Chapter 26: Acute oncology
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Bowel obstruction (malignant)
Definition
It is important to differentiate between constipation and malignant bowel obstruction (MBO). Constipation is the irregular and infrequent or difficult evacuation of the bowels and can be associated with obstruction or diverticulitis and also hypercalcaemia or metastatic spinal cord compression (MSCC) (London Cancer Alliance [151]). A generic definition of both benign and malignant bowel obstruction is any mechanical or functional obstruction of the intestine that prevents physiological transit and digestion (Tuca et al. [288]). The diagnostic criteria of MBO are: (i) clinical evidence of bowel obstruction, (ii) obstruction distal to the Treitz ligament, (iii) the presence of primary intra‐abdominal or extra‐abdominal cancer with peritoneal involvement, and (iv) the absence of reasonable possibilities for a cure (Anthony et al. [6]).
Anatomy and physiology
Abdominal tumour growth may cause MBO by extrinsic intestinal compression, endoluminal obstruction, intramural infiltration or extensive mesenteric infiltration (Ripamonti et al. [250]). Intraluminal tumours may occlude the bowel lumen or provoke intussusception. Intramural infiltration through the mucosa may obstruct the lumen or impair peristaltic movements. Mesenteric and omental tumour involvement may angulate the bowel and provoke extramural bowel occlusion. Infiltration of the enteric or coeliac plexus may cause severe impairment in peristalsis and consequent obstruction due to dysmotility.
Fluid retention and intestinal gases proximal to the occlusive level produce a marked increase in endoluminal intestinal pressure. This abdominal distension favours the release of 5‐HT3 by the intestinal enterochromaffin cells which, in turn, activates the enteric interneuronal system through its different mediators (substance P, nitric oxide, acetylcholine, somatostatin and vasoactive intestinal peptide). This stimulates the secretomotor neurones that are especially mediated by vasoactive intestinal peptide, which leads to splanchnic vasodilatation and hypersecretion of the cells of the intestinal crypts. The consequences of these phenomena are the appearance of intense intestinal oedema, an increase in the secretions retained, and endoluminal pressure, all of which are mechanisms that perpetuate the physiopathological process of MBO.
Related theory
MBO may appear at any time during the evolution of the patient's cancer but is more frequent in cases of advanced cancer (Ferguson et al. [77], Tuca et al. [288]). MBO is estimated to occur in 2% of all patients with advanced malignancy but has a greater frequency in colorectal (10–28.4%) and ovarian (5.5–42%) malignancies (Tuca et al. [288]). Obstruction may originate in the small (61%) or large bowel (33%) or in both simultaneously (20%) (Ripamonti et al. [250]). Obstruction may be complete or partial and may appear as a sub‐occlusive crisis or may involve one or multiple intestinal levels. Factors that may favour the appearance of MBO but are not directly dependent on abdominal tumour growth include paraneoplastic neuropathies, chronic constipation, intestinal dysfunction induced by opioids, inflammatory bowel disease, renal insufficiency, dehydration, mesenteric thrombosis, surgical adhesions, and radiogenic fibrosis (Ripamonti et al. [251]). In advanced and inoperable patients, multiple occlusive levels are presented in 80% of cases and peritoneal carcinomatosis is previously diagnosed in more than 65% of cases (Tuca et al. [288]). The prognosis of advanced oncological patients from the diagnosis of inoperable MBO is estimated at an average of 4 weeks (Tuca et al. [288]).
Diagnosis
MBO can present subacutely with the presence of colic pain, abdominal distension, nausea and vomiting which spontaneously cease (sub‐occlusive crisis) (Tuca et al. [288]). The prevalence of symptoms in consolidated MBO is: nausea 100%, vomiting 87–100%, colic pain 72–80%, pain due to distension 56–90%, and the absence of stools or emission of gases in the previous 72 hours (85–93%) (Ripamonti et al. [251]). In upper MBO, the nausea is intense and presents early; vomiting is frequent, has an aqueous, mucous or biliary appearance and has little odour. Vomiting in lower obstruction usually occurs later, is dark, and has a strong odour (Tuca et al. [288]). Bacterial liquefaction of the retained intestinal content in the zone proximal to the obstruction confers the characteristic appearance and smell of faecaloid vomit (Ripamonti et al. [250]).
Patients with partial obstruction may present with liquid stools due to bacterial liquefaction of the digestive content and intestinal hypersecretion. The colic pain is due to giant peristaltic waves and spasms in the bowel with increased endoluminal pressure and no possibility of effective transit. Intestinal distension and tumoural infiltration of the abdominal structures are responsible for the continuous pain.
Assessment
The nurse can start the assessment of the patient suspected of MBO by undertaking a focused history, asking questions such as:
- What is their current cancer treatment?
- When did bowels last move (what consistency/colour/smell/amount)?
- What is their normal bowel habit; medication history and any laxatives, change of medication, oral intake, nausea or vomiting (faecal smelling), abdominal swelling, discomfort or pain (Ferguson et al. [77])?
- What the stool consistency was like prior to the loose stool (many patients will present with liquid or loose stools, before presuming diarrhoea, always ask as this could be overflow, but a stool sample should always be sent for MC&S (Tradounsky [286])?
The patient should be cannulated and blood samples taken (FBC, U&Es, LFTs, calcium, magnesium, CRP); the results can be helpful in the evaluation of hydration or presentation with a metabolic disturbance (Tradounsky [286]). SACT should be stopped until clinical review and the diagnosis is confirmed as this may exacerbate symptoms and underlying pathophysiology (Ferguson et al. [77]).
The healthcare professional should undertake an abdominal assessment. If MBO is present, inspection of the abdomen will often show abdominal distension, but other important signs such as previous abdominal incisions and abdominal wall hernias must be noted for accurate diagnostic synthesis. Abdominal palpation may identify a specific tumour mass, or indeed a ‘woody’ abdomen secondary to diffuse malignant infiltration. Percussion of the abdomen is useful to differentiate the tympanic note of intestinal obstruction from the dull percussion note in cases where malignant ascites predominates as the cause of abdominal distension. In cases of true intestinal obstruction, hyperactive bowel sounds may be present, as may borborygmi. However, if a paralytic picture predominates, bowel sounds may be absent. This clinical sign is a useful discriminating factor when cross‐sectional imaging is unavailable.
A digital rectal examination is essential as severe constipation can mimic, worsen or co‐exist with symptoms of intestinal obstruction. A full rectum should be emptied by the use of local suppository or enema preparations before presuming a diagnosis of bowel obstruction. Stercoral perforation can and does occur in terminal disease, often due to the combination of long‐term opiate medication and immobility, so obstructive symptoms, especially pain, should be treated seriously even when constipation is suspected (Ripamonti et al. [250], [251], Tuca et al. [288]). In patients with advanced cancer, MBO is also associated with anaemia (70%), hypoalbuminaemia (68%), alterations in hepatic enzymes (62%), dehydration and pre‐renal renal dysfunction (44%), cachexia (22%), ascites (41%), palpable abdominal tumour masses (21%) and marked cognitive deterioration (23%) (Ferguson et al. [77]).
An abdominal X‐ray is usually the initial radiological test requested; signs of MBO are distension of the intestinal loops, fluid retention and gases, with the presence of air–fluid levels in the zone proximal to the occlusion as well as a reduction in gas and stools in the segments distal to the obstruction. The presence of gas in the large bowel is usually a sign of subacute obstruction (Ferguson et al. [77], Tuca et al. [288]).
Management
Management of MBO depends on the obstruction. A collaborative approach by surgeons and the oncologist and/or palliative care physician as well as an honest discourse between physicians and patients can offer an individualized and appropriate symptom management plan (Ferguson et al. [77], Ripamonti et al. [251]).
The cancer nurse's role is to work with the patient to ensure advice and support is given regarding the symptoms and management of MBO. Additional support may be necessary for patients who are aware of the symptoms of MBO in the context of their disease (Tradounsky [286]). For patients who have not had a bowel movement for the last 48 hours (constipation), advice regarding diet and fluid intake along with a review of medication (stopping or changing constipating medication) and possible change of laxatives to include a softener and stimulant is appropriate. The patient must feel listened to and encouraged to report if symptoms worsen. For patients who have not had a bowel motion in the last 72 hours admission may be required to manage associated symptoms such as pain and nausea and vomiting. Reviewing medication, including laxatives, and dietary advice remains the same.
If the patient is considered to be in bowel obstruction (paralytic ileus) then admission is essential. Initially, efforts should be made to correct any biochemical imbalance that may be contributing to intestinal dysmotility, most commonly hypercalcaemia or hypokalaemia (Ferguson et al. [77]). Intravenous fluids, emesis control and pain management are essential, along with recognizing when surgical management may be an option and therefore keeping the patient nil by mouth until a decision has been made. Total parenteral nutrition (TPN) is often discussed in the context of managing MBO, however it is only recommended in MBO for those patients who are undergoing surgery to enable subsequent chemotherapy and have a post‐operative survival likely to be more than 3 months (Shariat‐Madar et al. [269]). Surgery is recommended as the primary treatment for selected patients with MBO, however patients known to have poor prognostic criteria for surgical intervention such as intra‐abdominal carcinomatosis, poor performance status and massive ascites should be managed conservatively (Ripamonti et al. [251]). A number of treatment options are now available for patients unfit for surgery.
Conservative management consists of two mechanisms: obviating any precipitating factors, and decreasing the intraluminal pressure associated with MBO (Ferguson et al. [77]). Certain medications commonly used in advanced malignancy can worsen the obstructive picture, notably opioids and antispasmodic medications. A careful symptom exploration should be performed to ascertain if it is possible to stop or reduce these medications without precipitating symptomatic crises. Opioids can rarely be omitted, as acute pain also needs to be addressed, and have originally been commenced for ongoing significant pain. Conversion of background opioids to fentanyl can markedly reduce gastrointestinal dysmotility in appropriate cases (Ferguson et al. [77]). Active medical palliation in MBO focuses around the use of corticosteroids, antisecretory medications and antiemetics, with sufficient analgesia. Bowel rest is an aspect of medical management (Tuca et al. [288]). If the patient has nausea and vomiting, antisecretory drugs or/and antiemetics may be used. The insertion of a nasogastric Ryles tube may be necessary to aid stomach decompression and aid symptom control in severe nausea and vomiting but is only a temporary measure (Ripamonti et al. [251]). Somatostatin analogues (e.g. octreotide, from 300 to 600 µg per day) have been recommended, with good symptomatic outcomes reported; they reduce gastrointestinal secretions very rapidly and have a particularly important role in patients with high obstruction if hyoscine butylbromide fails (Ferguson et al. [77]).
The medical management of MBO will often take several days before there is a significant resolution of symptoms. Spontaneous resolution of MBO occurs in 36% (31–42%) of patients with inoperable MBO: 92% of those who settled spontaneously had done so by day 7, however 72% of those who settled spontaneously subsequently developed another episode of obstruction (Tuca et al. [288]).
Ongoing care
MBO is a frequent complication in advanced cancer patients, especially in those with abdominal tumours. Clinical management of MBO requires a specific and individualized approach that is based on disease prognosis and the objectives of care. Surgery should always be considered for patients in the initial stages of the disease with a preserved general status and a single level of occlusion. The priority of care for inoperable and consolidated MBO is to control symptoms and promote the maximum level of comfort possible. The spontaneous resolution of an inoperable obstructive process is observed in more than one‐third of patients. Patients with consolidated MBO have a mean survival of no longer than 4–5 weeks.