Section 5: Specialty Consultation—What the Consulting Hospitalist Needs to Know

INTRODUCTION

Obesity is a global problem and a major contributor to morbidity and mortality in the United States. The World Health Organization (WHO) estimates that 1.9 billion adults worldwide are overweight (BMI > 25 kg/m²) and 600 million are obese (BMI > 30 kg/m²). In the United States, 67% of adults are overweight, 35% of adults are considered obese, and 6.4% are morbidly obese (BMI > 40 kg/m²). While there is increasing knowledge about obesity and efforts to reduce the epidemic in the United States, the prevalence of obesity has remained largely unchanged over the past 10 years. In addition, the number of obese children has more than doubled over the past 3 decades to 17%. The more than 50 million obese Americans are at risk of developing numerous obesity-related health problems, including hypertension, diabetes, and coronary artery disease (Table 63-1).

Currently, the annual cost for treating obesity and its related comorbid conditions are estimated at $147 billion and those who are obese have approximately $1400 more in annual medical costs. Obesity accounts for more than 100,000 premature deaths annually and is considered the second most preventable cause of death after cigarette smoking.

To date, surgery is the most effective means of achieving and maintaining long-term weight loss in obese patients. It is also consistently found to be more effective than medical weight loss alone for the improvement or remission of type 2 diabetes and other major comorbid illnesses. In a 2014 Cochrane Review of randomized controlled trials, all seven included trials comparing outcomes of bariatric surgery to nonsurgical interventions found significantly more weight loss in the surgical groups (weight loss is often measured as percentage of excess body weight loss, EBWL, calculated as weight loss/excess weight × 100). Another meta-analysis including more recent trials showed that the mean decrease in BMI for all bariatric surgical procedures was 13.4 kg/m² with 55% of EBWL, and 65% of patients experienced remission of diabetes. These outcomes are far superior to medical interventions for obesity and its associated comorbid conditions as long-term maintenance of more than 10% EBWL is uncommon with diet, exercise and other medical interventions alone.

INDICATIONS FOR REFERRAL FOR BARIATRIC SURGERY

Based on the 1991 consensus statement on bariatric surgery for morbid obesity issued by the NIH, it is recommended that patients who have failed lifestyle and medical interventions with a BMI greater than 40 kg/m² or 35 kg/m² with two or more significant obesity-related comorbidities (Table 63-1) be referred to a bariatric surgeon.

PREOPERATIVE RISK ASSESSMENT SPECIFIC TO BARIATRIC SURGERY

Once a patient has been referred for bariatric surgery, a thorough screening must be conducted by a multidisciplinary team, to determine eligibility for surgical management (Table 63-2). Bariatric teams include specialists from bariatric medicine, bariatric surgery, nutrition and behavioral medicine.

Nutrition counseling is extremely important preoperatively to educate the patient about healthy eating habits that lead to long-term success. These habits include regular eating patterns throughout the day (no skipping meals), intake of an adequate amount of protein at each meal so that total protein intake per day is 40 to 60 g, avoidance of high-carbohydrate snack foods that could lead to dumping syndrome after intestinal bypass procedures, and the need for lifetime vitamin supplementation. Patients are also taught that the intense effects of bariatric surgery (such as repression of hunger and decreased appetite) are time-limited to approximately 2 years after surgery. Therefore, long-term success requires permanent lifestyle changes, including modifications in eating habits, dietary changes, and increased exercise and physical activity.

In addition to being seen by a nutritionist, prospective patients are seen by a psychiatrist, psychologist, or social worker during the initial evaluation process to determine the patient’s capacity to fully understand the risks and benefits of a life-changing operation. These patients are also counseled on mindful eating; that is, they need to understand whether they are eating to satisfy hunger or to satisfy an emotional need. Counseling may also include addressing the prospective patient’s expectations for weight loss, health outcomes, as well as the psychosocial impact of bariatric surgery.

The psychiatrist/psychologist/social worker must also be able to identify if any overt psychoses or mental illnesses are present that would require treatment before surgery. Eating disorders, such as binge eating, are screened for since they are associated with poor outcomes after bariatric surgery. Also important is identification of any signs of substance abuse or severe situational stress that would adversely affect the patient after surgery and hinder compliance with strict dietary and lifestyle modifications. Smoking cessation is strongly encouraged for roux-en-y gastric bypass and biliopancreatic diversion and some surgeons will decline performing such procedures if continuing to smoke, as it places patients at a higher risk of ulcer formation at the gastrojeunostomy and GI bleeding. It is important that patients seriously considering bariatric surgery are evaluated to determine whether they would be able to comply with a strict postoperative diet and lifestyle change, whether they have a support system in place, and whether or not long-term follow-up is in place before surgery.

Since morbidly obese patients have had poor results and often-negative experiences with exercise, it is important that physical activity, both aerobic and strength training, be stressed. It is often extremely helpful for patients to be seen by a clinical exercise physiologist to receive advice on implementing an exercise regimen and the benefits of combining cardiovascular activity with strength training. In addition, a clinical exercise physiologist can offer strategies to compensate for weight bearing joint pain during physical activity. These referrals are often quite helpful in reducing barriers to adopting exercise programs, which are necessary for long-term success after any bariatric procedure. Although the help of an exercise physiologist may be quite beneficial, not all bariatric programs have one in their multidisciplinary team, since it is not yet a requirement. When this is the case, it is important for the physician to refer a patient to a clinical exercise physiologist who is certified by the American College of Sports Medicine. Referrals are especially useful for patients with multiple medical problems. Often exercise physiologists working in the cardiac or pulmonary rehabilitation units within the same health care system can be helpful in guiding patients in their exercise regime. When severely overweight individuals begin an exercise program, early weight loss is often quite remarkable. This weight loss can be a strong positive reinforcement for an individual. After significant weight loss though, the effect of exercise becomes less impressive.

The remainder of the preoperative assessment focuses on factors that predispose the patient to increased surgical risk such as age, cardiovascular risk factors (coronary artery disease, congestive heart failure, cardiomyopathy, hypertension, pulmonary hypertension), pulmonary risk factors (asthma, obstructive pulmonary disease, obstructive sleep apnea, smoking), and vascular risk factors (venous stasis, hypercoaguable states secondary to obesity, prior deep venous thromboses, use of oral contraceptives). Some imaging studies such as right upper-quadrant ultrasound and contrasted upper GI may be ordered depending on the patient’s clinical history of biliary colic or hiatal hernia, for which the patient may benefit from cholecystectomy and repair of the hiatal hernia at the time of surgery.

There are few absolute contraindications for surgery, but severe cardiopulmonary disease based on the preoperative work-up may prohibit bariatric surgery if the operative mortality is deemed significant. Patients who weigh >500 pounds are at an increased risk of complications and death, and may require hospitalization prior to surgery for monitored weight loss. Inability to walk is also a contraindication. There is no defined age cut-off and it may be determined by surgeon preference and assessment of potential longevity to have a meaningful benefit from surgery.

BARIATRIC SURGICAL PROCEDURES

Bariatric surgical procedures are proposed to work in two primary mechanisms—restriction (reduces intake of food) and malabsorption (limits absorption of food); although other physiologic mechanisms have been proposed, they are not entirely understood. Alterations in ghrelin and incretin are also demonstrated, which act to increase satiety and postprandial insulin levels, respectively.

ROUX-EN-Y GASTRIC BYPASS

The Roux-en-Y gastric bypass (RYGB) is currently the most common bariatric procedure performed worldwide and is primarily performed laparoscopically. The procedure consists of creating a small gastric pouch (approximately 30 mL) and creating a gastrojejunal anastomosis with roux-en-y anatomy, leading to bypass of the duodenum of ingested food (Figure 63-1). Its efficacy was once thought to be due to its restrictive mechanism, but it is also effective due to the exclusion of the first part of the small bowel, decreasing incretin release. Now that most are performed laparoscopically, most patients are discharged in 2 to 3 days postoperatively. The Swedish Obese Subjects Study, the largest study on weight loss surgery to date with the longest follow-up, reports a mean percent weight loss of 32.5% of total body weight (percent of total weight loss is roughly equal to half of EBWL) 1 to 2 years after gastric bypass and 25% 10 years postbypass. A 2004 meta-analysis by Buchwald et al. reported an average weight loss of 46 kg and a mean EBWL of 61.6% after 1 to 2 years, which is comparable to the Swedish Obese Subjects Study.

Roux-en-Y gastric bypass also provides excellent improvement and even remission of comorbid conditions (Table 63-3). A meta-analysis showed >80% of patients with diabetes undergoing RYGB had remission of their diabetes and >90% demonstrated improved glycemic control, with remission defined as discontinuation of all diabetes-related medications as well as the ability to maintain blood glucose levels within the normal range.

Roux-en-Y gastric bypass patients also have remission of their hypertension in 65% to 85% of patients. Hyperlipidemia, hypercholesterolemia, and hypertriglyceridemia are also greatly improved in >90% of patients after gastric bypass surgery, with total cholesterol levels decreasing by 0.96 mmol/L, LDL by 0.89 mmol/L, triglycerides by 1.07 mmol/L, and HDL increasing by 0.05 mmol/L. Obstructive sleep apnea is improved or resolved in 80% to 90%, and gastroesophageal reflux disease (GERD) is resolved in 85% of patients after RYGB. Although more difficult to quantify, patients have also reported improvements in depression, joint pain, stress incontinence, infertility, self-esteem, and overall quality of life.

SLEEVE GASTRECTOMY

Laparoscopic sleeve gastrectomy (SG) has recently gained popularity as an operation for weight loss and is now commonly performed. The procedure entails creating an elongated gastric tube that remains in continuity with the pylorus and duodenum, and the resected gastric remnant is removed (Figure 63-2). It was initially thought to be a purely restrictive procedure. However, a recent study by Peterli et al. has shown a post-SG impact on incretin secretion similar to post-RYGB and it reduces ghrelin, which increases satiety. Studies show that the weight loss achieved with sleeve gastrectomy is similar to RYGB. In a review series, 24 studies of 1749 patients demonstrated a mean EWL of 46.6% and low complication rate. A recent meta-analysis comparing RYGB to sleeve gastrectomy in 32 studies found that RYGB resulted in greater (but nonsignificant) weight loss and fewer complications/reoperations, but RYGB had significantly better reductions in HTN, cholesterol, GERD, diabetes, and arthritis.

There are occasions in which SG may be the procedure of choice in patients with relative or absolute contraindications for a bypass procedure or a malabsorptive procedure. These include patients with severe pre-existing iron deficiency anemia and other vitamin deficiencies that rely on adequate and specific anatomic small bowel surface area for absorption. Transplant patients and patients with inflammatory bowel disease on chronic steroids, and patients with severe osteoarthritis relying on NSAIDs are better candidates for SG due to the risk of anastomotic leaks and gastrojenunostomy ulceration with NSAID use. Small bowel length should be preserved in patients with inflammatory bowel disease.

LAPAROSCOPIC ADJUSTABLE GASTRIC BANDING

Laparoscopic adjustable gastric banding (LAGB) used to be the most commonly performed bariatric procedure, but has fallen out of favor in recent years due to the demonstrated superiority of other surgical procedures that offer restrictive and metabolic benefits, and due to the potential long-term complications of banding. The procedure involves placing an inflatable band around the stomach just below the GE junction and an injectable port is anchored below the subcutaneous tissue on the fascia that attaches to the band via a silastic tube. Saline is then injected into the port incrementally to provide increased restriction and limited intake (Figure 63-3). Although technically less challenging than RYGB, the LAGB requires frequent clinic visits in order to properly adjust the band with saline injections and maintain the proper amount of gastric restriction to achieve weight loss. Studies have shown good weight loss results with LAGB. The Swedish Obese Subjects Study reports 20% total body weight loss 1 to 2 years after LAGB and 14% 10 years postbanding. Meta-analysis data shows a similar 47.5% EBWL after 1 to 2 years and an average of 34.8 kg.

LAGB may also lead to remission and improvement in comorbidities although less so than the previously described methods because it is purely a restrictive procedure—it does not have physiologic or metabolic effects seen with bypass procedures or sleeve gastrectomy. Multiple studies report remission of diabetes in 50% to 80%, improvement and remission of hypertension in 45% to 70%, and improvement in hyperlipidemia, hypercholesterolemia, and hypertriglyceridemia in 60%, 80%, and 75%. Based on meta-analysis data, total cholesterol, LDL, and triglyceride levels decrease by an average of 0.3, 0.11, and 0.76 mmol/L, respectively, while HDL increased by an average of 0.12 mmol/L. Symptoms of sleep apnea improve in 95% of patients, and many also report improvements in menstrual irregularities and GERD after LAGB as well.

MALABSORPTIVE PROCEDURES

Malabsorptive procedures include jejunal-ileal bypass (which is now never performed), and biliopancreatic diversion (BPD) and duodenal switch (DS). In BPD-DS, the stomach is resected from the duodenum (pylorus preserved) and the intestinal tract is reconstructed to allow a short common-channel of small bowl anastomosed with the stomach and ileum just before the ileocecal valve, leaving about 250 cm of small bowel for absorption (Figure 63-4). Studies show that BPD-DS provides greater early weight loss than RYGB and sleeve gastrectomy, and data show superior weight loss in very obese patients (BMI > 50). A randomized study of 160 morbidly obese adults compared RYGB results to the results of their variation of BPD-DS. After 2 years, 100% of the BPD-DS patients maintained a greater than 50% EBWL while only 88.7% of RYGB patients were able to maintain similar weight loss. A smaller but more recent randomized trial of morbidly obese found after 5 years, total body weight loss was 40% in the BPD/DS group compared to 26.4% in the RYGP group, with the BPD-DS group losing a mean of 25 kg more than the RYGP group.

Although BPD-DS may be a more complex procedure, patients who undergo this procedure appear to have the best outcomes with regard to resolution of comorbidities. A randomized trial found at 2-year follow-up, glucose intolerance, hypercholesterolemia, hypertriglyceridemia, and sleep apnea had completely resolved in both the BPD-DS and RYGB groups; but in the BPD-DS, 100% experienced remission of diabetes (versus 70% of RYGB), 81% of hypertensive patients experienced normalization of blood pressures (versus 63% of RYGB), and changes in total cholesterol, LDL, and HDL in the BPD/DS group were significantly greater than in the RYGB group. Sleep apnea is also greatly improved after BPD-DS in 85% of patients. Additionally, although more difficult to quantify, patients have reported significant improvements in depression, joint pain, stress incontinence, infertility, self-esteem, and overall quality of life.

Although there is great improvement of comorbid conditions, this must be balanced against the increased likelihood for vitamin and nutritional deficiencies, and higher-operative mortality risk (1.1% for BPD/DS, compared to 0.1% for gastric bypass).

POSTOPERATIVE COMPLICATIONS OF BARIATRIC SURGERY

All bariatric surgery patients are at risk of developing the same postoperative complications as patients undergoing general surgery. General late complications from all abdominal surgery may occur including laparoscopic port site hernias or ventral hernias, and intra-abdominal adhesion formation. There are also several potentially life-threatening postoperative complications specific to bariatric surgery that clinicians need to be aware of in order to provide timely diagnosis and treatment.

EARLY POSTOPERATIVE COMPLICATIONS OF GASTRIC BYPASS

ANASTOMOTIC LEAK

Anastomotic leak (leak at the gastrojejonostomy or jejunostomy), although rare, is the most feared complication of bariatric surgery. Reported incidence after RYGB ranges from 0.5% to 5% but in most recent literature is often <2%. Risk factors include multiple comorbid conditions, smoking, and poor glycemic control. Smokers are counseled to quit smoking preoperatively and diabetics should keep their HgA1c < 7 preoperatively. Surgical technique risk factors include open gastric bypass technique, retrocolic anastomosis, single layer closure, and surgical revision.

Patients usually present in the first 3 days postoperatively with tachycardia, tachypnea, epigastric pain, and/or fevers. Tachycardia is an early sign, and often times the first and only sign of a leak. Diagnosis varies based on the institution, but usually includes UGI series with gastrografin and/or CT abdomen with oral contrast.

Based on the clinical status of the patient and the radiographic findings, surgeons may opt to treat the anastomotic leak conservatively or with reoperation. Conservative management includes keeping the patient NPO, on intravenous fluids, and antibiotics. If a collection is found on CT scan, this may be drained with CT-guided percutaneous drainage often performed by interventional radiology. Operative intervention is rarely indicated; however, when deemed necessary, many bariatric surgeons recommend placement of a Graham patch over the anastomosis and keeping the patient NPO until the leak heals. Resection and reanastomosis in this urgent setting is usually an extensive operation that is at high risk of releak given the inflamed tissue and contaminated surgical bed. A feeding gastrostomy tube may be placed into the remnant stomach at the time of reoperation if postoperative oral feeding is not anticipated for a prolonged period.

GASTROINTESTINAL BLEEDING

Gastrointestinal bleeding (GIB) is another complication that may occur early in the postoperative period. GIB during the first 72 hours is usually due to bleeding from the staple or suture lines. Risk factors include use of anticoagulation or antiplatelet therapy, and thick inflamed tissues, or thin tissues. Diagnosis of GIB in a postoperative RYGB patient is no different than diagnosis in any other patient; however, care must be taken in any invasive diagnostic technique performed, including nasogastric lavage and endoscopy. These procedures can distend the newly created gastric pouch and disrupt the staple or suture line. Most staple and suture line bleeding may be treated nonoperatively by keeping the patient NPO, providing fluid resuscitation, checking frequent hematocrits with administration of blood products as needed, and reversing any anticoagulation.

LATE POSTOPERATIVE COMPLICATIONS OF GASTRIC BYPASS

SMALL BOWEL OBSTRUCTION

Although rare, small bowel obstructions may occur after RYGB. The majority of intestinal obstructions after RYGB are due to adhesions, internal hernias resulting from small bowel herniating through one of the mesenteric defects created during the bypass, or kinking of the jejunojejunostomy. Symptoms can be typical of small bowel obstructions: abdominal pain, nausea, vomiting, and/or obstipation. However, they may be subtle with low-grade tachycardia and vague abdominal pain, accompanied by an abdominal exam that is difficult to assess due to body habitus. Clinical and laboratory findings are often nonspecific. Workup should consist of chemistries, complete blood count, radiologic tests including plain abdominal films, and CT scan of the abdomen with PO and IV contrast, which is the gold standard and should be done promptly if a SBO is suspected. If a mesenteric swirl is found on CT scan, an internal hernia—a loop of bowel herniated through an iatrogenic defect in the mesentery—should be suspected. Findings of an obstruction should prompt urgent surgical exploration; delay in doing so can lead to necrotic bowel or early perforation.

There should be a low threshold to surgically explore patients with previous RYGB who are suspected of having small bowel obstructions. There is little benefit to nasal-gastric tube placement in these patients. Before an operative intervention is undertaken, however, it is important to have imaging studies as a guide (CT scan is the gold standard). Laparoscopic exploration is feasible in the majority of these patients and a thorough exploration can be conducted to look for internal hernias or kinking of the jejunojejunostomy using this minimally invasive technique. Conversion to open surgery may occasionally be necessary. If an internal hernia or bowel kinking are found at the time of exploration, they can be fixed at that time. A revision of the RYGB can also be carried out as well in that setting if it is deemed necessary by the bariatric surgeon. If adhesions are present, they can be lysed at that time.

STOMAL STENOSIS

Stomal stenosis is another potential late complication of RYGB. Stomal stenosis is an anastomotic stricture at the gastrojejunostomy. The reported incidence is between 3% and 15%, making it one of the most common complications of gastric bypass. There is no clear single etiology of stomal stenosis. Risk factors include the method of creation of the anastomosis (circular stapler vs linear stapler vs hand-sewn), ischemia to the anastomosis, and marginal ulcers (discussed later). It most frequently occurs 4 to 6 weeks postoperatively, but may occur later, especially if the patient has developed a marginal ulcer. Symptoms of stomal stenosis include nausea, vomiting, dysphagia, and food intolerance.

The diagnosis of stomal stenosis may sometimes be made with history alone. However, it can be difficult to distinguish between someone who has stomal stenosis versus a patient who is eating too much, too quickly. Tests such as UGI or barium swallow may be of use to diagnose the condition; however, both tests lack sensitivity. Upper endoscopy can be both diagnostic and therapeutic and is a much more sensitive test.

Dilation of the stenosis using endoscopic balloon dilators remains the treatment of choice, and studies report 55% to 80% success. Complications such as perforation are uncommon and can be managed nonoperatively. Surgical repair or revision of the gastrojejunostomy is reserved for those who have complete obstruction or who have failed multiple attempts at endoscopic dilation. This is common when the stricture is due to ischemia or when long-term inflammation has been present, maturing the tissues into scar.

MARGINAL ULCER

Marginal ulcer, or ulcer at the gastrojejunostomy anastomosis, is also a potential complication of RYGB with rates ranging from 2% to 4% in recent studies. Marginal ulcers usually occur at the jejunal side of the gastrojejunostomy. These ulcers are thought to be due to exposure of gastric acid to the jejunal mucosa. Risk factors include NSAIDs, tobacco use, ischemia, H. pylori, alcohol, foreign body reaction, large gastric pouch, and gastrogastric fistula. Symptoms usually include unrelenting, severe epigastric pain, and patients may develop GI bleeding with hematemesis or melena. Endoscopy is the diagnostic treatment of choice and can be therapeutic if ongoing bleeding is present.

Treatment begins with acid suppression as well as treatment of the underlying cause, such as eradication of H. pylori, cessation of tobacco and alcohol, and starting an oral sucralfate slurry regimen. Patients must also be in maximal proton-pump inhibitor therapy, and many surgeons have patients on PPIs postoperatively. There is no definitive duration of such therapy, although studies have shown that 6 to 12 months appear to be adequate. Repeat upper endoscopy can help to guide therapy. If symptoms persist or if they become debilitating to the patient, surgical intervention may be warranted. Resection and revision of the gastrojejunostomy may be required to remove the ulcerated area. In the setting of an acute ulcer perforation, the patient should be taken to the operating room. Many bariatric surgeons opt for a Graham patch of the perforation in these cases. More extensive interventions are usually unnecessary and can potentially cause more problems.

GASTROGASTRIC FISTULA

Gastrogastric fistula (GGF) is a rare complication after RYGB. These are usually due to staple line disruptions and allow communication between the gastric pouch created for the RYGB and the excluded stomach. This communication allows gastric acid to flow from the excluded stomach to the gastric pouch and down into the jejunum. GGF are extremely rare, with a reported incidence ranging from 1% to 2%. Symptoms include heartburn, epigastric pain, nausea, and weight regain. Several options exist for the treatment of GGF including endoscopic injection of fibrin glue, endoscopic plication/suturing, and endoscopic clipping. Surgical interventions all start with resection of the fistula tract. Some surgeons separate the pouch from the excluded stomach via stapling or oversewing or resection. Others prefer to resect the excluded stomach all together to prevent any future GGF from forming.

POSTOPERATIVE COMPLICATIONS OF SLEEVE GASTRECTOMY

One of the most common early side effects of SG is significant nausea and emesis, occurring more frequently than other bariatric procedures. This can usually be managed with antiemetic agents, and symptoms tend to improve within the first month. Rarely patients may require rehospitalization for IV fluids and IV anti-emetics with gradual return to their diet.

Similar to RYGP, other important early complications include bleeding and leak at the staple line, and are managed the same way. Long-term complications of SG include sleeve stenosis and severe reflux. Stenosis occurs in less than 1% of patients, although the long-term data is limited. Stenosis most often occurs at the incisura angularis, and the clinical presentation includes symptoms of reflux; as the stenosis worsens symptoms include dysphagia and vomiting. It can be easily diagnosed with an upper GI contrast study, and can be managed by endoscopic dilation if identified early, but if presenting with severe symptoms may be operatively managed with conversion to RYGP.

POSTOPERATIVE COMPLICATIONS OF BILIOPANCREATIC DIVERSION-DUODENAL SWITCH (BPD/DS)

Mortality rates after BPD-DS are 0.9% to 1.1%. Similar to RYGP, postoperative risks include anastomotic leaks and marginal ulcers. In two meta-analyses, the leak rates were cited between 0.1% and 1.8%. The clinical symptoms, diagnosis and management are the same as previously mentioned. Marginal ulcer formation has become less common with efforts to preserve the pylorus when dividing the stomach with duodenal switching.

The most common postoperative complications result from malabsorption side effects. Bloating, abdominal pain and diarrhea are not uncommon; BPD-DS causes significantly higher rates of diarrhea compared to RYGP, with 63% reporting significant social limitations secondary to altered bowel function. One of the most common and potentially severe complications of ongoing malabsorption is protein malnutrition, occurring in 11.9% of patients and may require parenteral nutrition. Short term reoperation rate for BPD-DS is 4%, often from protein malnutrition; 44.8% of patients undergoing BPD-DS within 5 years require additional operative interventions related to the initial procedure, some due to severe protein malnutrition. This involves reversal of the BPD completely or lengthening the common channel to allow for more surface area for absorption. A late complication potential is Wernicke’s encephalopathy, which may result if the malnutrition is slower and later in onset. Vitamin deficiencies (reviewed later) are a common complication of BPD-DS.

POSTOPERATIVE COMPLICATIONS OF ADJUSTABLE GASTRIC BANDING

Several adjustable gastric band complications are possible and can either occur early or late. The mortality of AGB is <0.1%, but there are a number of potential complications including port or port-site infection, band infection, band slippage or gastric prolapse, hiatal hernia, band erosion and fibrosis. Banding is done less commonly due to its many complications; many now opt to remove the band and convert the patient to a RYGB or sleeve gastrectomy.

INFECTION

Port and port-site infections may initially be treated with antibiotics. If these infections occur in the late postoperative period, a prompt upper endoscopy is indicated to exclude a gastric erosion. The intra-abdominal portion of a band may also become infected both in the early and late postoperative period. Patients may initially present with port or port-site infections that do not resolve despite antibiotic treatment. As the infection progresses patients may develop fever, abdominal pain, abscesses, and peritonitis. Treatment is removal of the infected band. Patients should have intraoperative tests to determine whether there is a leak from the stomach or esophagus. Antibiotics are also warranted for 7 to 10 days postoperatively. Bands can usually be replaced after 3 months.

GASTRIC PROLAPSE OR BAND SLIPPAGE

Gastric prolapse or band slippage occurs in approximately 5% of patients, but was as high as 15% for earlier techniques employed for placement in the 1990s. This phenomenon refers to the cephalad herniation of the gastric fundus through the band. Symptoms of band slippage are secondary to a gastric outlet-type obstruction and include nausea, heartburn or reflux, and the inability to swallow liquids. Some patients may complain of erratic function of the band; some days they feel no restriction, whereas other days they are unable to eat anything. These symptoms of gastric prolapse and/or band slippage can sometimes be relieved by removing some of the fluid from the band. In patients with worsening or persistent symptoms and in patients in whom removing fluid from the band does not improve symptoms, urgent surgery is required to either remove the band or move the band to the correct position on the stomach. After reduction of the prolapse, it is important to test the stomach and esophagus for evidence of leak. If uncorrected, a functional stenosis may develop causing distal esophageal dilation.

HIATAL HERNIA

Hiatal hernias can be found preoperatively on UGI series. If found preoperatively, these hernias should be repaired at the time of placement of the adjustable gastric banding. Occasionally hiatal hernias are found intraoperatively at the time of the dissection performed to free the right crus. If hiatal hernias are not fixed at the time of band placement or develop after band placement, patients may have symptoms of heartburn and reflux when the band is tightened. These symptoms tend to be alleviated with loosening of the band. If symptoms are persistent or weight loss is suboptimal due to the small amount of fluid in the band, repair of the hernia is indicated. This often requires removal and replacement of the band in addition to repair of the hiatal hernia.

BAND EROSION

Erosion of the gastric wall by an adjustable gastric band can occur after the first few weeks of placement or after a prolonged period. Incidence of band erosion is between 0.5% and 1%. Early erosions are thought to be secondary to unrecognized operative trauma to the stomach and may be considered an intraoperative injury more than a true band erosion, but may be secondary to the band being too tight. These patients can present with peritonitis requiring emergent operation; however, the large majority of patients with band erosions have a silent, chronic course that may present with abdominal pain or port-site infection. A typical course of band erosion develops over months to years. As the gastric secretions slowly leak out, the body develops a local inflammatory response. The inflammation eventually tracks out to the subcutaneous port and skin via the tubing that connects the band and the port, leading to local port-site infection. The development of gastric ulcers can also lead to band erosion. Patients with band erosions often do not have overt symptoms; instead they often present with failure of the restrictive properties of the band and/or a nonfunctioning band.

Diagnosis of band erosion is best made with upper endoscopy. Most erosions occur between the gastric fundus anteriorly and the band at the location where the fundus has been plicated over the band. UGI series are rarely useful in diagnosing band erosion.

Treatment is removal of the gastric band and repair of any areas of perforation on the stomach. Intraoperative tests should be conducted to rule out the presence of a leak. If a leak is found, a drain should be placed. Some advocate an UGI series on the first postoperative day to rule out a persistent leak. Diets can usually be resumed after the UGI series, if no abnormalities are found. Most bariatric surgeons do not replace the band during removal of an eroded one given the degree of inflammation and contamination.

LATE COMPLICATIONS OF BARIATRIC SURGERY: NUTRITIONAL DEFICIENCIES

Despite having large stores of energy in the form of excess fat, morbidly obese patients usually have some underlying nutritional deficiencies, even preoperatively, due to poor dietary habits over a prolonged period of time. These deficiencies can be exacerbated postoperatively. The severity of these deficiencies is dependent on several factors: the patient’s preoperative nutritional status, the type of bariatric surgery, the patient’s compliance to the postoperative diet and vitamin supplement regimen, as well as routine follow-up with the bariatric surgeon, nutritionist, and primary care provider. All bariatric patients are instructed to take a multivitamin daily and undergo routine blood tests to check for any nutritional deficiencies.

Vitamin deficiencies are common after bariatric surgery. Vitamin B12 deficiency is common, especially after a RYGB. The parietal cells that secrete acid and intrinsic factor, and the chief cells that secrete pepsinogen are mainly located in the fundus and body of the stomach, which is excluded from the tiny pouch that is created in the RYGB. There is also no time for the intrinsic factor to mix with the vitamin B12 since the pylorus has been removed and can no longer slow gastric emptying. The small amount of acid secreted by the pouch combined with decreased production of intrinsic factor causes vitamin B12 to remain in the crystalline form, which is not readily absorbed in the terminal ileum. The prevalence of vitamin B12 deficiency is approximately 15% to 30%, and varies depending on compliance with supplementation. Because the body usually has large stores of vitamin B12, levels often do not drop significantly for 2 to 5 years after gastric bypass. For this reason, patients must continue to have vitamin B12 levels monitored long-term on a regular basis and continue with vitamin B12 supplementation. Routine vitamin B12 supplementation can lead to eventual supranormal levels and reduction of the amount of supplementation given.

Calcium deficiency can be seen after procedures such as RYGB and BPD-DS in which the duodenum and proximal intestines are bypassed. Normally calcium absorption occurs in the duodenum. All patients who have undergone RYGB or BPD require a high daily intake of calcium (2 g/d) as well as calcium supplementation (1200-1500 mg calcium/d). A lack of calcium can lead to increased levels of parathyroid hormone (PTH), which can then lead to the release of calcium from bone. Therefore, after RYGB, BPD, or other procedures that bypass the duodenum, patients should have regular tests for serum calcium, ionized calcium, serum phosphorus, alkaline phosphatase, and PTH.

In addition to vitamin B12 and calcium deficiencies, patients who have had a malabsorptive procedure, such as BPD-DS, will have malabsorption of fat-soluble vitamins (A, D, E, K). It is important for these patients to include supplementation of fat-soluble vitamins into their daily regimen and to be monitored for any deficiencies.

Mineral deficiencies are also common in bariatric patients. Iron deficiency and anemia occur frequently in both the preoperative and postoperative bariatric patient. Postoperative causes for iron deficiency include decreased absorption due to bypass of the duodenum, decreased gastric acid, which is needed to reduce iron to its more soluble form, and reduced iron intake. About 20–70% of patients develop iron deficiency after RYGB. Symptoms include fatigue, glossitis, stomatitis, and feeling cold due to impaired temperature regulation. Supplementation of ferrous sulfate 320 mg twice daily is often sufficient. Vitamin C supplementation has been shown to improve absorption of iron.

CONCLUSION

The National Institutes of Health recommend that bariatric surgery be considered in patients with a BMI of ≥40 or if they have a BMI of ≥35 with high-risk comorbid conditions after trying other nonsurgical approaches that augment weight loss. Surgical procedures are superior to alternative approaches in this patient population, and outcomes vary by bariatric procedures. Surgical procedures accomplish weight loss by restriction or by malabsorption, or a combination of the two. Gastric banding is less frequently performed due to long-term risks of band slippage and erosion, and superior weight loss and improvement of comorbid conditions seen with RYGP, SG and BPD-DS. These procedures offer a significant benefit of prolonged weight loss with a high rate of type 2 diabetes remission, better HTN and HLD control, and improvement of other conditions including GERD and OSA. Hospitalists encounter many eligible patients during hospitalization and can play a role in appropriately referring these patients to surgeons after they recover from their illness. As a growing patient population has undergone these procedures, it is imperative that hospitalists also recognize the unique postoperative risks that these patients have both early and late, and how to appropriately initiate the appropriate diagnostic work-up and treatment, and referral to surgical colleagues for management (Table 63-4).

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INTRODUCTION

Neurological surgery is a broad field encompassing a wide range of disorders throughout the body. As with any surgical subspecialty neurosurgery is prone to its own set of unique complications. Some of the more common complications in these patients are often recognized and treated by physicians outside of neurosurgery. The goal of this chapter is to highlight a few of the more common neurosurgical complications and give the hospitalist a better understanding of how to evaluate and treat these patients. This chapter is subdivided into intracranial and spine complications.

INTRACRANIAL COMPLICATIONS

PNEUMOCEPHALUS

The brain is enclosed within the meninges and is not, in the usual situation, communicative with the external environment. Obviously a neurosurgical procedure involving an open craniotomy creates an event in which the brain is exposed to air. At the end of a craniotomy, the closure of the dura, reattachment of the bone flap and reapproximation of the skin unavoidably seals at least a small amount of air inside. In response, the partial pressure differences of gaseous air will cause reabsorption back into the blood and tissues. In the interim, however, the collection of air around the brain can cause dysfunction and even injury. A minor amount of trapped pneumocephalus is usually inconsequential. A voluminous amount of pneumocephalus, however, can cause altered mental status and a depressed level of consciousness. In addition when a passageway to the bony sinuses is inadvertently or purposely created (such as an opening into the frontal sinus with the fashioning of a bone flap), there occurs the possibility of a one-way valve wherein air enters the cranium and is not allowed to escape. Under these situations, pneumocephalus can accumulate over time and occur under pressure hastening and magnifying the neural symptoms even unto coma or death.

Evaluation

Pneumocephalus can occur after any craniotomy or endonasal surgery. Even minor twist drill hole procedures can produce a minor amount of intracranial air (this is almost uniformly benign). Suspicion of this diagnosis should be considered when a postoperative patient does not return to their baseline mentation. An urgent/emergent CT scan is the imaging study of choice and will reveal the amount of air along with the point of entry in the occurrence of “sucking” pneumocephalus from an opened frontal sinus, ethmoid air cell, sphenoid sinus, etc. Severe pneumocephalus produces an “Mt Fuji sign” from the sagging frontal lobes (Figure 64-1). When diagnosed and followed, a “brow-up” skull film will demonstrate the bubble of intracranial air quite well and can be compared day to day for proof of improvement (Figure 64-2). Use of this imaging study significantly reduces the amount of total radiation exposure over serial CT scans.

Treatment

Supplemental oxygen is the initial treatment of choice for pneumocephalus. This reduces the partial pressure of nitrogen in the blood and helps drive the reabsorption of nitrogen (the main component of atmospheric air) into the CNS parenchyma and blood. A 100% nonrebreather mask is often used for 24 hours, after which the patient is reassessed with imaging if needed. A schedule of on-off administration rotating every 2 hours can also be used when there are concerns for oxygen toxicity. When an opened sinus cavity is the etiology, the leak must be sealed. This is accomplished either via reoperation or temporary CSF diversion via external ventricular drain or lumbar drain.

MENINGITIS

As with any surgical procedure, a craniotomy may succumb to a postoperative wound infection. Staphylococcus species and Gram-negative rods are the most commonly identified organism. Endonasal surgeries comprise a special circumstance wherein oral and nasal organisms have a higher prevalence.

Evaluation

Classic signs of high fever, chills, rigors, and sweating occur, as well as meningismus, suggested by a positive Kernig’s sign (pain with extension of a bent knee) and/or a positive Brudzinski’s sign (involuntary bending of the hips and knee with flexion of the head). Laboratory peripheral leukocytosis, raised erythrocyte sedimentation rate and raised C-reactive protein are also usually present. A lumbar puncture may be needed to differentiate sterile aseptic meningitis (chemical meningitis) from bacterial meningitis, as aseptic meningitis can also occur after any craniotomy. In the case of a bacterial infection, the lumbar puncture will show elevated nucleated white cells, decreased glucose, and will usually have a positive Gram stain and culture. Aseptic meningitis may have an elevated white cell count but will usually be lymphocytic predominant and the Gram stain will be negative. Protein counts may be high in both.

Treatment

CSF infection/ventriculitis implies a nonpurulent infection and is treated somewhat differently than purulent drainage of a wound with meningitis. A draining wound with purulence requires operative debridement and usually abandonment of the bone flap. This is followed with broad spectrum antibiotics which are narrowed with direction from final cultures. Initially fourth generation cephalosporins or carbapenems along with vancomycin are used. In the case of nonpurulent ventriculitis, operative intervention is not usually necessary and treatment resides in administration of antibiotics only. Final duration of treatment is determined by clinical response, down trending of laboratory abnormalities but is usually at least 2 weeks, often longer. Imaging is often repeated with purulent infections to ensure walled abscess formation does not occur.

POSTOPERATIVE HEMATOMA (EPIDURAL, SUBDURAL, INTRAPARENCHYMAL)

The incidence of postoperative hematoma formation is among patients that are not coagulopathic is low (neurosurgery should always be avoided in patients that are coagulopathic). Unrecognized or undiagnosed coagulopathy may contribute to postoperative clot formation although the most common reasons in elective surgery are lack of intraoperative hemostasis or postoperative hypertensive events. The collection of a significant postoperative clot usually presents within the first 24 hours following surgery.

Evaluation

Postoperative clot formation will produce a local mass effect on the brain tissue with subsequent dysfunction, the characteristics of which reflect the location of the clot. Clots also have the potential for obstruction of the CSF pathways resulting in hydrocephalus. Patients with worsening neurologic defect on postoperative check or over the following 24 hours should raise the concern for clot formation and should be evaluated with an urgent/emergent CT scan. Headache out of proportion is the most common clinical symptom (Figure 64-3).

Treatment

Symptomatic clots should prompt a return to the operating room for emergent evacuation, and hydrocephalus should be relieved with CSF diversion usually with an external ventricular drain. The search for an underlying coagulopathy should be concomitantly started via laboratory evaluations and replacement/reversal agents should be administered as indicated.

POSTOPERATIVE SEIZURE/STATUS EPILEPTICUS

The incidence of postoperative seizures is roughly 5%. Any variety of seizure may be represented including generalized, complex partial, and focal motor/sensory. In addition, subclinical status epilepticus should be considered in any patient with persistent altered mental status (it is estimated at 8% incidence in comatose trauma patients). Factors that increase the risk for postoperative seizures include prior seizure disorder (especially with low-antiepileptic medication levels), pathology of the frontal lobe, younger age, malignant pathology, incomplete resection and intraoperative complications.

Evaluation and treatment

Suspicion for seizures should begin with interrogation of those witnessing the event; untrained persons may confuse seizure activity with posturing from brainstem compression. Once suspicion is confirmed, administration of benzodiazepines and antiepileptic’s is indicated. For persistent altered mental status or concern for subclinical status epilepticus, patients should be placed on long term EEG monitoring with swift interpretation by an epileptologist so that further medical management may be instituted if necessary. New onset seizure activity after surgery may also herald a brewing intracranial complication such as an infarct or clot, which should be evaluated by a CT scan. In those with significant compromise in their mental status, they may need to be intubated for airway protection.

CSF LEAK

Cerebrospinal fluid is made at a volume of roughly 450 mL/d and the intracranial vault and spinal column hold roughly 150 mL thereby resulting in a three times turnover daily. This reabsorption into the bloodstream is driven mainly by the differential pressure between what is most commonly encountered as “opening pressure” on a lumbar puncture and central venous pressure. When a craniotomy is fashioned and then closed, care is taken to reapproximate the dura in at least a semiwatertight nature. Normal intracranial pressures test this seal at a minor level. Pathologic situations that raise the intracranial pressure (ie, postoperative hydrocephalus, aseptic meningitis, etc) can place an even higher stress on healing tissues and result in a spinal fluid leak. Post irradiated wounds, infection, persistent cancer, poor nutrition, surgery of the posterior fossa and poorly closed wounds are at higher risk for leakage of spinal fluid. The development of a subcutaneous pseudomeningocele implies an “internal” or “contained” spinal fluid leak through the dura (Figure 64-4).

Evaluation

Clear fluid drainage from the wound with postural headaches (worse with upright position, better with recumbence) should raise suspicion of a spinal fluid leak. If there is a question of whether the fluid is CSF or more routine serous drainage, the fluid can be sent for a chloride level (which should be higher than serum chloride levels given the high-salt concentration in CSF), or for β-2 transferrin, a protein only found in CSF. Of note, the chloride test is fast and cheap; β-2 transferrin is a send-out at most hospitals, will take days to come back, and is much more expensive “Haloing” of fluid leaked onto a sheet or pillow or testing for the presence of glucose can give some suspicion but is not diagnostic. On examination, pseudomeningoceles are found to be fluctuant or occasionally firm (when under pressure) fluid pockets under the skin flap used for the craniotomy. They may occasionally regress when upright and recur when lying down. Spinal fluid rhinorrhea can also occur when a craniotomy opens into the mastoid air cells, temporal bone air cells, ethmoid sinus, sphenoid sinus, or frontal sinus. Placing the patient in a nose-down position can usually elicit leakage of fluid from the nose to aid in the diagnosis.

Treatment

The underlying cause for a spinal fluid leak should be sought out and addressed. The most common cause for CSF leakage from a wound is hydrocephalus or infection. These should be treated accordingly (covered elsewhere). Prompt attention to the leak should be taken as its presence opens a pathway in which skin flora may enter the sterile CNS environment. Wounds should be over sewn at the bedside under sterile conditions or taken back to the operating room for repair. CSF diversion in the form of a lumbar drain or external ventricular drain may be necessary to lower the resting intracranial pressure. This provides a pressure-free period of time for the wound to heal. Prophylactic/empiric antibiotics are often administered to prevent meningitis/ventriculitis while the possibility of infection is investigated.

HYDROCEPHALUS

Maintenance of intracranial pressure and stable CSF volumes rely on matched production and reabsorption processes. Imbalance (blockage of CSF pathways, overproduction, or impaired reabsorption) leads to increased CSF volume (and subsequent elevation of pressure) known as hydrocephalus. Hydrocephalus is not uncommon in the neurosurgical patient as is evidenced by the prolific nature of ventriculoperitoneal shunts and external ventricular drains on the neurosurgery service. Left untreated, hydrocephalus in a crescendo nature will ultimately lead to death as intracranial pressure matches blood pressure and cerebral blood flow is halted. Hydrocephalus may occur in the postoperative patient in a variety of ways including blood clot obstruction of the intraventricular system, blood in the CSF causing impaired reabsorption, or edema of the cerebral tissues obstructing CSF pathways. Postoperative patients may demonstrate hydrocephalus through symptoms of headache and signs of vomiting, altered mental status and CSF leak. Papilledema may also be seen although this is not always present in an acute presentation. Surgeries that involve opening of the ventricular cavities, posterior fossa surgery, craniopharyngiomas, epidermoid’s, and infectious oriented surgery (cerebral abscess, empyema, etc) pose a higher risk for developing postoperative hydrocephalus.

Evaluation

Patients with suspected hydrocephalus should undergo an urgent/emergent CT scan. This should be compared to a symptom free scan with attention to size of the ventricular system. Comparisons of the width of the third ventricle, intercaudate nucleus distance, evidence of transependymal flow, and presence/size of the temporal horns aid in the diagnosis. In addition, characterization of the lateral, third, and fourth ventricles should be made to pinpoint a possible site of obstruction and differentiate communicative versus noncommunicative hydrocephalus (Figure 64-5).

Treatment

Upon the diagnosis of hydrocephalus, neurosurgical consultation is necessary to determine if CSF diversion is necessary. This may be done via lumbar puncture, lumbar drain or external ventricular drain depending on the circumstance. Under no situation should noncommunicative (obstructive) hydrocephalus be treated with a lumbar puncture or lumbar drain as this places the patient at risk for downward herniation. Permanent CSF diversion may ultimately be necessary via a lumbo-peritoneal shunt or ventriculo-peritoneal shunt procedure if temporary measures are unable to be weaned over time.

SURGERY SPECIFIC RISKS

Certain surgeries carry particular risks that hospitalists should be aware. These usually revolve around the particular anatomy of the location of the surgery. Three will be mentioned below in more detail:

Facial nerve palsy

While this complication can be seen in any surgery involving the cerebellopontine angle or the course of the facial nerve within the temporal bone, it is best understood in the context of microsurgical removal of vestibular schwannomas (acoustic neuromas). These tumors usually arise from the vestibular nerve but tumors of any significant size will cause the accompanying facial nerve to be quite adherent and stretched upon the tumor capsule. Removal of the tumor has the potential to injury the facial nerve with a subsequent facial palsy, the degree of which can vary from mild to complete. The ramifications of this most immediately include the inability to close the eyelid and poor function of the orbicularis oris muscle making eating and speaking difficult. To prevent a drying injury to the eye, lubrication must be applied intermittently day and night and the eyelid taped shut at night. Implantation of a gold or platinum weight in the upper lid by an oculoplastic surgeon aids in eyelid closure on a more permanent basis and should be considered with complete facial palsies while the patient is still an inpatient after surgery. Speech therapy should be consulted to aid in eating and speaking exercises.

Pituitary insufficiency

This complication may be seen most commonly with pituitary tumor surgery but can also be seen with craniotomies for pathology of the central skull base (meningiomas, craniopharyngiomas, third ventricular tumors, etc). Complete discussion of pituitary hormone function is outside the scope of this chapter but attention to a few points is worthwhile. Injury to the pituitary gland can cause both rapid and slow changes in hormone production. Rapid changes include steroid production under the hypothalamic-pituitary-adrenal axis (adrenal insufficiency) and maintenance of appropriately concentrated urine through the production of vasopressin (diabetes insipidus). The clinician should be watchful for deficiencies of these two hormones as aberrations can produce shock and dehydration quickly. Care should be taken in their replacement however as the post injury underproduction can be a variable thing and dosing can significantly change in the days after surgery. Laboratory evaluation should occur the first postoperative morning and daily sequentially thereafter. More frequent checks should be driven by urine output and clinical signs and symptoms.

Lower cranial nerve palsy

Surgery of the posterior fossa, especially of the jugular foramen region and mid to lower medulla, can produce injury to the lower cranial nerves (CN IX, X, XI). Identification is important as their injury produces a loss of gag reflex and pharyngeal dysmotility that can lead to aspiration. Severe cases may require the placement of a tracheostomy and a percutaneous endoscopic gastrostomy tube. Less severe cases can be managed with close collaboration with speech therapy.

SPINE COMPLICATIONS

Neurosurgeons perform spine surgery to treat a variety of conditions including pain syndromes (back pain, radiculopathies, neurogenic claudication), tumors, degenerative disease, deformity, and instability. Some surgeries allow for patients to be discharged the same day while others require long hospitalizations with extensive rehab and recovery. The average length of stay is around 4 days. Recent literature quotes an 8% complication rate after spine surgery. This includes minor complications (eg, IV site phlebitis, accidental lacerations) and major complications (eg, pulmonary embolus, wound infection, CSF leak). Complication rates are exacerbated by comorbidities such as smoking, obesity, heart disease, advanced age, osteoporosis, and a history of prior spine surgery. For more extensive spinal operations, including deformity surgeries, the complication profile can be much higher (20%-30% or more).

PAIN, NAUSEA, CONSTIPATION

The most common postoperative complaint from spine surgery patients is incisional pain. Patients are initially managed with IV opiate medications and transitioned to oral medications as tolerated. Postoperative nausea and vomiting is quite common, limiting this transition to oral medications. The nausea is related to anesthesia and inflammation from surgery. Muscle spasm is also frequent. Short and long acting muscle relaxants will provide significant relief for these patients. Some patients are at a higher risk of developing an ileus, including those undergoing trans-abdominal or retroperitoneal approaches. Neuro-monitoring is frequently used in more complicated cases. This has been implicated in higher rates of postoperative ileus since the anesthetic technique needs to be altered to give no paralytics and high-dose narcotics to allow for motor evoked potentials to be checked during the procedure. Newer medications including methylnaltrexone (Relistor), a mu-opioid antagonist, can be given preoperatively to help reduce this complication in higher-risk patients.

INFECTION

Evaluation

The surgical site infection rate from spine surgery is often cited in the literature at 1% or less, however the risk can be much higher in patients with multiple comorbidities and more extensive surgery. Identifying high-risk patients and modifying risk factors such a nicotine use, high-HbA1C levels, obesity, and poor nutrition is mandatory. Proper patient selection is key to keep this very costly complication rate as low as possible.

Some erythema of the skin edges is normal as part of the inflammatory healing process taking place, but significant and/or spreading erythema present weeks to months after spine surgery is rare and an underlying infection should be suspected. A small amount of drainage from the incision in the first days after surgery is expected. If this drainage does not subside or even increases, underlying infection or CSF leak may be suspected. When evaluating an incision be mindful for breakdown or dehiscence of skin edges, purulent drainage, fluctuant masses below the skin (these may also be painful), and spreading erythema.

Occasionally patients with a thin body habitus will have issues with hardware causing pressure points and skin erosion. In all of these cases, it is best to keep the incision clean and covered and consult with the neurosurgeon. Wound care consultation is also useful in those patients with chronic wound breakdown.

Treatment

Imaging is helpful, usually an MRI with and without IV contrast, but plain CT and CT myelogram can be useful in some cases. Inflammatory markers (ESR, CRP), CBC, and blood cultures should be sent. Management ranges from a short course of oral antibiotics for superficial infections to percutaneous IR drainage and in some cases open debridement/washout with a prolonged course of IV antibiotics. Rare and complex cases may even require lifelong oral suppressive antibiotic therapy.

HEMORRHAGE

The incidence of acute blood loss anemia requiring intraoperative and postoperative transfusion is highly variable depending on the type of procedure. Noninstrumented surgeries and single level fusions rarely require blood products, but a transfusion for more extensive operations is fairly common and standard for open deformity cases such as scoliosis corrections (even if a cell saver is used to return as many red cells back to the patient intraoperatively). A very rare complication associated with long operative times, high-blood loss, episodes of hypotension, and prone positioning is postoperative blindness from ischemic optic neuropathy. The exact mechanism behind this is not fully known and is likely multifactorial.

Patients will commonly have surgical drains in place postoperatively. The purpose of this is to limit hematoma formation, prevent compression of exposed neural elements such as the spinal cord, and to decrease the rate of surgical site infections. Immediate thought must be given to epidural compression in patients who have a neurologic decline after a spinal decompression surgery. These drains will be monitored for 1 to 3 days in most cases before being removed after the output gradually decreases. Some drains that have persistent drainage will remain in place longer.

Evaluation and treatment

Postoperative patients should be monitored with a CBC on post op day 1 and sooner if needed. Vitals should be monitored for hemodynamic stability. Older patients or those with cardiac dysfunction will have less reserve than others and may need a transfusion at a lower threshold. The transfusion threshold for most postoperative patients is a Hgb of 7, but patient specific factors will influence this and continuing blood loss through drains needs to be taken into consideration by trending the CBC. (See Chapter 57 [Blood Products in the Postoperative Period].) Output of more than 150 cc/d is typically considered significant. The color of the drainage will also change from frank blood to more cool-aid colored drainage termed serosangiunous drainage. This is a mixture of blood and serous fluid that fills the dead space after surgery.

Epidural hematomas can occur and cause weakness, sensory deficit, and/or pain (incisional or radicular). These are fortunately rare. MRI or CT myelogram is the study of choice to evaluate for this. CT myelogram may be needed in cases where there is extensive hardware that would obscure MRI imaging. Surgical evacuation in symptomatic cases is mandatory. Full neurological recovery and elimination of pain is dependent on the timing of clot evacuation, with rather expeditious clot evacuations associated with faster recoveries. Large clots can compress the spinal cord, cause cord contusions, and even with rapid clot removal, some patients can still have residual deficits from sustaining this spinal cord injury (Figure 64-6).

CSF LEAK

Cerebrospinal fluid (CSF) coats the spinal cord and nerve roots and can be encountered in spine surgery. Iatrogenic CSF leaks are usually identified at the time of the operation, are caused by unintentionally opening the dura and arachnoid, and are either repaired primarily or in some complex cases just contain the fluid below the fascial layer which creates a pseudo-meningocele. These leaks are problematic because they can cause positional headaches similar to postlumbar puncture headaches. The patient is also at risk of developing septic or aseptic meningitis, where inflammatory cells, protein and blood in the CSF can cause headaches and meningeal signs. In addition, they increase the hospital length of stay as the patients are typically kept flat in bed as the dural repair and wound heals. These leaks are also known to increase the rate of other in-hospital complications, particularly in the elderly, who don’t tolerate prolonged hospital stays much less kept in the flat in bed. If the fascia is not closed in a water tight fashion, the CSF can leak through the skin, which requires either placement of a lumbar drain to divert CSF until the wound heals or a formal operative repair.

Evaluation and treatment

In most cases, if clear liquid is emanating from the wound, CSF is the culprit. If there is a question of whether the fluid is CSF or more routine serous drainage, the fluid can be sent for a chloride level (which should be higher than serum chloride levels given the high-salt concentration in CSF), or for β-2 transferrin, a protein only found in CSF. Of note, the chloride test is fast and cheap; β-2 transferrin is a send-out at most hospitals, will take days to come back, and is much more expensive. Immediate neurosurgical consultation is recommended.

HARDWARE FAILURE

The incidence of a malpositioned screw averages 1% but varies depending on the area of surgery (cervical, thoracic, or lumbar) and type of surgery being performed. Patients may have pain and/or weakness associated with poorly placed hardware. Synthetic grafts may also cause spinal cord of nerve root compression. Over time, a patient’s hardware may fail. Screws can come loose and rods may bend or break. In most cases, the instrumentation is only meant to give the patient’s spine support while it heals and fuses new bone to compensate. There are early and late hardware failures sometimes seen years after an operation.

Evaluation and treatment

Patients who have worsening pain, pain in a new location, or increased weakness postoperatively should be evaluated with AP and lateral plain film radiographs as an initial evaluation. Further imaging with a CT scan and in some cases an MRI or CT myelogram may be needed but this should be discussed with the operative team in order to coordinate the most useful exam. Not all screws with a cortical breach are problematic and in need of revision. The patient’s neurological exam must be compared with the suspected hardware complication. Occasionally flexion/extension or supine/standing radiographs will be needed in order to determine whether the newly implanted hardware is stable and providing support. These concerns should be coordinated with the neurosurgical team (Figures 64-7 and 64-8).

ADDITIONAL COMPLICATIONS

It is not uncommon to see a transient postoperative peripheral neuropathy or an OR positioning-related injury. These patients are commonly in the prone positions for an hour or more and can suffer from skin tears, bruises, corneal abrasions, ulnar neuropathies, brachial plexus injuries, and meralgia paresthetica to name a few. Most of these issues are minor and resolve on their own without intervention, but some cases can take many months to resolve. It is frustrating for both the patient and surgeon to see this despite careful positioning and padding.

Additional complications seen in spine patients are not unique: this includes postoperative fevers, atelectasis, pneumonia, cardiac abnormalities, urinary tract infections, and thromboembolic events including deep venous thrombosis and pulmonary emboli. In the neurologically compromised population, including myelopathic patients, the DVT and PE rate is significantly higher as they tend to be more immobile from weakness in one or more extremities. Surveillance Dopplers are reasonable in high-risk patients preoperatively. Mechanical prophylaxis with sequential compression devices is standard. Chemical prophylaxis with subcutaneous heparin or lovenox should be initiated postoperative day one, and in high-risk cases, starting this intraoperatively may be wise.

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PERIOPERATIVE VOLUME AND BLOOD MANAGEMENT

EPIDEMIOLOGY

Exposed cancellous bone presents a hemostatic challenge, and consequently, nearly all patients undergoing major orthopedic procedures have some degree of acute blood loss anemia. The estimated blood loss for a total hip replacement is approximately 3.2 units or 4.07 g of hemoglobin, while total knee replacement patients may lose 1 to 1.5 L of blood or 3.85 g of hemoglobin. Blood loss after bilateral or revision joint replacement may be significantly more.

Historically, 10% to 38% of total joint-replacement patients received a postoperative blood transfusion, usually 1 to 2 units for primary arthroplasties and 3 to 4 units for revisions. While blood transfusions may restore oxygen-carrying capacity, replace fluid volume, and increase vigor, they expose patients to risks, including transfusion reactions, transfusion-related lung injury, antigen exposure, higher mortality, disease transmission, immunosuppression, and infection, as well as higher costs and length of stay.

RISK STRATIFICATION

While the most significant risk factor for acute blood loss anemia is the magnitude of the surgical procedure, several other issues must be considered. Patients on chronic anticoagulation are at high risk for development of postoperative anemia. If possible, medications such as warfarin, rivaroxaban, clopidogrel, aspirin, and even nonsteroidal anti-inflammatory drugs should be stopped preoperatively. Therapeutic anticoagulation should ideally be held postoperatively until adequate hemostasis has been assured and the wound has stabilized. Intraoperative bleeding complications are increased by 1.5 times if preoperative aspirin is not stopped, but discontinuation may increase the risk of postoperative cardiac and vascular complications. Thus, cardioprotective doses of aspirin can be continued for most orthopedic surgery patients who are at increased cardiac risk. Transfusion requirements increase by 50% if clopidogrel is continued perioperatively. Bridging anticoagulant therapy with therapeutic low-molecular-weight heparin is associated with a 92% incidence of bleeding complications, 69% occurrence of hematoma, and 15% development of a prosthetic joint infection; the perioperative use of these drugs in therapeutic doses should therefore be undertaken with caution.

Preoperative anemia should be identified, evaluated, and treated. Anemia is present in 21% of elderly patients who are undergoing elective orthopedic surgery. It is also common in patients with thrombocytopenia, chronic disease, and in menstruating females. Total joint-replacement patients with a preoperative hemoglobin <10 g/dL have a 90% risk of needing a transfusion postoperatively. Of note, preoperative autologous donation (PAD) of blood has declined in popularity because of cost, waste from overcollection, and increased transfusions. Current recommendations for the treatment of preoperative anemia include a thorough hematologic workup, correction of vitamin B12 or iron deficiencies, if present, and evaluation for other sources of ongoing blood loss, such as the gastrointestinal tract.

EVALUATION AND MANAGEMENT OF BLOOD LOSS

Intraoperative measures to limit blood loss and resultant anemia include the use of acute normovolemic hemodilution, tourniquets, hypotensive anesthesia, regional anesthesia, avoidance of hypothermia, blood salvage, meticulous hemostasis, topical hemostatic agents, and intravenous antifibrinolytics.

The use of antifibrinolytics has increased dramatically in the past decade. Tranexamic acid and aminocaproic acid are both lysine analogues that inhibit fibrinolysis by reversible competitive blockade of lysine binding sites on plasminogen and plasmin. By impeding conversion of plasminogen to plasmin, which is an enzyme that degrades fibrin clots, and interfering with the action of plasmin, tranexamic acid inhibits clot breakdown and reduces postoperative bleeding. By disturbing the physiologic balance between clot formation and clot dissolution, there is a theoretical concern that these agents may increase the risk of thromboembolic disease but to date the data have not borne out this concern. Numerous studies have demonstrated decreased blood loss, lower incidence of postoperative anemia, and fewer transfusions in total joint, spine, and orthopedic trauma patients. In some of these studies, high-risk patients with ischemic heart disease or previous thromboembolic disease were excluded, but there is increasing evidence that anti-fibrinolytic therapy does not increase risk of thrombosis in these patients. Nevertheless, rare case reports have documented cerebral thrombosis, arterial thrombosis, ARF, coronary graft occlusion, and PA catheter thrombosis. In our institution, the use of tranexamic acid has decreased the number of patients requiring a transfusion by 44%, with a 55% reduction in the number of units transfused per patient without an increase in thrombotic complications.

Intravenous crystalloid given intraoperatively quickly leaves the pressurized intravascular space and accumulates in the interstitial (or “third”) space. Intravascular normovolemia must be maintained perioperatively, but significant postoperative weight gain is a marker of excessive extravascular fluid and is frequently a poor prognostic sign. Pathologic interstitial fluid shifts occur with infection, large procedures, major trauma, and inflammation. Isotonic crystalloid for fluid maintenance and replacement decreases the interstitial shift by maintaining an intravascular osmotic gradient. Colloids (hetastarch, dextran, and albumin) are more effective in maintaining this gradient and are preferred to replace blood loss in major surgical procedures. While the majority of blood loss occurs during operation or in the first 24 hours thereafter, decreases in hemoglobin and hematocrit may not stabilize until postoperative day 2 or 3, as interstitial fluid becomes mobilized. Often the decline in lab values is dilutional during this period and does not necessarily indicate ongoing blood loss or create hemodynamic instability. Incremental postoperative blood loss can be reduced by compressive dressings, minimizing phlebotomy, avoidance of continuous passive motion machines, optimized nutrition, and judicious use of chemoprophylaxis for deep vein thrombosis. Therapeutic anticoagulation should be avoided.

Postoperative anemia results in fatigue, decreased vigor, slower recovery, and increased length of stay. More severe cases may lead to impaired cognition, hypotension, tachycardia, dyspnea, and decreased tissue oxygenation. American anesthesia guidelines suggest that transfusions are unnecessary if hemoglobin is >10 mg/dL and is recommended if <6 mg/dL. Decisions about transfusions for hemoglobin values between 6 and 10 should be based on a combination of factors including medical history, symptoms, laboratory studies, and an understanding of operative and ongoing postoperative blood loss. When given, packed red blood cells should be administered on a unit-by-unit basis rather than ordering the historic-standard of two units at a time.

Postoperative anemia substantially recovers between post-op day 7 and 28, but complete recovery may be delayed by iron and nutritional deficiency. Oral iron supplementation is frequently administered, but is of questionable benefit. Gastrointestinal side-effects are frequent, and randomized trials have not shown an increase in hemoglobin recovery in the first 3 weeks of FeSO₄ administration, when return to 85% of the pre-op values occurs. There is a statistically-significant improvement of 3% to 3.5% in the next 3 weeks with iron administration, but the clinical importance of this change is questionable.

SURGICAL SITE INFECTION

EPIDEMIOLOGY

Surgical site infections are estimated to complicate 0.5% to 2.5% of clean orthopedic cases, including elective joint replacements. Currently, approximately 1 million hip and knee joint-replacement procedures are done in the United States annually. At a rate of 1%, approximately 10,000 post-op joint replacements will become infected annually. At an estimated cost of over $75,000 per case, the cost to the US health care system is approaching $1 billion. In most large centers, infection has replaced aseptic loosening, osteolysis, dislocation, and implant failure as the most frequent cause of revision total joint arthroplasty.

RISK STRATIFICATION

The most effective strategy for managing orthopedic infections is prevention, making risk stratification and modification essential. Development of a postoperative infection requires introduction of a bacterial load of sufficient quantity and virulence in a favorable environment, which often suggests an immunocompromised host. Knowledge of these factors helps us understand which patients are at risk for development of this serious complication.

There are numerous risk factors associated with the development of postoperative orthopedic infections (Table 65-1). These include factors related to the initial contamination of the wound, the patient’s intrinsic bacterial flora, the wound environment, and host factors which may limit the patient’s ability to eradicate potential contamination.

Assessment of potentially modifiable patient-associated risk factors is an important part of perioperative care of the elective orthopedic patient. It has been shown that 80% of primary total joint replacements and 93% of revision replacements have at least one modifiable risk factor:

• Diabetes is a well-established risk factor for SSI. Perioperative hyperglycemia affects the microvascular circulation, impairs oxygen delivery, and inhibits chemotaxis, complement function, and phagocytosis. Each of these factors contribute to problems with wound healing and infection. Uncontrolled perioperative diabetes has been associated with 2.25 times increased risk of wound infection.

• There is a strong association of postoperative urinary tract infections with prosthetic joint infection, but the significance of preoperative urinary tract infections is unknown. The most important factor is whether patients are symptomatic with obstructive symptoms in the preoperative setting; such patients should have urologic consultation prior to elective surgery. Pre- or postoperative urine cultures demonstrating bacterial counts of >100,000 colonies/mL require treatment even in the asymptomatic patient. Lower-bacterial counts may also warrant treatment in the presence of obstructive or irritative symptoms. Postoperatively, attention toward prevention of bladder distention and stasis is essential, and catheters should be removed as soon as possible to prevent colonization.

• Malnutrition is identified by transferrin levels <200 mg/dL, albumin <3.5 g/dL, or a total lymphocyte count <1500 cells/mm³. Patients that are malnourished have a 5 to 7 times higher risk of major wound complications.

• Patients with morbid obesity have a risk of deep infection that is more than twice that of normal controls, and in some cases the risks may outweigh the benefits of surgery.

• Patients with rheumatoid arthritis have a 2 to 3 times increased risk of infection compared to patients with osteoarthritis due to a combination of innate autoimmune immunosuppression and the use of immunosuppressive medications. Anti-inflammatories, prednisone, methotrexate, and biologic agents are all associated with wound healing complications and infections. Perioperative cessation of methotrexate and biologic agents is controversial, but frequently recommended. Prednisone has a high association with immunosuppression and perioperative infection, but is not usually stopped because of the risk of disease flares and acute adrenal insufficiency.

• Smoking is a frequently occurring modifiable risk factor. Smokers have 3 times the risk of wound healing complications with 3 to 4 times higher rates of nonunion in fractures and spinal fusions. Nicotine-containing products should be stopped 4 to 6 weeks prior to surgery, if possible.

EVALUATION AND MANAGEMENT OF SSI

There is no single reliable diagnostic test to rule-in or rule-out early postoperative infection, making evaluation difficult. Fever and elevated white cell count in the immediate postoperative period are common and often due to atelectasis and small amounts of embolized fat in patients undergoing orthopedic surgery. Disproportionate pain, prolonged wound drainage, or excessive erythema most commonly occur. Wounds with purulent drainage or a sinus tract should be considered infected. Serologic testing is nonspecific, and therefore only marginally useful in the perioperative period. Both erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are typically elevated in the early postoperative setting; the CRP returns to normal in about 3 weeks and ESR in 6 weeks.

Aspiration or biopsy of a suspected orthopedic surgical site infection is the gold standard diagnostic test. Fluid obtained should be sent for cell count with differential, as well as aerobic and anaerobic cultures. In the early postoperative setting, the white blood cell count in a total joint replacement can be as high as 27,000 WBCs/µL, but should be below 3000 in the nonacute setting. A neutrophil count of greater than 89% is highly sensitive and specific for infection even in the first 6 weeks following surgery. Fluid culture has relatively low sensitivity at about 75%, but is 95% specific for infection. False negative cultures are frequently associated with administration of antibiotics, which should be held for at least 2 weeks prior to sending cultures for reliable results.

Treatment of orthopedic surgical site infection requires both operative and medical management. Since there are large amounts of surface area around implants that are not exposed to blood and vascularized tissue, antibiotics alone are ineffective in eradicating most hardware associated infections. Moreover, the biofilm layer that forms within days of acute infection and is associated with many bacteria is usually not cleared even with surgical debridement. Most acute postoperative or hematogenous infections warrant a trial of surgical irrigation, debridement, and implant retention followed by IV antibiotic therapy. Chronic infections usually require hardware removal, IV antibiotics, and a staged reconstruction for successful eradication of the infection.

The goals of treatment of orthopedic infections are listed in Table 65-2. It is important to realize that management may be variable depending on numerous patient factors, and achieving all of the stated goals may not be possible in all patients. This requires extensive collaboration between the orthopedic surgeon, the hospitalist, and the infectious disease consultants.

Patients should maintain a sterile dressing over the wound until all serous drainage has stopped and the wound has become sealed. Persistent drainage beyond 2 weeks usually warrants operative investigation and debridement for early detection and eradication of a potential infection. Oral antibiotics for erythematous or draining wounds are rarely indicated and may complicate diagnosis via false-negative culture results as a deep infection progresses. Administration of oral antibiotics is associated with poor outcomes if debridement and implant retention is attempted as they often lead to a delay in diagnosis, establishment of a mature biofilm, and development of antibiotic resistance. Fever or an increase in pain or swelling may be the first signs of an infection, and should be thoroughly evaluated.

Long-term protection of previously implanted orthopedic hardware is also important. Patients should be informed of potential risks and understand the importance of prompt treatment of remote infections, particularly of the hands, feet, and mouth. Antibiotic prophylaxis for dental and other procedures is controversial but favored by most orthopedic surgeons.

PERIOPERATIVE PAIN MANAGEMENT

EPIDEMIOLOGY

Acute pain following orthopedic surgery remains one of the most vexing challenges impacting patient experience and outcome. Historically, general anesthesia (GA) combined with either oral or parenteral narcotic medications have been the preferred strategies to address postoperative pain in the orthopedic patient. With classic opioid-centric postoperative pain regimens, the incidence of adverse drug events has been reported to be 8.5% among total joint-replacement (TJR) patients. This accounts for greater than half of all postoperative in-hospital complications and contributes to increased length of stay. In recent years, concerns regarding the side-effects of GA combined with high-dose opioids have prompted the evolution and popularity of multimodal analgesic regimens. Multimodal analgesia was first popularized among total joint-replacement patients, but has expanded to orthopedic trauma and spine patients as well.

RISK STRATIFICATION

Pain regimens need to be tailored to the individual patient, particularly with respect to opioids in the following situations:

• Elderly patients as well as those with known hepatic or renal dysfunction may have impaired drug clearance, and therefore may be more susceptible to side effects if dosages are not properly adjusted.

• Patients with obstructive sleep apnea have increased rates of cardiopulmonary complications, including arrest, following major surgery. Many analgesics, but most notably opioids, exacerbate hypoxia via reduction of respiratory drive, volume, and alertness, and may cause previously undiagnosed apnea to become clinically relevant in the postoperative setting.

• Patients taking regular doses of opioids preoperatively may develop a tolerance to postoperative narcotic pain medications. These patients are likely to present a challenge in terms of management of acute pain and may require significantly increased doses compared to the opiate-naïve patient.

• Obese patients can require dose adjustments of fat-soluble medications like opioids to avoid sequestration and effective dilution in excess adipose tissue.

EVALUATION AND MANAGEMENT OF PAIN

Acute pain that is poorly controlled postoperatively may lead to hypertension, tachycardia, increased tissue oxygen demand, myocardial ischemia, and decreased minute ventilation from respiratory depression with pulmonary complications (including pneumonia). Pain prevents patients from effectively mobilizing and participating in therapy, which may jeopardize the outcome of surgery. Additionally, acute pain affects two of the classic components of Virchow’s triad via indirect inhibition of fibrinolysis as well as limiting mobility and contributing to venous stasis. Safe and effective treatment of acute pain in the postoperative setting is of paramount importance for these reasons and also to improve the overall patient experience.

Now gaining popularity nationwide, the combination of regional plus multimodal anesthesia is replacing the historic strategy of general anesthesia plus opioid-centric analgesia as the new standard of care for orthopedic surgery patients. This concept aims to both prevent and treat acute pain by using a combination of agents with different mechanisms of action in order to maximize the analgesic effects while decreasing undesirable side effects of any single agent (Figures 65-1 and 65-2).

One of the principles of multimodal analgesia is the preemptive treatment of acute pain, and therefore medications are initiated prior to surgery and continued postoperatively. Though substantial variability exists between institutions, a typical multimodal protocol will include some combination of opioids, acetaminophen, peripheral as well as central nerve blockade, local anesthetics, steroids, NSAIDs, and anticonvulsants. The synergistic effects of combination agents allows each to be dosed more conservatively than with single medication therapy. Though the severity and likelihood of side effects of any individual agent may be diminished, the spectrum of possible concerns expands with the additional medications.

Regional as opposed to general anesthesia offers advantages including a decreased incidence of postoperative nausea and confusion, improved early postoperative comfort, and facilitates early mobilization. Several potential complications specifically related to neuraxial and peripheral regional anesthesia need to be considered:

• Epidural hematoma is a rare though potentially devastating complication of combined spinal-epidural (CSE) anesthesia, occurring in <1/100,000 patients who receive epidural or spinal anesthesia. Orthopedic patients commonly receive anticoagulants to prevent VTE in the postoperative period, theoretically increasing the risk of hematoma formation.

• Epidural abscess is also rare but can be devastating; it is likely to present with systemic signs of infection, including fever, chills, nausea, and malaise.

• Abnormal motor blockade in a postoperative CSE patient warrants close monitoring and likely requires further evaluation. Lumbar spine MRI is the most informative and appropriate diagnostic study.

• CSE may be associated with persistent hypotension in the early postoperative period. Anesthetic medications delivered to the lumbar epidural space can affect the lumbosacral sympathetic chain, thereby producing an effective transient sympathectomy. Resulting vasodilation produces hypotension, particularly with the patient erect and standing; it is generally responsive to IV fluid support until the medication wears off.

• Urinary retention is more likely following CSE than after GA; patients receiving CSE may benefit from bladder catheterization postoperatively.

CSE anesthesia is commonly supported by local and/or regional nerve blockade. Local anesthetic toxicity is a particular risk if all three modalities are employed. Depending on the specific type of local anesthetic agent, a mixture of cardiac (hypotension) and neurologic (seizures) symptoms may be present, with bupivacaine being the most common offending agent.

The side-effect profiles of individual components of a multimodal analgesia regimen are well established. A few relevant orthopedic considerations deserve mention here:

• NSAIDs are a mainstay of nonoperative treatment of many orthopedic conditions, but also play an important role in the management of acute postoperative pain. Aside from nephrotoxicity and gastrointestinal effects, animal models and basic science studies suggest interference of NSAIDs with both fracture healing and osseointegration of implants. These biologic pathways are critical not only in the setting of trauma, but also following many joint-replacement procedures, the long-term durability of which often requires ingrowth of native bone into and around the porous surface of metal prostheses. Though unsupported by clinical trials, most orthopedic surgeons prefer to avoid NSAIDs in the setting of either fracture or cementless arthroplasty despite their analgesic benefits. Similarly, NSAIDs inhibit platelet aggregation and contribute to risk of bleeding complications, particularly in patients who are also receiving prophylactic antithrombotic agents.

• Anticonvulsants such as pregabalin and gabapentin provide effective analgesia and reduce opioid requirements in postoperative orthopedic patients.

• Acetaminophen has long been utilized as an antipyretic as well as a central analgesic agent. Recently, intravenous formulations have been approved for use and proven efficacious as an adjunct for the management of postoperative pain.

COMPARTMENT SYNDROME

EPIDEMIOLOGY

Compartment syndrome in the extremities is most commonly encountered in the acute trauma patient. Tibial fracture remains the specific injury most commonly associated with compartment syndrome, and open fractures have a rate of compartment syndrome five times that of closed fractures. Patients with a vascular injury are far more likely to have compartment syndrome than those without. The consequences of unrecognized compartment syndrome may be devastating, including joint contractures, permanent loss of function, loss of limb, and even death.

RISK STRATIFICATION

It is important to know which patients are at risk for developing compartment syndrome, as well as those at risk for failure to recognize and diagnose compartment syndrome in a timely fashion. Patients incapable of providing an accurate history secondary to intubation, intoxication, or severe dementia can present a diagnostic dilemma. In these circumstances the clinician must rely solely upon physical examination and objective findings. Similarly, patients who have received a peripheral or central nerve blockade for the purpose of postoperative pain control may be unable to accurately report severity of pain, and this may delay the diagnosis of compartment syndrome. Postoperative orthopedic patients commonly experience swelling and pain, and occasionally neurologic symptoms in the recently operated extremity. Differentiation between expected symptomatology and those concerning for compartment syndrome can be challenging.

EVALUATION AND MANAGEMENT

An understanding of the pathophysiology of compartment syndrome is critical to performance of a thorough physical examination and achievement of an accurate diagnosis. Within each anatomic segment of the extremity, the soft tissue contents traversing the limb are contained within compartments bordered and contained by tough, nonexpansile fascial connective tissue. Upon traumatic injury, or other myriad events that increase the fluid content of a compartment, the fixed space within the compartment is unable to accommodate expanding volume and results in increased interstitial pressure. If the interstitial pressure exceeds the capillary perfusion pressure, oxygen-rich arterial blood cannot diffuse to the tissues, and relative hypoxemia occurs. This results in a positive feedback cycle by which the resulting hypoxemia exacerbates local inflammation and increases edema, which again increases volume and raises interstitial pressure, and further impairs oxygen delivery to tissues (Figure 65-3).

Once the positive feedback cycle has been established, it is difficult to reverse without operative intervention. Surgery for compartment syndrome entails extensile incisions and complete release of the restrictive fascial boundary of the affected compartment. Upon release, the liberated muscles within the compartment expand, often precluding primary closure of the wound. Open wounds pose risk for secondary infection and necessitate additional surgery for wound closure. Depending on the timeliness of initial diagnosis, serial debridement of necrotic muscle and soft tissues within the involved compartment(s) may also be necessary.

The goal of evaluation and management of the at-risk patient is to avoid if possible, but at the very least recognize in a timely fashion, the need for surgical treatment of compartment syndrome. This process starts with identification of the at-risk patient. Given the drastic consequences of a missed diagnosis, even low-energy trauma patients with relatively modest symptoms deserve to be screened for compartment syndrome via a careful physical examination. Those patients with more concerning mechanism of injury (high energy, crush injury, delayed discovery), or concerning initial physical exam should be aggressively treated with noninvasive measures to reduce inflammation and swelling in the affected extremity and subjected to serial examinations. Aggressive application of ice along with strict elevation can prevent development of compartment syndrome, yet elevation in the setting of an established or evolving compartment syndrome can exacerbate ischemia. Treatment of concomitant hypotension can maintain capillary perfusion pressure greater than interstitial pressure and ensure continued tissue perfusion.

Other injuries and comorbidities may conspire to conceal the diagnosis of compartment syndrome. A high index of suspicion is necessary to avoid missed diagnoses. Classic medical teaching refers to the six “P’s” for the diagnosis of compartment syndrome: pain, pallor, pulselessness, poikilothermia, paralysis, and paresthesias. With the exception of pain and perhaps paresthesias, all are late findings of compartment syndrome. If the diagnosis has not been established prior to the development of pulselessness and paralysis, the prognosis becomes dire as tissue necrosis is likely already ongoing.

Pain out of proportion to the injury is the hallmark physical exam finding of compartment syndrome. By definition, compartment syndrome cannot occur without swelling although it may be difficult to appreciate even significant edema contained within the deep posterior compartment in the lower leg. Compartments may be described as, in order of increasing concern, soft, full, tense or firm. The possibility of evolving or early compartment syndrome should be considered in the presence of severe pain despite less worrisome objective exam findings. In such instances, the patient should be reexamined frequently at regular intervals by the same physician who may therefore recognize trends and changes in serial examinations.

Certainly a worsening examination in a patient at risk for compartment syndrome is concerning and warrants further action. Pain with passive stretch of muscles in the suspect compartment is the most ominous physical finding. Compartment syndrome is a clinical diagnosis, and this scenario would indicate the need for emergent surgical fasciotomies. In instances where the patient and/or the exam is unreliable or equivocal—such as the obtunded or intubated patient—direct measurement of compartment pressures is indicated. This may be accomplished via the use of commercially available devices specifically designed for this purpose, or a modified arterial line setup (Figure 65-4). An absolute pressure value >30 mm Hg is consistent with a diagnosis of compartment syndrome. Of more precise diagnostic value is an absolute pressure within 20 mm Hg of the diastolic pressure, that is, the delta (diastolic blood pressure minus compartment pressure). A compartment with a pressure of 30 mm Hg may remain well-perfused in a normotensive patient with a diastolic blood pressure of 70 mm Hg, as opposed to a scenario where that same patient were hypotensive with a diastolic pressure of only 40 mm Hg. Early consultation with orthopedics is advisable if there is any question or concern of compartment syndrome.

VENOUS THROMBOEMBOLIC DISEASE

EPIDEMIOLOGY

Venous thromboembolism (VTE), specifically pulmonary embolism (PE), is the most common cause of readmission and death after elective hip and knee replacement. In the absence of prophylaxis, 80% to 85% of THA and TKA patients will develop deep venous thrombosis (DVT), as will patients following hip fracture. Polytraumatized patients are known to be at high risk for DVT; pelvic (60%), femoral (80%) and tibial (77%) shaft fractures, and spinal cord injury (81%) are associated with the highest risk. Compared to patients with head, chest, or abdominal injury, those with isolated femur or tibial shaft fracture have a 5 times greater DVT risk; spinal cord injury imparts an 8.5 times greater DVT risk. Following TKA, in excess of 90% of thrombi occur below the trifurcation of the popliteal vein, and “proximal” clots occur almost exclusively by contiguous extension of primary calf thrombi to the popliteal vein. In contrast, after THA approximately half of thrombi occur primarily in the proximal (popliteal and common femoral) veins, are typically not contiguous with calf clots, and are discontinuous and segmental in nature. Segmental femoral vein clots after THA typically occur in the region of the lesser trochanter and are thought to result from torsional injury to the intima incurred with positioning of the lower limb. Nearly 20% of postoperative calf clots will extend proximally and, once in the thigh, nearly 50% will embolize to the lung. Accordingly, conventional wisdom holds that patients undergoing THA and hip fracture repair have the greatest risk of PE by virtue of their high frequency of proximal thrombi.

Contemporary prophylaxis against VTE is considered standard of care subsequent to a 1986 NIH consensus conference on the subject. Venographic clot rates with potent new anticoagulants are <5% after THA and <20% after TKA. Reduction in DVT after TKA is relatively more refractory to anticoagulant prophylaxis than after THA; symptomatic VTE is now twice as common in-hospital (1% vs 0.5%) and symptomatic PE is twice as common after discharge (0.27% vs 0.14%) following TKA than THA, respectively. Despite these advancements, fatal PE occurs after 0.1% to 0.5% of total joint replacements, accounting for more than 1000 deaths each year. Appropriately, considerable effort has been directed at identifying the optimal prophylaxis regimen. However, use of potent anticoagulants to mitigate activation of thrombogenesis after orthopedic operations must necessarily be tempered by consideration of the bleeding risk following these procedures, where hemostasis is imperfect in the setting of exposed bony surfaces. It must represent a risk-benefit balance between the fear of fatal PE weighed against the morbidity of persistent wound drainage and hematoma, secondary infection, and reoperation resulting from bleeding associated with perioperative anticoagulant use.

RISK STRATIFICATION

Patients who have undergone disruption of the medullary canal of the long bones of the lower limb, either by virtue of traumatic injury or instrumentation for fracture fixation or prosthetic joint replacement, have the highest risk of venous thromboembolism (VTE) of any in the hospital. Intravasation of marrow fat contents is now known to be a potent thrombogenic stimulus and is largely responsible for the peculiar high risk of venous thromboembolism in the orthopedic patient population. Indeed, this risk is appreciated to be so high that all patients undergoing any lower-limb orthopedic procedure are considered “high risk” in the Surgical Care Improvement Project (SCIP) guidelines for VTE risk stratification and all are considered as automatic recipients of directed anticoagulant prophylaxis unless there exist specific contraindications to same. While heritable hypercoagulable conditions such as Factor V Leiden have been shown to account for a majority of spontaneous VTE events in the community, such markers have not been able to identify those among the joint-replacement population at greatest risk for VTE. Neuraxial (spinal or epidural) anesthesia is widely acknowledged to reduce the risk of lower-limb DVT by approximately 50% compared to general anesthesia, independent of the type of anticoagulant VTE prophylaxis employed in the perioperative period.

Orthopedic practitioners typically opt for one of three main regimens for perioperative VTE chemoprophylaxis; aspirin, low-intensity warfarin, or one of the newer anticoagulants such as fractionated heparins or direct factor X or II inhibitors. Choice of anticoagulant is driven by some approach to risk stratification among this group of high-risk patients; most surgeons agree that a past history of VTE warrants more intensive anticoagulation than provided by aspirin alone.

Guideline reconciliation finally occurred between the American Academy of Orthopedic Surgeons and the American College of Chest Physicians in February 2012, largely as a result of agreement that clinically important PE and VTE was the relevant endpoint and insufficient data existed to endorse any one specific prophylaxis regimen. Concurrently, the ACCP placed greater value on avoidance of bleeding events based on acknowledgement of patient preferences and aversion to surgical complications. Likewise, the exhaustive AHRQ Comparative Effectiveness Review on Venous Thromboembolism Prophylaxis in Orthopedic Surgery concluded, “The balance of benefits to harms is favorable for providing prophylaxis … and to extend the period of prophylaxis beyond the standard 7 to 10 days.” They noted that “interclass comparisons could not be made due to lack of data, similarities between classes on outcomes, or offsetting effects where benefits on efficacy were tempered by an increased risk of bleeding.” In 2014, SCIP added aspirin to its list of acceptable agents for VTE prophylaxis, making the list of appropriate agents uniform and all-inclusive among all groups, with no endorsement of any agent or regimen as best practice.

INPATIENT PROPHYLAXIS

Chemoprophylaxis (Figure 65-5) can by grouped into three main categories; warfarin, aspirin, and selective heparinoids or direct factor Xa or IIa inhibitors.

Warfarin. Low-intensity warfarin (INR target 2.0), despite its variable dosing and need for monitoring, is a time-honored option for orthopedic thromboprophylaxis, likely because it has an acceptably low-bleeding risk (1%-2%) coupled with efficacy in preventing clinically important PE. In 2008, it was the VTE prophylaxis of choice for nearly 50% of US orthopedic arthroplasty surgeons prior to the release of direct Xa and thrombin inhibitors. Warfarin remains popular in the US, despite the inconvenience and expense of monitoring, because many feel it represents the best available compromise of efficacy in preventing clinical VTE and safety in minimizing bleeding.

Critics have been most concerned with its erratic effect, need for monitoring, and associated bleeding. Early studies reported bleeding rates of 10% with a prothrombin time index (PTI) of 1.8 to 2.0, but efficacy is now proven with a PTI of 1.3 to 1.5 (INR 2.0) and reduced bleeding to <2%. Historically, low-intensity warfarin prophylaxis (INR 2.0) results in venographic DVT of 9% to 26% and proximal clot rates of 2% to 5% after THA compared with overall DVT of 35% to 55% and proximal clot rates of 2% to 14% after TKA performed with general anesthesia. Warfarin preferentially reduces proximal compared with distal DVT after THA and, when combined with epidural anesthesia/analgesia, the residual DVT rate dropped below 10%. Most importantly, extended low-intensity warfarin continued for 6 weeks after THA or TKA in 3293 patients was associated with readmission for clinical VTE in 0.3% in THA and 0.2% in TKA with a major bleed rate of 0.1%. In the aggregated THA and TKA groups, 6 weeks of warfarin after hospital discharge eliminated the risk of PE, and reduced VTE-related readmissions 0.2% versus 1.6%.

Optimal use of warfarin remains challenging and labor intensive; it ideally begins the night before surgery because of its 48-hour latency to anticoagulant effect. Indeed, this lag in activity is likely responsible for its popular safety margin with low-perioperative bleeding rates.

Aspirin. Aspirin, acetylsalicylic acid, is traditionally considered an arterial drug but has been used in conjunction with mechanical compression devices for venous thromboembolism prophylaxis by a consistent minority (10%-20%) of surgeons. Conventional wisdom holds that aspirin reduces arterial thrombosis through inhibition of platelet cyclooxygenase-1, which decreases synthesis of thromboxane A2 (platelet-activating eicosanoid) and related platelet activation, and has demonstrated substantial arterial thrombotic event reduction as well as survival benefit relative to stroke, myocardial infarction, and related deaths in high-risk patients. Conversely, clotting experts often regard aspirin as an inferior and inconsistent agent in mitigating venous thrombosis.

Since 2006, three large observational studies and the British joint-replacement registry have rekindled the notion that aspirin can prevent clinical PE after total joint arthroplasty, especially in conjunction with regional anesthesia. In nearly 10,000 THA and TKA patients managed with neuraxial anesthesia, in-hospital pneumatic compression, and 6 weeks of aspirin (325 mg bid or 150 md qd), overall VTE-related readmission was 3.2% after THA with a clinical PE rate of 0.6% compared with overall VTE-related readmission after TKA of 0.5% with a clinical PE rate of 0.36%. In 2009, National Joint Registry data matched nearly 23,000 patients receiving aspirin or LMWH and revealed no difference in 90-day outcomes related to clinical PE (0.7%), DVT (0.95%), stroke or gastrointestinal bleeding (0.75%), or reoperation (0.35%). Yet, patients receiving LMWH had a survival advantage over those receiving aspirin (all-cause mortality 0.49% vs 0.65%; p = 0.02).

In two studies of >1200 patients randomized to aspirin or placebo for prevention of recurrent VTE after standard therapy, aspirin was associated with a 32% reduction in recurrent VTE and a 34% reduction in major adverse vascular events, without an accompanying increase in bleeding. Given its apparent efficacy without a compromise in safety, the role of aspirin in VTE prophylaxis and prevention of embolization of existing venous thrombi is being reassessed.

Newer Agents. Many new selective anticoagulants have been introduced since the 1986 NIH conference, but the risk of fatal PE after THA and TKA has changed very little. Despite venographic clot rates up to 5 times greater than with these newer agents, low-intensity (INR 2.0) warfarin and aspirin offer comparable clinical PE rates and two- to three-fold less major bleeding complications.

Low-molecular-weight (fractionated) heparins and pentasaccharide are incrementally smaller sugar molecules with increasing specificity in binding antithrombin III (AT-III) as the critical intermediary prior to deactivating factor X or II (thrombin). Indeed, synthetically derived pentasaccharide exactly corresponds to the five sugar AT-III binding site and enjoys enhanced specificity to bind factor Xa. Due to its more proximal location in the coagulation cascade, this affinity for factor Xa greatly augments the potency of LMW heparins and pentasaccharide. Accordingly, LMWH reduced overall venographic DVT from 44% to 31% after THA compared with unfractionated heparins; DVT reduction was also significant after TKA, but less dramatic. Fondaparinux (pentasaccharide) further reduced venographic DVT by 50% compared with enoxaparin after THA, TKA, and hip fracture. It was the first agent to reduce DVT to <20% after TKA and the most extensively studied agent after hip fracture, but its bleeding rate of 3% to 6% exceeded even that seen with enoxaparin. One meta-analysis demonstrated a two- to three-fold increase in bleeding after THA and TKA with LMWH compared with warfarin prophylaxis.

New direct factor X and II inhibitors require no monitoring and are administered orally. Rivaroxaban, a direct factor Xa inhibitor, has been most extensively studied in two THA and two TKA trials. Compared with enoxaparin, pooled analysis of the four studies demonstrated a 58% reduction in all-cause mortality and symptomatic VTE (0.6% vs 1.3%; p < 0.001) but aggregate bleeding data revealed an increase in major plus clinically relevant nonmajor bleeding events (3.2% vs 2.6%; p = 0.039). Rivaroxaban has enjoyed rapid growth in popularity in the VTE prophylaxis market, but an increase in bleeding events has dampened enthusiasm for its widespread adoption by the orthopedic community. One observational study demonstrated all-cause mortality after total hip and knee replacement in patients who had been given potent anticoagulants was more than twice that in patients receiving aspirin, pneumatic compression, and regional anesthesia. Another report specifically noted the “failure” of low-molecular-weight heparin compared with warfarin prophylaxis; symptomatic DVT (3.8%), nonfatal PE (1.3%), persistent wound drainage resulting in readmission (4.7%) and reoperation (3.4%) all occurred at rates exceeding prior experience with low-intensity warfarin. Finally, one retrospective review of 1048 consecutive THA and TKA reported a two-fold increase in 30-day reoperation for wound complications with rivaroxaban compared with tinzaparin prophylaxis. Not surprisingly, the orthopedic community has been slow to adopt these newer agents in favor of a more balanced strategy that offers less bleeding risk with comparable protection against clinical VTED.

INPATIENT MANAGEMENT OF ACUTE VENOUS THROMBOEMBOLISM

Management of perioperative DVT requires more vigilant treatment than a spontaneous event in an ambulatory patient. Typically, routine prophylaxis is continued for 35 days after operation and the occurrence of a symptomatic clot may further prolong anticoagulation to mitigate the risk of clot propagation and embolization.

With the advent of multidetector computed tomography for definitive diagnosis of PE, the prevalence of PE has increased 10-fold in the past decade, from 0.2% to >2%, without any explicable change in the operation or perioperative management. It is likely that this increment is largely explained by the recognition of very small peripheral subsegmental filling defects with this more sensitive CT technology. The clinical significance of these lesions has been questioned and it has been proposed that they represent embolization of marrow elements from instrumentation of the medullary canal rather than a conventional PE. When clinically silent hypoxemia is recognized with pulse oximetry, a 10-minute 2 L/min oxygen challenge has been proposed; resolution of hypoxemia has been suggested to indicate the absence of a meaningful PE and no need for further intervention. Persistence of hypoxemia deserves further workup. The observed frequency of PE has returned to less than 1% with this pragmatic clinical protocol.

Acute postoperative PE is conventionally managed with more intensive anticoagulation. There is increasing interest in outpatient management with the newer oral agents, however the substantial risk of bleeding in the early period after hip and knee replacement should temper the enthusiasm for outpatient management of PE within 5 to 10 days of the index operation. Indeed, when initiating therapeutic anticoagulation with an IV heparin bolus for clinically significant PE within 5 days of operation, the risk of major wound hemorrhage is 50% and within 1 week the bleeding rate decreases to 15%. In general, intravenous heparinization should be initiated with a constant continuous infusion without bolus therapy in the first week after total joint replacement.

In general, it is accepted that the risk of VTE after orthopedic surgical procedures extends far beyond the time of operation and hospital discharge. Clinical guidelines endorse 35 days of prophylaxis after THA and 10 to 35 days after TKA.

FAT EMBOLISM SYNDROME

EPIDEMIOLOGY

The fat embolism syndrome (FES) was initially described by Zenker in 1861 in a patient following a thoracoabdominal crush injury. It may be practically defined as a complex alteration in coagulation homeostasis that occurs as an infrequent complication of fracture of the pelvis and long bones and is manifest clinically as acute respiratory insufficiency secondary to the filtering function of the lung. The full blown clinical syndrome is evident in 0.5% to 2% of patients after isolated long bone fractures and approaching 5% to 10% of patients with multiple fractures and pelvic injuries following polytrauma. In contrast, fat embolization occurs as a subclinical event following all fractures as well as instrumentation of the medullary canal during total joint replacement. The likelihood that this event results in the clinical manifestations characterized by florid respiratory failure is determined by the quantity of fat intravasated into the systemic circulation and the ability of the patient’s cardiopulmonary system to withstand the collection of this material in the lung.

RISK STRATIFICATION

Conditions that increase the size and fatty content of the marrow cavity, such as collagen vascular diseases and osteoporosis, increase the risk of FES. Children develop clinical FES nearly 100 times less commonly than adults, secondary to persistence of hematopoietic marrow and a paucity of fatty marrow. Instrumentation of the medullary canal during THA and TKA always results in embolization of marrow fat to the lung; concurrent bilateral TKA under the same anesthetic increases this risk and has been largely curtailed. Whether it is clinically manifest as FES is largely determined by the magnitude of the embolic load, the intrinsic cardiopulmonary reserve, and the ability to maintain oxygenation in the presence of pulmonary capillary occlusion.

EVALUATION AND MANAGEMENT

The initial insult after embolic fat to the lungs is characterized by increased right heart pressures and cardiovascular collapse, evidenced by hypotension, hypoxemia, confusion, and bradycardia, and is infrequently clinically evident in humans. It has, however, been reported after cementation of the femoral component during total hip arthroplasty, especially in the elderly osteoporotic patient treated for hip fracture and after intramedullary nailing of the femur for an impending pathologic fracture with concurrent filling of the medullary canal with methylmethacrylate. Autopsy evaluation typically demonstrates embolic marrow elements in the capillary bed of the brain, suggesting a lung filter overloaded with embolic material that leaks into the systemic circulation. Transient aphasia and other central neurologic deficits have been observed after bilateral total knee arthroplasty in patients with a patent foramen ovale; embolic intracerebral events can be seen by magnetic resonance imaging.

The more typical fat embolism syndrome is “delayed” in its appearance; clinical signs and symptoms typically develop in 85% of patients within 48 hours after fracture or instrumentation of the medullary canal. This temporal delay is thought to result from the evolving effects of vasoactive substances in the lung and the resulting decrement in gas exchange. Clinical manifestations are primarily cardiopulmonary in nature and include arterial hypoxemia; oxygen desaturation, sinus tachycardia, and fever comprise the classic triad of early findings. Nonspecific changes of pulmonary congestion may be seen on the chest radiograph and the EKG often exhibits ST segment elevation from ischemia or right heart strain. Alterations in cognition are common and may include lethargy, delirium, and/or seizures secondary to hypoxemia or fat embolization to the brain. Petecchiae develop in more than half of patients and typically occur in the axilla (Figure 65-6), over the chest and base of the neck, and in the conjunctivae; they often appear after a 24- to 48-hour delay and are evanescent in nature. Skin biopsy demonstrates embolic fat in capillaries with local hemorrhage. A variety of laboratory coagulation abnormalities are present but clinical bleeding is rare. While this constellation of findings is uncommon, the mortality rate approaches 10% to 15% after full-blown FES. A high index of suspicion is necessary for early diagnosis and proper treatment.

No specific treatment exists for FES. Rather, acute management is predicated upon provision of supportive pulmonary care, often with intubation, oxygen, and mechanical ventilation with airway pressure support in an effort to mitigate the effects of the adult respiratory distress syndrome. In many circumstances high-dose steroids are empirically utilized as a general measure to blunt the lung reaction, stabilize the pulmonary capillary bed, and improve gas exchange.

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INTRODUCTION

Organ transplantation is a complex but effective treatment for end-stage organ failure. Since the advent of more potent immunosuppressive medications, the demand for transplantation has far exceeded the supply. Every year in the United States more than 25,000 people undergo organ transplantation, while at the same time more than 100,000 people remain on the waiting list. The combination of complex surgery, immunosuppression, and very ill and debilitated patients make postoperative management very challenging.

Complications related to transplantation are most often divided into early (typically technical in nature) and late (typically related to immunosuppression or other medications). All of the complications associated with less complicated general surgical procedures can also be seen after transplantation. This chapter will focus on the complications that are particular to transplantation and that are most likely to be encountered by Hospitalists.

COMPLICATIONS OF KIDNEY TRANSPLANT

POSTOPERATIVE OLIGURIA/GRAFT DYSFUNCTION

The causes of early graft dysfunction range from the benign to the truly emergent and include, but are not limited to, thrombus in the Foley catheter, acute tubular necrosis, thrombosis of the renal artery or vein, ureteric leak or stenosis, and rejection. Prompt diagnosis and appropriate management are necessary to salvage the graft (Figure 66-1).

Low or absent urine output may be attributable to the renal parenchyma (ATN), the renal vasculature, ureteral issues, or Foley catheter obstruction/malfunction. ATN is the most likely cause for poor/delayed graft function and complicates approximately 20% to 30% of kidney transplants. It is more common in the setting of long cold ischemic times, older donors, and highly sensitized recipients. It typically improves spontaneously over the first few weeks posttransplant. Although ATN is the most likely etiology of poor initial function, it is a diagnosis of exclusion, and a rapid and systematic evaluation must occur to rule out the other more worrisome possibilities:

• The Foley catheter should be irrigated to ensure that clot or tissue has not affected its patency.

• The adequacy of resuscitation should be evaluated by reviewing the vital signs, central pressures, and fluid balances; intravascular depletion should be treated with a bolus of an appropriate crystalloid fluid.

• The patency of the renal artery and vein should be evaluated using duplex Doppler ultrasonography. Urgent surgical exploration is indicated when vascular compromise is demonstrated by imaging or when clinical suspicion is high. Renal scintigraphy can be used as a confirmatory test after ultrasound.

• Acute cellular rejection is unlikely early after transplant but must be a part of the differential if the clinical scenario is appropriate (ie, high panel reactive antibodies or PRA, marginal crossmatch, absence of other explanation). When rejection is suspected, either an open renal biopsy (if the patient is post-op day <7) or percutaneous biopsy (if the patient is post-op day >7) is indicated.

• Hyperacute rejection, mediated by preformed antibodies against the donor, is extremely uncommon in the modern era, but leads almost inevitably to graft loss.

Other common surgical complications after kidney transplant are outlined in Table 66-1.

OTHER POSTOPERATIVE COMPLICATIONS

Most of the early complications after kidney transplantation may be diagnosed by either ultrasonography or renal scintigraphy. CT scan with IV contrast should be avoided in the posttransplant setting due to the nephrotoxic effects of the contrast. Small perinephric hematomas are very common, particularly in recipients receiving anticoagulants, antiplatelet agents, thymoglobulin, or plasmapheresis. Most small hematomas will resolve spontaneously and require no intervention. Hematomas with pressure effect on the graft need to be evacuated surgically (percutaneous drainage is almost never sufficient). Thrombosis of the renal artery or vein is uncommon with a cumulative incidence of approximately 2%; when present it is almost invariably due to technical issues (ie, kink, malposition, intimal flap). Such vascular thrombosis typically presents with sudden onset of oliguria/anuria, and in the case of venous thrombosis, frank hematuria and pain over the graft. Confirmation of the diagnosis (best by duplex Doppler ultrasound) requires emergent return to the operating room for exploration. Grafts with venous thrombosis may be salvageable with prompt identification and treatment, but arterial thrombosis is almost universally associated with graft loss.

The most common urological complication following kidney transplantation is hematuria. The source of the bleeding, which is usually minor, is the new anastomosis between the transplanted ureter and the native bladder. In the rare instance that the bleeding does not stop spontaneously, revision of the anastomosis or cystoscopic ablation may be necessary. Care must be taken to avoid (or at least quickly identify) Foley catheter occlusion with clot. Most often gentle irrigation is sufficient to relieve the occlusion, but occasionally Foley replacement is necessary. Urologic consultation is well advised for frank hematuria (after ruling out venous thrombosis) or persistent slow bleeding.

Urine leak, most commonly from the neoureterocystostomy, is a common early postoperative complication, the clinical presentation of which can range from the very subtle to the very obvious. The most obvious presentations typically include an abrupt decrease or cessation of urine output, associated with the development of copious clear wound drainage or drain output. More subtle presentations might include new onset abdominal pain or an unexplained elevation in the serum creatinine. Urine leak should be in the differential diagnosis in the early posttransplant period whenever there is poor urine output, a new fluid collection, new wound drainage, new abdominal pain, or delayed graft function. Any new fluid drainage or aspirated fluid collection should be sent for creatinine measurement and the value checked against the serum value. Diagnostic imaging choices include CT cystogram, contrast cystogram, and renal scintigraphy (the most sensitive test choice).

For small, distal leaks, management typically begins with reinstitution of Foley bladder drainage, placement/replacement of ureteral stent, and percutaneous drainage. Cystoscopic placement of a stent can be challenging due to the ectopic ureteral location and lack of periureteral support. Percutaneous nephrostomy is an option, although this may be technically difficult in the absence of hydronephrosis. If this approach is effective, the catheter should remain in place for at least 2 weeks and a cystogram performed prior to catheter removal. Treatment failure, whether manifest by uncontrolled drainage or persistence of the leak beyond two weeks, suggests ureteral necrosis and is an indication for operative exploration and revision of the neoureterocystostomy.

The development of a lymphocoele after renal transplantation is common and is thought to be related to the disruption of the lymphatics surrounding the iliac vessels. Most collections are small (<100 cc), identified on ultrasound, and clinically silent. Spontaneous resolution of these small collections is the normal course. Larger collections may become apparent clinically and usually do so between 1 week and 6 months after transplantation, with incidence peaking at around 30 days posttransplant. They commonly present with complaints related to nocturnal urinary frequency as a consequence of bladder impingement by the lymphocoele. A sensation of pelvic fullness and ipsilateral painless leg edema are other common complaints. Deteriorating renal function subsequent to ureteral stent removal can be the first presentation of a lymphocoele that is compressing the donor ureter. For symptomatic lymphoceles, percutaneous drainage is successful in about 50% of the cases. A fraction of the remaining 50% will respond to an attempt at ablation with the instillation of a sclerosant into the cavity. Surgical drainage via creation of a peritoneal window is a last resort and can be done open or laparoscopically.

COMPLICATIONS OF LIVER TRANSPLANT

INTRAOPERATIVE HEMORRHAGE AND COAGULOPATHY

Patients in need of liver transplantation often have concomitant portal hypertension and coagulopathy as a consequence of their liver disease (Figure 66-2). This combination results in a tremendously high risk for significant intraoperative blood loss. Additionally, patients with a history of any upper abdominal surgery or past spontaneous bacterial peritonitis (SBP) portends an even greater intraoperative risk, as they are associated with the presence of extensive and heavily collateralized adhesions. As with any procedure associated with massive blood loss, there is a real possibility that the resulting derangements in temperature, fluid homeostasis, and the coagulation cascade will create a vicious cycle that can be extremely difficult, if not impossible, to recover. In these situations, the most prudent action is often to truncate the operation and get the patient off of the operating table and into the ICU as quickly as possible. The transplant can be completed if and when the patient is resuscitated and stabilized.

HEPATIC ARTERY THROMBOSIS

The literature suggests that the overall incidence of hepatic artery thrombosis (HAT) is between 1.6% and 8% in adult liver transplant recipients. The clinical presentation of HAT ranges from an asymptomatic patient with minimal alterations in liver function to a critically ill-patient with fulminant hepatic necrosis. The most common presentations begin with postoperative biliary complications, including leaks, strictures, and ischemic intrahepatic cholangiopathy.

Suspicion of HAT should be raised whenever there is evidence of biliary complication or significant worsening of liver chemistries. Initial investigation is made with duplex ultrasonography. If the duplex is suspicious, further evaluation by visceral angiography or CT angiography is needed, as failure to make a rapid diagnosis can result in hepatic necrosis and graft loss.

The approach to HAT in the early postoperative period, regardless of whether or not symptoms are present, should be an aggressive attempt at the reestablishment of arterial flow to the liver. This often requires urgent operative exploration and revision of the anastomosis or replacement of the artery with conduit (usually a donor iliac artery). Some surgeons attempt to reestablish flow using thrombolystics, but this will be successful only when there are no technical factors contributing to the thrombosis. In most cases of HAT, patients ultimately require retransplantation as a consequence of ischemic biliary cholangiopathy.

PORTAL VEIN THROMBOSIS

Portal vein thrombosis after transplantation is an uncommon complication in the immediate postoperative period, and is usually the result of a technical issue, such as incomplete recipient portal vein thrombectomy or a mechanical issue with the anastomosis. A high index of suspicion is needed to make the diagnosis, and investigation by duplex Doppler ultrasound is usually initiated with one or more of the following signs: new or persistent ascites, lower-body anasarca, persistent varices, and new or persistent encephalopathy. Early thrombosis is best treated with reoperation, thrombectomy, and anastomotic revision followed by systemic anticoagulation. The treatment of late thrombosis is more controversial as direct repair is technically challenging and not very durable.

BILIARY LEAKS

The reported incidence of biliary leaks after liver transplantation varies widely from 10% to 50%. Leaks are observed most commonly at the site of choledochal anastomosis. Anastomotic leaks encountered in the early postoperative period are most often related to either technical errors (ie, tension, twisting, denuding, malpositioned stitch) or ischemic necrosis following HAT. Signs and symptoms include bilious drainage, abdominal or shoulder pain, increased serum bilirubin, nausea, vomiting, fever, or copious ascites. The diagnosis can be made by HIDA scan, endoscopic retrograde cholangiography (ERC), or percutaneous transhepatic cholangiography (PTC). ERC is preferred because it offers an opportunity to treat with endoscopic stent placement without the risk associated with the indwelling transhepatic catheters used during PTC. HIDA is useful very early after transplantation when manipulation of the anastomosis is best avoided in the absence of a confirmed leak. CT scan is useful as an adjunct to identify fluid collections that require percutaneous drainage. Large leaks or leaks associated with ischemic necrosis require surgical intervention, usually with conversion to a Roux-en-Y hepaticojejunostomy. The development of early postoperative leaks is associated with late stricture formation and may also be a contributor to late HAT.

BILIARY STRICTURE OR OBSTRUCTION

Biliary obstruction occurs in approximately 7% to 15% of patients after liver transplantation. Anastomotic stricture accounts for 50% of obstruction cases and can occur early in the postoperative period secondary to edema, or later, as a result of compromised blood supply. The diagnosis of biliary stricture or obstruction is suggested by an obstructive pattern on routine liver function tests. Commonly, patients present with constitutional symptoms of rigors, fever, headache, and fatigue. Occasionally, patients will present with symptoms of cholangitis and sepsis.

After appropriate fluid resuscitation and antibiotic coverage, ERC or PTC is indicated to confirm the diagnosis and to relieve the obstruction by either stenting or proximal drainage. An unpassable stricture or obstruction is indication for surgical revision or, more likely, conversion to Roux-en-Y hepaticojejunosotomy. The rare intrahepatic strictures are best treated with percutaneous balloon dilatation.

PRIMARY GRAFT NONFUNCTION

Primary graft nonfunction (PNF) following liver transplantation is an infrequent but life-threatening complication wherein the transplanted liver does not recover function after engraftment. This usually fatal complication occurs in approximately 5% to 6% of cases and is, by definition, without identifiable cause. PNF is usually heralded by severely elevated and rising serum transaminases (often >8000 IU/L) within the first 24 to 48 hours after transplant and a rising PT and INR. The clinical picture also often includes rising serum bilirubin and worsening renal function. PNF is multifactorial and putative causes include all manner of donor, recipient, and procedure-related variables. Patients with PNF require urgent retransplantation, usually within 24 to 72 hours, if mortality is to be avoided. Explantation of the nonfunction liver and creation of a portocaval shunt has some role in patients with PNF and refractory or profound acidemia.

RENAL DYSFUNCTION

Renal dysfunction is observed to some degree in nearly every patient who undergoes liver transplantation. In patients with normal preoperative serum creatinine and good initial graft function, the usual mechanism is prerenal azotemia secondary to periods of hypotension and hypovolemia during the operative procedure, as well as the temporary partial occlusion of the inferior vena cava (IVC) that occurs during the implantation. Additionally, the postoperative administration of nephrotoxic agents, especially the calcineurin inhibitors (CNIs) cyclosporine and tacrolimus, contribute to impaired renal function. Management is largely expectant with dialysis as necessary until renal function recovers. Delayed administration of CNIs is prudent in patients at particular risk of renal dysfunction after transplant.

COMPLICATIONS OF PANCREATIC TRANSPLANT

Presently there are more than 1,000,000 individuals with type 1 diabetes in the United States. A successful pancreas transplant will produce a normogylcemic insulin independent state and prevent progression of diabetic nephropathy, stabilize diabetic retinopathy, and potentially reverse diabetic peripheral sensory neuropathy. The vast majority of pancreas transplants are performed as a simultaneous kidney and pancreas transplant (85%-90%) for patients with diabetes and concomitant renal failure. A smaller number are done following a prior successful kidney transplant, and fewer still are done as an isolated transplant for patients with very labile type 1 diabetes complicated by recurrent episodes of hypoglycemic unawareness or diabetic ketoacidosis. When considering isolated pancreas transplantation, it is important to weigh the potential benefits of normoglycemia against the risk of lifelong immunosuppression. In the case of simultaneous kidney and pancreas transplantation or pancreas transplantation following kidney transplant, the risk of the immunosuppression is clearly outweighed by the avoidance of dialysis (Figure 66-3).

THROMBOSIS

Thrombosis of the donor portal vein is a common complication after pancreas transplantation and is attributable to a the relatively low flow state of the pancreas graft, as compared to normal portal vein flow. Arterial thrombosis is much less common and is usually the result of a technical error at the time of transplantation. Postoperative hyperglycemia suggests the possibility of graft thrombosis and necessitates urgent evaluation with duplex Doppler ultrasound. There is a potential for graft salvage with rapid identification of thrombosis and operative thrombectomy. Approximately 3% to 5 % of the pancreas grafts are lost due to graft thrombosis.

PANCREATITIS OF THE GRAFT

Graft pancreatitis is not uncommon and will manifest as elevations in the serum amylase and lipase, usually without associated abdominal pain. Treatment is largely expectant but in some cases the development of phlegmon or abscess will require operative debridement or percutaneous drainage.

COMPLICATION OF THE ENTERIC DRAINED TRANSPLANT

Duodenal stump leak or anastomotic leak is one of the most serious complications of a pancreas transplant. Patients present with fever, pain, and a leukocytosis. CT scan is helpful in making the diagnosis. Surgical exploration and repair of the leak is necessary. Removal of the graft might be required if it is not salvageable.

COMPLICATIONS SPECIFIC FOR BLADDER DRAINED PANCREAS

There is a greater incidence of urinary infection due to the bicarbonate-rich fluid draining into the bladder. Sterile cystitis, urethritis and balanitis may occur after bladder drainage. Reflux of the urine through the ampulla can result in reflux pancreatitis, which is initially managed by Foley catheterization. Patients might require a work up for bladder dysfunction. Urine leak due to the duodenal stump breakdown will necessitate re-exploration.

GENERAL COMPLICATIONS AFTER TRANSPLANTATION

ACUTE IMMUNOSUPPRESSIVE DRUG TOXICITY

Immunosuppression after transplantation must achieve a balance between the beneficial effects of the drugs in preventing or reversing rejection, and the dangers of excess immunosuppression with the development of acute toxicity symptoms, nosocomial infection, and lymphoproliferative disorders. The most common agents used for immunosuppression in liver transplant patients are cyclosporine and tacrolimus (FK506) in combination with steroids. Mycophenolate mofetil has essentially replaced azathioprine in the immunosuppression regimen after liver and kidney transplantation. After the initiation of immunosuppression therapy, development of infection and acute toxicity are usually seen early during treatment, whereas lymphoproliferative disorders and other malignancies are long-term sequelae.

The side-effect profiles of cyclosporine and tacrolimus are similar and include gastrointestinal disturbances, headache, and tremor. Gingival hyperplasia and hirsutism are encountered frequently during cyclosporine and steroid treatment, whereas glucose intolerance is reported more often with tacrolimus treatment than with cyclosporine therapy. Hyperkalemia, hyperuricemia, hypophosphatemia, and hypomagnesemia are manifestations of renal tubular dysfunction and usually can be controlled by adjusting the dose according to drug levels. Nephrotoxicity is the most clinically significant adverse effect of both drugs and is manifested as acute azotemia. This effect is largely reversible after reducing the dose of the drug and providing adequate hydration. Occasionally, progressive chronic renal disease can develop, which is usually irreversible. In such a situation, dialysis or kidney transplantation is required.

NEUROPSYCHIATRIC COMPLICATIONS

In addition to the acute neurophysiologic changes associated with fluid and electrolyte shifts during the perioperative period, anxiety and depression are common psychiatric conditions observed in many transplant patients. Seizures, alterations of the levels of consciousness, and infections of the central nervous system are infrequent but are significant causes of morbidity and mortality. Encephalopathy observed after liver transplantation can be related to poor initial graft function, but it is more commonly multifactorial in etiology. Metabolic derangements, hypoxia, sedation, and drug interactions all can contribute.

Neurologic signs and symptoms associated with immunosuppression toxicity related to cyclosporine and tacrolimus include tremors, headaches, and seizures. These can be avoided by close monitoring of drug levels. High-dose steroids can result in emotional liability or mania. Any patients presenting with new neuropsychiatric symptoms should have a cranial CT scan and lumbar puncture to rule out other causes of mental status changes, such as intracerebral bleeding or an infectious etiology. Posterior reversible encephalopthay syndrome (PRES) often manifests in the setting of drug toxicity and hypertension. Clinically, PRESS manifests with headaches, seizures and visual loss. These patients require and urgent MRI and intensive care unit admission and aggressive control of hypertension with minimization of their cyclosporine and tacrolimus.

FLUID AND ELECTROLYTE DISTURBANCES

Fluid and electrolyte disturbances and alterations in acid-base status are common after transplantation. Preoperative protein calorie malnutrition and end-stage liver disease lead to derangements in total body water and electrolyte balance that are worsened initially by the metabolic stress of surgery and massive fluid and blood product resuscitation. The rapidity of recovery depends in large part on the patient’s renal and liver allograft function postoperatively. For a patient with stable postoperative renal and liver graft function, little metabolic manipulation is required to correct such derangements.

The early development of metabolic alkalosis secondary to metabolism of citrate in blood products is a favorable sign of graft function but can be serious if alkalemia develops. Excess total body water and excess sodium are best treated with gentle diuresis with furosemide. Careful repletion of potassium should be instituted, but it must be monitored closely in the setting of medications such as tacrolimus and cyclosporine, which tend to increase serum potassium levels by afferent arteriolar constriction and direct distal tubular toxicity. Derangements in serum calcium, magnesium, and phosphorus are common and should be repleted to avoid neurologic, skeletal, and cardiac muscle dysfunction.

POSTTRANSPLANT INFECTIONS

Infection risk is determined by a patient’s “net state of immunosuppression,” a balance contributed to by factors such as the dose, type, and duration of immunosuppressive therapy, the presence of indwelling devices such as catheters, nutritional status, metabolic conditions, certain immunomodulating viral infections, graft function, and underlying diseases. Signs and symptoms of infection are often attenuated in the setting of immunosuppression. The variety of possible pathogens is quite broad but is influenced by the timing of infection in relation to transplantation (Figure 66-4). Antimicrobial agents used to treat infections can have important drug interactions with immunosuppressive medications, and consultation with a pharmacist is strongly recommended. Infections in these patients may be more severe and progress more rapidly compared with immunocompetent hosts.

LATE TRANSPLANT COMPLICATIONS

HYPERTENSION

Hypertension is common after renal transplantation with nearly 70% of the patients requiring antihypertensive medications. Hypertension can be caused by preexisting disease, medications (tacrolimus, cyclosporin, prednisone) and rarely due to stenosis of the renal artery anastomoses. The treatment of posttransplant hypertension is same as in the nontransplant population.

HYPERLIPIDEMIA

Hyperlipidemia is common in the posttransplant patient, and the cause is often multifactorial. Some of the medications used (tacrolimus, cyclosporin, prednisone) are prone to cause hyperlipidemia. The management of these patients should follow the guidelines used to treat general population with dyslipidemias.

NEW ONSET DIABETES AFTER TRANSPLANTATION (NODAT)

Exposure to immunosuppressive agents such as tacrolimus, cyclosporin, and steroids can predispose to the development of diabetes after transplantation. The incidence of NODAT can range from 5% to 40%. Tacrolimus has a higher propensity to cause hyperglycemia than cyclosporine. Most of the patients tend to become insulin dependent and the same guidelines used to treat non transplant patients should be used in these patients.

SKELETAL COMPLICATIONS

Osteoporosis is common after renal transplantation and seems directly related to amount of steriods used. Treatment involves steroid-free regimens, calcium supplements and bisphosphonates.

POSTTRANSPLANT MALIGNANCIES

The incidence of skin cancer, lymphoma and kaposi sarcoma are significantly increased in posttransplant patients. Kaposi’s sarcoma is thought to be related to HSV-8 and is generally treated by minimizing immunosuppression. Squamous cell cancers and melanomas appear to be more frequent in the posttransplant population and they tend to have a more aggressive course. Early detection and aggressive management is necessary. Posttransplant patients should minimize sun exposure and should have regular skin examination. Posttransplant lymphoproliferative disorder (PTLD) is a type of B-cell lymphoma related to Epstein Barr virus (EBV) infection. These are most commonly extra nodal in presentation. Treatment of PTLD involves minimizing immunosuppression; some patients will require chemotherapy or radiotherapy.

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PREOPERATIVE RISK STRATIFICATION

Any patient undergoing urology surgery should have a preoperative risk assessment. Obesity significantly contributes to the increased incidence and progression of urologic condition requiring surgery (eg, neoplasms, BPH, stress incontinence, erectile dysfunction, infertility, and urolithiasis); obese patients are also at increased risk for general postoperative complications. Increased peripheral androgen conversion to estrogen and secretion of prothrombin activator inhibitor-1 adipocytes contributes to a hypercoagulable state. Poor wound healing is more common in obese patients because of the proinflammatory state of the body, decreased peripheral perfusion, decreased local angiogenesis, and inhibited cell tissue response. The body habitus of obese patients also predisposes them to complications such as urethral-vesical anastomotic leak (UVAL) due to inadequate surgical exposure.

On the other end of the spectrum, poor preoperative nutritional status has also been well established as a risk factor for developing postoperative complications. Patients with one of four abnormalities in preoperative nutritional parameters have significantly higher-postoperative complication rates as well as longer hospital stays (low body mass index <24, preoperative weight loss >5%, arm muscle circumference <5th percentile, and low-serum albumin [below reference range]).

Risk factors that predispose patients to developing complicated UTIs include older age, external instrumentation, ureteral stent or other foreign body placement, metabolic dysfunction (obesity, diabetes mellitus, poor nutritional status), urinary tract obstruction (anatomic or functional), immunosuppression, and recent antibiotic use.

URINARY RETENTION

Under normal physiologic conditions, the urgency to void is sensed when the bladder reaches a threshold of approximately 250 to 300 mL. Maximum bladder capacity for the average adult is 400 to 600 mL. Afferent pelvic sensory nerves are stimulated to transmit a signal to the parasympathetic ganglia in the spinal cord. Parasympathetic efferent fibers then fire a signal to the detrusor muscle of the bladder to initiate micturition when socially appropriate. Conversely, if micturition is not desired, afferent fibers will cause activation of the sympathetic nervous system and inhibit contraction of the detrusor muscle and cause contraction of the internal urethral sphincter (visceral efferent) and external sphincter (somatic efferent).

The incidence of postoperative urinary retention (POUR) ranges from 4% to 29%. Factors that contribute to POUR include prior history of urinary retention, the type of surgery performed and whether performed on an emergency basis (anorectal and total knee replacement amongst the highest with incidences of 16% to 20% and 19% to 70%, respectively), method and duration of anesthesia (>2 hours), emergency surgeries, certain medications (those with anticholinergic properties, opioids), constipation, and inability to ambulate postoperatively (Table 67-1).

Evaluation of a patient with suspected POUR includes ultrasound of the bladder, bladder catheterization (when indicated), and postvoid ultrasonography of the bladder. Sedated patients may not be able to mount an urgency to void even if their bladder holds an amount of urine that would typically instigate such a sensation. One study found that as many as 61% of patients in the postanesthesia care unit (PACU) did not verbalize that they needed to void despite having 600 mL of urine (confirmed by ultrasound).

If POUR is suspected, an ultrasound is indicated to confirm urinary retention, obtain an approximate amount of retained urine, and to avoid unnecessary catheterizations. Studies have shown good correlation between volumes measured on ultrasound and those determined by catheterization. Ultrasound has been shown to improve detection of POUR at larger volumes in patients who cannot appreciate the need to void. False positive results of bladder scan technology commonly occur in patients with generalized anasarca, gravid uterus or peritoneal dialysis fluid.

Assuming no contraindications, catheterization follows sonography in patients with bladder volumes greater than 250 to 300 mL and the urine is sent to for routine microscopy and culture if indicated. Nurse-driven algorithms (Figure 67-1) can help determine the clinical necessity of indwelling catheters and assess for the possibility of early removal.

Complications of POUR include bladder overdistention leading to hypotonia, renal insufficiency, and infection from urine stagnation. Intermittent catheterization (IC) is justified as an acceptable and appropriate alternative to indwelling catheterization. Both the CDC and the American Urological Association (AUA) recommend clean intermittent catheterization over indwelling catheterization for intermediate and long-term bladder decompression when feasible.

Alpha-adrenergic antagonists, particularly those with favorable affinity for the alpha-1a receptor such as tamsulosin, may reduce the incidence of POUR if initiated preoperatively. If no contraindication to the medication, tamsulosin should be instituted at the time of POUR diagnosis if it was not used prior to surgery. In general, alpha-blockers should be used with caution in patients with hypotension, or a history of cataract or glaucoma surgery. Tamsulosin specifically can stimulate an allergic reaction in someone with a hypersensitivity to sulfonamides.

Although intermittent catheterization is widely accepted for management of POUR for outpatient procedures, the duration of catheterization for inpatient surgeries remains controversial (Figure 67-2).

Patients with chronic urinary retention will have a rapid diuresis (>200 mL/h), which usually resolves spontaneously. They need to be closely monitored for dehydration and electrolyte imbalances. If patients have access to water, most can compensate for any deficit. If unable to drink, patients may receive IV fluid supplementation using a hypotonic solution (0.45% normal saline) with replacement of half the urine output every 2 to 4 hours.

URETERAL INJURY

Fifty percent of all ureteral injuries occur during gynecologic procedures (with radical hysterectomies and abdominal hysterectomies accounting for 50% and 40% of these, respectively). The injury generally involves the distal one-third of the ureter, where the ureter is in closest proximity to the uterus and associated structures. Risk of injury to the ureter is highest during ligation and division of the cardinal ligaments in abdominal hysterectomies. Other injuries observed intraoperatively include kinking, laceration, burn injury from electrocautery, and insults that compromise the blood supply to the ureter.

Radical prostatectomy, ureterolysis, retroperitoneal lymph node dissection, and female incontinence procedures pose the highest risk of injury amongst the urological procedures. Risk factors for ureteral injury include abnormal anatomy, intraoperative hemorrhage, and failure to recognize the ureter intraoperatively.

Failure to recognize ureteral injury and treat appropriately may result in permanent renal damage and may ultimately result in nephrectomy. Patients with ureteral injury and a urine leak may have fever, ileus secondary to uroperitoneum, abdominal swelling, and flank pain. Laboratory abnormalities include leukocytosis, elevated BUN and creatinine secondary to peritoneal absorption, hematuria and pyuria. Hematuria is absent in 23% to 45% of all ureteral injuries. Imaging may reveal the presence of ascites and pleural effusion. Intraperitoneal drain fluid may be sent for analysis of a creatinine level if there is a higher output than expected. The fluid in the drain contains some urine if the value is much higher than the patient’s serum creatinine.

The following tests may diagnose ureteral injury:

• Intraoperative retrograde pyelogram (the gold standard)

• Renal ultrasound to identify urinoma, hydronephrosis

• CT with contrast and delayed images to evaluate function of the kidney ipsilateral to the injury and the integrity of the affected ureter

If a minor ureteral injury is recognized intraoperatively, the surgeon may place a ureteral stent to facilitate the healing process. These stents are typically removed 4 to 6 weeks after the procedure. Ureteral injuries that are not corrected intraoperatively tend to be more complex in nature, require more extensive surgical repairs, and have more associated complications. The vast majority of ureteral injuries will not resolve on their own and require emergent urologic consultation.

TRANSURETHRAL RESECTION SYNDROME

Transurethral resection syndrome (TURS) is commonly associated with transurethral resection of the prostate (TURP), but may occur in any endourological procedure using hypotonic solution for mechanical bladder irrigation. After many patients were noted to exhibit extensive hemolysis following irrigation with deionized water, nonelectrolyte hypotonic fluids such as glycine, sorbitol, and mannitol were introduced to decrease this complication.

TURS primarily occurs by direct infusion of the irrigating solution into the venous sinuses of the prostate and by reabsorption of extravasated fluid following prostatic capsule and/or bladder wall perforation. Hyponatremia develops secondary to the dilutional effect of the irrigant as well as from a natriuretic response from increased extracellular fluid volume. This complication may be associated with a postobstructive diuresis, following surgical relief of chronic obstruction.

The progression and presentation of these patients depends on the rate, amount, and type of fluid used during the procedure. TUR syndrome may present acutely or insidiously over 24 hours; while direct venous sinus infusion of the irrigant will lead to an acute presentation, resorption of extravasated fluid from prostatic capsule or bladder perforation may cause a more insidious onset (Table 67-2).

If risk factors for the development of TURS are present (procedure length >90 minutes, open venous sinuses, high-pressure irrigation, and large volume of resection [>45 g]) and no intraoperative or postoperative sodium level was obtained, serum sodium and serum osmolalities should be ordered immediately.

Patients with TURS will need their volume status stabilized and hyponatremia corrected. Blood pressure may transiently increase due to aggressive fluid replacement; this will resolve as fluid passes through the cellular membrane into the cell. Usually the patient should be managed in a step-down or intensive care unit.

HEMATURIA FOLLOWING ENDOSCOPIC SURGERY

With any endourologic resection, the amount of postoperative bleeding will largely depend on the extent of tissue resected. Arterial bleeds typically present with acute onset of hematuria, while venous bleeds will develop gradually. Postoperative bleeds may be due to patient-specific factors such as increased blood pressure as the patient emerges from anesthesia, or a coagulopathic state. A bleeding vessel is compressed with bladder distension during surgery; reinspection with a reduced volume in the bladder will often identify bleeding vessels before the surgery is complete.

A three-way catheter in place following endourological procedures allows for continuous bladder irrigation (CBI), which helps prevent the formation of any blood clots that may obstruct the outflow of urine, and helps to quell the bleeding. Urine return that is light-red to pink in color indicates that the current rate of irrigation is likely sufficient to prevent clot formation.

The lumen of the three-way catheter may become obstructed due to the relatively small size. Any obstruction in the catheter may lead to excessive urine retention and ultimately bladder wall perforation. If CBI is utilized, it should be gravity fed only and never connected to an intravenous pump. If there is any obstruction to the flow of CBI, the catheter should be flushed (by hand) with 60 to 120 mL of saline to remove any blood clots or debris. This is best performed by repeatedly instilling saline with a catheter-tip syringe and withdrawing the fluid present in the bladder, until the majority of clot material is extracted.

The nursing staff should monitor the amount of irrigation and return, to accurately calculate urine output, and should replace the irrigation bag as soon as it is nearly empty. Similarly, the drainage bags can fill up quickly, and need to be emptied frequently so that CBI flow is not reduced (any lull in CBI flow may lead to clot formation). If a clot forms, it needs to be manually extracted before resuming CBI. These patients are at risk for bladder wall perforation, as the wall may be significantly weakened after endourologic procedures, and stretched thin if intravesical pressures are high from obstructed CBI. The use of CBI is contraindicated in patients with confirmed or assumed bladder perforation. CBI should also be avoided or used with extreme caution in patients with fresh anastomoses of the GU tract.

All patients will have some bleeding after a transurethral resection of the prostate (TURP) and are managed postoperatively with a three-way catheter and CBI. The source of bleeding is generally from the venous sinuses of the prostate, so the catheter balloon is inflated to larger volumes than normal (30 mL vs the standard 10 mL) to fill and compress the prostatic fossa or defect left by the TURP. In cases with excessive bleeding, the catheter may be put on gentle traction (with a heavy fabric tape secured to the leg) to force the catheter balloon into the defect. Bed rest is generally necessary during this maneuver to avoid irritation of the bleeding sinus. This traction should be released each morning to reassess the hematuria and release the tension on the tissues. If heavy traction is left for too long, it can result in necrosis of the urethral sphincter muscle or prostate tissue.

Significant and early postoperative hematuria is likely of arterial origin and usually requires a return to the OR for inspection and potentially fulguration. Patients that develop hemodynamic instability nonresponsive to fluid resuscitation may also require re-exploration in the OR. The urologist should be consulted immediately for assessment.

URETHRAL-VESICAL ANASTOMOTIC LEAK IN RADICAL PROSTATECTOMY

Urethral-vesical anastomotic leak (UVAL) is one of the most common postoperative complications in radical prostatectomy. UVAL usually occurs early, with the incidence highest in the first 7 to 10 postoperative days. UVAL occurs in 1% to 10% of laparoscopic cases and 2% to 10% of radical retropubic prostatectomy cases. Robotic-assisted laparoscopic prostatectomy has advantages over pure laparoscopic techniques due to better visualization of the surgical field and the ability to perform a running anastomosis. The majority of anastomotic leaks are located in the posterior segment of the anastomosis, which is the site of the initial suture placement.

After surgery, the patients overall clinical condition and surgical drain output should be monitored. Drain output should significantly decrease over the first 24 to 48 hours; continued high output may indicate an injury to the ureter, and the fluid should be sent for a creatinine level. The majority of patients with mild urinary leak will be asymptomatic and the diagnosis is made based on drain output creatinine level (Figure 67-3). If symptomatic, the patient may have signs of peritonitis or paralytic ileus, which may indicate extravasation of urine into the peritoneum.

Initial management of a urine leak is conservative; the surgical drain and a transurethral catheter are left in place for a period of time (to aspirate urine from the anastomosis, and decompress the bladder, respectively). The urologist may apply gentle traction or manipulate the transurethral catheter (correct catheter placement can facilitate healing the anastomosis) and may repeatedly switch the surgical drain from active to passive drainage (releasing the pressure of the bulb) and slightly withdrawing the drain over time. If the creatinine content of the drain fluid persists following manipulation of the catheter and drain, a cystogram is indicated to rule out injury to the bladder and/or determine the severity of UVAL (alternative imaging includes CT cystography or retrograde urethrogram). If a ureteral injury is suspected, the best imaging is a CT scan using delayed images or a retrograde study of the ureter in the operating room. Longer term urine leaks are managed with prolonged catheterization, and further interventions may include urinary diversion with a suprapubic catheter or nephrostomy tubes, endoscopic evaluation, or ultimately reoperation.

URINE LEAK FOLLOWING PARTIAL NEPHRECTOMY

As partial nephrectomies have become the standard of care for excision of smaller renal parenchymal masses, the incidence of postoperative urinary leak has risen, and currently occurs between 0.5% to 21%, and is more common in excisions that remove endophytic masses involving the collecting system of the kidney.

Urinary leak following partial nephrectomy may present acutely or as a more insidious process. Early leak is typically due to unrecognized insult to the collecting duct system or a defect that was not repaired sufficiently; this should be suspected if drain output exceeds 30 to 40 mL/shift more than 48 hours after surgery. If present, the drain fluid creatinine will be markedly elevated (relative to the serum creatinine). The suspected leak should be evaluated with a noncontrast CT or sonogram to evaluate the drain placement, ensure the kidney is not obstructed (leading to higher pressures in the collecting system thereby perpetuating the leak), and ensure there is no urinoma present.

Delayed urinary leak will present anywhere between 5 and 14 days. The specific etiology of a delayed urine leak is unclear, but it is hypothesized that most are simply unrecognized early leaks. The patient with a delayed urine leak may present with fever, drain site tenderness, flank pain and/or drainage from a port site or incision. The suspected leak should be evaluated with CT with IV contrast (with delayed images to uncover any extravasation of contrast) or sonogram (to identify any perirenal fluid collections). Healing of the leak occurs most rapidly when there is maximal kidney drainage; therefore, a percutaneous drain may be required to evacuate an urinoma if it is impeding kidney drainage. In addition, if the bladder has high voiding pressures, the patient may need a short-term (1-3 days) indwelling catheter to reduce those pressures and allow the kidney to drain properly. The patient can be discharged with the drain and/or the Foley in place; they should be instructed to record daily drain volumes and have close follow-up (within a week) with the surgeon.

COMPLICATIONS FOLLOWING ADRENALECTOMY

Adrenalectomies are most commonly performed for the removal of pheochromocytomas, aldosteronomas, and glucocorticoid-producing tumors, and the physician should be able to recognize the symptoms that arise following abrupt removal of the hormones these tumors produce. Pheochromocytoma, aldosteronoma, and glucocorticoid-producing tumors produce norepinephrine/epinephrine, aldosterone, and cortisol, respectively, which predisposes the patient to a relative deficiency of these hormones. Other complications associated with adrenalectomy include postoperative bleeding or pneumothorax. The proximity of the adrenal glands to the liver, spleen and pancreas, as well as the posterior-inferior border of the diaphragm predispose surgical interventions to problems involving these organs.

Patients with a pheochromocytoma are usually on alpha-blockade perioperatively to control hypertension and often have contracted blood volumes due to the chronic exposure to catecholamines (and resulting increase in vascular tone). These patients are very vulnerable to the development of perioperative hypotension due to the abrupt decrease in norepinephrine. Aggressive fluid resuscitation should be started before surgery and continued throughout the procedure; vasopressors may also be required. Hypoglycemia is also a risk, due to a rebound increase in insulin and should be closely monitored.

Patients with an aldosteronoma are at increased risk of developing either hyperkalemia or hypokalemia in the perioperative period. Due to the excess preoperative aldosterone production, hypokalemia is more typical. Alternatively, in some patients the renin-angiotensin-adrenal-axis is down-regulated (due to the chronic hypernatremia associated with primary hyperaldosteronism). Thus, renin production by the renal juxtaglomerular apparatus is suppressed. If the contralateral adrenal gland cannot compensate for the abrupt decrease in aldosterone levels, patients may actually develop a temporary hyperkalemia and salt-wasting. Therefore, close monitoring of electrolytes and blood pressure is needed, and potassium-sparing diuretics should be immediately discontinued postoperatively.

Patients with a glucocorticoid-producing adenoma are at risk for adrenocortical insufficiency (also known as adrenal crisis). Adrenal crisis symptoms include hypoglycemia, hypotension, fever, nausea, vomiting, abdominal pain, hyponatremia, and hyperkalemia. The symptoms are due to the abrupt decrease in serum glucocorticoids from surgical removal, as well as the suppression of the contralateral adrenal gland from negative feedback at the level of the anterior pituitary. Perioperative administration of mineralocorticoids and glucocorticoids can prevent (or at least attenuate) postoperative adrenal crises. Patients who have undergone bilateral adrenalectomy will require long-term steroid replacement therapy. Patients who have had partial or unilateral adrenalectomy may or may not require supplementation.

Due to the anatomy and vascular supply of the adrenal gland, these surgeries have a high risk of hemorrhage; although this is usually recognized intraoperatively, hemodynamic instability shortly after surgery should be considered an unrecognized vascular insult until proven otherwise. Significant bleeding may require exploration in the operating room and will require the immediate notification of the surgeon. Similarly, respiratory difficulties may be related to an unrecognized or increasing pneumothorax, which should be confirmed on chest radiograph. Lastly, pancreatitis can occur from manipulation or injury to the tail of the pancreas, and should be considered in patients with severe back pain, abdominal pain and inability to tolerate oral intake. This finding may be confirmed with elevated amylase and lipase levels and may require bowel rest with parenteral nutrition.

UROLITHIASIS

Kidney stones affect approximately 1/11 US adults at some point during their lives. Any patient with unilateral flank or groin pain, with or without hematuria, should raise the suspicion of urolithiasis, particularly in a patient with prior history of stones or known risk factors (ie, diabetes, obesity, metabolic syndrome, gout, Caucasian ethnicity, dehydration, etc).

If an obstructing, symptomatic kidney stone is suspected, imaging should be obtained. Ultrasonography can identify the presence or absence of hydronephrosis, and can often identify stones as well, but the sensitivity is poor and is often inadequate for surgical planning. A low-dose, noncontrasted CT scan of the abdomen and pelvis (CT IVP) is a sensitive and specific modality for determining stone size, location and degree of consequent obstruction, if present. Moreover, it can assess a stone’s hardness or composition by noting the Hounsfield Units (HU), which measures the radiodensity relative to distilled water at standard temperature and pressure. An abdominal radiograph of the kidney, ureter and bladder (KUB) can be helpful in patients who can be managed conservatively for stone disease. Additionally, if shock wave lithotripsy is desired, a KUB must be obtained to ensure that the stone is visible prior to scheduling. However, not all stones are visible on KUB, and bowel gas and other artifacts can intermittently obscure the image.

If infection or urosepsis is suspected (based on fever, chills, dysuria, unstable vital signs, leukocytosis, or findings on urinalysis) definitive stone treatment should be delayed and a ureteral stent or percutaneous nephrostomy tube should be placed to relieve the obstruction and allow for decompression of the collecting system. The stent or nephrostomy tube should be left in place while the infection is treated with an appropriate course of antibiotics. After resolution of symptoms and a negative urine culture, the patient can undergo definitive stone treatment.

If the stone is small (generally <6-8 mm), without marked hydroureteronephrosis, acute kidney injury, or infection, and the patient is tolerating fluids with adequate pain control on oral medications, it is reasonable to pursue medical expulsive therapy (MET). This consists of 2 to 4 weeks of daily tamsulosin, anti-inflammatory medications (if no contraindication), oral hydration, and pain/nausea control as needed. The hope is the patient passes the stone without surgical intervention. This is most likely in patients with small, distal stones, particularly those who have passed stones from the same ureter previously or who have been treated instrumented for stones previously, as these patients tend to have more dilated ureters. If the patient fails to pass the stone after 2 to 4 weeks on MET, surgical intervention is warranted.

If prior stone analysis data is available, the patient should be educated on proper dieting to avoid stone recurrences. Recommendations vary based on the type of stone, but in general should consist of ample water, low sodium, low oxalate, low animal protein and normal calcium. Urinary citrate is a known stone inhibitor and is in high concentration in lemon and orange juice. Additional dietary and medical intervention, such as urinary alkalinization or thiazide therapy, is dependent on the type of stone as well as the patient’s 24-hour urine collection.

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