulse pressure
  • Aortic blood flow peak velocity
  • Left ventricular outflow tract velocity-time integral
  • Brachial artery blood flow velocity are considered dynamic measures of fluid responsiveness
  • Serum lactate in patients with sepsis should be assessed until the lactate value has clearly fallen.

Vasopressors

References

  1. Ibrahim EH, Sherman G, Ward S, Fraser VJ, Kollef MH (2000). "The influence of inadequate antimicrobial treatment of bloodstream infections on patient outcomes in the ICU setting". Chest. 118 (1): 146–55. PMID 10893372.
  2. ProCESS Investigators. Yealy DM, Kellum JA, Huang DT, Barnato AE, Weissfeld LA; et al. (2014). "A randomized trial of protocol-based care for early septic shock". N Engl J Med. 370 (18): 1683–93. doi:10.1056/NEJMoa1401602. PMC 4101700. PMID 24635773. Review in: Ann Intern Med. 2014 Jun 17;160(12):JC9
  3. ARISE Investigators. ANZICS Clinical Trials Group. Peake SL, Delaney A, Bailey M, Bellomo R; et al. (2014). "Goal-directed resuscitation for patients with early septic shock". N Engl J Med. 371 (16): 1496–506. doi:10.1056/NEJMoa1404380. PMID 25272316. Review in: Ann Intern Med. 2015 Mar 17;162(6):JC4
  4. Mouncey PR, Osborn TM, Power GS, Harrison DA, Sadique MZ, Grieve RD; et al. (2015). "Trial of early, goal-directed resuscitation for septic shock". N Engl J Med. 372 (14): 1301–11. doi:10.1056/NEJMoa1500896. PMID 25776532. Review in: Ann Intern Med. 2015 Aug 18;163(4):JC10
  5. Caironi P, Tognoni G, Masson S, Fumagalli R, Pesenti A, Romero M; et al. (2014). "Albumin replacement in patients with severe sepsis or septic shock". N Engl J Med. 370 (15): 1412–21. doi:10.1056/NEJMoa1305727. PMID 24635772. Review in: Ann Intern Med. 2014 Jul 15;161(2):JC6
  6. Asfar P, Schortgen F, Boisramé-Helms J, Charpentier J, Guérot E, Megarbane B; et al. (2017). "Hyperoxia and hypertonic saline in patients with septic shock (HYPERS2S): a two-by-two factorial, multicentre, randomised, clinical trial". Lancet Respir Med. 5 (3): 180–190. doi:10.1016/S2213-2600(17)30046-2. PMID 28219612.
  7. Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R; et al. (2017). "Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016". Intensive Care Med. 43 (3): 304–377. doi:10.1007/s00134-017-4683-6. PMID 28101605.
  8. De Backer D, Biston P, Devriendt J, Madl C, Chochrad D, Aldecoa C; et al. (2010). "Comparison of dopamine and norepinephrine in the treatment of shock". N Engl J Med. 362 (9): 779–89. doi:10.1056/NEJMoa0907118. PMID 20200382.
  9. Marik PE, Mohedin M (1994). "The contrasting effects of dopamine and norepinephrine on systemic and splanchnic oxygen utilization in hyperdynamic sepsis". JAMA. 272 (17): 1354–7. PMID 7933396.