State of the Art Review

Critical Care Management of Bariatric Surgery Complications

Journal of Intensive Care Medicine 1-18 ª The Author(s) 2015 Reprints and permission: sagepub.com/journalsPermissions.nav DOI: 10.1177/0885066615593067 jic.sagepub.com

Bipan Chand, MD, FACS, FASMBS, FASGE1 and Pornthep Prathanvanich, MD, FRCST, FACS1

Abstract Obesity remains a major medical disease that often requires surgical intervention in morbidly obese patients. Surgical procedures have evolved and are performed routinely in most major medical centers. Outcomes are often dependent on patient characteristics, type of procedure, and preoperative planning. Risk stratification often depends on screening and optimizing known comorbidities often encountered in this patient population. A thorough understanding of the physiologic changes seen in obese patient and the commonly performed operations will allow the physician to perform optimal treatment strategies. Keywords critical care, critical illness, decision making, intensive care, knowledge

Obesity has become a major world public health issue. The World Health Organization predicts that approximately 2.3 billion adults will be overweight and >700 million will be obese by 2015.1 The prevalence of obesity has dramatically increased over the past 3 decades, and among Americans aged 20 years and older, 78.4 million were found to be obese (body mass index [BMI]  30 kg/m2) in 2012.2 In recognition of an increased mortality rate with being obese, as well as evidence for risk reduction with weight loss surgery (WLS), the National Institutes of Health has recommended WLS in carefully selected individuals with morbid obesity (Class III obesity [BMI  40] or obesity Class IIc [BMI ¼ 35-39.9] with comorbid conditions).3,4 According to the American Society for Metabolic and Bariatric Surgery, the number of bariatric procedures in the United States has doubled in the last 6 years with approximately 220 000 surgeries in 2008. Approximately 344 221 bariatric procedures were performed worldwide the same year.5 Initial bariatric procedures originated in the 1950s and 1960s.6 Mason and Ito,7 Scopinaro et al,8 and Kuzmak9 proposed the modern bariatric procedures that were initially endorsed by the National Institutes of Health in 1991 and later by all bariatric surgical associations.10,11 In 1994, Wittgrove et al12 published results of their first 5 laparoscopic gastric bypass procedures. Soon thereafter, all surgical weight loss procedures enjoyed an evolution to less invasive laparoscopic methods. Complication rates declined as surgeons and centers gained experience. Over 95% of bariatric operations are now being performed laparoscopically. The most common operations include the laparoscopic roux-en-y gastric bypass (LRYGB), laparoscopic vertical sleeve gastrectomy, and laparoscopic adjustable gastric banding (LAGB).5 In a recent study by Nguyen et al,13 data obtained from the University Health System consortium between 2008 and

2012 showed a change in trend of 60 738 bariatric procedures. Laparoscopic sleeve gastrectomy (LSG) rose from the third most popular procedure to the second, accounting from 0.9% to 36.3% of operations. The LAGB decreased from 23.8% to 4.1%. There was also a concurrent decrease in the use of LRYGB from 66.8% to 56.4% and open gastric bypass from 8.6% to 3.2%. Bariatric surgery remains safe when performed in specialized centers. The overall mortality rate remains 55 Kg/m2 3. Rhabdomyolysis: BMI > 60, OR time > 5 hrs 4. Wernicke Encephalopathy: Chronic vomiting in young women, Poor diet Step 4: Consider Non Procedure-specific complications. A. Perioperative pulmonary complications B. Venous Thromboembolism (VTE) complications C. Rhabdomyolysis D. Wernicke Encephalopathy E. Early Hemorrhage F. Early small bowel obstruction (SBO)

Step 5: Consider Procedure-specific complications. 1. LSG: Leak and Obstruction 2. LRYGB: Anastomotic leak and Marginal ulcer 3. LAGB: Slippage and band erosion Figure 1. Algorithm for recognition and management protocol in case of emergency readmission after bariatric surgery.

Table 1. Complications of Laparoscopic Bariatric Procedures.

Bleeding Intestinal leak Wound infection VTE40,41,45,47,48 MR15,16,19,22

LRYGB

LAGB

LSG

0.4-4%55 0-6.1%58,59 0-8.7% 0-0.64% 0-0.3%

0.1%56 0.5-0.8%60 0.1-8.8% 0-0.16% 0-0.3%

0-8.7%57 0.7-7%61-65 0-8.1% 0.32-1.21% 0-0.6%

Abbreviations: LRYGB, laparoscopic roux-en-y gastric bypass; LAGB, laparoscopic adjustable gastric banding; VTE, venous thromboembolism; LSG, laparoscopic sleeve gastrectomy; MR, marginal ulcer.

exertional dyspnea, OSA, OHS, PE, and aspiration pneumonia. Obesity hypoventilation syndrome is associated with abnormalities of pulmonary physiology from long-standing severe obesity, pulmonary hypertension, right-sided cardiac failure, and abnormalities of arterial gas exchange at rest. These patients have high resting arterial PCO2 levels, depressed arterial PO2 levels, elevated hematocrits, and dyspnea at minimal exertion or at rest. They are at high risk of pulmonary complications from any surgical intervention, and have an increased risk for VTE complications as well.72,73 Preoperative blood gas levels, intensive care unit (ICU) or step-down continuous monitoring postoperatively, and consideration of pulmonary artery catheter monitoring in the postoperative setting are all appropriate for severe OHS74 (Figure 2). These patients are at a

greater risk of rapid oxygen desaturation, difficulty with mask ventilation, and laryngoscopy/intubation. Before induction of anesthesia, both reverse Trendelenburg position and CPAP should be applied to improve preoxygenation and mask ventilation.75 Elevating the upper body and head of a morbidly obese patient aligns their sternum and ear in a horizontal line (‘‘ramped position’’) and results in an improved laryngoscopic view.77 The ‘‘ramped position’’ is obtained by placing blankets under the patient’s upper body. Moreover,  the reverse Trendelenburg position (>30 ) may also improve ventilation by decreasing impaired diaphragmatic excursion caused by increased intra-abdominal pressure (IAP). This position also reduces the risk of aspiration by lowering IAP. In addition, optimal preoxygenation avoids rapid desaturation. The use of CPAP to maintain a positive end-expiratory pressure of 10 cm H2O during induction may prolong nonhypoxic apnea by 50% in the morbidly obese patient.78 Both strategies, reverse Trendelenburg position and CPAP, may improve pulmonary gas exchange. The new video laryngoscopies may improve the laryngeal view depending on the anesthesiologists’ expertise and may be an alternative to the Macintosh laryngoscope for intubation. If awake intubation is deemed necessary, intubation should be performed with fiber-optic bronchoscope after providing adequate topical anesthesia and sedation with short-acting drugs, such as remifentanil.75

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Bariatric Surgery

Non-OSA or

- Moderate to severe OSA

Obesity Hypoventilation-

Mild OSA

- BMI > 60

syndrome

-Baseline pulse-

-Baseline pulse oximetry and -Preoperative blood gas

oximetry

capnography

-Consideration of

-Prepare to use own CPAP mask Continuous oximetry

pulmonary artery catheter monitoring -Prepare to use own CPAP

monitoring

mask

Continuous monitoring with CPAP in ICU setting Hypoxemia

No

Yes Patients can be safely discharged from-

Increased FiO2

the monitored setting once: Continuous oxymetry monitoring

1.Oxygen saturation > 90% can be maintained on room air including during-

Hypoxemia

No

Yes

sleep 2. There is no hypoxemia/airway-

CPAP

obstruction when the patient is leftUndisturbed 3. Patients no longer require parenteralnarcotics

Figure 2. Algorithm for perioperative airway management after laparoscopic bariatric surgery.73-76

Postoperative monitoring and care of morbidly obese patients after bariatric surgery. Bariatric patients are at increased risk of perioperative pulmonary complications including atelectasis, pneumonia, and acute respiratory failure (ARF; Figure 2). The overall incidence of ARF after bariatric surgery remains low. However, when it does occur, it is associated with significant morbidity and mortality. Masoomi et al79 demonstrated that the overall ARF rate was 1.35% in the Nationwide Inpatient Sample database, from 2006 to 2008. A total of 304 515 patients underwent bariatric surgery during the 3-year period. The greatest rate of ARF (4.10%) was observed after open gastric bypass surgery. The ARF rate was lower after laparoscopy (0.94% vs 3.87%,

respectively for laparoscopy and open approach; P < .01) and after nongastric bypass versus gastric bypass (0.82% vs 1.54%, respectively; P < .01). Using multivariate regression analysis, congestive heart failure (adjusted odds ratio [AOR] 5.1), open surgery (AOR 3.3), chronic renal failure (AOR 2.9), gastric bypass (AOR 2.5), peripheral vascular disease (AOR 2.4), male gender (AOR 1.9), age >50 years (AOR 1.8), alcohol abuse (AOR 1.8), chronic lung disease (AOR 1.6), diabetes mellitus (AOR 1.2), and smoking (AOR 1.1) were factors associated with greater rates of ARF. Compared to patients without ARF, patients with ARF had significantly greater in-hospital mortality (5.69% vs 0.04%, P < .01).

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Morbidly obese patients are predisposed to basal atelectasis because of a reduction in forced vital capacity and forced expiratory volume.80 Atelectasis typically manifests during the immediate 24 to 48 hours after surgery and can present with mild tachypnea, fever, leukocytosis, and loss of lung volume on one or both sides on a CXR. Untreated, it may progress to a basal bronchopneumonia. Prevention includes optimal pain management, early ambulation, and aggressive incentive spirometry usage. All maneuvers attempt to reduce the tendency of atelectactic collapse by increasing forced vital capacity. Postoperative monitoring of the bariatric surgical patient with OSA depends on a variety of factors including type of procedure, approach (laparoscopic vs open), severity of sleep apnea, patient comorbidities, and individual facility capabilities. Minimum requirements include pulse oximetry and/or capnography in the postanesthesia care unit and in the surgical ward. The majority of patients with OSA can be safely monitored in this fashion.76 Select higher risk patients, including males, BMI > 60, and severe OSA, may require monitoring in an ICU setting (Figure 2). In these high-risk patients, CPAP should be strongly encouraged preoperatively to allow for accommodation of the therapy and placed relatively early in the postoperative course. Use of CPAP use should be continued until clinical evaluation demonstrates resolution of OSA. Patients should be allowed to bring their CPAP machines, or at least their masks, to allow for appropriate fitting of the device. Venous thromboembolism complications. Patients with high risk of VTE include those with lower limb venous stasis, BMI > 55 kg/ m2, history of previous VTE, and OHS with a mean pulmonary artery pressure 40 mm Hg. Pulmonary embolism must be considered in any postoperative patient with diaphoresis, tachycardia, or hypoxia, especially in the absence of a fever or leukocytosis. Findings may be indistinguishable from pulmonary atelectasis or intestinal leak. Occasionally, findings may be subtle and include, mild shortness of breath or pleuritic pain on deep inspiration. Confirmation with computed tomography pulmonary angiography (CTPA) should ideally precede institution of therapeutic anticoagulation to prevent the risk of hemorrhage. The CTPA was more useful for detection of acute PE when compared to ventilation-perfusion (V/Q) scanning and PA.81 The V/Q scanning may need to be used in patients with major renal impairment or anaphylaxis to intravenous contrast. Magnetic resonance angiography may serve as an alternative imaging modality.82 When a VTE is detected, patients are treated with anticoagulation. Standard treatment is 3 to 6 months with warfarin therapy unless an underlying coagulation disorder is uncovered or the risk is longer. New evidence has shown that following D-dimer levels in patients with PE may help predict the duration of anticoagulation therapy.83 Inferior vena cava filter. In a minority of patients with VTE, anticoagulant therapy may be contraindicated. Because patients with an acute episode of VTE are at substantial risk

of recurrence in the absence of anticoagulation, IVCF represents a valuable treatment option.52,84 The 2012 American College of Chest Physicians Evidence-Based Clinical Practice guideline recommends placement of an IVCF in patients with acute proximal lower extremity DVT in whom anticoagulation is contraindicated.85 Once the bleeding risk resolves, a conventional course of anticoagulation therapy should be administered. Similarly, the British Committee for standards in hematology considers IVCF in cases where anticoagulants are contraindicated.86 Any patient with recurrent VTE, despite anticoagulation should be carefully evaluated for causes of recurrent VTE prior to considering IVCF placement. Failures can occur because of subtherapeutic anticoagulant doses or hypercoagulable syndromes (eg, antiphospholipid syndrome) that require more intensive or alternative forms of anticoagulation. Heparininduced thrombocytopenia is a common cause of early anticoagulation failure. In this prothrombotic immune thrombocytopenia, patients typically present after a recent hospitalization with new moderate thrombocytopenia and a new thrombotic event. Use of heparin in this setting can result in worsening thrombocytopenia and progressive thrombosis. The only effective therapy is to discontinue all forms of heparin exposure and initiate therapy with a direct thrombin inhibitor (lepirudin, argatroban, or bivalirudin) or possibly fondaparinux. Systemic thrombolysis of proximal DVT (particularly iliofemoral or IVC thrombi) has been temporally associated with several cases of fatal and nonfatal PE. Therefore, prophylactic placement of IVCF has been proposed as a strategy for preventing PE from IVC thrombi released as a result of thrombolysis. Clinicians should consider filters on a case-by-case basis after reviewing the patient’s risk of embolization (eg, poorly adherent IVC and iliac thrombi) and mortality from PE (eg, patients with concomitant PE and those with limited cardiopulmonary reserve). Rhabdomyolysis (RML). Rhabdomyolysis typically affects the super-obese male patient who lies supine during a long operative procedure. In bariatric surgery, RML occurs due to prolonged muscle compression in many nonphysiological surgical positions but mainly in procedures longer than 4 to 5 hours.87 Rhabdomyolysis can be defined as a disorder that consists of striated muscle disintegration. This results in the release of muscle toxic cell constituents, myoglobin, and intracellular enzymes into the bloodstream, which leads to electrolyte imbalance, hypovolemia, and acute kidney injury. The incidence may be as high as 6% after bariatric surgery.87-89 Renal failure may be seen in up to 33% of all cases with RML and patients who develop acute renal injury are at an increased risk of death (up to 50%). In a recent meta-analysis,89 risk factors for developing RML include male gender (53% in the RML group compared to 29% in the non-RML group, respectively [P < .0001]), higher mean BMI (52 [range 45-67] vs 48 [range 42-56] kg/m2, P < .01), and longer operating time (255 [range 221-342] vs 207 [range 173251] minutes, P < .01). Other important factors include the

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Figure 3. Algorithm for risk stratification of rhabdomyolysis (RML) in bariatric surgery. Adapted from Chakravartty et al.89

presence of diabetes, treatment with statins, and ASA physical status >II.90 In establishing risk stratification, a creatinine kinase (CK) of >5000 and postoperative myalgia have led to increased risk of acute renal failure which can have a higher mortality. Patients with an epidural may not complain of pain, and therefore regular postoperative CK levels may be required in nonambulatory patients in order to identify RML early. Routine CK measurements should also be considered in high-risk patients (BMI > 50 kg/m2, operating time >4 hours; Figure 3). The diagnosis can often be delayed due to postoperative analgesia, late extubation, and preexisting myoskeletal symptoms. The morbidly obese patient often has discomfort in the lumbar and gluteal region. Laboratory and imaging tests must be done to confirm RML (Figure 4). Once RML is suspected, the diagnosis can be confirmed by identifying high levels of creatinine phosphokinase (CPK). A serum CPK 5 times the normal value is considered a biochemical diagnosis of RML.88 An elevation in the CPK level is the most sensitive diagnostic evidence of muscle injury and is present in 100% of cases with RML.87,89 The classic pattern of laboratory findings when RML is present as follows: 1.

Myoglobinuria provokes a typical reddish-brown or tea color. Khuara et al91 found in a prospective study that a urine myoglobin concentration >300 ng/mL was associated with an increased risk of RML and ARF.

2.

3. 4. 5.

6. 7. 8.

9.

Urinalysis in patients with RML will also reveal the presence of protein, brown casts in tubules, and uric acid crystals. Increase in blood urea nitrogen and creatinine due to prerenal ARF from dehydration and myoglobinuria. Increase in serum levels of potassium and phosphate as these components are released from cells. Serum calcium initially decreases as calcium moves into the damaged muscle cells, and then gradually increases during the recovery phase due to the release of calcium from injured muscle and elevated 1,25dihydroxyvitamin D levels. Severe hyperuricemia may develop because of the release of purines from damaged muscle cells. Coagulation studies are useful for detecting any indication of disseminated intravascular coagulation. Serum aspartate aminotransferase, alanine aminotransferase, aldolase, troponin I, and lactate dehydrogenase enzymes can increase due to muscular injury. Hypoxemia and metabolic acidosis is detected from arterial blood gas analysis. Venous bicarbonate lesser than 17 mmol/L is significantly predictive of acute renal failure development.92

Aggressive treatment must be immediately initiated to avoid complications (Figure 4). The first step is to preserve the affected zones and avoid RML in new areas of pressure,

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Figure 4. Algorithm for diagnosis and treatment of rhabdomyolysis (RML) in bariatric surgery.127

encourage early ambulation, and the use of special mattresses or pneumatic beds. Early administration of fluid, bicarbonate, and mannitol must be started to prevent volume depletion, tubular obstruction, aciduria, and free radical release. All of these are the causes of renal failure. Treatment of RML requires aggressive administration of fluids to ensure urine output >1.5 mL/kg/h or 150 to 300 mL/h until myoglobinuria has ceased.87,88 Maintaining a urine output this high may require intravenous infusion of fluids between 500 and 1000 mL/h. Dialysis is necessary if the kidneys no longer respond to the above-mentioned supportive measures and severe renal dysfunction has set in. Dialysis is indicated in patients with overt hyperkalemia and acidosis. Decompressive fasciotomy, muscular debridement, and escharotomies should also be considered in patients with evidence of compartment syndrome with neurovascular compression and decubitus ulcer if the compartment pressure is >30 mm Hg.93 Creatinine phosphokinase levels should be determined every 6 to12 hours, and all patients with RML require continuous electrocardiographic monitoring for signs of hyperkalemia or cardiac irritability.

Wernicke encephalopathy after bariatric surgery. Wernicke encephalopathy (WE) can occur after all types of bariatric surgical procedures and usually presents with the classic triad of confusion, ataxia with unsteadiness of gait, and nystagmus with diplopia. Wernicke encephalopathy typically follows a period of nutritional deprivation during which vitamin B1 is not supplemented. The usual clinical setting is a patient with nausea and vomiting for more than a week, or a patient maintained on a prolonged clear liquid diet postoperatively without oral multivitamin supplementation, or a patient on intravenous feeding, typically in the first 4 to 12 weeks after bariatric surgery.94 Wernicke encephalopathy has been reported more often in young women with persistent vomiting. Characteristic radiographic findings such as hyperintense signals in the periaqueductal gray area and the dorsal medial nucleus of the thalamus may be absent, making an early clinical diagnosis essential.95 Parenteral thiamine is the treatment of choice (500 mg every 8 hours). It is important to note that attempts to rehydrate the patient with a solution containing glucose that does not include thiamine may in fact precipitate and aggravate the neurological damage. Some authors recommend enteral or

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Post-bariatric surgery Suspected hemorrhage -

Tachycardia (sustained heart rate > 100 beats/min) Hypotension Fall in Hb or transfusion requirement > 2 U

Extra-luminal hemorrhage

Intraluminal hemorrhage (Hematemesis, Melena)

- Endosocpy

Unstable

± Laparoscopy for clamping bowel - ET in OR if unstable

Reoperation

Differential diagnosis (LRYGB) 1. 2. 3. 4.

G-J anastomosis Gastric pouch J-J anastomosis Gastric remnant

Stable

CT scan J-J hematoma

Reoperation

Trocar site Success and Stable

Staple line Mesentery

Observe

No success

Observe

Omentum Spleen

Stable

Unstable

Liver biopsy

Reoperation Figure 5. Algorithm for management of early postbariatric hemorrhage.

parenteral nutrition immediately after obesity surgery (such as the routine addition of thiamine 100 mg in addition to 1 mg folic acid and multivitamin to a 1 L bag of lactated Ringers intravenous fluids once a day for patients with bariatric surgery on a restricted oral intake) to ensure adequate thiamine supplementation and prevent this complication.96 The prognosis is favorable for most patients, but residual neurologic effects, including Korsakoff psychosis, memory loss, ataxia, nystagmus, and neuropathy, may persist in some patients. Early hemorrhage after bariatric surgery. Early postoperative GI hemorrhage after bariatric surgery is a potentially lifethreatening situation (Figure 5). Usually, this complication appears in the first 48 hours after surgery, when the patient is still

under the care of the bariatric specialist. However, with shorter hospital stays and earlier discharge policies, postoperative bleeding may present to the emergency department. Indications to return to the operating room for intervention include hemodynamic instability with a sustained heart rate >100 beats/min or a decrease in systolic blood pressure to 2 U, melena, or hematemesis will benefit from early surgical or endoscopic intervention. However, the site of bleeding and therefore corresponding control can be the challenge. The strategy for finding the site of bleeding is depicted in Figure 5. Early bleeding can be classified as either intraluminal or extraluminal bleeding. Most intraluminal hemorrhage will manifest with hematemesis or melena. Management is similar

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to any other cause of GI hemorrhage as in a nonbariatric patient. In all cases, management includes serial blood counts, adequate intravenous access, fluid and blood administration, stop of anticoagulants, monitoring of vital signs, and upper GI endoscopy in a safe, controlled, and monitored environment. This may be in the operating room or in an ICU setting. If the endoscopist is familiar with the anatomic changes related to the bariatric procedure, endoscopy might reveal bleeding from the staple line. Control can be obtained by adrenaline injection, electrocoagulation, or hemostatic endoclips.97 Endoscopic treatment has been very effective in most studies with 17% requiring a second endoscopic intervention.97,98 However, refractory bleeding from the gastric remnant or other more distal site can be difficult to reach endoscopically and may require surgical intervention. Hemorrhage from the staple line of the jejunojejunostomy (J-J) is often self-limited; however bleeding from this site can lead to an obstructing blood clot. This clot can lead to fluid filling the biliary limb and gastric remnant, thereby increasing pressure in the gastric remnant resulting in a potential leak from the staple line. Several bleeding sites can occur after bariatric surgery. The most common location is along staple lines. These include the gastrojejunostomy, gastric pouch, excluded stomach (gastric remnant), and J-J. The clinical presentation can help the endoscopist determine the bleeding site in some cases. Hematemesis most likely indicates bleeding from the gastric pouch or gastrojejunostomy. Melena most likely indicates distal bleeding from the J-J or excluded stomach staple line. Aspiration on induction of anesthesia is a major risk and must be taken into consideration prior to endoscopy. Maintaining the patient in a semiupright position with awake, fiber-optic intubation will reduce the risk of aspiration. Extraluminal bleeding can appear through a wound or drain. If the patient is hemodynamically unstable, an urgent reoperation is required. The bleeding source can vary but often is from the staple line, retrogastric vessels, short gastric vessels, omentum, splenic or liver injury, and trocar site.99 The laparoscopic approach is often employed but only where experience is available. Upper GI bleeding can occur any time after LAGB. Peptic ulcer disease, Mallory–Weiss tear, erosive gastritis, and esophagitis as well as band erosions can be a source. The initial treatment of upper GI bleeding after LAGB, as of any other GI bleeding, is a conservative therapy (adequate resuscitation, close monitoring, assessment of the severity of bleeding, blood transfusions, and emergency endoscopy when necessary). When surgery becomes necessary, the patient should be referred to the bariatric center, when the clinical situation permits.

common, SBO after laparoscopic bariatric surgery is caused primarily by nonadhesive disease. The most common cause of SBO in the bariatric patient is an abdominal wall or internal hernia.103 It may be difficult to identify small incisional hernias (trocar site hernia) in an obese patient. Physicians who are not adequately familiar with these alterations may be misled in their evaluation. Internal hernia is widely recognized as the most frequent cause of SBO (> 50%) in bariatric patients. There are 3 classic locations where SBO can occur after LRYGB: Petersen space (between Roux limb’s mesentery and transverse mesocolon), at the transverse mesocolon defect (in retrocolic Roux limb), and at the J-J Nasogastric decompression may be ineffective on a substantial portion of the GI tract (gastric remnant, biliopancreatic limb) and prolonged nonoperative management may be ineffective and dangerous (Figure 6). Other causes of SBO include constriction at a mesocolic defect, anastomotic strictures, intussusception, and volvulus or kinking of the gastric sleeve. Diagnosis is based on clinical presentation and radiologic imaging. Imaging may include plain abdominal X-ray, upper GI studies, and computerized tomography (CT) scan of the abdomen and pelvis. The CT has become the standard diagnostic tool and can demonstrate dilatation of the Roux limb, gastric remnant, or of the biliopancreatic limb, depending on site and cause of the obstruction. Laparoscopic exploration is usually the preferred initial approach and in the vast majority of obstructive complications the obstruction can be alleviated in this manner. The exploration should always include evaluation of bowel viability and often is performed in a retrograde fashion from the ileocecal valve toward the site of obstruction. If an internal hernia is found, gentle reduction should be performed with closure of the mesenteric defect. Early and aggressive management of intestinal obstruction after bariatric surgery is essential to prevent further morbidity and mortality (Figure 6). Acute dilatation of the gastric remnant after LRYGB is a potentially catastrophic event. This may lead to an accumulation of a large volume of digestive fluids with possible evolution to gastric wall necrosis and/or perforation. Obstructions may even manifest as pancreatitis or biliary obstruction. Severe epigastric pain and hypovolemic shock (evidenced by tachycardia) in conjunction with gastric dilatation on a plain abdominal X-ray or CT scan is diagnostic. Management includes urgent gastrostomy tube decompression (surgically or radiologically) and subsequent management of the underlying biliary limb obstruction (Figure 6).

Procedure-Specific Acute Complications 1.

Early Small Bowel Obstruction (SBO) after bariatric surgery. The incidence of SBO following open bariatric surgery has been reported to range from 1% to 5%.100,101 Similar rates have been reported with the laparoscopic approach (0.6%-2.7%).102 In a recent review of nearly 10 000 laparoscopic gastric bypasses, Martin et al reported an overall incidence of 3.6%.103 Unlike open bariatric procedures, where adhesive disease is more

Laparoscopic sleeve gastrectomy: 1.1. Gastric leaks represent one of the most dangerous complications of bariatric surgery. In the literature, the incidence of gastric leak after LSG ranges from 0% to 7%.104-106 Most leaks appear in the proximal third of the stomach, close to the esophagogastric (EG) junction or the angle of His. Burgos et al reported 85.7% of leaks in the

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Suspected obstruction - Persistent nausea,vomiting, or dysphagia - Abdominal colicky pain

Investigation: Abdominal X-ray, UGI studies ± CT abdomen with contrast

Clinical abdominal colicky pain - Operative if positive for SBO - LRYGB: Urgent decompression and explore if found gastric remnant dilatation

Post-LRYGB EGD G-J anastomosis stenosis: Endoscopic balloon dilatation

Clinical persistent nausea, vomiting or dysphagia

Post-LAGB Differential diagnosis: 1. Adjusted band too tight or 2. Slippage or 3. Food bolus - Immediate band deflation - IV fluid, PPI - EGD

Normal UGI study and/or Symptoms resolve Routine F/U

Post-LSG

Abnormal UGI study and/or Symptoms persist

EGD

Responder: Repeat dilation

Short-segment stenosis

Long-segment stenosis

EGD + Dilation ± Stent

- EGD + Dilation + Stent - Lap. Seromyotomy - Lap. RYGB

Non-Responder: Operative revision (LRYGB or Lap stricturoplasty)

Figure 6. Algorithm for management of postbariatric obstruction.

proximal third and only 14.3% in the distal third.107 Etiologies included are as follows:  

Final staple line is placed across the EG junction or distal esophagus causing poor staple line configuration. Devascularization by crossing staple lines in the critical area near the EG junction.

The signs and symptoms of a leak are similar to patients with other causes of abdominal sepsis. The clinical presentation ranges from an asymptomatic patient (identified by fluoroscopic study) to localized or generalized peritonitis (pain, fever

tachycardia, tachypnea, left pleural effusion, persistent hiccup, and pain in the left shoulder). Abdominal plain X-rays and contrast studies may assist in the diagnosis. If a surgical drain is present, amylase-rich fluid is often found. In certain cases, or in order to increase sensitivity, abdominal CT scan with oral Gastrografin can be helpful. The CT imaging can also provide additional information in regard to fluid collections or abscess in the left upper quadrant or the presence of subdiaphragmatic air. In hemodynamic instability or in patients with an uncontained leak, emergent operative intervention is often necessary (Figure 7). Laparoscopy is often the initial approach. The

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Post-bariatric surgery Suspected leakage

Investigation - Contrast studies - CT scans with contrast - Drain fluid amylase

- Unexplained tachycardia (> 100/min) - Fever (> 38°C) - Abdominal pain, Diaphoresis - Persistent hiccups, Oliguria

Unstable - Signs of sepsis

Stable

Uncontrolled

Controlled

Reoperation Laparoscopy or Laparotomy 1. Washout of the infected collection 2. Wide adequate drainage (closed suction or sump drains) 3. Feeding jejunostomy (if the patient is stable during the case)

More surrounding inflammatory reaction

Yes Omental graft

Adequate drainage

No Primary closure defect

± Endoscopic stenting (if test leak positive)

- PCD - Antibiotics - Nutritional support : TPN or NJ tube

Endoluminal therapies - Endoluminal stenting - Endoscopic clips - Fibrin glue - Bioabsorbable fistula plugs

Figure 7. Algorithm for management of postbariatric gastric leak.

operation includes peritoneal washout, identification of the fistula site, and closed suction drainage. Attempts at closure of the staple line defect is often fraught with failure secondary to the significant surrounding inflammatory reaction. The tissue often will not hold suture material. Use of omental fat to cover the area is recommended. Combined endoluminal therapy, in particular stenting, is often used to provide further diversion of oral content. Three main objectives should be accomplished: sepsis control, prevention of abdominal recontamination, and nutritional (parenteral and enteral such as feeding jejunostomy tube) support. In the presence of hemodynamic stability or a contained leak, nonoperative management is often used (Figure 7). This

approach is safe and consists of eliminating oral intake, initiating intravenous antibiotics, percutaneous drainage of a localized collection or abscess, and feeding parenterally or via a nasojejunal tube. If drainage is adequate, endoluminal therapies can be used to facilitate closure of the leak. This process often includes placement of endoscopic clips, fibrin glue, or bioabsorbable fistula plugs. Further diversion of oral contents can be accomplished by endoluminal stenting across the leak. However, current stent technology is not ideal for sleeve anatomy. Problems include different lumen diameters and the curvature of the gastric lumen. Before attempts at stenting, all extraluminal collections must be adequately addressed. Endoscopic management is successful

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50% to 100% of the time with stent migration rates of 8% to 58%.105,108-110

only independent risk factor for ulcer persistence after treatment.117 The most common presenting symptom is pain (63%) followed by bleeding (24%). Rarely a perforation can be the presenting sign. Pouch ulceration heals with proton pump inhibitors and/or sucralfate along with cessation of NSAIDs, smoking, or elimination of any other offending agent. In patients with a large pouch (in which acid production can still persist), ulcer recurrence with medical therapy alone is common. Consideration, in these cases, should be given to pouch size reduction along with ulcer excision. Occasionally, a chronic ulcer can lead to gastro-gastric fistula with persistent acid from the remnant bathing the ulcer and thereby preventing healing. The incidence of a perforated marginal ulcer is 1%. The clinical picture is similar to any other visceral perforation, with often severe epigastric pain, tachycardia, fever, and leukocytosis. Pneumoperitoneum is often seen on plain radiographs or CT scan. Surgical management is required and can be performed by laparoscopy or laparotomy. In cases with a chronic marginal ulcer, definitive therapy may require surgical revision of the anastomosis. Other strategies have included coverage of the perforation with an omental patch.118,119 A gastrostomy tube in the excluded stomach should be considered for enteral nutrition, and high doses of PPI are always used.

1.2. Obstruction after LSG: Sleeve stenosis can occur due to unintentional narrow tubularization of the stomach and is reported to occur in 0.26% to 4% of LSG operations.111,112 The management algorithm is shown in Figure 6. Patients presenting with persistent nausea, vomiting, or dysphagia should undergo an Upper Gastrointestinal (UGI) contrast study. If the study demonstrates an abnormal finding or if the symptoms persist over time, an esophagogastroduodenoscopy should be performed with anticipation of performing dilation. Repeat dilation can be performed as long as the patient demonstrates improvement in oral tolerance. Placement of a can also be considered. Stenting for a mechanical obstruction are often poorly tolerated due to pain and discomfort. Failure of progression to a normal diet warrants consideration of operative revision. Clinical significant short-segment stenoses may be treated successfully with endoscopic balloon dilation and stent. Long-segment stenoses are less likely to respond to endoscopic techniques and may ultimately require conversion to RYGB. 2.

Laparoscopic roux-en-y gastric bypass: 2.1. Anastomotic leak: The incidence is from 0% to 6.1%.113 The presentation is similar as leaks in sleeve gastrectomy. The diagnosis is often made with contrast imaging (Gastrografin swallow or CT scan). Treatment often includes fluid resuscitation, antibiotics, analgesia, drainage, and endoluminal therapy. Surgical intervention should be considered in a hemodynamically unstable patient or in a patient with severe, persistent symptoms. Intense washout of the abdominal cavity and multiple drain placements should be considered (Figure 7). Laparoscopy often identifies the site and allows for adequate washout and drainage. 2.2. Marginal ulcer is often seen at the gastrojejunal anastomosis and can occur early (1-3 months) or late after LRYGB. It is located either on the gastrojejunal anastomosis (50%) or the jejunum (40%).114 Its reported incidence ranges between 0.3% and 16%, and several risk factors are often identified (operative technique, type of absorbable/nonabsorbable suture, patient age, history of previous gastric surgery, preoperative diabetes, coronary artery disease, prior peptic ulcer disease, and use of nonsteroidal anti-inflammatory medications or tobacco).115,116 In a large cohort study, prior or current tobacco use remained the

3.

Laparoscopic adjustable gastric banding: 3.1. Slippage: Slippage of the adjustable gastric banding is the most common leading to reoperation. It can develop early or late, but most often occurs late in the postoperative period with a reported incidence of 1 to 20.120-123 Acute abdominal pain, vomiting, and eventually obstructive symptoms characterize an acute slippage. The bariatric surgeon usually manages this complication with deflation of the system and possible urgent reoperation (Figure 6). Radiological imaging shows the band in a horizontal orientation, and when contrast is orally administered the gastric pouch is enlarged with slow passage of contrast and significant reflux. Emergency treatment consists of complete band deflation through the subcutaneous port, nothing per mouth, and intravenous administration of fluids, antiemetics, and proton pump inhibitors. This should allow for significant symptom improvement andreferral to a bariatric center. If symptoms persist or worsen, signs of gastric obstruction or necrosis should be sought after. This includes the presence of tachycardia,

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Journal of Intensive Care Medicine complications that are either specific or nonspecific procedure related. Bariatric surgeon consultation should be obtained early, and referral to a bariatric center should be taken into consideration at any time if permitted by the patient’s conditions.

Postoperative adjusted gastric banding Suspected Band erosion - Recurrent port site infection

Declaration of Conflicting Interests 1. 2. 3. 4. 5.

Abdominal X-ray Contrast swallow Culture and antibiotics Diagnostic puncture, abscess drainage and port removal Referral to bariatric center

Figure 8. Postlaparoscopic adjustable gastric banding (LAGB) band erosion.

inability to tolerate saliva, or a raised lactate level and acidosis. If any of these signs or symptoms persist, emergency surgery is required. 3.2. Gastric band erosion: Intraoperative gastric wall trauma and tight band placement may account for early erosion. High band pressure, band overinflation, and dietary noncompliance can lead to late band erosion. Band removal is mandatory because of the risk of infectious complications as well as hemorrhage (Figure 8). The incidence ranges from 0.8% to 4%.124,125 Most cases do not require emergency surgery, as the erosion is often over a long period of time with the capsule and inflammatory process walling off the erosion. Chronic melena, anemia, and the absence of abdominal symptoms with a loss of restriction or even weight regain are often seen in a latent band erosion. Exsanguinating hemorrhage from an eroded band has been reported.126 Port site infection may also be a sign of band erosion, as the infection transcends from the gastric lumen to the subcutaneous port. Acute port infection, with evident local signs, such as port site inflammation, abscess, or cutaneous fistulas, requires urgent surgical drainage and referral to the bariatric center for further investigations. Upper endoscopy is the best test in determining whether an erosion exits or not.

Conclusion Obesity is characterized by a chronic proinflammatory state, changes in cellular immunity, hypercoagulability, and insulin resistance. A thorough understanding of these physiologic derangements are required in order to safely and effectively manage the bariatric patient undergoing complex operations with the potential of complications. Knowledge of the presentation of these complications is necessary in order to effectively diagnose and treat them. After initial resuscitation, a systematic stepwise approach should be performed in order to identify

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.

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