This chapter explores recent insights from preclinical and clinical studies of cancer induced bone pain (CIBP). There are various neuropathic, nociceptive, and inflammatory pain mechanisms that contribute to CIBP. Neuropathic pain can be induced as tumor cell growth injures distal nerve fibers that innervate bone and pathological sprouting of both sensory and sympathetic nerve fibers. These changes in the peripheral sensory neurons result in the generation and maintenance of tumor induced pain. CIBP is usually described as dull in character, constant in presentation, and gradually increasing in intensity with time. A component of bone cancer pain appears to be neuropathic in origin as tumor cells induce injury or remodeling of the primary afferent nerve fibers that normally innervate the tumor bearing bone. The treatment of pain from bone metastases involves the use of multiple complementary approaches including radiotherapy, chemotherapy, surgery, bisphosphonates, and analgesics.
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Cancer can affect the autonomic nervous system in a variety of ways: direct tumor compression or infiltration, treatment effects (irradiation, chemotherapy), indirect effects (e.g., malabsorption, malnutrition, organ failure, and metabolic abnormalities), and paraneoplastic/autoimmune effects. This chapter focuses on a diagnostic approach and treatment of cancer patients with dysautonomia, with an emphasis on immune-mediated autonomic dysfunction, a rare but potentially highly treatable cause of dysautonomia. Autonomic dysfunction can be divided into nonneurogenic (medical) and neurogenic (primary or secondary) causes. Orthostatic hypotension is a cardinal symptom of dysautonomia. The autonomic testing battery includes sudomotor, vasomotor, and cardiovagal function testing and defines the severity and extent of dysautonomia. Conditions encountered in the cancer setting that are associated with autonomic dysfunction include Lambert-Eaton Myasthenic Syndrome, anti-Hu antibody syndrome, collapsin response-mediator protein 5, subacute autonomic neuropathy, neuromyotonia (Isaacs’ syndrome), and intestinal pseudo-obstruction. The chapter describes various pharmacologic and nonpharmacologic therapies for treatment of orthostatic hypotension.
Intracranial imaging is vital to the initial evaluation, staging and treatment planning, and posttreatment follow-up of brain tumor patients. The modalities used to evaluate the brain are CT and MRI. A familiarity with basic radiologic concepts can enable a provider to better translate the intracranial process to clinical care. This chapter is intended to give the clinician a baseline for interpreting images independently in either the acute or chronic setting. Imaging of the brain using CT and MRI techniques is essential to the evaluation of patients with intracranial malignancy, both in the acute and chronic setting. Knowledge of basic imaging principles related to the presence of an intracranial mass and familiarity with findings unique to certain malignancies are useful tools for the clinician. These skills can be built over time by reviewing patient images independently, utilizing the kinds of fundamentals discussed in this chapter.
Interventional pain procedures are an adjunct to pharmacologic therapy for cancer pain. While pain at the location of the tumor might be the primary cause of pain, cancer patients may also have non-cancer related pain as a result of altered anatomy or biomechanics, for example, myofascial pain. Myofascial pain is pain or autonomic phenomena referred from active trigger points in the muscles, fascia, and tendons. This chapter discusses about the therapies for muscular pain which includes the trigger point, botulinum toxin, acupuncture, therapies for peripheral nerve mediated pain, local blockade, ultrasound guided procedures, sympathetic blocks, complex regional pain syndrome, spinal procedures, epidural steroid injections, neuromodulation, vertebral procedures and facet arthropathy. Kyphoplasty and vertebroplasty not only have been studied most extensively in stabilizing compression fractures from osteoporosis, but have also been used to treat fractures resulting from osteolytic metastasis, myeloma, vertebral osteonecrosis, and hemangioma.
This chapter provides a brief description on principles of breast reconstruction in cancer. Breast cancer will impact one in eight women over the course of their lifetime. While breast conserving therapy is a mainstay of surgical treatment with outcomes equivalent to mastectomy in many cases, some women require or elect to have mastectomy to treat their cancer or high-risk state. Breast reconstruction is an essential aspect of the overall postmastectomy treatment, with important psychosocial impacts on patient well-being, as the reconstruction is an attempt to improve their outward appearance, their sense of femininity, and ultimately, their self-esteem. Postmastectomy reconstruction can be categorized into three modalities: implant-based reconstruction, autologous tissue-based reconstruction utilizing the patient’s own tissue, or a combination of implant and autologous-based reconstruction. Immediate postmastectomy reconstruction is currently considered the standard of care in breast reconstruction. Breast reconstruction has a positive impact on postmastectomy physical and mental quality of life.
Involvement of neural plexus structures in a patient with cancer may result from direct invasion by tumors originating within nerve tissue, local metastatic extension or distant spread from diseased organs, or compression by adjacent tumor masses. The function of the neural components may also be severely affected by sequelae or complications of surgical intervention or radiation therapy. Clinical history may suggest a possible etiology; however, physical examination may be of limited value in evaluation of plexopathy depending on the structure affected. Conventional radiologic methods are usually nonrevealing, although they may be helpful in advanced disease. As new techniques are introduced, improved resolution and ability to analyze chemical composition of tissues advanced MRI to the method of choice in diagnosis and assessment of treatment response in patients with plexopathy. This chapter discusses the role of conventional and new modalities in evaluation of plexus disease, including indications, current techniques, advantages, and pitfalls.
Endocrine late effects are among the common late effects seen in cancer survivors, and can be quite complex for the patients, their caregivers, and the medical providers to delineate. This chapter educates the importance of basic concepts and facts that can help in caring for survivors at risk for endocrinopathies. It discusses risk factors, evaluation and management of growth hormone deficiency, thyroid disorders, gonadal dysfunction, adrenal gland disorders, disorders of glucose homeostasis, fluid and sodium homeostasis disorders, calcium homeostasis and bone health disorders, bone density in cancer patients, and endocrine complications resulting from abnormal body mass index (BMI). It is important to evaluate and optimize bone mineral density (BMD) in cancer survivors. Long-standing underweight or overweight/obesity may negatively impact morbidity and quality of life in cancer survivors; monitoring/intervention according to guidelines is thus advised.
Gastrointestinal (GI) complications of cancer are significant and can be challenging to manage. Dysphagia, nausea, vomiting, diarrhea, constipation, fecal impaction, bowel obstruction, and infections are just a few of the adverse effects experienced by the cancer patient. This chapter discusses the current strategies for diagnosis and treatment. The treatment of cancer with chemotherapy agents, immunotherapy, and radiotherapy has dramatically improved the prognosis and survival of many patients diagnosed with cancer. However, these interventions may cause significant GI side effects that can limit tolerability of treatment. The prevention and treatment strategies often utilize a combined pharmacological approach and target the receptors located in the chemoreceptor trigger zone and periphery. Cancer rehabilitation includes vigilant monitoring for GI complications of cancer. GI complications resulting from cancer treatment are variable in presentation and often multifactorial. Proper diagnosis of treatment related symptoms and more serious sequelae are imperative.
Neurologic paraneoplastic disorders are nonmetastatic syndromes that are not attributable to toxicity of cancer therapy, cerebrovascular disease, coagulopathy, infection, or toxic/metabolic causes. Paraneoplastic disorders can affect any part of the central or peripheral nervous systems. Several syndromes should always raise the possibility of a paraneoplastic etiology, including limbic encephalopathy, subacute cerebellar degeneration, opsoclonus–myoclonus, severe sensory neuronopathy, Lambert–Eaton myasthenic syndrome, and dermatomyositis. Most types of tumor can be associated with paraneoplastic disorders, but the most common and best known are thymoma with myasthenia gravis and small cell lung carcinoma with Lambert–Eaton myasthenic syndrome. Paraneoplastic encephalomyelitis is characterized clinically and pathologically by patchy, multifocal involvement of any or all areas of the cerebral hemispheres, limbic system, cerebellum, brainstem, spinal cord, dorsal root ganglia, and autonomic ganglia. The most common clinical manifestation of paraneoplastic encephalomyelitis is subacute sensory neuronopathy reflecting involvement of the dorsal root ganglia.
This chapter discusses dermatological toxicities of anticancer therapies and mainly focuses on two adverse events: hand–foot syndrome (HFS) and paronychia. HFS is a well-documented reversible adverse effect of many chemotherapeutic therapies, causing a wide variety of cutaneous symptoms ranging from erythema, dysesthesia, pain, and desquamation of the palms and soles to impairing daily activities of living. The standard approach used in the management of HFS is treatment interruption or dose modification, with symptom improvement reported within 1 to 2 weeks. Paronychia is the inflammation of the nail folds, jeopardizing the nail fold barrier and potentially exposing the nail matrix to damage. Paronychia is also an adverse effect of chemotherapeutic agents. The known causes of acute paronychia prior to the introduction of epidermal growth factor receptor (EGFR) inhibitors included staphylococci, streptococci, and pseudomonas, whereas, Candida albicans was frequently associated with chronic paronychia, with diabetes mellitus being a predisposing factor.