Luis D. Pacheco, MD

INTRODUCTION

INITIAL EVALUATION

COMMON ETIOLOGIES OF LOWER GASTROINTESTINAL BLEEDING

   • Ulcerative Colitis

   • Crohn Disease

PREGNANCY CONSIDERATIONS

UPPER GASTROINTESTINAL BLEEDING

INTRODUCTION

The American College of Gastroenterology defines acute lower gastrointestinal bleeding (LGIB) as a bleeding episode from the gastrointestinal tract originating distal to the ligament of Treitz that may lead to unstable vital signs, anemia, or requirement of a blood transfusion.¹ Acute LGIB most commonly presents as hematochezia and often necessitates hospital admission, immediate workup, and treatment. In this section, we will be focusing on the initial evaluation of acute hematochezia associated with inflammatory bowel disease (IBD), the major etiology of LGIB in the young adult population.

INITIAL EVALUATION

It is essential to obtain a thorough history and physical examination in patients presenting with acute LGIB. Clinicians should inquire about the duration and nature of bleeding, stool color, and frequency. Patients may present with symptoms of fever, shortness of breath, dyspnea, palpitations, orthostatic symptoms, abdominal pain, weight loss, urgency/tenesmus, or change in bowel habits. One should also note any past history of abdominal surgeries, prior bleeding episodes, radiation exposure, inflammatory bowel disorders, previous peptic ulcer disease, recent trauma, or liver disease. Exposure of medications (NSAIDS, Aspirin, or anticoagulants) that may cause or exacerbate LGIB should be enquired. Initial patient monitoring with basic vital signs assessment, and fetal monitoring should be ensured if indicated. Large bore intravenous access and initial laboratory workup should be obtained. Laboratory workup should include a complete blood count, coagulation panel, type and screen, electrocardiogram, and basic metabolic panel. Resuscitative measures such as fluid resuscitation with crystalloids or blood transfusion (hemoglobin <7 g/dL) should be initiated. If the patient does not respond to initial interventions, admission to an intensive care unit should be considered. After initial evaluation and resuscitative maneuvers, determining the source of bleeding becomes imperative. Diagnosis and management of this clinical scenario should involve a multidisciplinary team consisting of the obstetrician (usually the primary care physician), maternal fetal medicine specialist, surgeon, and gastroenterologist. The first step in working up the source of LGIB is to rule out an upper gastrointestinal source as up to 11% of patients with hematochezia have a proximal source of bleeding.² The latter may require placement of a nasogastric tube and if its aspirate is negative for blood, the patient should undergo a colonoscopy. If the latter is negative, small bowel studies (enteroscopy, capsule video assisted endoscopy, small bowel radiography) may be required. If the source is not identified by conventional studies, an arteriography (+/−nuclear scan) with potential surgical consultation may be indicated. The overall yield to identify correctly the source of bleeding of a colonoscopy is 69% to 80%,³ and of arteriography is 40% to 78%.^4,5 Arteriography is a useful tool to localize the site of bleeding presuming that the minimum rate of bleeding of 1 to 1.5 mL/min is met. The rate of bleeding for optimal results using a nuclear scan is 0.1 to 0.4 mL/min. The detection yield for the latter is 26% to 72%.⁶ If surgical intervention is required for saving life, it should be pursued irrespective of the gestational age. Continuous fetal monitoring during any procedure should be performed if pregnancy is viable.

COMMON ETIOLOGIES OF LOWER GASTROINTESTINAL BLEEDING

In the general population, the three most common pathologies responsible for LGIB encompass diverticular disease, colonic vascular ectasia, and inflammatory bowel disease. IBD affects a large number of women during childbearing age. Consequently, it is the most common cause of LGIB during pregnancy (together with hemorrhoids). The exact incidence of IBD during pregnancy remains unknown. IBD is an illness of the modern society. It has been linked to westernized lifestyle, high-fat/sugar diets, stress, medication usage, and high socioeconomic status.⁷ In this chapter, we will be emphasizing on diagnosis and management of ulcerative Colitis (UC) and Crohn disease (CD) during pregnancy.

Ulcerative Colitis

UC affects 500,000 Americans yearly and its frequency has been stable over the past 50 years.^8,9 UC affects exclusively the colon, and is characterized by symmetrical continuous mucosal inflammation of the large intestine. The rectum is involved in 95% of cases. Tenesmus, rectal urgency, and bloody diarrhea are characteristics of the disease. When a patient presents with these symptoms, stool testing, sigmoidoscopy, or colonoscopy with biopsy should be performed for diagnosis. Endoscopic findings and histologic characteristic of the disease, in the absence of an infectious etiology, confirms the diagnosis of UC. Endoscopic findings typical of UC consist of absence of mucosal vascularity, granularity, and mucosal denudation.¹⁰ UC classically involves the rectum and extends proximally in a symmetric, circumferentially, and uninterrupted pattern. Biopsy reveals typical mucosal separation, crypt’s atrophy, inflammatory cells invading the lamina propria, and basal lymphoid aggregates.¹¹ Infectious diseases that mimic UC include bacterial (Escherichia coli 0157:H7 and Shigella) and parasitic infections (ameba). All new patients need to be tested for these microbes and stools examined for Clostridium difficile by PCR.¹² Management of UC patients should be directed toward inducing and maintaining remission of the disease in order to improve quality of life, decrease chronic corticosteroid usage, and decrease cancer risk. Therapy is guided according to severity. Mild disease is characterized by less than four bowel movements a day with a normal erythrocyte sedimentation rate (ESR). Bleeding may be present. Moderate disease presents with more than four bowel movements per day.

Mild and moderate distal colitis is commonly treated with 5-aminosalicylic acid derivatives, such as sulfasalazine 4 to 6 g/day, balsalazide 2.25 g tid, or mesalamine 2 to 4 g/day. Proctitis may also be managed with topical mesalamine (500 mg bid or 1 g/day). Actually, topical 5-aminosalicylic acid derivatives are first line therapy in mild to moderate disease and many patients will be adequately managed with the sole use of these agents.¹³ Combination of topical and oral mesalamine could be more efficient than each agent alone.¹⁴ Steroids (either systemic or topical) may be required to induce remission if no response to the latter agents is achieved. Oral prednisone (20-60 mg/day) should be initiated. After adequate response is achieved, steroid taper should be initiated by decreasing the dose by 5 to 10 mg/week until a dose of 20 mg/day is achieved. The latter is followed by 2.5-mg weekly decrements until the steroid is discontinued. If corticosteroids fail to treat moderate disease or tapering is not tolerated, 6-mercaptopurine or azathioprine (1.5-2.5 mg/kg) treatment may be considered. Both agents are safe during pregnancy and should be used if clearly indicated. If the patient is unable to tolerate the latter therapy or no response is achieved, infliximab induction should be considered. Contraindications to infliximab therapy include demyelinating disorders, untreated latent or active tuberculosis, optic neuritis, malignancies, or congestive heart failure.

Most patients will achieve remission 4 weeks after therapy initiation.¹⁵ After induction of remission or improvement/resolution of the flare, maintenance doses of rectal or oral 5-aminosalicylic acid derivatives are usually initiated. Steroids (rectal or oral) should not be used to maintain remission of UC. Azathioprine is an option in patients with history of sulfasalazine/mesalamine intolerance or in patients requiring multiple courses of steroids due to recurrent exacerbations.

Severe colitis is defined as more than six bloody stools per day with symptoms of fever, tachycardia, anemia, and increased ESR.¹⁶

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