Pain is the way the body shows abnormal function and, usually, the reason that leads someone to use the healthcare system. There are numerous causes of pain in Chronic Kidney Disease and their manifestations vary. Pain can result from the primary kidney disease, such as Polycystic Kidney Disease (PKD) or Systemic Lupus Erythematous (SLE), or comorbid situations, such as Diabetes Mellitus (DM), Peripheral Vascular Disease (PVD), and Cardiovascular Disease (CVD). There are, also, several other conditions that cause pain and are associated with renal disease (calcific uremic arteriolopathy, secondary hyperparathyroidism, nephrogenic fibrosing dermopathy), or RRT (steal syndrome from an arteriovenous fistula for HD, abdominal distension from PD, needle insertion, and muscle cramps) (Davison 2007a, Salisbury et al. 2009, Bagheri-Nesami et al. 2014, Moss & Davison 2015). Furthermore, painful ischaemic neuropathies can be caused by chronic infections, such as discitis or osteomyelitis; complications from central venous catheters used for dialysis or infected arteriovenous fistulas. Finally, pain between the twelfth thoracic (T12) and the third lumbar (L3) vertebra could be misdiagnosed as caused by injury to back muscles or the spine, when in fact could be caused by renal problems, such as Polycystic Kidney Disease (Manias & Williams 2007, Heiwe & Bjuke 2009). It is advised that any pain in the particular area to be further investigated in order to determine the exact cause.
4.1.1 Primary or secondary disease initiated pain 4.1.1.1 Polycystic Kidney Disease (PKD)
Polycystic Kidney Disease (PKD) is the most common renal hereditary disease, which can be found either as autosomal dominant or autosomal recessive type. A gene mutation or defect is responsible for the disease. The prevalence of PKD in Europe and USA is ranging from 1/200 to 1/1000 individuals. Moreover, its prevalence among Chronic Kidney Disease stage 5 patients is around 10-15% in the USA, 6-10% in Europe and 11% in Greece. Almost half the patients with PKD will reach Chronic Kidney Disease stage 5 by the time they are 60 years old, or earlier if haematuria occurs before the age of thirty (Mavromatidis 2003, Badani et al.
2004, Tellman et al. 2015). It is characterised by progressive enlargement of the kidneys due to cyst growth and development, and can be accompanied by hepatic cysts, intracranial aneurysms, cardiac disease, hernias, and diverticular disease. Pain in patients with PKD can either begin with an acute episode and persist as chronic after the elevation of its cause, or develop gradually and become more severe over time. Either type of pain (acute or chronic) is the source of great frustration and distress for PKD patients, as it affects almost 60% of them (Steinman 2000, Bajwa et al. 2004, Torres et al. 2007, Shetty et al. 2012, Walsh & Sarria 2012, Savige et al. 2015).
During cyst formation or enlargement, the surrounding tissues are compressed, the pedicle of the kidney is pulled and renal capsule becomes swollen (Steinman 2000, Cohen et
al. 2006, Torres et al. 2011, Shetty et al. 2012). These mechanisms will cause chronic and localised pain, usually in the anterior abdominal area and can be explained in details as Walsh & Sarria (2012) explained in their study. According to the researchers, afferent fibers from the renal capsule, parenchyma, and vasculature go to neuraxis, passing through sympathetic nerves and prevertebral ganglia, and join the lesser and least splanchnic nerves.
These nerves then travel cranially along the retrocrural space to the T10-T12 and L1 spinal levels through the respective paravertebral ganglia and rami communicans. Intercostal somatic nerves are nerving part of the renal capsule and nearby musculoskeletal structures, corresponding to T7-T12 dermatomal levels. Large cysts result in bigger pelvic angle and lumbar lordosis causing mechanical low back pain, as the abdomen projects, more strain is forced to lower back muscles and disc disease is established in the lumbosacral area (Steinman 2000, Bajwa et al. 2004, Tozzi et al. 2012). Infected renal cysts can cause diffuse, generalised unilateral or bilateral pain accompanied by fever, unrelieved by changes in position. This type of pain is similar to pyelonephritis in general population. Raptured cysts, on the other hand, manifested by haemorrhage – haematuria- are the cause of acute flank pain which is, usually, localised and finger pointed by patients. It can, also, reflect to anterior abdominal area (Hogan & Norby 2010, Haseebuddin et al. 2012) or even the shoulder if the cysts are larger and compressing the surrounding tissues. Haematuria can be present in almost half of the patients with PKD (Bajwa 2001). In case of ruptured cysts which are on the surface of the kidney, sub-capsular hematoma is caused, resulting in mild and steady pain persisting until it is absorbed (Steinman 2000). Clots within the renal cysts can lead to urinary tract obstruction, similar to the one caused by kidney stones, and renal colic. Renal colic caused by kidney stones (calcium oxalate, calcium phosphate, calcium carbonate or uric acid) can be found in almost 20% of patients with PKD. Anatomic deformity caused by the cysts may contribute to the formation of kidney stones, possibly due to increased urinary stasis (Grampsas et al. 2000). Furthermore, liver cysts is a common comorbidity found in 85% of the individuals older than 30 years in the multicentre study CRISP (Bae et al. 2006). Liver cysts are, too, associated with more severe pain and abdominal distension while in standing position.
Headache or migraine in the PKD population could be an early sign of cerebral aneurysm, even though the prevalence is between 4%-6% of the total ADPKD group (Bajwa et al. 2001).
In the cases of positive family history of cerebral aneurysms, the incidence of aneurysms increases to 26% (Chapman et al. 1993).
4.1.1.2 Hyperparathyroidism
Secondary hyperparathyroidism, a serious complication of Chronic Kidney Disease, originates from deregulation of serum calcium, phosphorus and vitamin D, resulting in elevated levels of parathyroid hormone and, furthermore, in abnormal bone metabolism and muscle weakness, skeletal deformities and bone pain, called renal osteodystrophy.
Ergocalciferol (vitamin D2), cholecalciferol (vitamin D3), and their metabolites and derivatives are involved in this process. Vitamin D3 is produced after the conversion of skin’s 7-Dehydrocholesterol in the presence of sunlight. As it is not active, it has to be hydroxylated in the liver to produce 25-hydroxyvitamin D3. Then in the normal kidney it is converted into calcitriol (1.25 dihydroxyvitamin D3). The same process happens with vitamin D2, which comes from plants and fungus, producing 1.25 dihydroxyergocalciferol. Both forms of vitamin D maintain normal calcium homeostasis via the vitamin D receptor increasing intestinal calcium absorption and modulating mineral mobilization from bone (Palmer et al.
2009). These mineral and hormonal abnormalities start early in Chronic Kidney Disease process, usually in Stage 3 or when GFR is <60mL/min/1.73m2. If left untreated, hyperparathyroidism can lead to onset of purpuric plagues, discolored skin and nodules, signs of calciphylaxis, and could evolve in necrotic ulcers, gangrene, and unavoidable amputation. Painful proximal myopathy can accompany the skin manifestations, resembling
Neuropathic pain, on the other hand, in the general population has a very low prevalence of 7-8% (Smith et al. 2007) compared to around 45% in Chronic Kidney Disease population (Atalay et al. 2013, Santoro et al. 2013).
Pain in Chronic Kidney Disease patients is undertreated as it is shown in various international observational researches. Davison (2005) reports that 74% of patients with pain that affected negatively their work had no analgesic prescribed to them. The same researcher in a previous study (Davison 2003) found that 35% of haemodialysis patients with chronic pain were not prescribed any analgesics and less than 10% were prescribed strong opioids.
Furthermore, 74% of Chronic Kidney Disease stages 4-5 patients with moderate to severe pain or pain that interfered with their work were undertreated (Bailie et al. 2004, Bulter et al.
2014, Wu et al. 2015).
4.1 AETIOLOGY OF PAIN IN CHRONIC KIDNEY DISEASE PATIENTS
Pain is the way the body shows abnormal function and, usually, the reason that leads someone to use the healthcare system. There are numerous causes of pain in Chronic Kidney Disease and their manifestations vary. Pain can result from the primary kidney disease, such as Polycystic Kidney Disease (PKD) or Systemic Lupus Erythematous (SLE), or comorbid situations, such as Diabetes Mellitus (DM), Peripheral Vascular Disease (PVD), and Cardiovascular Disease (CVD). There are, also, several other conditions that cause pain and are associated with renal disease (calcific uremic arteriolopathy, secondary hyperparathyroidism, nephrogenic fibrosing dermopathy), or RRT (steal syndrome from an arteriovenous fistula for HD, abdominal distension from PD, needle insertion, and muscle cramps) (Davison 2007a, Salisbury et al. 2009, Bagheri-Nesami et al. 2014, Moss & Davison 2015). Furthermore, painful ischaemic neuropathies can be caused by chronic infections, such as discitis or osteomyelitis; complications from central venous catheters used for dialysis or infected arteriovenous fistulas. Finally, pain between the twelfth thoracic (T12) and the third lumbar (L3) vertebra could be misdiagnosed as caused by injury to back muscles or the spine, when in fact could be caused by renal problems, such as Polycystic Kidney Disease (Manias & Williams 2007, Heiwe & Bjuke 2009). It is advised that any pain in the particular area to be further investigated in order to determine the exact cause.
4.1.1 Primary or secondary disease initiated pain 4.1.1.1 Polycystic Kidney Disease (PKD)
Polycystic Kidney Disease (PKD) is the most common renal hereditary disease, which can be found either as autosomal dominant or autosomal recessive type. A gene mutation or defect is responsible for the disease. The prevalence of PKD in Europe and USA is ranging from 1/200 to 1/1000 individuals. Moreover, its prevalence among Chronic Kidney Disease stage 5 patients is around 10-15% in the USA, 6-10% in Europe and 11% in Greece. Almost half the patients with PKD will reach Chronic Kidney Disease stage 5 by the time they are 60 years old, or earlier if haematuria occurs before the age of thirty (Mavromatidis 2003, Badani et al.
2004, Tellman et al. 2015). It is characterised by progressive enlargement of the kidneys due to cyst growth and development, and can be accompanied by hepatic cysts, intracranial aneurysms, cardiac disease, hernias, and diverticular disease. Pain in patients with PKD can either begin with an acute episode and persist as chronic after the elevation of its cause, or develop gradually and become more severe over time. Either type of pain (acute or chronic) is the source of great frustration and distress for PKD patients, as it affects almost 60% of them (Steinman 2000, Bajwa et al. 2004, Torres et al. 2007, Shetty et al. 2012, Walsh & Sarria 2012, Savige et al. 2015).
During cyst formation or enlargement, the surrounding tissues are compressed, the pedicle of the kidney is pulled and renal capsule becomes swollen (Steinman 2000, Cohen et
al. 2006, Torres et al. 2011, Shetty et al. 2012). These mechanisms will cause chronic and localised pain, usually in the anterior abdominal area and can be explained in details as Walsh & Sarria (2012) explained in their study. According to the researchers, afferent fibers from the renal capsule, parenchyma, and vasculature go to neuraxis, passing through sympathetic nerves and prevertebral ganglia, and join the lesser and least splanchnic nerves.
These nerves then travel cranially along the retrocrural space to the T10-T12 and L1 spinal levels through the respective paravertebral ganglia and rami communicans. Intercostal somatic nerves are nerving part of the renal capsule and nearby musculoskeletal structures, corresponding to T7-T12 dermatomal levels. Large cysts result in bigger pelvic angle and lumbar lordosis causing mechanical low back pain, as the abdomen projects, more strain is forced to lower back muscles and disc disease is established in the lumbosacral area (Steinman 2000, Bajwa et al. 2004, Tozzi et al. 2012). Infected renal cysts can cause diffuse, generalised unilateral or bilateral pain accompanied by fever, unrelieved by changes in position. This type of pain is similar to pyelonephritis in general population. Raptured cysts, on the other hand, manifested by haemorrhage – haematuria- are the cause of acute flank pain which is, usually, localised and finger pointed by patients. It can, also, reflect to anterior abdominal area (Hogan & Norby 2010, Haseebuddin et al. 2012) or even the shoulder if the cysts are larger and compressing the surrounding tissues. Haematuria can be present in almost half of the patients with PKD (Bajwa 2001). In case of ruptured cysts which are on the surface of the kidney, sub-capsular hematoma is caused, resulting in mild and steady pain persisting until it is absorbed (Steinman 2000). Clots within the renal cysts can lead to urinary tract obstruction, similar to the one caused by kidney stones, and renal colic. Renal colic caused by kidney stones (calcium oxalate, calcium phosphate, calcium carbonate or uric acid) can be found in almost 20% of patients with PKD. Anatomic deformity caused by the cysts may contribute to the formation of kidney stones, possibly due to increased urinary stasis (Grampsas et al. 2000). Furthermore, liver cysts is a common comorbidity found in 85% of the individuals older than 30 years in the multicentre study CRISP (Bae et al. 2006). Liver cysts are, too, associated with more severe pain and abdominal distension while in standing position.
Headache or migraine in the PKD population could be an early sign of cerebral aneurysm, even though the prevalence is between 4%-6% of the total ADPKD group (Bajwa et al. 2001).
In the cases of positive family history of cerebral aneurysms, the incidence of aneurysms increases to 26% (Chapman et al. 1993).
4.1.1.2 Hyperparathyroidism
Secondary hyperparathyroidism, a serious complication of Chronic Kidney Disease, originates from deregulation of serum calcium, phosphorus and vitamin D, resulting in elevated levels of parathyroid hormone and, furthermore, in abnormal bone metabolism and muscle weakness, skeletal deformities and bone pain, called renal osteodystrophy.
Ergocalciferol (vitamin D2), cholecalciferol (vitamin D3), and their metabolites and derivatives are involved in this process. Vitamin D3 is produced after the conversion of skin’s 7-Dehydrocholesterol in the presence of sunlight. As it is not active, it has to be hydroxylated in the liver to produce 25-hydroxyvitamin D3. Then in the normal kidney it is converted into calcitriol (1.25 dihydroxyvitamin D3). The same process happens with vitamin D2, which comes from plants and fungus, producing 1.25 dihydroxyergocalciferol. Both forms of vitamin D maintain normal calcium homeostasis via the vitamin D receptor increasing intestinal calcium absorption and modulating mineral mobilization from bone (Palmer et al.
2009). These mineral and hormonal abnormalities start early in Chronic Kidney Disease process, usually in Stage 3 or when GFR is <60mL/min/1.73m2. If left untreated, hyperparathyroidism can lead to onset of purpuric plagues, discolored skin and nodules, signs of calciphylaxis, and could evolve in necrotic ulcers, gangrene, and unavoidable amputation. Painful proximal myopathy can accompany the skin manifestations, resembling
dermatomyositis. Biopsy findings show varying degrees of calcification of the media layer of the blood vessel walls of subcutaneous or digital arteries causing ischaemic necrosis of the skin and other organs (Perlman 2005, Terzibasioglu et al. 2005, Strippoli et al. 2010).
4.1.1.3 Dialysis-related amyloidosis (DRA)
Dialysis-related amyloidosis (DRA) is common among patients that have been on dialysis, HD or PD, for more than 5 years (Moss 2008). B2-microglobulin is deposited in bone, synovium, tendons and peripheral nerves and is manifested as arthritis, bone cysts, carpal tunnel syndrome and fractures along with pain. In renal osteodystrophy, the abnormality is happening in the metabolic process itself, causing bone turnover whereas in DRA the amyloid deposits interfere with normal bone tissue dynamics (Kelly et al. 2007). It is a cause of musculoskeletal pain in 51% of dialysis patients, as described by Davison (2003) and 37%
of another HD population studied by Carreon et al. (2008). Nephrogenic fibrosing dermopathy is a dermatologic disorder that has recently been recognised causing considerable amounts of pain (Cowper et al. 2001, Daram et al. 2005).
4.1.1.4 Diabetes Mellitus (DM)
Diabetic peripheral neuropathy, affecting large and small fibres, is another cause of pain in Chronic Kidney Disease patients and is correlated with duration of Diabetes Mellitus (DM), degree of glycaemic control and level of uraemia (Edwards et al. 2008). Sensory deficits overshadow motor nerve dysfunction and appear first in the distal portions of the extremities and progress proximally in a “stocking-glove” distribution causing difficulty in walking as well as loss of sensitiveness (Pop-Busui et al. 2010).
4.1.2 Clinically inflicted pain
In addition to pain caused by medical conditions or diseases, primary or secondary, HD patients are, quite often, exposed to clinically inflicted pain, caused by insertion of Central Venous Catheter (CVC) for HD or cannulation of vascular access (Arteriovenous fistula or graft). Haemodialysis sessions are held, usually, three times a week and involve at least one puncture at the arterial and one at the venous part of the vascular access for every session, a total of 320 punctures each year. This repeated puncturing leads to a considerable pain, due to the tearing of the skin, and passing through the walls of the vessel (Montero et al. 2004, Verhallen et al. 2007, Figueiredo et al. 2008). Due to irritation of the skin’s nerve endings, pain perception mechanism is triggered and pain is experienced. On the other hand, PD patients experience pain during the placement of the PD catheter, as this procedure is performed under local anaesthesia, and during episodes of peritonitis.
5 Assessment of pain in renal patients
Pain assessment in renal patients is based on sufficient co-operation and communication between healthcare professionals and patients, themselves, despite variances in beliefs and perspectives. Literature emphasizes on the importance of the person experiencing pain and defines pain as “whatever the experiencing person says it is, exists whenever she/he says it does” (McCaffery 1968) or “as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” (Merskey &
Bogduk 2012). Nonetheless, the response to the patient’s experience of pain is dominated by the healthcare professional’s knowledge and attitudes (Watt-Watson et al. 2001, Lovering 2006).
The process of assessment is the act of determining the importance, amount or value of something, in particular pain. Pain cannot be easily measured as heart rate or blood pressure can, but it can be measured using a variety of valid and reliable approaches, scales or questionnaires during assessment time. Pain assessment is the first step towards an effective pain management and a critical constituent of high quality patient care (Greek Act of Patients Rights 1992). A full and detailed assessment during nursing process is necessary in order to understand the patients’ situation, to choose appropriate analgesic treatment, to program necessary interventions, to evaluate their effectiveness and to further modify management according to patient’s response. Information obtained helps nurses and other healthcare professionals to plan and implement an individualised care plan within the bio-psychosocial model of care.
Pain assessment and management is an interactive procedure between individuals (patients and nurses) with different perspectives regarding health beliefs and practices. Pain is a very subjective feeling and can only be measured accurately by the person who is experiencing it, as it is already stated. Frequency, tolerance and intensity vary among individuals. Pain intensity can be affected by multiple factors, such as sleep deprivation, previous experiences of pain, and family situations (Sherwood et al. 2000, Heiwe & Bjuke 2009). Furthermore, the recollection of a painful stimulus and/or situation affects both the patients’ response to future similar situations as well as the choices regarding pain management (Ylinen et al. 2009). In addition, pain tolerance can be influenced by the person’s expectations, behaviors, physical and emotional health as well as ethnical and cultural background (Lasch 2002, Heiwe & Bjuke 2009, Khan et al. 2015, Lin et al. 2015).
Patients of different ethnic origin, with differing occupational, economic and educational status, have different responses to health and illness (Kourakos & Kafkia, 2007). Research has shown that it was trice more likely for minorities to have inadequate cancer pain management than natives (Cleeland & Ryan 1994), whereas in another research, Asian patients received, postoperatively, 24% lower dose of analgesics and had lower mean of analgesic consumption compared to European patients (Houghton et al. 1992). In accordance with these, are the findings of Faucett et al. (1994) who states that Europeans reported less severe postoperative pain than black American or Latino patients.
According to the Canadian Nurses Pain Association (2005) the main goals of pain assessment are to give a detailed report of the phenomenon of pain and the factors that affect it, to assist in the diagnosis and planning of pain management interventions, to evaluate their
According to the Canadian Nurses Pain Association (2005) the main goals of pain assessment are to give a detailed report of the phenomenon of pain and the factors that affect it, to assist in the diagnosis and planning of pain management interventions, to evaluate their