LAPAROTOMY AND LAPAROSCOPY
UPPER GASTROINTESTINAL TRACT DISORDERS
UPPER GASTROINTESTINAL BLEEDING
DISORDERS OF THE SMALL BOWEL AND COLON
INFLAMMATORY BOWEL DISEASE
During normal pregnancy, the gastrointestinal tract and its appendages undergo remarkable anatomical, physiological, and functional changes. These changes, which are discussed in detail in Chapter 4 (p. 66), can appreciably alter clinical findings normally relied on for diagnosis and treatment of gastrointestinal disorders. Moreover, as pregnancy progresses, gastrointestinal symptoms become more difficult to assess. Physical findings are often obscured by a large uterus that displaces abdominal organs and can alter the location and intensity of pain and tenderness.
Various methods can evaluate the gastrointestinal tract during pregnancy without reliance on x-ray techniques. Fiberoptic endoscopic instruments have revolutionized diagnosis and management of most gastrointestinal conditions, and these are particularly well suited for pregnancy. With endoscopy, the esophagus, stomach, duodenum, and colon can be inspected (Cappell, 2006, 2011). The proximal jejunum can also be studied, and the ampulla of Vater cannulated to perform endoscopic retrograde cholangiopancreatography—ERCP (Fogel, 2014; Kamani, 2012; Tang, 2009). Experience in pregnancy with videocapsule endoscopy for small-bowel evaluation is limited (Storch, 2006).
Upper gastrointestinal endoscopy is used for management as well as diagnosis of several problems. Common bile duct exploration and drainage are used for choledocholithiasis as described in Chapter 55 (p. 1096). It is also used for sclerotherapy as well as placement of percutaneous endoscopic gastrostomy (PEG) tubes. A number of concise reviews have been provided (Cappell, 2011; Fogel, 2014; Gilinsky, 2006).
Flexible sigmoidoscopy can be used safely in pregnant women (Siddiqui, 2006). In nonpregnant patients, colonoscopy is indispensible for viewing the entire colon and distal ileum for diagnosis and management of inflammatory bowel disease. Except for the midtrimester, reports of colonoscopy during pregnancy are limited, but preliminary results indicate that it should be performed if indicated (Cappell, 2010, 2011). Bowel preparation is completed using polyethylene glycol electrolyte or sodium phosphate solutions. With these, serious maternal dehydration that may cause diminished uteroplacental perfusion should be avoided.
Noninvasive Imaging Techniques
The obvious ideal technique for gastrointestinal evaluation during pregnancy is abdominal sonography. Because computed tomography (CT) use is limited in pregnancy due to radiation exposure, magnetic resonance (MR) imaging is now commonly used to evaluate the abdomen and retroperitoneal space (Khandelwal, 2013). One example is magnetic-resonance cholangiopancreatography—MRCP (Oto, 2009). These and other imaging modalities, and their safe use in pregnancy, are considered in more detail in Chapter 46 (p. 933).
Laparotomy and Laparoscopy
Surgery is lifesaving for certain gastrointestinal conditions—perforative appendicitis being the most common example. From the Swedish Registry database through 1981, abdominal exploration by laparotomy or laparoscopy was performed in 1331 of 720,000 pregnancies—approximately 1 in every 500 (Mazze, 1989). A similar incidence of 1 in 635 in nearly 50,000 pregnancies was described by Kort (1993). In both studies, the most common indications for surgery were appendicitis, an adnexal mass, and cholecystitis.
Laparoscopic procedures have replaced traditional surgical techniques for many abdominal disorders during pregnancy (Carter, 2004). In an updated report from the Swedish Registry database, there were 2181 pregnant women who underwent laparoscopy and 1522 who had laparotomy for nonobstetrical indications (Reedy, 1997). Use of these procedures was similar to their first study—approximately 1 in every 800 pregnancies. Both approaches were used usually before 20 weeks, and they were found to be safe. Long-term surveillance studies also suggest no deleterious effects for mother or fetus (Rizzo, 2003).
The most common nongynecological laparoscopic procedures performed during pregnancy are cholecystectomy and appendectomy (Fatum, 2001; Rollins, 2004). For more details and for descriptions of surgical technique, see Chapter 46 (p. 928) as well as Operative Obstetrics, 2nd edition (Gilstrap, 2002). Guidelines for diagnosis, treatment, and use of laparoscopy for surgical problems during pregnancy have been provided by the Society of American Gastrointestinal and Endoscopic Surgeons (Pearl, 2011).
Specialized nutritional support can be delivered enterally, usually via nasogastric tube feedings, or parenterally with nutrition given by venous catheter access, either peripherally or centrally.
When possible, enteral alimentation is preferable because it has fewer serious complications (Bistrian, 2012; Hamaoui, 2003). In obstetrical patients, very few conditions prohibit enteral nutrition as a first effort to prevent catabolism. Even in extreme cases, such as recalcitrant hyperemesis gravidarum, percutaneous endoscopic gastrostomy with a jejunal port—PEG (J) tube—has been described (Saha, 2009).
The purpose of parenteral feeding, or hyperalimentation, is to provide nutrition when the intestinal tract must be kept quiescent. Central venous access is necessary for total parenteral nutrition because its hyperosmolarity requires rapid dilution in a high-flow vascular system. These solutions provide 24 to 40 kcal/kg/day, principally as a hypertonic glucose solution.
There have been a variety of conditions for which total parenteral nutrition has been employed during pregnancy (Table 54-1). Gastrointestinal disorders are the most common indication, and in the many studies cited, feeding duration averaged 33 days. It is imperative to emphasize that complications of parenteral nutrition are frequent, and they may be severe (Guglielmi, 2006). In an early report of 26 pregnancies, a 50-percent rate of complications, which included pneumothorax, hemothorax, and brachial plexus injury, was described (Russo-Stieglitz, 1999).
TABLE 54-1. Some Conditions Treated with Enteral or Parenteral Nutrition During Pregnancya
Preterm labor/ruptured membranes
Short gut syndrome
aRisk are listed alphabetically.
From Folk, 2004; Guglielmi, 2006; Ogura, 2003; Russo-Stieglitz, 1999; Saha, 2009; Spiliopoulos, 2013.
The most frequent serious complication is catheter sepsis, and Folk (2004) reported a 25-percent incidence in 27 women with hyperemesis gravidarum. Although bacterial sepsis is most common, Candidasepticemia has been described (Paranyuk, 2006). The Centers for Disease Control and Prevention (2002) has published detailed guidelines to prevent catheter-related sepsis, and these have served to lessen the dangers of serious infections. Perinatal complications are uncommon, however, fetal subdural hematoma caused by maternal vitamin K deficiency has been described (Sakai, 2003).
There is also appreciable morbidity from long-term use of a peripherally inserted central catheter (PICC). Ogura (2003) reported infection with long-term access in 31 of 52 pregnant women. Holmgren (2008) reported complications in 21 of 33 women in whom a PICC line was placed for hyperemesis. Infections were the most common, and half of infected women also had bacteremia. From a review of 48 reports of nonpregnant adults, Turcotte and associates (2006) concluded that there were no advantages to peripherally placed catheters compared with centrally placed ones. Still, it seems reasonable for short-term nutrition—weeks—that PICC placement has a greater benefit-versus-risk ratio (Bistrian, 2012).
DISORDERS OF THE UPPER GASTROINTESTINAL TRACT
Mild to moderate nausea and vomiting are especially common in pregnant women until approximately 16 weeks (Chap. 9, p. 187). In a small proportion of these, however, it is severe and unresponsive to simple dietary modification and antiemetics. In an attempt to quantify nausea and vomiting severity, Lacasse and colleagues (2008) have proposed a pregnancy-unique quantification of emesis and nausea (PUQE) scoring index. Severe unrelenting nausea and vomiting—hyperemesis gravidarum—is defined variably as being sufficiently severe to produce weight loss, dehydration, ketosis, alkalosis from loss of hydrochloric acid, and hypokalemia. Acidosis develops from partial starvation. In some women, transient hepatic dysfunction develops, and there is accumulation of biliary sludge (Matsubara, 2012). Other causes should be considered because hyperemesis gravidarum is a diagnosis of exclusion (Benson, 2013).
Study criteria have not been homogeneous, thus reports of population incidences vary. There does, however, appear to be an ethnic or familial predilection (Grjibovski, 2008). In population-based studies from California and Nova Scotia, the hospitalization rate for hyperemesis gravidarum was 0.5 to 0.8 percent (Bailit, 2005; Fell, 2006). Up to 20 percent of those hospitalized in a previous pregnancy for hyperemesis will again require hospitalization (Dodds, 2006; Trogstad, 2005). In general, obese women are less likely to be hospitalized for this (Cedergren, 2008).
The etiopathogenesis of hyperemesis gravidarum is likely multifactorial and certainly is enigmatic. It appears to be related to high or rapidly rising serum levels of pregnancy-related hormones. Putative culprits include human chorionic gonadotropin (hCG), estrogens, progesterone, leptin, placental growth hormone, prolactin, thyroxine, and adrenocortical hormones (Verberg, 2005). More recently implicated are other hormones that include ghrelins, leptin, nesfatin-1, and PYY-3 (Albayrak, 2013; Gungor, 2013).
Superimposed on this hormonal cornucopia are an imposing number of biological and environmental factors. Moreover, in some but not all severe cases, interrelated psychological components play a major role (Buckwalter, 2002; Christodoulou-Smith, 2011; McCarthy, 2011). Other factors that increase the risk for admission include hyperthyroidism, previous molar pregnancy, diabetes, gastrointestinal illnesses, some restrictive diets, and asthma and other allergic disorders (Fell, 2006; Mullin, 2012). The vestibular system has been implicated (Goodwin, 2008). An association of Helicobacter pylori infection has also been proposed, but evidence is not conclusive (Goldberg, 2007). And for unknown reasons—perhaps estrogen-related—a female fetus increases the risk by 1.5-fold (Schiff, 2004; Tan, 2006; Veenendaal, 2011). Finally, Bolin and coworkers (2013) reported an association between hyperemesis gravidarum and preterm labor, placental abruption, and preeclampsia.
Vomiting may be prolonged, frequent, and severe, and a list of potentially fatal complications is given in Table 54-2. Various degrees of acute kidney injury from dehydration are encountered (Nwoko, 2012). We have cared for a number of women with markedly impaired renal function. The extreme example was a woman who required 5 days of dialysis when her serum creatinine level rose to 10.7 mg/dL (Hill, 2002). Complications from continuous retching include a Mallory-Weiss tear, such as that shown in Figure 54-1. Others are pneumothorax, pneumomediastinum, diaphragmatic rupture, and gastroesophageal rupture, which is Boerhaave syndrome (Chen, 2012; Schwartz, 1994; Yamamoto, 2001).
TABLE 54-2. Some Life-Threatening Complications of Recalcitrant Hyperemesis Gravidarum
Acute kidney injury—may require dialysis
Depression—cause versus effect?
Esophageal rupture—Boerhaave syndrome
Hypoprothrombinemia—vitamin K deficiency
Mallory-Weiss tears—bleeding, pneumothorax, pneumomediastinum, pneumopericardium
Wernicke encephalopathy—thiamine deficiency
FIGURE 54-1 Endoscopic view of Mallory-Weiss tear. (From Song, 2012, with permission.)
In more severe cases, plasma zinc levels are increased, copper levels decreased, and magnesium levels unchanged (Dokmeci, 2004). At least two serious vitamin deficiencies have been reported with hyperemesis in pregnancy. Wernicke encephalopathy from thiamine deficiency has been reported with increasing frequency (Di Gangi, 2012; Palacios-Marqués, 2012). In a review of 49 such cases, Chiossi (2006) reported that only half had the triad of confusion, ocular findings, and ataxia. With this encephalopathy, an abnormal electroencephalogram (EEG) may be seen, and usually there are MR imaging findings (Vaknin, 2006; Zara, 2012). At least three maternal deaths have been described, and long-term sequelae include blindness, convulsions, and coma (Selitsky, 2006). Last, vitamin K deficiency has been reported to cause maternal coagulopathy and fetal intracranial hemorrhage (Kawamura, 2008; Robinson, 1998; Sakai, 2003).
One algorithm for management of nausea and vomiting of pregnancy is shown in Figure 54-2. A Cochrane review reported a salutary effect from several antiemetics given orally or by rectal suppository as first-line agents (Jewell, 2000). The Food and Drug Administration (2013) recently approved Diclegis—a combination of doxylamine-pyridoxine—for morning sickness. When simple measures fail, intravenous Ringer lactate or normal saline solutions are given to correct dehydration, ketonemia, electrolyte deficits, and acid-base imbalances. There are no benefits to using 5-percent dextrose along with crystalloids (Tan, 2013). Thiamine, 100 mg, is given to prevent Wernicke encephalopathy (Niebyl, 2010).
FIGURE 54-2 Algorithm for outpatient and inpatient management of hyperemesis gravidarum.
If vomiting persists after rehydration and failed outpatient management, hospitalization is recommended (American College of Obstetricians and Gynecologists, 2013). Antiemetics such as promethazine, prochlorperazine, chlorpromazine, or metoclopramide are given parenterally. There is little evidence that treatment with glucocorticosteroids is effective. Two small trials found no benefits of methylprednisolone compared with placebo, but the corticosteroid-treated group had significantly fewer readmissions (Duggar, 2001; Safari, 1998). In another study from Parkland Hospital, Yost (2003) compared placebo with intravenous methylprednisolone plus two different tapered oral steroid regimens. They noted that a third in each group required readmission. In a study reported by Bondok (2006), pulsed hydrocortisone therapy was superior to metoclopramide to reduce vomiting and readmissions. Serotonin antagonists are most effective for controlling chemotherapy-induced nausea and vomiting (Hesketh, 2008). But when used for hyperemesis gravidarum, ondansetron was not superior to promethazine (Sullivan, 1996). Serotonin antagonist use in pregnancy is limited, but these drugs appear to be safe (Briggs, 2011).
With persistent vomiting after hospitalization, appropriate steps should be taken to exclude possible underlying diseases as a cause of hyperemesis. In one study, endoscopy did not change management in 49 women (Debby, 2008). Other potential causes include gastroenteritis, cholecystitis, pancreatitis, hepatitis, peptic ulcer, and pyelonephritis. In addition, severe preeclampsia and fatty liver are more likely after midpregnancy. And although clinical thyrotoxicosis has been implicated as a cause of hyperemesis, it is more likely that abnormally elevated serum thyroxine levels are a surrogate for higher-than-average serum hCG levels (Chap. 5, p. 103). This was termed “chemical hyperthyroidism” by Tan (2002). And of interest, Panesar and associates (2006) showed that a cohort of women with hyperemesis had lower serum thyrotropin levels. In our experiences, serum free thyroxine levels normalize quickly with hydration.
With treatment, most women will have a salutary response and may be sent home with antiemetic therapy. Their readmission rate is 25 to 35 percent in most prospective studies. If associated psychiatric and social factors contribute to the illness, the woman usually improves remarkably while hospitalized (Swallow, 2004). That said, symptoms may relapse in these women, and some go on to develop posttraumatic stress syndrome (Christodoulou-Smith, 2011; McCarthy, 2011). For some women, hyperemesis can be an indication for elective termination (Poursharif, 2007).
In the small percentage of women who continue to have recalcitrant vomiting, consideration is given for enteral nutrition. Vaisman (2004) described successful use of nasojejunal feeding for up to 21 days in 11 such women. Use of sonography to confirm correct placement of the tube has been described (Swartzlander, 2013). Percutaneous endoscopic gastrostomy with a jejunal port has also been reported (Saha, 2009; Schrag, 2007).
In our experiences, only a very few women will require parenteral nutrition (Yost, 2003). In a study of 166 women, Folk (2004) reported that 16 percent had central venous access established for nutrition. The litany of complications included line sepsis in 25 percent and thrombosis and infective endocarditis in one woman each.
Gastroesophageal Reflux Disease (GERD)
Reflux disease is seen in up to 15 percent of nonpregnant individuals (Kahrilas, 2012). Heartburn, or pyrosis, is especially common in late pregnancy, and it appears at some point in 50 to 80 percent of pregnancies (Mehta, 2010). The retrosternal burning sensation is caused by esophagitis from gastroesophageal reflux related to relaxation of the lower esophageal sphincter (Hytten, 1991). According to Costigan and colleagues (2006), common folklore is confirmed in that women with excessive heartburn do give birth to infants with more hair! Long-term complications are chronic esophagitis and adenocarcinoma.
Reflux symptoms usually respond to tobacco and alcohol abstinence, small meals, head of the bed elevation, and avoidance of postprandial recumbency and “trigger” foods. Oral antacids are first-line therapy. If severe symptoms persist, sucralfate is given with an H2-receptor antagonist such as cimetidine or ranitidine. If these are not successful, commonly used proton-pump inhibitors such as omeprazole or pantoprazole are also safe for use in pregnancy (Briggs, 2011; Mahadevan, 2006b). If there is still no relief, then endoscopy should be considered. Misoprostol is contraindicated because it stimulates labor (Chap. 26, p. 529).
For medical treatment failures in nonpregnant patients, surgical fundoplication is performed (Kahrilas, 2012). Although the procedure was not done during pregnancy, Biertho (2006) described 25 women who had undergone laparoscopic Nissen fundoplication before pregnancy. Only 20 percent had reflux symptoms during pregnancy.
The older literature is informative regarding hiatal hernias in pregnancy. Upper gastrointestinal radiographs performed in 195 women in late pregnancy showed that 20 percent of 116 multiparas and 5 percent of 79 nulliparas had a hiatal hernia (Rigler, 1935). Of 10 women studied postpartum, hernia persisted in three at 1 to 18 months.
The relationship of hiatal hernia with reflux esophagitis, and thus symptoms, is not clear. One study demonstrated no relationship between reflux and hernia and showed that the lower esophageal sphincter functioned effectively even when displaced intrathoracically (Cohen, 1971). Nevertheless, during pregnancy, these hiatal hernias may cause vomiting, epigastric pain, and bleeding from ulceration. Schwentner (2011) reported severe herniation requiring surgical repair in a woman with a 12-week gestation. Curran (1999) described a 30-week pregnancy complicated by gastric outlet obstruction from a paraesophageal hernia.
These are caused by herniations of abdominal contents through either the foramen of Bochdalek or that of Morgagni. Fortunately, they rarely complicate pregnancy. Kurzel and associates (1988) reviewed the outcomes of 18 pregnant women with such a hernia and who developed acute obstruction. Because the maternal mortality rate was 45 percent, they recommend repair during pregnancy even if a woman is asymptomatic. Herniation has been reported in one pregnant woman from a previous traumatic diaphragmatic defect and in another who had antireflux surgery in early pregnancy (Brygger, 2013; Flick, 1999). Several case reports also describe spontaneous diaphragmatic rupture from increased intraabdominal pressure during delivery (Chen, 2012; Ortega-Carnicer, 1998; Sharifah, 2003).
A rare disorder, achalasia is a motility disorder in which the lower esophageal sphincter does not relax properly with swallowing. There is also nonperistaltic contraction activity of the esophageal muscularis to cause symptoms (Kahrilas, 2012; Khudyak, 2006). The defect is caused by inflammatory destruction of the myenteric (Auerbach) plexus within smooth muscle of the lower esophagus and its sphincter. Postganglionic cholinergic neurons are unaffected, thus, there is unopposed sphincter stimulation. Symptoms are dysphagia, chest pain, and regurgitation. Barium swallow radiography demonstrates bird beakor ace of spades narrowing at the distal esophagus. Endoscopy is performed to exclude gastric carcinoma, and manometry is confirmatory. If dilatation of the esophagus and medical therapy does not provide relief, myotomy is considered (Torquati, 2006).
During pregnancy, normal relaxation of the lower esophageal sphincter in those with achalasia theoretically should not occur. Even so, in most women, pregnancy does not seem to worsen achalasia. One report of 20 affected pregnant women found no excessive reflux esophagitis (Mayberry, 1987). Khudyak and coworkers (2006) reviewed 35 cases and described most women as symptom free, although esophageal dilatation was needed in a few. A maternal death at 24 weeks associated with perforation of a 14-cm diameter megaesophagus has been reported (Fassina, 1995).
Management of achalasia includes soft diet and anticholinergic drugs. With persistent symptoms, other options include nitrates, calcium-channel antagonists, and botulinum toxin A injected locally (Khudyak, 2006; Wataganara, 2009). Balloon dilatation of the sphincter may be necessary, and 85 percent of nonpregnant patients respond to this. Satin (1992) and Fiest (1993) and their associates reported successful use of pneumatic dilatation in pregnancy. One caveat is that esophageal perforation is a serious complication of dilatation. Spiliopoulos and colleagues (2013) described a 29-week pregnant woman with achalasia treated for 10 weeks with parenteral nutrition with surgical correction done postpartum.
Erosive ulcer disease more often involves the duodenum rather than the stomach in young women. Gastroduodenal ulcers in nonpregnant women may be caused by chronic gastritis from H pylori, or they develop from use of aspirin or other nonsteroidal antiinflammatory drugs. Neither is common in pregnancy (McKenna, 2003; Weyermann, 2003). Acid secretion is also important, and thus underlies the efficacy of antisecretory agents (Suerbaum, 2002). Gastroprotection during pregnancy is probably due to reduced gastric acid secretion, decreased motility, and considerably increased mucus secretion (Hytten, 1991). Despite this, ulcer disease may be underdiagnosed because of frequent treatment for reflux esophagitis (Cappell, 1998; Mehta, 2010). In the past 45 years at Parkland Hospital, during which time we have cared for more than 500,000 pregnant women, we have encountered very few who had symptomatic ulcer disease. Before appropriate therapy was commonplace, Clark (1953) studied 313 pregnancies in 118 women with proven ulcer disease. They noted a clear remission during pregnancy in almost 90 percent. However, benefits were short lived. Symptoms recurred in more than half by 3 months postpartum and in almost all by 2 years.
Antacids are first-line therapy, and H2-receptor blockers or proton-pump inhibitors are safely prescribed for those who do not respond (Briggs, 2011; Diav-Citrin, 2005; Mahadevan, 2006b). Sucralfate is the aluminum salt of sulfated sucrose that inhibits pepsin. It provides a protective coating at the ulcer base. Approximately 10 percent of the aluminum salt is absorbed, and it is considered safe for pregnant women (Briggs, 2011).
With active ulcers, a search for H pylori is undertaken. Diagnostic aids include the urea breath test, serological testing, or endoscopic biopsy. If any of these are positive, antimicrobial therapy is indicated. There are several effective oral treatment regimens that do not include tetracycline and that can be used during pregnancy. These 14-day regimens include amoxicillin, 1000 mg twice daily along with clarithromycin, 500 mg twice daily; or metronidazole, 500 mg twice daily (Dzieniszewski, 2006; Mehta, 2010).
Upper Gastrointestinal Bleeding
In some women, persistent vomiting is accompanied by worrisome upper gastrointestinal bleeding. Occasionally, there is a bleeding peptic ulceration, however, most of these women have small linear mucosal tears near the gastroesophageal junction—Mallory-Weiss tears, as shown in Figure 54-1. Bleeding usually responds promptly to conservative measures, including iced saline irrigations, topical antacids, and intravenously administered H2-blockers or proton-pump inhibitors. Transfusions may be needed, and if there is persistent bleeding, then endoscopy may be indicated (O’Mahony, 2007). With persistent retching, the less common, but more serious, esophageal rupture—Boerhaave syndrome—may develop from greatly increased esophageal pressure.
DISORDERS OF THE SMALL BOWEL AND COLON
The small bowel has diminished motility during pregnancy. Using a nonabsorbable carbohydrate, Lawson (1985) showed that small bowel mean transit times were 99, 125, and 137 minutes in each trimester, compared with 75 minutes when nonpregnant. In a study cited by Everson (1992), mean transit time for a mercury-filled balloon from the stomach to the cecum was 58 hours in term pregnant women compared with 52 hours in nonpregnant women.
Muscular relaxation of the colon is accompanied by increased absorption of water and sodium that predisposes to constipation. This complaint is reported by almost 40 percent of women at some time during pregnancy (Everson, 1992). Such symptoms are usually only mildly bothersome, and preventive measures include a high-fiber diet and bulk-forming laxatives. Wald (2003) has reviewed treatment options. We have encountered several pregnant women who developed megacolon from impacted stool. These women almost invariably had chronically abused stimulatory laxatives.
Most cases of acute diarrhea are caused by infectious agents. The large variety of viruses, bacteria, helminths, and protozoa that cause diarrhea in adults inevitably also afflict pregnant women. Some of these are discussed in Chapter 64. Evaluation of acute diarrhea depends on its severity and duration. According to Camilleri and Murray (2012), some indications for evaluation include profuse diarrhea with dehydration, grossly bloody stools, fever ≥ 38.5°C, duration of > 48 hours without improvement, recent antimicrobial use, immunocompromise, and new community outbreaks. Cases of moderately severe diarrhea with fecal leukocytes or gross blood may best be treated with empirical antibiotics rather than evaluation. Some features of the more common acute diarrheal syndromes are shown in Table 54-3.
TABLE 54-3. Causative Agents and Clinical Features of Common Acute, Infectious Diarrheal Syndromes
The mainstay of treatment is intravenous hydration using normal saline or Ringer lactate with potassium supplementation in amounts to restore maternal blood volume and to ensure uteroplacental perfusion. Vital signs and urine output are monitored for signs of sepsis syndrome. For moderately severe nonfebrile illness without bloody diarrhea, antimobility agents such as loperamide may be useful. Bismuth subsalicylate may also alleviate symptoms.
Judicious use of antimicrobial agents is warranted. For moderate to severely ill women, some recommend empirical treatment with ciprofloxacin, 500 mg twice daily for 3 to 5 days. Specific pathogens are treated as needed when identified. Syndromes for which treatment is usually unnecessary include those caused by Escherichia coli, staphylococcus, Bacillus cereus, and Norwalk-like virus. Severe illness caused by Salmonella is treated with trimethoprim-sulfamethoxazole or azithromycin; Campylobacter with azithromycin; Clostridium difficile with oral metronidazole or vancomycin; and Giardia and Entamoeba histolytica with metronidazole (Mehta, 2010).
Inflammatory Bowel Disease
The two presumably noninfectious forms of intestinal inflammation are ulcerative colitis and Crohn disease. Differentiation between the two is important because treatment differs. That said, they both share common factors, and sometimes are indistinguishable if Crohn disease involves the colon. The salient clinical and laboratory features shown in Table 54-4 permit a reasonably confident diagnostic differentiation in most cases. The etiopathogenesis of both disorders is enigmatic, but there is genetic predisposition toward either. Inflammation is thought to result from dysregulated mucosal immune function in response to normal bacterial flora, with or without an autoimmune component (Friedman, 2012).
TABLE 54-4. Some Shared and Differentiating Characteristics of Inflammatory Bowel Disease
This is a mucosal disorder with inflammation confined to the superficial luminal layers of the colon. It typically begins at the rectum and extends proximally for a variable distance. In approximately 40 percent, disease is confined to the rectum and rectosigmoid, and 20 percent have pancolitis. Endoscopic findings include mucosal granularity and friability that is interspersed with mucosal ulcerations and a mucopurulent exudate (Fig. 54-3).
FIGURE 54-3 Causes of colitis. A. Chronic ulcerative colitis with diffuse ulcerations and exudates. B. Crohn colitis with deep ulcers. C. Pseudomembranous colitis with yellow pseudomembranes. (From Song, 2012, with permission.)
Major symptoms of ulcerative colitis include diarrhea, rectal bleeding, tenesmus, and abdominal cramps. The disease can be acute or intermittent and is characterized by exacerbations and remissions. For unknown reasons, prior appendectomy protects against development of ulcerative colitis (Friedman, 2012; Selby, 2002). Toxic megacolon and catastrophic hemorrhage are particularly dangerous complications that may necessitate colectomy. Extraintestinal manifestations include arthritis, uveitis, and erythema nodosum. Another serious problem is that the risk of colon cancer approaches 1 percent per year. With either ulcerative colitis or Crohn disease, there is also concern for possible increased risks for thromboembolism (Kappelman, 2011; Novacek, 2010).
Also known as regional enteritis, Crohn ileitis, and granulomatous colitis, Crohn disease has more protean manifestations than ulcerative colitis. It involves not only the bowel mucosa but also the deeper layers, and sometimes there is transmural involvement. Lesions can be seen throughout the entire gastrointestinal tract, from the mouth to the anus (Friedman, 2012). It is typically segmental. Approximately 30 percent of patients have small-bowel involvement, 25 percent have isolated colonic involvement, and 40 percent have both, usually with the terminal ileum and colon involved. Perirectal fistulas and abscesses develop in a third of those with colonic involvement.
Symptoms depend on which bowel segment(s) is involved. Thus, complaints may include right-sided lower cramping abdominal pain, diarrhea, weight loss, low-grade fever, and obstructive symptoms. The disease is chronic with exacerbations and remissions, and importantly, it cannot be cured medically or surgically (Lichtenstein, 2009). Approximately a third of patients require surgery within the first year after diagnosis, and thereafter, 5 percent per year. Reactive arthritis is common, and the gastrointestinal cancer risk, although not as great as with ulcerative colitis, is increased substantially.
Inflammatory Bowel Disease and Fertility
Subfertility is commonly linked to chronic medical disease. That said, Mahadevan (2006a) cited a normal fertility rate for inflammatory bowel disease unless severe disease warranted surgery. Alstead (2003) reported that decreased female fertility from active Crohn disease returned to normal with remission. For women requiring surgical resection, laparoscopic anastomosis has a higher subsequent fertility rate (Beyer-Berjot, 2013). Even though fertility is improved after colectomy, up to half of women will still be infertile (Bartels, 2012; Waljee, 2006). Subfertility may also be partially due to sulfasalazine, which causes reversible sperm abnormalities (Feagins, 2009).
Inflammatory Bowel Disease and Pregnancy
Because ulcerative colitis and Crohn disease are relatively common in young women, they are encountered with some frequency in pregnancy. In this regard, a few generalizations can be made. The consensus is that pregnancy does not increase the likelihood of an inflammatory bowel disease flare. To the contrary, in a 10-year surveillance of women in the European Collaborative on Inflammatory Bowel Disease, the likelihood of a flare during pregnancy was decreased compared with the preconceptional rate (Riis, 2006). This diminished rate persisted for years after pregnancy and was attributed to close attention and monitoring of enrolled women.
Although most of those with quiescent disease in early pregnancy uncommonly have relapses, when a flare develops, it may be severe. Conversely, active disease in early pregnancy increases the likelihood of poor pregnancy outcome. In general, most usual treatment regimens may be continued during pregnancy. If needed to direct management, diagnostic evaluations should be undertaken, and if indicated, surgery should be performed. For women who successfully complete pregnancy, half experience improvement in their health-related quality of life (Ananthakrishnan, 2012).
At first glance, it appears that adverse pregnancy outcomes are increased with inflammatory bowel disease (Bush, 2004; Cornish, 2012; Elbaz, 2005; Mahadevan, 2005). Initially, this was attributed to the fact that most studies included women with either form of disease. Specifically, Crohn disease was noted to be linked to excessive morbidity (Dominitz, 2002; Stephansson, 2010). But, according to Reddy (2008) as well as others, these adverse outcomes were in women with severe disease and multiple recurrences. Indeed, in the prospective European case-control ECCO-EpiCom study of 332 pregnant women with inflammatory disease, Bortoli and coworkers (2011) found similar outcomes in women with ulcerative colitis or Crohn disease compared with normally pregnant women. Importantly, even reports of adverse outcomes found that perinatal mortality rates are not appreciably increased.
Ulcerative Colitis and Pregnancy. Pregnancy has no significant effects on ulcerative colitis. In a metaanalysis of 755 pregnancies, Fonager (1998) reported that ulcerative colitis quiescent at conception worsened in approximately a third of pregnancies. In women with active disease at the time of conception, approximately 45 percent worsened, 25 percent remained unchanged, and only 25 percent improved. These observations are similar to those previously described in an extensive review by Miller (1986) and a report from Oron and colleagues (2012).
Calcium supplementation is provided for osteoporosis. Folic acid is given in high doses to counteract the antifolate actions of sulfasalazine. Flares may be caused by psychogenic stress, and reassurance is important. Management for colitis for the most part is the same as for nonpregnancy. Treatment of active colitis, as well as maintenance therapy, is with drugs that deliver 5-aminosalicyclic acid (5-ASA) or mesalamine. Sulfasalazine is the prototype, and its 5-ASA moiety inhibits prostaglandin synthase in colonic mucosa. Others include olsalazine (Dipentum) and coated 5-ASA derivatives (Asacol, Pentasa, Lialda). Glucocorticoids are given orally, parenterally, or by enema for more severe disease that does not respond to 5-ASA. Recalcitrant disease is managed with immunomodulating drugs, including azathioprine, 6-mercaptopurine, or cyclosporine, which appear relatively safe in pregnancy (Briggs, 2011; Moskovitz, 2004). Importantly, methotrexate is contraindicated in pregnancy. High-dose intravenous cyclosporine may be beneficial for severely ill patients and used in lieu of colectomy. Parenteral nutrition is occasionally necessary for women with prolonged exacerbations.
Colorectal endoscopy is performed as indicated (Katz, 2002). During pregnancy, colectomy and ostomy creation for fulminant colitis may be needed as a lifesaving measure, and it has been described during each trimester. Dozois (2006) reviewed 42 such cases and found that, in general, outcomes have been good in recent reports. Most women underwent partial or complete colectomy, but Ooi and colleagues (2003) described decompression colostomy with ileostomy in a 10- and a 16-week pregnancy.
More commonly for nonpregnant women undergoing proctocolectomy for ulcerative colitis, an ileal pouch is constructed and an anal anastomosis completed. For women with this procedure performed before pregnancy, sexual function and fertility are improved (Cornish, 2007). Disadvantages include frequent bowel movements, fecal incontinence that includes nocturnal soilage in almost half of patients, and pouchitis. Pouchitis is an inflammatory condition of the ileoanal pouch, probably due to bacterial proliferation, stasis, and endotoxin release. It usually responds to cephalosporins or metronidazole. Although these disadvantages temporarily worsen during pregnancy, they typically abate postpartum. In one rare case, adhesions to the growing uterus led to ileal pouch perforation (Aouthmany, 2004).
Women who have had a prior proctocolectomy and ileal pouch–anal anastomosis can safely deliver vaginally (Ravid, 2002). Hahnloser (2004) reviewed routes of delivery in women with 235 pregnancies before and 232 pregnancies after ileoanal pouch surgery. Functional outcomes were similar, and it was concluded that cesarean delivery should be reserved for obstetrical indications. Postcesarean delivery ileoanal pouch obstruction has been described (Malecki, 2010).
As previously discussed, ulcerative colitis likely has minimal adverse effects on pregnancy outcome. Modigliani (2000) reviewed perinatal outcomes in 2398 pregnancies and reported them to be not substantively different from those in the general obstetrical population. Specifically, the incidences of spontaneous abortion, preterm delivery, and stillbirth were remarkably low. In a population-based cohort study of 107 women from Washington state, perinatal outcomes, with two exceptions, were similar to those of 1308 normal pregnancies (Dominitz, 2002). One exception was an inexplicably increased incidence of congenital malformations, and the other was a cesarean delivery rate that was increased from 20 to 29 percent compared with normal controls. The previously described ECCO-EpiCom study reported similar outcomes in 187 women with ulcerative colitis compared with their normal controls (Bortoli, 2011). There are smaller studies in which the risks for preterm birth and low birthweight are increased (Emerson, 2013).
Crohn Disease and Pregnancy. In general, Crohn disease activity during pregnancy is related to its status around the time of conception. In a cohort study of 279 pregnancies, for 186 women whose disease was inactive at conception, a fourth relapsed during pregnancy (Fonager, 1998). In 93 with active disease at conception, however, two thirds either remained active or worsened. Miller (1986) had described similar findings from his earlier review as did Oron and associates (2012).
Calcium and folic acid supplementation are given as for ulcerative colitis. There is no regimen that is universally effective for maintenance during asymptomatic periods. Sulfasalazine is effective for some, but the newer 5-ASA formulations are better tolerated. As a class, they appear to be safe in pregnancy (Briggs, 2011; Rahimi, 2008). Prednisone therapy may control moderate to severe flares but is less effective for small-bowel involvement. Immunomodulators such as azathioprine, 6-mercaptopurine, and cyclosporine are used for active disease and for maintenance and appear relatively safe during pregnancy (Briggs, 2011; Moskovitz, 2004; Prefontaine, 2009). As discussed in Chapter 12 (p. 248), methotrexate, mycophenolate mofetil, and mycophenolic acid are contraindicated in pregnancy (Briggs, 2011; Food and Drug Administration, 2008). Anti-tumor necrosis factor (TNF)-α antibodies, which include infliximab, adalimumab, and certolizumab, are also effective for active Crohn disease and maintenance (Casanova, 2013; Colombel, 2010; Cominelli, 2013; Friedman, 2012; Sandborn, 2007; Schreiber, 2007). This class of immunomodulators is considered safe in pregnancy, but data are limited (Katz, 2004; Roux, 2007; Schnitzler, 2011). Parenteral hyperalimentation has been used successfully during severe recurrences (Russo-Stieglitz, 1999).
Endoscopy or conservative surgery is indicated for complications. Patients with small-bowel involvement more likely will require surgery for complications that include fistulas, strictures, abscesses, and intractable disease. An abdominal surgical procedure was required during 5 percent of pregnancies described by Woolfson (1990). Those with an ileal loop colostomy may have significant problems as discussed below. Women with a perianal fistula—unless these are rectovaginal—usually can undergo vaginal delivery without complications (Forsnes, 1999; Takahashi, 2007).
As discussed, there seems to be a greater likelihood that Crohn disease may be associated with adverse pregnancy outcomes compared with ulcerative colitis (Stephansson, 2010). Outcomes are probably related to disease activities. For example, based on a 20-year review, Korelitz (1998) concluded that perinatal outcomes were generally good with quiescent disease. That said, in a case-control Danish study, Norgård (2007) reported a twofold risk of preterm births. Dominitz (2002) reported a two- to threefold increase in preterm delivery, low birthweight, fetal-growth restriction, and cesarean delivery in 149 women with Crohn disease. Recall, however, that the prospective ECCO-EpiCom study found outcomes to be similar to those for normal pregnancies.
Ostomy and Pregnancy
A colostomy or an ileostomy can be problematic during pregnancy because of its location (Hux, 2010). In a report of 82 pregnancies in 66 women with an ostomy, stomal dysfunction was common, but it responded to conservative management in all cases (Gopal, 1985). Surgical intervention was necessary, however, in three of six women who developed bowel obstruction and in another four with ileostomy prolapse—almost 10 percent overall. In this older study, only a third of 82 women underwent cesarean delivery, but Takahashi (2007) described six of seven cesarean deliveries in women with Crohn disease and a stoma. Fortunately, Farouk and coworkers (2000) reported that pregnancy did not worsen long-term ostomy function.
The incidence of bowel obstruction is not increased during pregnancy, although it generally is more difficult to diagnose. Meyerson (1995) reported a 20-year incidence of 1 in 17,000 deliveries at two Detroit hospitals. In one study, adhesive disease leading to small bowel obstruction was the second most common cause of an acute abdomen in pregnancy following appendicitis—15 versus 30 percent, respectively (Unal, 2011). As shown in Table 54-5, approximately half of cases are due to adhesions from previous pelvic surgery that includes cesarean delivery (Al-Sunaidi, 2006; Andolf, 2010; Lyell, 2011). Another 25 percent of bowel obstruction is caused by volvulus—sigmoid, cecal, or small bowel. These have been reported in late pregnancy or early puerperium (Alshawi, 2005; Biswas, 2006; Lal, 2006). Wax and colleagues (2013) described small bowel obstruction in pregnancy following the currently popular Roux-en-Y gastric bypass. Intussusception is occasionally encountered (Gould, 2008; Harma, 2011). Bowel obstruction subsequent to colorectal surgery for cancer was increased threefold in women who had open versus laparoscopic surgery (Haggar, 2013).
TABLE 54-5. Causes of Intestinal Obstruction During Pregnancy and the Puerperium
Most cases of intestinal obstruction during pregnancy result from pressure of the growing uterus on intestinal adhesions. According to Davis and Bohon (1983), this more likely occurs: (1) around midpregnancy, when the uterus becomes an abdominal organ; (2) in the third trimester, when the fetal head descends; or (3) immediately postpartum, when there is an acute change in uterine size. Perdue (1992) reported that 98 percent of pregnant women had either continuous or colicky abdominal pain, and 80 percent had nausea and vomiting. Abdominal tenderness was found in 70 percent, and abnormal bowel sounds noted in only 55 percent. Plain abdominal radiographs following soluble contrast showed evidence of obstruction in 90 percent of women. Plain radiographs, however, are less accurate for diagnosing small-bowel obstruction, and we and others have found that CT and MR imaging can be diagnostic (Biswas, 2006; Essilfie, 2007; McKenna, 2007). Colonoscopy can be both diagnostic and therapeutic for colonic volvulus (Dray, 2012; Khan, 2012).
During pregnancy, mortality rates with obstruction can be excessive because of difficult and thus delayed diagnosis, reluctance to operate during pregnancy, and the need for emergency surgery (Firstenberg, 1998; Shui, 2011). In an older report of 66 pregnancies, Perdue and associates (1992) described a 6-percent maternal mortality rate and 26-percent fetal mortality rate. Two of the four women who died were in late pregnancy, and they had sigmoid or cecal volvulus caused by adhesions. Perforation from massive bowel dilation such as that shown in Figure 54-4 causes severe sepsis syndrome.
FIGURE 54-4 Massively dilated colon in a pregnant woman with colonic volvulus. (Courtesy of Dr. Lowell Davis.)
Also known as Ogilvie syndrome, pseudo-obstruction is caused by adynamic colonic ileus. It is characterized by massive abdominal distention with cecal and right-hemicolon dilatation. Approximately 10 percent of all cases are associated with pregnancy. The syndrome usually develops postpartum—most commonly after cesarean delivery—but it has been reported antepartum (Tung, 2008). Although this is unusual, the large bowel may rupture (Singh, 2005). Treatment with an intravenous infusion of neostigmine, 2 mg, usually results in prompt decompression (Ponec, 1999). In some cases, colonoscopic decompression is performed, but laparotomy is done for perforation (De Giorgio, 2009; Rawlings, 2010).
Suspected appendicitis is one of the most common indications for abdominal exploration during pregnancy. The frequency for suspected appendicitis approximated 1 in 1000 women in the Swedish registry of 720,000 pregnancies (Mazze, 1991). Disease was confirmed in 65 percent for an incidence of approximately 1 in 1500 births. Inexplicably, the incidence was much lower in the Danish registry of more than 320,000 pregnancies—the confirmed appendicitis rate was only 1 per 5500 pregnancies (Hée, 1999).
It is repeatedly—and appropriately—emphasized that pregnancy makes the diagnosis of appendicitis more difficult. Nausea and vomiting accompany normal pregnancy, but also, as the uterus enlarges, the appendix commonly moves upward and outward from the right-lower quadrant (Baer, 1932; Pates, 2009). Another often-stated reason for late diagnosis is that some degree of leukocytosis accompanies normal pregnancy. For these and other reasons, pregnant women—especially those late in gestation—frequently do not have clinical findings “typical” for appendicitis. Thus, it commonly is confused with cholecystitis, preterm labor, pyelonephritis, renal colic, placental abruption, or uterine leiomyoma degeneration.
Most reports indicate increasing morbidity and mortality rates with increasing gestational age. And as the appendix is progressively deflected upward by the growing uterus, omental containment of infection becomes increasingly unlikely. It is indisputable that appendiceal perforation is more common during later pregnancy. In the studies by Andersson (2001) and Ueberrueck (2004), the incidence of perforation was approximately 8, 12, and 20 percent in successive trimesters.
Persistent abdominal pain and tenderness are the most reproducible findings. Right-lower quadrant pain is the most frequent, although pain migrates upward with appendiceal displacement (Mourad, 2000). For evaluation, sonographic abdominal imaging is reasonable in suspected appendicitis, even if to exclude an obstetrical cause of right-lower quadrant pain (Butala, 2010). That said, graded compression sonography is difficult because of cecal displacement and uterine imposition (Pedrosa, 2009). Appendiceal computed tomography is more sensitive and accurate than sonography to confirm suspected appendicitis (Gearhart, 2008; Katz, 2012; Raman, 2008). Specific views can be designed to decrease fetal radiation exposure (Chap. 46, p. 933). In one study, the negative appendectomy rate was 54 percent with clinical diagnosis alone, but only 8 percent if sonography and CT scanning were used (Wallace, 2008). MR imaging may be preferable, and as shown in Figure 54-5, we and others have had good results with its use (Dewhurst, 2013; Israel, 2008). One metaanalysis cited positive- and negative-predictive values of 90 and 99.5 percent, respectively (Blumenfeld, 2011). Using a decision-analysis model, CT and MR imaging were found to be cost effective (Kastenberg, 2013).
FIGURE 54-5 Anterior-posterior magnetic resonance image of a periappendiceal abscess in a midtrimester pregnancy. The abscess is approximately 5 × 6 cm, and the appendiceal lumen (arrow) is visible within the right-lower quadrant mass.
When appendicitis is suspected, treatment is prompt surgical exploration. Although diagnostic errors may lead to removal of a normal appendix, surgical evaluation is preferable to postponed intervention and generalized peritonitis. In earlier reports, the diagnosis was verified in only 60 to 70 percent of pregnant women. However, as indicated above, with CT and MR imaging, these figures have improved (Blumenfeld, 2011; Wallace, 2008). Importantly, the accuracy of diagnosis is inversely proportional to gestational age (Mazze, 1991).
Laparoscopy is almost always used to treat suspected appendicitis during the first two trimesters. There were similar perinatal outcomes reported from the Swedish database of nearly 2000 laparoscopic appendectomies compared with those of more than 1500 open laparotomies done before 20 weeks (Reedy, 1997). Conversely, from their review, Wilasrusmee and coworkers (2012) reported a higher fetal loss with laparoscopy. It has evolved that in many centers, laparoscopic appendectomy is performed in most cases during the third trimester (Barnes, 2004; Donkervoort, 2011). This is sanctioned and encouraged by the Society of American Gastrointestinal and Endoscopic Surgeons (Pearl, 2011; Soper, 2011). Some are of the opinion that laparoscopic surgery in pregnancy after 26 to 28 weeks should be performed only by the most experienced endoscopic surgeons (Parangi, 2007).
Before exploration, intravenous antimicrobial therapy is begun, usually with a second-generation cephalosporin or third-generation penicillin. Unless there is gangrene, perforation, or a periappendiceal phlegmon, antimicrobial therapy can usually be discontinued after surgery. Without generalized peritonitis, the prognosis is excellent. Seldom is cesarean delivery indicated at the time of appendectomy. Uterine contractions are common, and although some clinicians recommend tocolytic agents, we do not. De Veciana (1994) reported that tocolytic use substantially increased the risk for pulmonary-permeability edema caused by sepsis syndrome (Chap. 47, p. 947).
Appendicitis increases the likelihood of abortion or preterm labor, especially if there is peritonitis. In two studies, spontaneous labor after 23 weeks ensued with greater frequency following surgery for appendicitis compared with surgery for other indications (Cohen-Kerem, 2005; Mazze, 1991). In one study, the fetal loss rate was 22 percent if surgery was performed after 23 weeks. There are at least two large population-based studies that attest to the adverse outcomes from appendicitis in pregnancy. From the California Inpatient File of 3133 pregnant women undergoing surgery for suspected appendicitis, the fetal loss rate was 23 percent, and it was doubled—6 versus 11 percent—with simple versus complicated disease (McGory, 2007). A nationwide study from Taiwan found that there were 1.5- to twofold increased risks for low birthweight and preterm delivery when outcomes in 908 women with acute appendicitis were compared with those of controls (Wei, 2012).
Long-term complications are not common. The possible link between sepsis and neonatal neurological injury has not been verified (Mays, 1995). Finally, appendicitis during pregnancy does not appear to be associated with subsequent infertility (Viktrup, 1998).
Postpartum Acute Appendicitis
Although new-onset appendicitis during the immediate puerperium is uncommon, in some women it is undiagnosed before delivery. Appendicitis in these women often stimulated labor and when the large uterus rapidly empties, walled-off infection may be disrupted to result in an acute surgical abdomen. In some cases, acute appendicitis or a periappendiceal abscess or phlegmon may be found at the time of cesarean delivery or puerperal tubal ligation (see Fig. 54-5). It is important to remember that puerperal pelvic infections typically do not cause peritonitis.
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