Chapter 57. Gastrointestinal Disorders

 Gastrointestinal Disorders

BS. Nguyễn Hồng Anh

During normal pregnancy, the gastrointestinal (GI) tract

and its appendages undergo remarkable anatomical, physiological, and unctional alterations. Tese changes, which

are discussed in detail in Chapter 4 (p. 70), can appreciably

alter clinical ndings normally relied on or diagnosis and

treatment. Moreover, as pregnancy progresses, GI ndings

become more dicult to assess. Te clinical examination is

oten obscured by a large uterus that displaces abdominal

organs and can alter the location and intensity o pain and

tenderness.

GENERAL CONSIDERATIONS

■ Diagnostic Techniques

Endoscopy

Several endoscopic methods can be used to evaluate the gastrointestinal (GI) tract during pregnancy without reliance on

radiographic techniques. With beroptic endoscopic instruments, the esophagus, stomach, duodenum, and colon can be

inspected (Savas, 2014; Song, 2018). Te proximal jejunum

also can be studied, and the ampulla o Vater cannulated to

perorm endoscopic retrograde cholangiopancreatography—ERCP

(Fogel, 2014; Hedström, 2017). Experience in pregnancy with

video capsule endoscopy or small-bowel evaluation remains limited (Bandorski, 2016). Normal pregnancy-related slowing

o GI motility and thus increased transit time as well as the

recorder capsule’s electromagnetic eld are theoretical concerns.

Upper gastrointestinal endoscopy is used or diagnosis and

management o several problems. Common bile duct exploration and drainage are used or choledocholithiasis (Chap. 58,

p. 1043). Sclerotherapy and placement o percutaneous endoscopic

gastrostomy (PEG) tubes also are perormed endoscopically.

Colonoscopy is indispensible or viewing the entire colon and

distal ileum. Except or the midtrimester, reports o colonoscopy during pregnancy are limited, but most results suggest

that it should be perormed i necessary (De Lima, 2015; Ludvigsson, 2017). Pregnancy indications include chronic abdominal pain, hematochezia, and diarrhea (Cappell, 2011). Bowel

preparation is completed using polyethylene glycol electrolyte

(GoLYELY) or sodium sulate (Suprep) solutions (American

Society or Gastrointestinal Endoscopy, 2015). With these,

most women avoid serious dehydration that may cause diminished uteroplacental perusion. In select cases, tap water enemas

TABLE 57-1. Preprocedural Considerations for Gastrointestinal Endoscopy During Pregnancy

Plan consultation with an obstetrician, gastroenterologist, and anesthesiologist

Place patient in let lateral decubitus position

Use lowest eective dose o sedation necessary

Give prophylactic antibiotics as indicated. Penicillin, cephalosporin, erythromycin, and clindamycin are sae options

Minimize procedure time

Obtain etal heart tones at the discretion o the obstetrician. In general, pre- and post-procedure heart tones are adequate

For colonoscopy, avor preparation with PEG-ES or with tap water enemas depending on GI level to be evaluated

GI = gastrointestinal; PEG-ES = polyethylene glycol electrolyte solution.

From American Society or Gastrointestinal Endoscopy, 2012, 2015.

TABLE 57-2. Some Conditions Treated with Enteral or

Parenteral Nutrition During Pregnancya

Achalasia

Anorexia nervosa

Appendiceal rupture

Bowel obstruction

Burns

Cholecystitis

Crohn disease

Diabetic gastropathy

Esophageal injury

Hyperemesis gravidarum

Jejunoileal bypass

Malignancies

Ostomy obstruction

Pancreatitis

Preeclampsia syndrome

Short bowel syndrome

Stroke

Ulcerative colitis

aComplications arranged alphabetically.

From Billiauws, 2017; Folk, 2004; Guglielmi, 2006;

Mahadevan, 2019; Porter, 2014; Russo-Stieglitz, 1999; Saha,

2009; Spiliopoulos, 2013.

nutrition as a rst eort to prevent catabolism. For extreme

cases, such as recalcitrant hyperemesis gravidarum, percutaneous endoscopic gastrostomy with a jejunal port (PEG-J tube)

has been described.

Parenteral nutrition provides nutrients when the intestinal

tract must be quiescent. Peripheral parenteral nutrition (PPN)

administers dilute nutrient admixtures and is appropriate or

short-term use. Central venous access is necessary or central

parenteral nutrition (CPN) because its hyperosmolarity requires

rapid dilution in a high-ow vascular system (Robinson, 2018;

Worthington, 2017). Tese solutions provide 24 to 40 kcal/

kg/d, principally as a hypertonic glucose solution. Various

conditions may prompt CPN during pregnancy (Table 57-2).

Te most common indications are short bowel syndrome and

dysmotility disorders, and eeding duration averages 33 days

(Billiauws, 2017).

may be an alternative or rectosigmoidoscopy to avoid some o

these risks.

Endoscopic procedures should be perormed when indicated and ideally in the second trimester (American Society or

Gastrointestinal Endoscopy, 2012; Ludvigsson, 2017). A multidisciplinary approach with obstetricians, gastroenterologists,

and anesthesiologists is prudent. Table 57-1 outlines preprocedural considerations in pregnancy.

Noninvasive Imaging Techniques

Te ideal technique or GI tract imaging during pregnancy

is abdominal sonography. However, the gravid uterus may

obscure abdominal organs making evaluation dicult. Magnetic resonance (MR) imaging allows inspection o the abdomen and retroperitoneal space yet avoids radiation exposure

rom computed tomography (C) (Khandelwal, 2013).

Examples are MR cholangiopancreatography (MRCP) and

MR enterography (MRE) (Oto, 2009; Stern, 2014). Tese and

other imaging modalities, and their sae use in pregnancy, are

discussed in Chapter 49.

Laparotomy and Laparoscopy

Surgery is liesaving or certain GI conditions—perorative

appendicitis being the most common example. Intraabdominal

surgery is the most requently perormed nonobstetrical procedure during pregnancy (Devroe, 2019). Laparoscopic procedures have replaced traditional surgical techniques or many

abdominal disorders during pregnancy (Ye, 2019). Tese are

discussed in detail with descriptions o surgical technique in

Chapter 49 (p. 867) and in Cunningham and Gilstrap’s Operative Obstetrics, 3rd edition (Kho, 2017). Guidelines or laparoscopy during pregnancy have been provided by the American

College o Obstetricians and Gynecologists (2019) and the

Society o American Gastrointestinal and Endoscopic Surgeons

(Pearl, 2017).

■ Nutritional Support

Specialized nutritional support can be delivered enterally, usually via nasogastric tube eedings, or parenterally by venous

catheter access, either peripherally or centrally.

When possible, enteral alimentation is preerable because it

has ewer serious complications (Hoer, 2018; Stokke, 2015).

In obstetrical patients, very ew conditions prohibit enteral1014

Section 12

Medical and Surgical Complications

Parenteral nutrition complications are requent and may be

severe (Hoer, 2018). Te most common is catheter sepsis, and

Folk (2004) reported a 25-percent incidence in 27 women with

hyperemesis gravidarum. Te Centers or Disease Control and

Prevention provides detailed guidelines to prevent catheterrelated sepsis (O’Grady, 2011). Other maternal complications

include upper-extremity venous thrombosis, volume overload,

and reversible liver dysunction. Perinatal complications are

rare, however, etal subdural hematoma caused by maternal

vitamin K deciency has been described (Sakai, 2003).

Appreciable morbidity is also associated with long-term

use o a peripherally inserted central catheter (PICC). Again,

inection is the most common serious long-term complication

(Hoer, 2018; Holmgren, 2008). In a series o 84 such catheters inserted in 66 pregnant women, Cape and coworkers

(2014) reported a 56-percent complication rate, and bacteremia was the most requent. For short-term nutrition lasting a

ew weeks, PICC placement and its greater benet-versus-risk

ratio seems reasonable (Worthington, 2017).

UPPER GASTROINTESTINAL

TRACT DISORDERS

■ Hyperemesis Gravidarum

Mild to moderate nausea and vomiting are especially common

in pregnant women until approximately 16 weeks’ gestation

(Chap. 10, p. 191). In a small but signicant proportion o

these, however, it is severe and unresponsive to simple dietary

modication and antiemetics. Hyperemesis gravidarum is

dened variably as severe unrelenting nausea and vomiting that

produces weight loss, dehydration, ketosis, alkalosis rom loss

o hydrochloric acid, and hypokalemia. Acidosis develops rom

partial starvation. In some women, transient hepatic dysunction develops, and biliary sludge accumulates (able 58-1, p.

1031). Other causes should rst be considered because hyperemesis gravidarum is a diagnosis o exclusion.

Study criteria are not standardized, and thus population

incidences vary (Koot, 2018). However, an ethnic or amilial

predilection has been described (London, 2017). In several

population-based studies, the hospitalization rate or hyperemesis gravidarum was 0.5 to 2.1 percent (Fiaschi, 2019;

Vikanes, 2013). Up to 25 percent o those hospitalized in a

previous pregnancy or hyperemesis will again require admission (Nurmi, 2018).

Te etiopathogenesis o hyperemesis gravidarum is unknown

and is likely multiactorial. High or rapidly rising serum levels o pregnancy-related hormones such as human chorionic

gonadotropin (hCG), estrogen, progesterone, placental growth

hormone, prolactin, thyroxine, and adrenocortical hormones

are implicated (London, 2017; Verberg, 2005). Other associated hormones include ghrelins, leptin, nesatin-1, and peptide

YY 3–36 (Albayrak, 2013; Gungor, 2013).

Superimposed on this hormonal cornucopia are many biological and environmental actors. Moreover, in some but not

all severe cases, interrelated psychological components play a

major role (Mitchell-Jones, 2017; Senturk, 2017). Factors

that increase the risk or admission include hyperthyroidism,

previous pregnancy complicated by hyperemesis, diabetes,

GI illnesses, some restrictive diets, and asthma (Fell, 2006;

Fiaschi, 2016; Mullin, 2012). An association o Helicobacter

pylori inection has been proposed, but evidence is inconclusive

(Goldberg, 2007; London, 2017). Chronic marijuana use may

cause the similar cannabinoid hyperemesis syndrome (Alaniz, 2015;

Andrews, 2015). And or unknown reasons—perhaps estrogenrelated—a emale etus raises the risk but smoking and obesity decrease it by 1.5-old (Cedergren, 2008; Fiaschi, 2016).

Some have reported a relationship between severe hyperemesis

gravidarum and anemia, venous thromboembolism (VE),

gestational hypertension, and preeclampsia (Fiaschi, 2018). An

association between hyperemesis and preterm birth is unclear

(Kleine, 2017). Koren and colleagues (2018) suggested that

prolonged vomiting may cause metabolic abnormalities that

interere with etal brain development. No long-term maternal

consequences ollow hyperemesis. Specically, two populationbased studies ound no unavorable cardiovascular risks in

Norwegian women (Fossum, 2017, 2018).

Complications

Vomiting may be prolonged, requent, and severe, and a

list o potentially atal complications is given in Table 57-3.

Various degrees o acute kidney injury rom dehydration are

encountered, and rhabdomyolysis may be contributory (Lassey,

2016). Rarely, we and others have encountered women with

renal ailure requiring dialysis (Dayangan Sayan, 2018; Hill,

2002). Mallory-Weiss tears result rom continuous retching.

Other complications include pneumothorax, pneumomediastinum, diaphragmatic rupture, and gastroesophageal rupture—

Boerhaave syndrome (American College o Obstetricians and

Gynecologists, 2018; Chen, 2012).

At least two serious vitamin deciencies have been reported

with hyperemesis in pregnancy. One is Wernicke encephalopathy

rom thiamine deciency (Di Gangi, 2012; Palacios-Marqués,

2012). A systematic review reported that ocular signs, conusion, and ataxia were common, and approximately 60 percent

had this triad (Oudman, 2019). In some women, an abnormal

electroencephalogram (EEG) may be seen, and usually MR

imaging shows ndings (Oudman, 2019; Vaknin, 2006; Zara,

TABLE 57-3. Some Serious and Life-Threatening

Complications Reported with Hyperemesis

Gravidaruma

Acute kidney injury—may require dialysis

Depression—cause versus eect?

Diaphragmatic rupture

Esophageal rupture—Boerhaave syndrome

Hyperalimentation complications

Hypokalemia—arrhythmias, cardiac arrest

Hypoprothrombinemia—vitamin K deiciency

Mallory–Weiss tears—bleeding, pneumothorax,

pneumomediastinum, pneumopericardium

Rhabdomyolysis

Wernicke encephalopathy—thiamine deiciency

aComplications arranged alphabetically.Gastrointestinal Disorders 1015

CHAPTER 57

institution, or cost savings, we prescribe these two agents individually. Te ormula is one hal o a 25-mg Unisom (doxylamine) tablet plus a 25-mg vitamin B6 (pyridoxine) tablet. Te

same graduated dosing is used but does not exceed three total

daily doses.

Ondansetron (Zoran) is slightly more eective than the

combination o doxylamine and pyridoxine (Oliveira, 2014;

Pasternak, 2013). In some studies, the ormer has been associated with birth deects (Briggs, 2017). However, ater a recent

systematic review o Cochrane and Reprotox databases, authors

concluded that ondansetron is not teratogenic (Kaplan, 2019).

Other drawbacks include potential maternal eects rom prolonged Q-interval and serotonin syndrome. For these reasons

it is preerably reserved or severe cases ater 8 weeks’ gestation

(Lavecchia, 2018).

When simple measures ail, intravenous (IV) crystalloid

solutions are given to correct dehydration, ketonemia, electrolyte decits, and acid-base imbalances. Hypokalemia is common, and cardiac arrest has been reported (Walch, 2018). No

benets are gained by inusing 5-percent dextrose along with

crystalloids (an, 2013). Tiamine,

100 mg, is usually diluted in 1 L o

the selected crystalloid to prevent Wernicke encephalopathy or women who

require IV hydration and have vomited or more than 3 weeks (Giugale,

2015). It is inused at the maintenance

rate desired or patient hydration. Tis

thiamine dose is provided daily or the

next 2 to 3 days and is ollowed by IV

multivitamins i IV hydration continues (Levichek, 2002).

I vomiting persists ater rehydration and ailed outpatient management, hospitalization is recommended

(American College o Obstetricians

and Gynecologists, 2018). IV hydration is continued and antiemetics such

as promethazine, prochlorperazine,

chlorpromazine, or metoclopramide

are given parenterally (Table 57-4).

Several antiemetics are associated with

the long-Q syndrome, discussed in

Chapter 52 (p. 936). Outpatient treatment regimens at the hospital also are

eective (McCarthy, 2014).

Some, but not all, studies indicate

that treatment with glucocorticosteroids

is not eective (Sridharan, 2020; Yost,

2003). Tey are recommended only or

reractory cases because o their putative teratogenicity (American College

o Obstetricians and Gynecologists,

2018).

With persistent vomiting ater hospitalization, appropriate steps should

be taken to exclude possible underlying diseases as a cause o hyperemesis.

FIGURE 57-1 Algorithm or outpatient and inpatient management o pregnancy nausea

and vomiting, and hyperemesis gravidarum.

2012). One woman had recurrent encephalopathy in a subsequent pregnancy (Stephens, 2019). Maternal deaths have been

described, and long-term sequelae include blindness, convulsions, and coma (Oudman, 2019; Selitsky, 2006). Vitamin K

is a second potential deciency. Maternal coagulopathy, etal

intracranial hemorrhage, and vitamin K embryopathy have

been reported (Kawamura, 2008; Lane, 2015; Nijsten, 2021).

Management

One management algorithm or nausea and vomiting o pregnancy is shown in Figure 57-1. Most women with mild to

moderate symptoms respond to outpatient therapy with any

o several rst-line antiemetic agents (Boelig, 2018, McParlin,

2016). One mainstay is Diclegis—a combination o doxylamine

(10 mg) plus pyridoxine (10 mg). Te usual dose is two tablets orally at bedtime, and it appears sae and eective (Briggs,

2017; Koren, 2014). I relie is insucient, one additional

rst-morning tablet is added to the bedtime dose. Tis can be

urther escalated to include one rst-morning, one midaternoon, and two bedtime tablets (Duchesnay Inc., 2018). At our1016

Section 12

Medical and Surgical Complications

Tat said, in one study, endoscopy did not change management

in 49 women (Debby, 2008). Other potential sources include

gastroenteritis, cholecystitis, pancreatitis, hepatitis, peptic

ulcer, and pyelonephritis. In addition, severe preeclampsia and

atty liver are more likely ater midpregnancy. Although clinical

thyrotoxicosis has been implicated as a cause o hyperemesis, it

is more likely that abnormally elevated serum thyroxine levels

are a surrogate or higher-than-average serum hCG levels (Sun,

2014). Tis is discussed urther in Chapter 5 (p. 97). In our

experiences, serum ree thyroxine levels normalize quickly with

hydration and emesis treatment.

With treatment, most women will have a positive response

and may be sent home with oral antiemetic therapy. Te readmission rate is 25 to 35 percent in most prospective studies.

Risks or anxiety and depression are increased in these women

(Mitchell-Jones, 2017; Senturk, 2017). At Parkland Hospital,

more than one third o women with hyperemesis required readmission. Patient characteristics had limited utility in predicting

the risk o readmission. For example, maternal demographics, substance use, psychiatric illness, and initial hospitalization length were not associated with readmission (White,

2018). I psychiatric and social actors contribute to the illness,

the woman usually improves remarkably while hospitalized

(Swallow, 2004). However, symptoms relapse in a ourth o these

TABLE 57-4. Medications for Gastrointestinal Disorders in Pregnancy

Medication (Brand Name) Usual Dosing Route(s)

Options for nausea and vomiting

Antihistamine

Doxylamine + pyridoxine (Diclegis)a At bedtime; up to 4 times daily PO

Phenothiazines Every 6 hr

Promethazine (Phenergan)c 12.5–25 mg IM, IV, PO, PR

Prochlorperazine (Compazine)c 5–10 (25 PR) mg IM, IV, PO, PR

Chlorpromazine (Thorazine)c 25–50 mg IM, PO

Serotonin antagonist Every 8 hr

Ondansetron (Zoran)b 8 mg IV, PO

Benzamides Every 6 hr

Metoclopramide (Reglan)b 5–15 mg IM, IV, PO

Trimethobenzamide (Tigan) 300 mg PO

Oral options for gastroesophageal reflux disease (GERD)

Proton-pump inhibitors

Pantoprazole (Protonix)b 40 mg daily or up to 8 wks

Lansoprazole (Prevacid)b 15 mg daily or up to 8 wks

Omeprazole (Prilosec, Zegerid)c 20 mg daily or 4–8 wks

Dexlansoprazole (Dexilant)c 30 mg daily or up to 4 wks

H2-receptor antagonists

Cimetidine (Tagamet)b 400 mg 4 times daily or up to 12 wks

800 mg twice daily or up to 12 wks

Nizatidine (Axid)b 150 mg twice daily

Famotidine (Pepcid)b 20 mg twice daily up to 6 wks

aFood and Drug Administration category A.

bFood and Drug Administration category B.

cFood and Drug Administration category C.

IM = intramuscularly; IV = intravenously; PO = orally; PR = rectally.

women, and some go on to develop posttraumatic stress syndrome

(Chap. 64, p. 1150) (Christodoulou-Smith, 2011; McCarthy,

2011; Nurmi, 2018). For some women, hyperemesis may be an

indication or elective termination (Pourshari, 2007).

Grooten and colleagues (2017) showed that early enteral tube

eeding has no advantages. However, in the small percentage o

women who have recalcitrant vomiting ater intensive therapy,

consideration is given or enteral nutrition (p. 1013). Stokke

and associates (2015) described successul use o nasojejunal

eeding or up to 41 days in 107 such women. Use o sonography to conrm correct tube placement has been described and

avoids radiation exposure (Swartzlander, 2013). PEG-J tubes

also have been reported (Saha, 2009; Schrag, 2007).

Only a very ew women will require parenteral nutrition

(American College o Obstetricians and Gynecologists, 2018;

Yost, 2003). In a study o 599 women, however, Peled and

coworkers (2014) reported that 20 percent required central

parenteral nutrition.

■ Gastroesophageal Reflux Disease

Symptomatic reux is seen in up to 15 percent o nonpregnant

individuals (Kahrilas, 2018). Te spectrum o sequelae includes

esophagitis, stricture, Barrett esophagus, and adenocarcinoma.Gastrointestinal Disorders 1017

CHAPTER 57

Te main symptom o reux is pyrosis (heartburn), which is

especially common in pregnancy. In one study, its prevalence

rose rom 26 percent in the rst trimester to 36 percent in

the second and 51 percent in the third trimester (Fill Malertheiner, 2017). Te retrosternal burning sensation stems rom

esophagitis caused by gastroesophageal reux o stomach acid,

which ollows relaxation o the lower esophageal sphincter. Te

diagnosis is typically made rom symptoms alone.

Symptoms usually respond to abstaining rom tobacco and

alcohol, eating small meals, elevating the head o the bed, limiting postprandial recumbency, and avoiding “trigger” oods.

Tese may include atty oods, tomato-based oods, and co-

ee. Oral antacids are rst-line therapy. I severe symptoms

persist, a proton-pump inhibitor is given and an H2-receptor

antagonist and sucralate can be added (see able 57-4). Both

classes are generally sae or use in pregnancy (Briggs, 2017).

From preliminary data, proton-pump inhibitors taken early

in pregnancy may increase the risk or preeclampsia (Hastie,

2019). Sucralate is the aluminum salt o sulated sucrose and

inhibits pepsin. Approximately 10 percent o the aluminum

salt is absorbed, and this agent is considered sae or pregnant

women (Briggs, 2017). A 1-g sucralate tablet is taken orally 1

hour beore each o the three meals and at bedtime or up to 8

weeks. Antacids are not used within a hal hour beore or ater

sucralate doses. Despite attempts with these options, i relie

is not attained, endoscopy should be considered. Misoprostol is

contraindicated because it stimulates labor (Chap. 26, p. 490).

In nonpregnant patients, surgical undoplication can be per-

ormed (Kahrilas, 2018). Although the procedure is not done

during pregnancy, Biertho and colleagues (2006) described 25

women who had undergone laparoscopic Nissen undoplication beore pregnancy. Only 20 percent had reux symptoms

during pregnancy.

■ Hiatal Hernia

Te older literature is inormative regarding hiatal hernias in

pregnancy. Upper gastrointestinal radiographs perormed in

195 women in late pregnancy showed that 20 percent o 116

multiparas and 5 percent o 79 nulliparas had a hiatal hernia

(Rigler, 1935). O 10 women studied postpartum, hernia persisted in three at 1 to 18 months.

Te relationship o hiatal hernia with reux esophagitis is

not clear. One study demonstrated no association and showed

that the lower esophageal sphincter unctioned eectively even

when displaced intrathoracically (Cohen, 1971). Nevertheless,

during pregnancy, hiatal hernias may cause vomiting, epigastric pain, and bleeding rom ulceration. Schwentner (2011)

reported severe herniation requiring surgical repair in a woman

with a 12-week gestation. Curran and coworkers (1999)

described a 30-week pregnancy complicated by gastric outlet

obstruction rom a paraesophageal hernia.

■ Diaphragmatic Hernia

Tese are caused by herniations o abdominal contents through

either the oramen o Bochdalek or Morgagni. Fortunately,

they rarely complicate pregnancy. In one review o 18 pregnant

women who developed acute obstruction within a diaphragmatic hernia, the maternal mortality rate was 45 percent

(Kurzel, 1988). Herniation has been reported in one woman

who had antireux surgery in early pregnancy (Brygger, 2013).

Several case reports also describe spontaneous diaphragmatic

rupture rom elevated intraabdominal pressure during delivery

(Chen, 2012; Shariah, 2003). Surgical treatment is considered in symptomatic gravidas and is individualized according

to gestational age and clinical setting (Ménassa, 2019; Whang,

2018).

■ Achalasia

In this rare motility disorder, the lower esophageal sphincter ails to relax properly with swallowing. Te esophageal

muscularis also displays nonperistaltic contraction activity

(Kahrilas, 2018). Te deect is caused by inammatory destruction o the myenteric (Auerbach) plexus within smooth muscle

o the lower esophagus and its sphincter. Postganglionic cholinergic neurons are unaected, and thus sphincter stimulation

is unopposed.

Symptoms are dysphagia, chest pain, and regurgitation. Barium swallow radiography demonstrates bird beak or ace o spades

narrowing at the distal esophagus. Endoscopy is perormed to

exclude gastric carcinoma, and manometry is conrmatory.

During pregnancy, normal physiological relaxation o the

lower esophageal sphincter in women with achalasia theoretically should not occur. In one series, hal o these women had

worsened symptoms, but reux is uncommon (Vogel, 2018).

In other pregnancy studies, most women did not have worsening symptoms (Khudyak, 2006). At least one maternal death

was reported at 24 weeks’ gestation and peroration o a 14-cmdiameter megaesophagus was implicated (Fassina, 1995).

Management o achalasia includes a sot diet and anticholinergic drugs. With persistent symptoms, other options include

nitrates, calcium-channel antagonists, and botulinum toxin A

injected locally (Hoot, 2015; Kahrilas, 2018). Balloon dilation

o the sphincter may be necessary, and 85 percent o nonpregnant patients respond (Vogel, 2018). One caveat is that esophageal peroration is a serious complication o dilation. I dilation or

medical therapy ail to provide relie, myotomy is considered.

In one report, a 29-week pregnant woman with achalasia was

treated or 10 weeks with peripheral parenteral nutrition, and

surgical myotomy was done postpartum (Spiliopoulos, 2013).

■ Peptic Ulcer Disease

Te lietime prevalence o acid peptic disorders in women is

10 percent (Del Valle, 2018). Erosive ulcer disease involves the

stomach and duodenum. Gastroduodenal ulcers commonly

are caused by chronic gastritis rom Helicobacter pylori, or they

develop rom nonsteroidal antiinammatory drug (NSAID)

use. Neither is common in pregnancy (McKenna, 2003;

Weyermann, 2003). Rosen and coworkers (2021) reported

2535 pregnant women with peptic ulcer disease and ound that

complications were less requent than in nonpregnant controls.

Acid secretion also is important, and this underlies the e-

cacy o antisecretory agents. Natural gastroprotection during1018

Section 12

Medical and Surgical Complications

pregnancy probably originates rom physiological changes

that include reduced gastric acid secretion, decreased motility,

and considerably increased mucus secretion (Hytten, 1991).

Despite this, ulcer disease may be underdiagnosed because

o requent treatment or reux esophagitis (Mehta, 2010).

In the past 55 years at Parkland Hospital, during which time

we have cared or more than 600,000 pregnant women, we

have encountered very ew who had proven ulcer disease. Per-

oration is rare (Goel, 2014). Beore appropriate therapy was

commonplace, Clark (1953) studied 313 pregnancies in 118

women with ulcer disease and noted a clear remission during

pregnancy in almost 90 percent. However, benets were short

lived. Symptoms recurred in more than hal by 3 months postpartum and in almost all by 2 years.

Te mainstay o management is eradication o H pylori and

prevention o NSAID-induced disease. Antacids are usually

sel-prescribed, but other rst-line therapy is a proton-pump

inhibitor or H2-receptor blocker (see able 57-4) (Del Valle,

2018; Laine, 2012). Sucralate can be added and provides a

protective coating at the ulcer base.

With active ulcers, a search or H pylori is undertaken. Diagnostic aids include the urea breath test, serological testing, ecal

testing, or endoscopic biopsy. I any o these yield positive

results, combination antimicrobial plus proton-pump inhibitor

therapy is indicated (Chey, 2017). Several eective oral treatment regimens do not include tetracycline and can be used during pregnancy. One 14-day regimen includes clarithromycin,

500 mg twice daily, which is paired either with amoxicillin,

1000 mg twice daily or with metronidazole, 500 mg three times

daily. Tese antibiotics are given with a proton-pump inhibitor

(Del Valle, 2018).

■ Upper Gastrointestinal Bleeding

In some women, persistent vomiting is accompanied by worrisome upper gastrointestinal bleeding. Occasionally, a peptic

ulcer is the source. However, most o these women have small

linear mucosal tears near the gastroesophageal junction—

Mallory-Weiss tears (p. 1014). Bleeding usually responds

promptly to conservative measures that include IV protonpump inhibitors and topical antacids (Laine, 2012). rans-

usions may be needed, and i bleeding persists, endoscopy is

usually indicated (O’Mahony, 2007). With sustained retching,

the less common, but more serious, esophageal rupture—Boerhaave syndrome—may develop rom high esophageal pressure.

SMALL BOWEL AND COLON DISORDERS

Te small bowel has diminished motility during pregnancy.

Lawson and colleagues (1985) showed that the small bowel

mean transit times o 99, 125, and 137 minutes in each successive trimester, respectively, were slower than 75 minutes when

nonpregnant. Muscular relaxation o the colon is accompanied

by increased absorption o water and sodium that predisposes to

constipation. Tis complaint is reported by almost 25 percent

o women at some time during pregnancy and the puerperium

(Everson, 1992). Symptoms are usually only mildly bothersome, and initial treatment includes increasing uid intake

(>8 glasses/d) and ber consumption (20 to 35 g/d) (Body,

2016). I these liestyle modications ail, bulk-orming agents

such as methylcellulose may be added, and in severe cases the

stimulant laxative bisacodyl. We have encountered several pregnant women who developed megacolon rom impacted stool.

Tese women almost invariably had chronically abused stimulatory laxatives.

■ Acute Diarrhea

Te estimated monthly prevalence o diarrhea among adults

is 3 to 7 percent (DuPont, 2014). Diarrhea can be classied

as acute (<2 weeks), persistent (2 to 4 weeks), and chronic

(>4 weeks). Most cases o acute diarrhea are caused by inectious agents, and a third result rom oodborne pathogens. Te

large variety o viruses, bacteria, helminths, and protozoa that

cause diarrhea in adults also afict pregnant women. Tese are

usually accompanied by vomiting, ever, and abdominal pain.

Some o these are discussed in Chapter 64 (p. 1197).

Evaluation o acute diarrhea depends on its severity and

duration. Some indications or evaluation include prouse

watery diarrhea with dehydration, grossly bloody stools, ever

>38°C, duration >48 hr without improvement, recent antimicrobial use, and diarrhea in the immunocompromised patient

(Camilleri, 2018; DuPont, 2014). Cases o moderately severe

diarrhea with ecal leukocytes or gross blood may be treated

with empirical antibiotics rather than evaluation. However,

risks and benets should be considered, and it is reasonable to

withhold treatment until stool testing is completed to exclude

inection. Some eatures o the more common acute diarrheal

syndromes and their treatment are shown in Table 57-5.

Te mainstay o treatment is IV hydration using normal

saline or Ringer lactate and potassium supplementation in

amounts to restore maternal blood volume and to ensure uteroplacental perusion. Vital signs and urine output are monitored

or signs o sepsis. For moderately severe nonebrile illness

without bloody diarrhea or recent travel, antimotility agents

such as loperamide (Imodium) may be useul. An initial 4-mg

(two capsules) dose can be ollowed with another 2-mg capsule ater subsequently passed watery stools. Dosages should

not exceed 8 mg/d, and loperamide is not used or more than

48 h. Bismuth subsalicylate (Pepto-Bismol) also may alleviate

symptoms. Te recommended dosage is 30 mL (525 mg) o its

liquid orm or two tablets (263 mg/tablet) chewed well each 30

to 60 min and not to exceed eight doses in 24 h. Te drug will

produce harmless black stools (Riddle, 2016).

Judicious use o antimicrobial agents is warranted. For moderately to severely ill women, some recommend empirical treatment with ciprooxacin, 500 mg twice daily or 3 days. Specic

pathogens are treated as needed when identied (see able 57-5).

Syndromes or which treatment is usually unnecessary include

those caused by Escherichia coli, staphylococcal species, Bacillus cereus, and norovirus. Severe illness caused by Salmonella

species is treated with ciprooxacin or trimethoprim-sulamethoxazole; by Campylobacter species with azithromycin; by

Clostridioides dicile with oral vancomycin or daxomicin; and

by Giardia species and Entamoeba histolytica with metronidazole (DuPont, 2014; McDonald, 2018; Rocha-Castro, 2016).Gastrointestinal Disorders 1019

CHAPTER 57

Clostridioides difficile Infection

Formally known as Clostridium dicile, this anaerobic grampositive bacillus is transmitted by the ecal-oral route. In a study

rom China, 3.7 percent o normal gravidas were colonized

(Ye, 2016). It is the most requent nosocomial inection in the

United States. In 2011, 453,000 cases o C dicile and 29,000

associated deaths were reported by the Centers or Disease

Control and Prevention (Lessa, 2015). Its incidence in pregnant women has doubled during the past decade (Ruiter-Ligeti,

2018). Te most important risk actor is antibiotic use, and the

highest risk is with aminopenicillins, clindamycin, cephalosporins, and uoroquinolones. Other risk actors include inammatory bowel disease, immunosuppression, advanced age,

and gastrointestinal surgery. Most cases are hospital-acquired,

however, 10 percent are community-acquired cases (Gerding,

2018). With severe colitis, the inection-related mortality rate

is 5 percent.

Laboratory diagnosis rom a stool sample uses nucleic-acid

amplication testing (NAA) or C dicile itsel or uses an

enzyme-immunoassay-based algorithm or a unique C dicile

enzyme or its toxins A and B (McDonald, 2018). Less oten,

inection may be diagnosed endoscopically (Fig. 57-2). Only

patients with new-onset diarrhea and ≥3 unormed stool o

unexplained etiology should be tested, and posttreatment testing is not recommended. Prevention is by soap-and-water hand

TABLE 57-5. Etiology, Clinical Features, and Treatment of Common Acute Diarrheal Syndromes

Agents Incubation Emesis Pain Fever Diarrhea Treatment

Toxin producers

1. Staphylococcus spp.

2. C perringens

3. E coli (enterotoxin)

4. B cereus

1–72 hr 3–4+ 1–2+ 0–1+ 3–4+, watery

1. None

2. None

3. Ciprofoxacin

4. None

Enteroadherent

1. E coli

2. Giardia spp.

3. Helminths

1–8 days 0–1+ 1–3+ 0–2+ 1–2+, watery,

mushy 1. Ciprofoxacin

2. Tinidazole

3. As detected

Cytotoxin producers

1. C difcile

2. E coli (hemorrhagic)

1–3 days 0–1+ 3–4+ 1–2+ 1–3+, watery,

then bloody 1. Vancomycin

2. None

Inflammatory

Minimal

1. Rotavirus

2. Norovirus

Variable

3. Salmonella spp.

4. Campylobacter spp.

5. Vibrio spp.

Severe

6. Shigella spp.

7. E coli

8. Entamoeba histolytica

1–3 days

12 hr–11 days

12 hr–8 days

1–3+

0–3+

0–1+

2–3+

2–4+

3–4+

3–4+

3–4+

3–4+

1–3+, watery

1–4+ watery or

bloody

1–2+, bloody

1. None

2. None

3. Ciproloxacin

4. Azithromycin

5. Doxycycline

6. Ciproloxacin

7. Ciproloxacin

8. Metronidazole

B cereus = Bacillus cereus; C diicile = Clostridioides diicile; C perringens = Clostridium perringens; E coli = Escherichia coli;

spp. = species.

Modiied rom Camilleri, 2018; DuPont, 2014; McDonald, 2018.

A B

C D

FIGURE 57-2 Causes o colitis. A. Ulcerative colitis with diuse

ulcerations and exudates. B. Crohn colitis with deep ulcers.

C. Pseudomembranous colitis with yellow, adherent membranes.

D. Ischemic colitis. (Reproduced with permission rom Song LM,

Topazian M: Gastrointestinal endoscopy. In Jameson JL, Fauci AS,

Kasper DL, et al (eds): Harrison’s Principles o Internal Medicine,

20th ed. New York, NY: McGraw Hill; 2018.)1020

Section 12

Medical and Surgical Complications

Major symptoms o ulcerative colitis include diarrhea, rectal bleeding, tenesmus, and abdominal cramps. Te disease is

characterized by exacerbations and remissions. Toxic megacolon

and catastrophic hemorrhage are particularly dangerous complications that may necessitate colectomy. Extraintestinal mani-

estations include arthritis, uveitis, and erythema nodosum. Te

risk o associated colon cancer approaches 1 percent per year.

With either ulcerative colitis or Crohn disease, risks or VE

are higher in even asymptomatic women (Friedman, 2018;

Mahadevan, 2019).

Crohn Disease

Also known as regional enteritis, Crohn ileitis, or granulomatous colitis, Crohn disease has more protean maniestations than

ulcerative colitis. It involves not only the mucosa but also the

deeper bowel layers (see Fig. 57-2). Lesions can be seen throughout the entire GI tract, rom the mouth to the anus, but it typically is segmental (Friedman, 2018). Approximately 30 percent

o patients have only small-bowel involvement, 25 percent have

isolated colonic involvement, and 40 percent have both, usually

with the terminal ileum and colon involved. Perianal stulas and

abscesses develop in a third o those with colonic involvement.

Symptoms depend on which bowel segment(s) is involved.

Tus, complaints may include lower-right-sided cramping

abdominal pain, diarrhea, weight loss, low-grade ever, and

obstructive symptoms. Te disease is chronic with exacerbations and remissions, and importantly, it cannot be cured medically or surgically. Approximately a third o patients require

surgery within the rst year ater diagnosis, and thereater, the

rate is 5 percent per year. Reactive arthritis is common, and the

GI cancer risk, although not as great as with ulcerative colitis,

is increased substantially.

TABLE 57-6. Some Shared and Differentiating Characteristics of Inflammatory Bowel Disease

Ulcerative Colitis Crohn Disease

Shared Characteristics

Hereditary More than 100 disease-associated genetic loci–a third shared; Jewish predominance; amilial in

5–10% o cases; Turner syndrome; immune dysregulation

Other Chronic and intermittent with exacerbations and remissions; extraintestinal maniestations: arthritis,

erythema nodosum, uveitis

Differentiating Characteristics

Major symptoms Diarrhea, tenesmus, rectal bleeding, cramping pain;

chronic, intermittent; anemia

Fibrostenotic–recurrent RLQ colicky pain; ever

Fistulizing–cutaneous, bladder, interenteric

Bowel involvement Mucosa and submucosa o large bowel; usually

begins at rectum (40% proctitis only); continuous

disease

Deep layers small and large bowel; commonly

transmural; discontinuous involvement;

strictures and istulas

Endoscopy Granular and riable erythematous mucosa;

bleeding; rectal involvement

Patchy; segmental colitis; rectum spared;

perianal involvement

Serum antibodies Antineutrophil cytoplasmic (pANCA) ∼70% Anti–S cerevisiae ∼50%

Complications Toxic megacolon; strictures; arthritis; cancer (3–5%) Fistulas; arthritis; toxic megacolon; small bowel

obstruction

Management Medical; proctocolectomy curative Medical; segmental and istula resection

RLQ = right lower quadrant; S cerevisiae = Saccharomyces cerevisiae.

From Friedman, 2018; Lichtenstein, 2009.

washing, and inected individuals are isolated. reatment consists o stopping the oending antibiotics and giving 10 days

o oral vancomycin, 125 mg our times daily, or daxomicin

(Dicid), 200 mg twice daily (McDonald, 2018). Te risk o

recurrence ater an initial episode is 20 percent. Fecal microbial

transplantation may become standard or recurrent clostridial

colitis (Saeedi, 2017).

■ Inflammatory Bowel Disease

wo presumably noninectious orms o intestinal inammation are ulcerative colitis and Crohn disease. Dierentiation

between these is important because treatment diers. Tat said,

they both share common eatures, and sometimes are indistinguishable i Crohn disease involves the colon. Te eatures

shown in Table 57-6 permit a reasonably condent diagnostic

dierentiation in most cases. Te etiopathogenesis is enigmatic

in both, but a genetic predisposition is suspected, especially or

Crohn disease. Inammation is thought to result rom dysregulated mucosal immune unction in response to commensal microbiota, with or without an autoimmune component

(Friedman, 2018).

Ulcerative Colitis

Tis is a mucosal disorder with inammation conned to the

supercial luminal layers o the colon. It typically begins at the

rectum and extends proximally or a variable distance. In approximately 40 percent o cases, disease is conned to the rectum or

the rectosigmoid, but 20 percent have pancolitis. For unknown

reasons, prior appendectomy protects against ulcerative colitis

(Friedman, 2018). Endoscopic ndings include mucosal granularity and riability that is interspersed with mucosal ulcerations

and a mucopurulent exudate (see Fig. 57-2).Gastrointestinal Disorders 1021

CHAPTER 57

Inflammatory Bowel Disease and Fertility

Subertility in women is linked to active disease, but normal

ertility is likely with quiescent colitis (Mahadevan, 2019). Sub-

ertility may also be partially attributed to sulasalazine, which

causes reversible sperm abnormalities (Feagins, 2009).

For women requiring surgical resection, a laparoscopic

approach has a higher subsequent ertility rate (Beyer-Berjot, 2013). With colectomy, however, although ertility is

improved, up to hal o women will be persistently inertile (Bartels, 2012; Lee, 2019a). Sexual unction and ertility

are only modestly aected by ileal pouch–anal anastomosis

(Hor, 2016).

Inflammatory Bowel Disease and Pregnancy

Because ulcerative colitis and Crohn disease are relatively common in young women, these disorders are encountered with

some requency in pregnancy. In many studies, the outcomes

are grouped together or both entities. For example, in a study

rom Australia, Shand and colleagues (2016) reported a prevalence o 1 inammatory bowel disease (IBD) case in 320 births.

In this regard, some generalizations can be made. First, consensus supports that pregnancy does not increase the likelihood o

an IBD are (Mahadevan, 2019). Indeed, in a 10-year surveillance o women in the European Collaborative on Inammatory Bowel Disease, the likelihood o a are during pregnancy

was lower than the preconceptional rate (Riis, 2006). Although

most women with quiescent disease in early pregnancy do not

have relapses, when a are develops, it may be severe. Also,

and as discussed subsequently, active disease in early pregnancy

increases the likelihood o disease relapse during pregnancy (de

Lima-Karagiannis, 2016).

In general, most usual treatment regimens may be continued during pregnancy. Diagnostic evaluations should be undertaken i needed to direct management, and surgery should be

perormed i indicated (Mahadevan, 2019). Fecal calprotectin,

an inammatory biomarker in stool samples, is a valid tool in

pregnancy to identiy IBD ares (Julsgaard, 2017; Lichtenstein,

2018; Rubin, 2019).

At rst glance, it appears that adverse pregnancy outcomes

are increased with IBD (Boyd, 2015; Getahun, 2014). Initially, this was attributed to the act that most studies included

women with either orm o disease. Specically, Crohn disease

was noted to be linked to excessive morbidity. But, according

to Reddy (2008) and others, these adverse outcomes were in

women with severe disease and multiple recurrences. Indeed,

in the prospective European case-control ECCO-EpiCom

study o 332 pregnant women with IBD, outcomes were

similar in women with ulcerative colitis or Crohn disease

compared with unaected pregnant women (Bortoli, 2011).

Still, women with active disease during pregnancy have an

increased requency o preterm births (Kammerlander, 2017;

Shand, 2016). Importantly, perinatal mortality rates are not

appreciably increased.

Ulcerative Colitis and Pregnancy. In one review o 755 pregnancies, colitis that was quiescent at conception worsened

in approximately a third o pregnancies (Fonager, 1998). In

women with active disease at the time o conception, approximately 45 percent worsened, 25 percent remained unchanged,

and only 25 percent improved. Tese observations are similar

to those described in a review by Miller (1986) as well as in

later reports (de Lima-Karagiannis, 2016; Oron, 2012).

Osteoporosis is a signicant complication in up to a third

o aected women. Tus, vitamin D—800 IU daily—and

calcium—1200 mg daily—are given. Folic acid, 2 to 4 mg

orally daily, is recommended preconceptionally and during the

rst trimester or neural-tube deect prevention (Mahadevan,

2019). Tis high dose counteracts the antiolate actions o sul-

asalazine. Flares may be caused by psychogenic stress, and reassurance is important. Last, the venous thromboembolism risk

is doubled, but thromboprophylaxis is not routinely provided

(Hansen, 2017).

Management or colitis or the most part mirrors that

outside o pregnancy. reatment o active colitis and maintenance therapy incorporate drugs that deliver 5-aminosalicyclic acid (5-ASA), also known as mesalamine. Sulasalazine

(Azulfdine) is the prototype, and its 5-ASA moiety inhibits

prostaglandin synthase in colonic mucosa. Others include

olsalazine (Dipentum), balsalazide (Colazal), and delayedrelease 5-ASA derivatives (Apriso, Asacol, Pentasa, Lialda).

Glucocorticoids are benecial and are given orally, parenterally, or by enema or moderate or severe disease that does not

respond to 5-ASA. Corticosteroids provide a high remission

rate or active disease, but they are not given or maintenance

therapy (Friedman, 2018). Recalcitrant disease is managed

with immunomodulating drugs, including azathioprine,

6-mercaptopurine, cyclosporine, or tacrolimus, which all appear

relatively sae in pregnancy (Briggs, 2017; Mozaari, 2015).

Importantly, methotrexate is teratogenic and contraindicated

in pregnancy (Chap. 8, p. 152).

In the past, biologics were reserved or recalcitrant, moderate to severe disease. Because o their considerable ecacy,

however, these medications are now requently given initially

or this severity o disease to prevent uture complications.

Tese agents are antibodies against tumor necrosis actor alpha

(NF-α). Tose recommended or IBD treatment are shown in

Table 57-7 (Mahadevan, 2019). Women who begin pregnancy

while taking biologics should continue these through pregnancy

until several weeks beore delivery to help avoid maternal inections rom immunosuppression. Tese agents are administered

TABLE 57-7. Biologics Used to Treat Inflammatory

Bowel Disease in Pregnancy

Drug (Brand Name) Recommendations

Adalimumab (Humira) Last dose 2–3 wks beore EDC

Certolizumab pegol

(Cimzia)

Continue throughout pregnancy

Inliximab (Remicade) Last dose 6–10 wks beore EDC

Natalizumab (Tysabri) Last dose 4–6 wks beore EDC

Ustekinumab (Stelara) Last dose 6–10 wks beore EDC

Vedolizumab (Entyvio) Last dose 6–10 wks beore EDC

EDC = estimated date o coninement.1022

Section 12

Medical and Surgical Complications

IV or subcutaneously. Several studies support their saety in

pregnancy, although there are concerns that their discontinuance may prompt a relapse (Chaparro, 2018; Friedman, 2018;

Luu, 2018). Another worry is that they may cause immunosuppression in the newborn, and early neonatal vaccination with

live-attenuated agents are delayed or at least 6 months (EsteveSolé, 2017; Julsgaard, 2016).

Colorectal endoscopy is perormed as indicated. Surgical

management is tailored to disease severity (Killeen, 2017).

During pregnancy, colectomy and ostomy creation or ulminant colitis may be needed as a liesaving measure, and it has

been described during each trimester. Dozois (2006) reviewed

42 such cases and ound that, in general, outcomes have been

good with partial or complete colectomy. Parenteral nutrition is

occasionally needed or women with prolonged exacerbations.

For women with an ileal pouch and an anal anastomosis,

requency o bowel movements, ecal incontinence, and pouchitis may temporarily worsen with pregnancy. Te last is an

inammatory condition o the ileoanal pouch probably due to

bacterial prolieration and stasis. Pouchitis usually responds to

ciprooxacin or metronidazole. In one rare case, adhesions to

the growing uterus led to ileal pouch peroration (Aouthmany,

2004).

In general, women with uncomplicated colitis can be delivered vaginally (Foulon, 2017). Tat said, the cesarean delivery

rate in these women is increased (Burke, 2017). It is controversial whether women who have had a prior proctocolectomy and

ileal pouch–anal anastomosis can be saely delivered vaginally.

Hahnloser (2004) reviewed delivery routes in women with 235

pregnancies beore and 232 pregnancies ater ileoanal pouch

surgery. Functional outcomes were similar, and it was concluded that cesarean delivery should be reserved or obstetrical

indications. o the contrary, ollowing their systematic review,

Foulon and coworkers (2017) recommended cesarean delivery

with the caveat that uncomplicated vaginal delivery was sae.

As discussed, quiescent ulcerative colitis likely has minimal adverse eects on pregnancy outcome. Modigliani (2000)

reviewed perinatal outcomes in 2398 pregnancies and reported

them to be not substantively dierent rom those in the general

obstetrical population. Specically, the incidences o spontaneous abortion, preterm delivery, and stillbirth were remarkably

low. Tese authors and others also describe a cesarean delivery

rate that was substantially higher than that or normal controls

(Burke, 2017; Mahadevan, 2015). Te previously described

ECCO-EpiCom study reported similar outcomes in 187

gravidas with ulcerative colitis compared with normal control

women (Bortoli, 2011).

Crohn Disease and Pregnancy. In general, Crohn disease

activity during pregnancy is related to its status around the

time o conception. In a cohort study o 279 pregnancies conceived by 186 women whose disease was inactive at conception, a ourth relapsed during pregnancy (Fonager, 1998). In

93 with active disease at conception, however, two thirds either

remained active or worsened. Other reviews describe similar

ndings (Miller, 1986; Oron, 2012).

Calcium, vitamin D, and olic acid supplementation mirror

that or ulcerative colitis. For maintenance during asymptomatic

periods, no regimen is universally eective. Sulasalazine is

eective or some, but the newer 5-ASA ormulations are better

tolerated. Glucocorticoids induce a 60- to 70-percent remission

rate (Friedman, 2018). Prednisone therapy may control moderate

to severe ares but is less eective or small-bowel involvement.

Immunomodulators such as azathioprine, 6-mercaptopurine,

cyclosporine, and tacrolimus are used or active disease and or

maintenance. Tese appear relatively sae during pregnancy

(Chaparro, 2018; Luu, 2018). As discussed in Chapter 8

(p. 152), methotrexate is contraindicated in pregnancy. As with

ulcerative colitis, treatment with NF-α inhibitors is oten

used initially or active Crohn disease and maintenance (see

able 57-7) (Friedman, 2018; Mahadevan, 2019).

Endoscopy or conservative surgery is indicated or complications (Killeen, 2017). Patients with small-bowel involvement

are more likely to require surgery or complications that include

stulas, strictures, obstruction, abscesses, and intractable disease. In an earlier study, an abdominal surgical procedure was

required during 5 percent o pregnancies (Woolson, 1990).

Parenteral nutrition has been used successully during severe

recurrences. Tose with an ileal loop colostomy may have signicant problems. Unless there is a perianal stula or active

perianal disease, women with Crohn disease usually can

undergo vaginal delivery without complications (Foulon, 2017;

Mahadevan, 2019).

As discussed, Crohn disease compared with ulcerative colitis is associated with higher adverse pregnancy outcome rates.

Outcomes are probably related to disease activities. In a casecontrol Danish study, Norgård (2007) reported a twoold risk

o preterm births. Dominitz (2002) reported a two- to three-

old increased risk or preterm delivery, low birthweight, etalgrowth restriction, and cesarean delivery in 149 women with

Crohn disease. Recall, however, that the ECCO-EpiCom study

ound pregnancy outcomes to be similar to those in unaected

women.

■ Ostomy and Pregnancy

A colostomy or an ileostomy can be problematic during pregnancy because o its location (Hux, 2010). In a report o 82

pregnancies in 66 women with an ostomy, stomal dysunction

was common, but it responded to conservative management in

most cases (Gopal, 1985). Surgical intervention was necessary,

however, in three o six women who developed bowel obstruction and in another our with ileostomy prolapse—almost 10

percent overall. In this older study, only a third o 82 women

underwent cesarean delivery, but akahashi (2007) described

six o seven cesarean deliveries in women with Crohn disease

and a stoma. Although adhesions usually are involved with an

obstructed ileostomy, the enlarging uterus may act to cause

obstruction (Porter, 2014). Last, Farouk and coworkers (2000)

reported that pregnancy did not worsen long-term ostomy

unction.

■ Intestinal Obstruction

Te incidence o bowel obstruction is not increased during

pregnancy, although it generally is more dicult to diagnose.

Meyerson (1995) reported a 20-year incidence o 1 case inGastrointestinal Disorders 1023

CHAPTER 57

17,000 deliveries at two Detroit hospitals. O acute abdomen

cases in pregnancy, adhesive disease leading to small-bowel

obstruction was second only to appendicitis—15 versus 30

percent, respectively (Unal, 2011). Approximately hal o cases

are due to adhesions rom previous pelvic surgery that includes

cesarean delivery (Andol, 2010; Lyell, 2011). Another 25 percent o bowel obstruction is caused by volvulus, which may

involve sigmoid colon, cecum, or small bowel. Tese have been

reported in late pregnancy or early puerperium (Al Maksoud,

2015; Bade, 2014). Bokslag (2014) and Wax (2013) and their

colleagues described small-bowel obstruction in pregnancy ollowing the currently popular Roux-en-Y gastric bypass, which

is perormed or weight loss. Intussusception is occasionally

encountered (Bosman, 2014; Moliere, 2019). Bowel obstruction subsequent to colorectal surgery or cancer was increased

threeold in women who had open versus laparoscopic surgery

(Haggar, 2013). Last, Serra and coworkers (2014) described a

massive ventral hernia with intestinal obstruction.

Most cases o intestinal obstruction during pregnancy result

rom pressure o the growing uterus on intestinal adhesions.

Tis is more likely around midpregnancy when the uterus

becomes an abdominal organ; in the third trimester when the

etal head descends; or immediately postpartum when uterine

size acutely shrinks (Davis, 1983). Perdue (1992) reported

that 98 percent o aected pregnant women had either continuous or colicky abdominal pain, and 80 percent had nausea

and vomiting. Abdominal tenderness was ound in 70 percent,

and abnormal bowel sounds noted in only 55 percent. Plain

abdominal radiographs ollowing soluble contrast showed evidence o obstruction in 90 percent o aected women. Plain

radiographs, however, are less accurate or diagnosing smallbowel obstruction, and we and others have ound that C

and MR imaging can be diagnostic (Essile, 2007; Moliere,

2019). Colonoscopy can be both diagnostic and therapeutic or

colonic volvulus (Dray, 2012; Khan, 2012).

During pregnancy, mortality rates with obstruction can be

excessive because o dicult and thus delayed diagnosis, reluctance to operate during pregnancy, and the need or emergency

surgery (Firstenberg, 1998; Shui, 2011). In an older report o

66 pregnancies, Perdue and associates (1992) described 6-percent maternal and 26-percent etal mortality rates. wo o the

our women who died were in late pregnancy, and they had

bowel peroration rom sigmoid or cecal volvulus caused by

adhesions.

■ Colonic PseudoObstruction

Also known as Ogilvie syndrome, pseudo-obstruction is caused

by adynamic colonic ileus. It is characterized by massive

abdominal distention with cecal and right-hemicolonic dilation

(Fig. 57-3). Approximately 10 percent o all cases are associated with pregnancy, and its reported requency is 1 case in

1500 births (Reeves, 2015). Te syndrome usually develops

postpartum—90 percent ater cesarean delivery—but it has

been reported antepartum. In a review, peroration was common, especially i the cecal diameter exceeded 12 cm (Jayaram,

2017). More recently, treatment with an IV inusion o neostigmine, 2 mg, given during cardiac monitoring usually results

in prompt decompression (Song, 2018). In some cases, colonoscopic decompression is perormed, and in others, laparotomy

is needed or peroration (Rawlings, 2010).

■ Appendicitis

Te lietime incidence or appendicitis ranges rom 7 to 10 percent (Flum, 2015). Tus, evaluation or possible appendicitis is

relatively common during pregnancy. Teilen and colleagues

(2017) studied 171 such women during a 5-year period, but

only 14 women ultimately were ound to have pathologically

conrmed appendicitis. Ater clinical and imaging evaluation,

the requency o suspected appendicitis drops and that o con-

rmed appendicitis in more than 8 million women ranged

rom 1 case in 1000 to 5500 births (Abbasi, 2014; Hée, 1999;

Mazze, 1991).

It is repeatedly—and appropriately—emphasized that pregnancy makes the diagnosis o appendicitis more dicult. Nausea

A B

FIGURE 57-3 Ogilvie syndrome. Massive dilation o colon due to pseudo-obstruction in a woman ollowing cesarean delivery. A. Abdominal radiograph. B. Axial image rom computed tomography.1024

Section 12

Medical and Surgical Complications

and vomiting accompany normal pregnancy, but also, as the

uterus enlarges, the appendix commonly moves upward and outward rom the right lower quadrant (Baer, 1932; Erkek, 2015;

Pates, 2009). Another oten-stated reason or late diagnosis is

that some degree o leukocytosis accompanies normal pregnancy. Tat said, Teilen and coworkers (2017) observed that a

white cell count >18,000/μL made the diagnosis tenold more

likely. Neutrophilic shit is another (Gentles, 2020). Pregnant

women—especially in late gestation—requently do not have

clinical ndings “typical” or appendicitis. Tus, it commonly

is conused with cholecystitis, labor, pyelonephritis, renal colic,

placental abruption, or uterine leiomyoma degeneration.

Most reports indicate increasing morbidity and mortality

rates with advancing gestational age. And, as the appendix is

progressively deected upward by the growing uterus, omental

containment o inection becomes increasingly unlikely. It is

indisputable that appendiceal peroration is more common during later pregnancy (Abbasi, 2014). In the studies by Andersson

(2001) and Ueberrueck (2004), the incidence o peroration was

approximately 8, 12, and 20 percent in successive trimesters.

Diagnosis

Persistent abdominal pain and tenderness are the most reproducible ndings. Right lower quadrant pain is the most

requent, although pain migrates upward with appendiceal displacement (Mourad, 2000). For initial evaluation, sonographic

abdominal imaging is reasonable in suspected appendicitis,

even i to exclude an obstetrical cause o pain (Butala, 2010).

Tat said, graded compression sonography is dicult because o

cecal displacement and uterine imposition (Pedrosa, 2009).

Appendiceal computed tomography is more sensitive and accurate than sonography to conrm suspected appendicitis (Katz,

2012; Raman, 2008). Specic views can be designed to diminish etal radiation exposure (Chap. 49, p. 873).

When available, MR imaging is the preerred modality or

evaluation o suspected appendicitis in pregnancy (Fig. 57-4).

MR imaging has high diagnostic yield and accuracy, and it also

provides alternative diagnoses (Fonseca, 2014; Teilen, 2015).

One metaanalysis o 30 studies cited positive- and negativepredictive values o 96 and 99.5 percent, respectively, or MR

imaging (Duke, 2016). Others report similar ndings (Burke,

2015; Kave, 2019). However, Aguilera and colleagues (2018)

ound a sensitivity o only 18 percent in pregnant women.

Management

When appendicitis is suspected, most recommend prompt

surgical exploration. Although diagnostic errors may lead to

removal o a normal appendix, surgical evaluation is preerable

to postponed intervention and generalized peritonitis (Abbasi,

2014). In earlier reports, the diagnosis was veried in only 60

to 70 percent o pregnant women. As indicated above, however, with C and MR imaging, these gures have improved

(Duke, 2016; Teilen, 2015). Still and importantly, the accuracy o diagnosis is inversely proportional to gestational age.

Currently, laparoscopic resection is almost always used to treat

suspected appendicitis during the rst two trimesters. In a report

rom a Swedish database o nearly 2000 laparoscopic appendectomies, perinatal outcomes were similar to those o more than

1500 open laparotomies done beore 20 weeks’ gestation (Reedy,

1997). Conversely, in their review, Wilasrusmee and coworkers (2012) reported a higher rate o etal loss with laparoscopy.

Authors o three more recent systematic reviews indicate that

the level o evidence is not strong enough to demonstrate a pre-

erred approach to appendectomy (Frountzas, 2019; Lee, 2019b;

Walker, 2014). It has evolved that in many centers, laparoscopic

appendectomy is also perormed in most cases during the third

trimester (Donkervoort, 2011). Tis is encouraged by others,

including the Society o American Gastrointestinal and Endoscopic Surgeons (Pearl, 2017; Sekar, 2019; Soper, 2011).

Beore exploration, IV antimicrobial therapy is begun, usually with a second-generation cephalosporin or third- generation

penicillin. Unless there is gangrene, peroration, or a periappendiceal phlegmon, antimicrobial therapy can usually be discontinued ater surgery. Without generalized peritonitis, the

prognosis is excellent. Seldom is cesarean delivery indicated at

the time o 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 or pulmonary-permeability edema

caused by sepsis (Chap. 50, p. 883).

Antimicrobial versus Surgical Treatment

Because o European studies, some advocate that many cases

o appendicitis can be treated successully with IV antimicrobials alone (Flum, 2015; alan, 2019). In one study, 6 percent

o pregnant women with appendicitis were treated medically,

and these gravidas had “considerably” elevated risks or septic

shock, peritonitis, and VE compared with surgically managed

cases (Abbasi, 2014). In another study o 20 women, ailure

rate was 25 percent (Joo, 2017). At this time, we discourage

this practice until appropriate studies have been done with

pregnant women. Certainly, i elected, such treatment should

exclude women with obstructive appendicitis, and the threshold to convert to surgical treatment must be low.

FIGURE 57-4 Magnetic resonance T2 lair image o acute appendicitis in a midtrimester pregnancy. The bright signal is inlammation and the block dot is a ecalith that can be seen in the

midappendix (arrow). The etal trunk (T) and leg (L) and amnionic

luid (A) are seen within the gravid uterus superior to the appendix.

(Reproduced with permission by Dr. Christina Herrera.)Gastrointestinal Disorders 1025

CHAPTER 57

Pregnancy Outcomes

Appendicitis increases the likelihood o preterm labor, especially

i peritonitis has developed. Spontaneous labor ater 23 weeks

ensues with greater requency ollowing surgery or appendicitis

compared with surgery or other indications (Ibiebele, 2019;

Won, 2017). In one study, the etal loss rate was 22 percent

i surgery was perormed ater 23 weeks’ gestation. Tree large

population-based studies attest to the adverse outcomes rom

appendicitis in pregnancy. From the Caliornia State Inpatient

Database, the etal loss rate was 20 percent (Won, 2017). A

nationwide study rom aiwan ound that risks or low birthweight and preterm delivery rose 1.5- to 2-old when outcomes

in 908 women with acute appendicitis were compared with

those o controls (Wei, 2012). Last, an Australian populationbased study reported an almost twoold increased incidence o

preterm birth ollowing appendectomy (Ibiebele, 2019).

Nhận xét