Pharmacologic Management of Malignant Bowel Obstruction: When Surgery Is Not an Option
Malignant bowel obstruction (MBO) complicates 3%-15% of cancers and often necessitates inpatient admission. Hospitalists are increasingly involved in treating patients with MBO and coordinating their care across multiple subspecialties. Direct resolution of the obstruction via surgical or interventional means is always preferable. When such options are not possible, pharmacological treatments are the mainstay of therapy. Medications such as somatostatin analogs, steroids, H2-blockers, and other modalities can be effective in palliation and possible resolution of obstruction. Awareness of these pharmacologic therapies can aid hospitalists in treating patients who are confronted with this devastating condition.
© 2019 Society of Hospital Medicine
Malignant bowel obstruction (MBO) is a catastrophic complication of cancer that often requires hospitalization and a multidisciplinary approach in its management. Hospitalists frequently collaborate with such specialties as Hematology/Oncology, Surgery, Palliative Medicine, and Interventional Radiology in arriving at a treatment plan.
Initial management is focused on hydration, bowel rest and decompression via nasogastric (NG) tube. Surgical resection or endoscopic stenting should be considered early.1 However, patients who present in the terminal stages may be poor candidates for these options due to diminished functional status, multiple areas of obstruction, complicated anatomy limiting intervention, or an associated large volume of ascites.
Presence of inoperable MBO portends a poor prognosis, often measured in weeks.2 Presentation often occurs in the context of a sentinel hospitalization, signifying a shift in disease course.3,4 It is essential for hospitalists to be familiar with noninvasive therapies for inoperable MBO given the increasing role of hospitalists in providing inpatient palliative care. Palliative pharmacologic management of MBO can reduce symptom burden during these terminal stages and will be the focus of this paper.
BACKGROUND AND PATHOPHYSIOLOGY
Malignant bowel obstruction occurs in about 3%-15% of patients with cancer.2 A consensus definition of MBO established the following specific criteria: (1) clinical evidence of bowel obstruction, (2) obstruction distal to the ligament of Treitz, and (3) the presence of primary intra-abdominal cancer with incurable disease or extra-abdominal cancer with peritoneal involvement.5 The most common malignancies are gastric, colorectal, and ovarian in origin.1,2 The most common extra-abdominal malignancies associated with MBO are breast, melanoma, and lung. MBO is most frequently diagnosed during the advanced stages of cancer.2 The obstruction can involve a partial or total blockage of the small or large intestine from either an intrinsic or extrinsic source. Peristalsis may also be impaired via direct tumor infiltration of the intestinal walls or within the enteric nervous system or celiac plexus. Other etiologies of MBO include peritoneal carcinomatosis and radiation-induced fibrosis.1,6 The obstruction can occur at a single level or involve multiple areas, which usually precludes surgical intervention.2
Symptoms of MBO can be insidious in onset and take several weeks to manifest. The most prevalent symptoms are nausea, vomiting, constipation, abdominal pain, and distension.2,6 The intermittent pattern of symptoms may evolve into continuous episodes with spontaneous remission in between. The etiology of symptoms can be attributed to distension proximal to the site of obstruction with concomitantly increased gastrointestinal and pancreaticobiliary secretions.
The distension creates a “hypertensive state” in the intestinal lumen causing enterochromaffin cells to release serotonin which activates the enteric nervous system and its effectors including substance P, nitric oxide, acetylcholine, somatostatin, and vasoactive intestinal peptide (VIP). These neurotransmitters stimulate the secretomotor actions that cause hypersecretion of mucus from cells of the intestinal crypts. Additional water and sodium secretions accumulate due to the expanded surface area of the bowel.1,2 Overloaded with luminal contents, the bowel attempts to overcome the obstruction by contracting, which leads to colicky abdominal pain. Tumor burden can also damage the intestinal epithelium and cause continuous pain.
