Cancer‐related bone pain has overlapping but distinct features of both inflammatory and neuropathic pain. The most important changes are in bone homeostasis. These changes correspond with events in the peripheral and central nervous system.

In healthy bone osteoclasts and osteoblasts are highly regulated to maintain balanced reabsorption and formation of bone respectively (Kane and Bennett [114]). In the presence of bone metastases this relationship is disrupted leading to increased osteoclast activity and bone destruction.

Cancer cells also stimulate local inflammatory mediators, creating a highly acidic environment. This sensitizes the peripheral nerve endings within the bone marrow and bone matrix (Mantyh [136]). Combined with the destruction of nerve endings through cancer invasion, the resulting pain is a mixture of ongoing inflammatory and neuropathic processes, leading to central sensitization in the spinal cord (Mantyh [136]).

For patients, cancer bone pain is constant, with high sensitivity for movement. Bone pain remains one of the most difficult to control, as metastases are often not limited to one site. This can be extremely debilitating in patients who may already have limited life expectancy.

Management of bone pain includes a thorough assessment to diagnose this as the cause of the pain.

Once diagnosed, the treatment of bone pain may include the following:

These include oncological treatment of the primary tumour, analgesia, surgery or interventional radiology procedures to relieve obstructed ducts, vessels or organs. After careful assessment of the position of the tumour to assess suitability, a coeliac plexus block may be considered.

These include oncological treatment of the primary tumour, analgesia, surgery or interventional radiology procedures to relieve obstructed ducts, vessels or organs or interventional analgesia procedures (sacral nerve blocks, saddle blocks, epidural or intrathecal analgesia).

Treatment options for thoracic pain caused by tumour include:

Chemotherapy‐induced peripheral neuropathy (CIPN) can be argued to be the most common and debilitating symptom following cancer treatment (Majithia et al. [132]). It is becoming a major issue in cancer survivorship as chemotherapy agents are increasingly being used as first‐line treatment (Majithia et al. [132]).

The exact incidence of CIPN is difficult to determine due to the variety of cancer treatments being used and under‐reporting from patients. Under‐reporting is often due to the fear of having treatment doses reduced or stopped in consequence. It is most commonly associated with platinum‐ and taxane‐based treatments (Brewer et al. [21], Kuroi and Shimozuma [119]). Hershman et al. ([96]) estimated the incidence of CIPN in patients receiving multiple agent treatment at 38% and Brown et al. ([26]) estimated its prevalence at 30%.

Ventzel et al. ([226]) found that out of 174 patients 63.6% reported CIPN 1 year after completion of treatment. Majithia et al. ([132]) found that patients were reporting symptoms lasting years after completion of treatment. In patients who report symptoms lasting longer than 6 months the condition becomes virtually irreversible. It is estimated that around 60% of patients fall into this group (Beijers et al. [11]).

The exact pathophysiology of CIPN is complex and not fully understood as it is highly dependent on the chemotherapy agent being administered (Brown et al. [26]).

Different theories have been suggested as to the cause of CIPN. Causes include: changes to the structure of mitochondria in cells (Flatters and Bennett [75]); alteration in pain mediators in peripheries and the central nervous system (Cavaletti et al. [33]); and abnormal transmission of pain impulses via A delta, A beta and C fibres in vincristine, paclitaxel and oxaliplatin treatment (Xiao and Bennett [237]). The alteration in pain mediators can also include a reduction in nerve growth factor that results in nerve damage (Cavaletti et al. [33]).

The side‐effect profiles of chemotherapy agents are well known and documented. However their neurotoxic effects can vary depending on the individual and this can make predicting CIPN challenging (Tzatha and DeAngelis [221]). There are associated risk factors and other co‐morbidities that can predispose the nervous system to injury. These include (Tzatha and DeAngelis [221]):

The initial presenting symptoms for CIPN normally include abnormal and/or loss of sensation, which usually starts in fingertips and toes and can spread to upper and lower extremities depending on severity (Tofthagen et al. [213]). Brown et al. ([26]) and Kuroi and Shimozuma ([119]) reported that the most common presenting symptoms included:

CIPN can have a negative impact on the patient's quality of life with many reporting difficulty with or inability to perform daily tasks such as buttoning clothes, holding objects, opening jars/bottles, loss of balance and pain on standing/walking/climbing stairs (Beijers et al. [11], Driessen et al. [57]).

A 2014 study (Beijers et al. [11]) surveyed 43 patients, of whom 48% reported a direct decrease in quality of life indicators as a result of CIPN symptoms. It also found that CIPN had a profound impact on emotional well‐being and patients became more dependent on others to assist with daily tasks.

Despite the wide use of treatments that cause CIPN and the severity of the side‐effects there is no clinical agreement on how best to assess severity and monitor changes in symptoms (Cavaletti et al. [33]). Tofthagen et al. ([213]) suggest that simple direct questioning of the patient at every visit (asking if they have any new altered sensation, i.e. numbness, pins and needles, etc.) would be the simplest way of identifying patients with CIPN. However, patients are often reluctant to report symptoms of CIPN for fear of having their treatment stopped or simply not wanting to disturb healthcare staff (Tofthagen [212]). As CIPN is not always painful, patients may not report this when asked about their pain, and because it falls out of the normal pain characteristics the patient may not make the association between CIPN and pain (Tofthagen et al. [213]).

Ellen et al. ([63]) surveyed 408 oncology nurses regarding their knowledge and assessment of patients with CIPN. They found that 86% were collecting data on patient‐reported sensory symptoms but only 41% were performing physical examination and the use of assessment tools was infrequent.

A wide variety of assessment tools can be used to aid CIPN diagnosis. However these rely heavily on subjective questions (Brown et al. [26]). The tools most commonly used are the World Health Organization (WHO) CIPN grading scale, the Eastern Cooperative Oncology Group (ECOG) neuropathy scale and the National Cancer Institute Common Toxicity Criteria (NCI‐CTC) neuropathy score (Cavaletti et al. [34]).

Given the subjective nature of the symptoms, the most accurate assessment tool is one that relies on the patient's report of their symptoms (Postma et al. [176]). The European Organisation for Research and Treatment of Cancer (EORTC) performed literature reviews and a survey of healthcare professionals on CIPN issues that led to the development of a 20‐item questionnaire to identify symptoms of CIPN. Called the EORTC CIPN20 (Postma et al. [176]), it has been shown to be a valid and accurate tool to score the severity of symptoms and impact on the patient's quality of life. The authors of this study went on to develop the Rasch‐built overall disability scale (R‐ODS) based on the limitations from CIPN20. They recommend the use of this scale in future research to ascertain validity (Binda et al. [15]).