Guidance on bowel management in patients with metastatic spinal cord compression
Executive Summary
Autonomic dysfunction is a critical late-stage manifestation of Metastatic Spinal Cord Compression (MSCC), leading to significant disturbances in bowel habits, including constipation, incontinence, and loss of rectal sensation. This document synthesizes clinical guidance from The Christie, Greater Manchester & Cheshire, regarding the management of bowel dysfunction in MSCC patients. The primary objective of clinical intervention is to achieve controlled continence, characterized by the regular evacuation of formed faeces every one to three days. Effective management is contingent upon accurate assessment of the vertebral lesion level, which determines whether the patient presents with a spastic (reflex) or flaccid bowel, and the implementation of a structured escalation protocol for faecal loading and maintenance.
Clinical Background and Classification
Bowel dysfunction in MSCC is categorized based on the anatomical level of the vertebral lesion. This distinction is vital for determining the appropriate manual or pharmacological intervention.
Spastic (Reflex) Bowel
Anatomical Level: Above T12–L1.
Characteristics: The cauda equina remains intact, and reflex arcs are preserved. The sacral reflex is generally maintained.
Management Note: Digital manual stimulation may be particularly useful in these cases.
Flaccid Bowel
Anatomical Level: Below T12–L1.
Characteristics: Reflex arcs are damaged due to involvement of the cauda equina.
Management Note: This presentation generally requires gentle digital manual evacuation of the rectum.
ABC Guidelines for Clinical Assessment
A thorough baseline assessment must be conducted for all clinicians managing MSCC patients to determine the severity of dysfunction and the risk of complications.
Level of Compression: Identify the specific vertebral level of the lesion.
Bowel Habit Documentation: Record the patient's current frequency and consistency of bowel movements.
Medication Review:
Identify current laxative or suppository use.
Identify constipating medications, particularly opiates.
Physical Examination: Conduct a per rectum (PR) exam to assess anal tone and identify faecal loading.
Bladder Function Assessment: Constipation may exacerbate bladder symptoms; therefore, urinary function must be monitored.
Diagnostic Imaging: Utilize a baseline abdominal X-ray if there is suspicion of obstruction or to confirm the extent of faecal loading.
Management and Control Protocols
The ultimate goal of treatment is regular evacuation every 1–3 days. Clinicians are advised that achieving controlled continence may take several weeks.
Protocol for Faecal Loading (Escalation Steps)
First Line: Insert two glycerine suppositories or a micro-enema deep into the rectum. Digital manual stimulation is recommended for spastic bowel (lesions above T12-L1).
Second Line: Arachis oil enema administered overnight.
Third Line: Phosphate enema administered the following morning.
Fourth Line: Gentle digital manual evacuation (specifically for flaccid bowel/lesions below T12-L1).
Establishing a Maintenance Routine
Dietary Adjustments: Review and implement a high-fibre diet and high fluid intake.
Pharmacological Support: Regular oral laxatives combined with PR interventions every 1–3 days.
Persistent Leakage: If faecal leakage continues, consider anti-diarrhoeal preparations such as loperamide or codeine as part of the control regime.
Recommended Pharmacological Regimes
Note: If these regimes fail, regular gentle manual evacuation may be required, following RCN clinical nursing guidelines.
Critical Complication: Autonomic Dysreflexia
Autonomic dysreflexia is a medical emergency that can occur if the spinal lesion is located above T7. It is triggered by a stimulus below the level of the lesion (such as a full bladder or faecal impaction) causing sympathetic autonomic overactivity.
Clinical Presentation
Pounding headache.
Profuse sweating and facial flushing.
Nasal stuffiness.
Hypertension and bradycardia.
Pathophysiology and Action
The stimulus causes vasoconstriction and hypertension below the lesion. This triggers a parasympathetic response above the lesion via carotid and aortic baroreceptors.
Required Action: Immediately identify and treat the cause. Check the urinary catheter and perform a PR assessment to resolve the underlying stimulus.