Books on the topic 'Pain aetiology'
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1
Chronic pain epidemiology: From aetiology to public health. Oxford: Oxford University Press, 2010.
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2
Mayou, Richard. Atypical chest pain. Oxford University Press, 2015. http://dx.doi.org/10.1093/med:psych/9780192627254.003.0015.
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Chapter 15 discusses atypical (or non-cardiac) chest pain. The prevalence, aetiology, and history of treatment are outlined, a psychological model of atypical chest pain, maintaining factors, approaches to management, delivery of care, practical guidelines for and evaluation of psychological treatment, treatment of panic disorder and anxiety, and treatment of hypochondriasis.
3
Neary, John. Loin pain haematuria syndrome. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0047.
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Loin pain haematuria syndrome is an uncommon but disabling condition which presents with recurrent severe loin pain and either microscopic or macroscopic haematuria. It predominantly affects young Caucasian females. The aetiology is unclear, but it seems to be most commonly initiated by glomerular bleeding. There are no defining features of the disorder on any investigation, and it is mostly termed a diagnosis of exclusion. A lack of a clear definition of the condition and uncertainty about the aetiology mean that this is still a poorly understood entity. A variety of medical and surgical treatments have been used with mixed results. The mainstays of treatment are effective analgesia management and involvement of a multidisciplinary team including psychological support.
4
Tighe, Mark, and Mark Beattie. Recurrent abdominal pain. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759928.003.0042.
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Recurrent abdominal pain occurs in 10–15% of school-aged children and is a frequent presenting complaint in general practice and general paediatric and paediatric gastroenterology clinics. Patients often have vague symptoms and investigation usually results in a low yield of organic disease. Treatment strategies are varied and often subjective with limited evidence upon which to base them. This chapter includes a general overview, classification, discussion of the complex and multifactorial aetiology, therapeutic approach, and outcome. It discusses a recommended clinical approach for the management of complex cases.
5
Wager, Julia, and Boris Zernikow. Pain in children. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198785750.003.0041.
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Pain management in children is a specialized service. Pain aetiology, assessment, and treatment vary at every age from pre-term foetuses at 23 weeks gestation to adolescence. In this chapter of European Pain Management advances in our understanding of pain assessment are reviewed, particularly in the use of developmentally relevant technology. Advances in acute pain, cancer pain, and in chronic pain are also reviewed, with a special focus on innovations in multidisciplinary treatments for chronic pain. There is a need to raise awareness and understanding of the needs of paediatric pain patients, and their family members. Education for all professionals who interact with pain patients is essential, as is the need to invest in specialized pain management services, and professionals, across Europe.
6
Atkins, Roger M. Complex regional pain syndrome. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.0011.
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♦ Complex regional pain syndrome (CRPS) is a disabling chronic pain condition of unknown aetiology♦ Traditionally it was thought to be rare; however, prospective studies demonstrate it to be common following both trauma and operative procedures involving the upper and lower limbs♦ The condition is usually self-limiting over a maximum period of 2 years, although minor abnormalities may remain♦ In a minority of cases it does not resolve and is responsible for severe chronic disability♦ Treatment is aimed at functional restoration of limb function supported by pharmacological intervention.
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Zeppetella, Giovambattista. Clarifying the concept of breakthrough pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0054.
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The 1990 publication ‘Breakthrough pain: Definition, prevalence and characteristics’ was the first to study to describe breakthrough pain as a discrete pain state. Using the definition that ‘breakthrough pain is a transient increase in the intensity of moderate or severe pain, occurring in the presence of well-established baseline pain’ the authors interviewed 90 cancer pain patients and identified 51 types of breakthrough pain; these varied widely with respect to severity, location, temporal characteristics, relationship to scheduled analgesia, precipitating events, predictability, pathophysiology, aetiology, and palliative factors. As a result of Portenoy and Hagen’s survey, breakthrough pain has been studied as a discrete pain state for almost 30 years, and recognized as an important clinical problem in its own right. An increasing number of published studies exist, with ongoing debate about the breakthrough pain definition, pain assessment, and pain management.
8
Kuttikat, Anoop, and Nicholas Shenker. Fibromyalgia and chronic widespread pain syndromes—adult onset. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0160.
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Fibromyalgia syndrome (FMS) is characterized by chronic widespread pain, excessive fatigue, unrefreshing sleep, and other associated somatic symptoms. FMS is common in the general population with an estimated prevalence of 2-4% and is about six times more common in females than males. FMS causes significant individual and societal costs. The precise aetiology of FMS remains unclear. Dysfunctional pain processing within the central nervous system is the primary abnormality. FMS is a clinical diagnosis based on pattern recognition and it can coexist with other conditions. A multidisciplinary approach, incorporating patient education, physical therapies, psychological therapies, and pharmacotherapy, is effective in managing these patients.
9
Lovell, Melanie, and Frances Boyle. Communication strategies and skills for optimum pain control. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198736134.003.0038.
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Pain is a subjective experience and as such, communication regarding the experience is essential for the clinician to comprehensively assess and manage it. It is also the most feared complication of the most feared diagnosis. Effective communication creates an environment of trust, in which a patient is able to relate their experiences, in their entirety, including hopes and fears. This expression enables diagnosis of the aetiology, mechanism, and the myriad modulators of the pain by the clinician and is therapeutic in its own right as the patient makes meaning of the pain experience in the telling. The clinician is then able to explain the cause of the pain, the possible treatment strategies, and negotiate a management plan with the patient. There are many misconceptions associated with opioid analgesics and these can also be explored and corrected.
10
Sandkühler, Jürgen. Making the link from “central sensitization” to clinical pain. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0047.
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The landmark paper discussed in this chapter is ‘Central sensitization: Implications for the diagnosis and treatment of pain’, published by C. J. Woolf in 2011. The phrase ‘central sensitization’ is often used as an umbrella term for all kinds of central nervous system (CNS) mechanisms contributing to pain hypersensitivity. The International Association for the Study of Pain (IASP) defines ‘central sensitization’ as the ‘increased responsiveness of nociceptive neurons in the CNS’. In the CNS, highly distinct mechanisms contribute to pain hypersensitivity depending upon pain aetiology and disease stage. These include modification of synaptic strength, inhibitory tone, and membrane excitability and often involve components of neuroinflammation. It is thus recommended to avoid using the phrase ‘central sensitization’ in the scientific literature all together and replace it with unambiguous technical terms such as ‘CNS mechanisms of pain hypersensitivity’ or with the specific mechanism(s) and CNS location(s) in mind.
11
Ramachandran, Manoj. The foot in childhood. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.013022.
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♦ Congenital foot anomalies are common: most are minor and do not affect function♦ Postural problems must be differentiated from structural anomalies♦ An underlying neuromuscular aetiology should be considered♦ A pain-free, functional foot is the goal of treatment.
12
Lal, Mira, and Johannes Bitzer. Disease severity, pain, and patient perception: themes in clinical practice and research. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198749547.003.0006.
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Chapter 6 begins with a discussion of how to assess disease severity. It then moves on to the concepts of physical and emotional pain, which are particularly useful for understanding pelvic floor problems, infertility, pregnancy loss, and chronic pelvic pain. All of these have biological, psychological, and social features associated with their aetiopathogenesis, and presentations. To manage these conditions effectively, it is crucial to understand the patient's perception. First, pelvic/perineal dysfunction is addressed. This includes the loss of urinary and bowel continence, with deleterious effects on biopsychosocial health. The condition is common, and can cause severe morbidity following any delivery mode, including a planned caesarean. This is illustrated by an evaluation of biopsychosocial morbidity, quantified by categorising patient perceptions of severity of incontinence, and related sexual problems. The psychosomatic repercussions of infertility, miscarriage, stillbirth, and chronic pelvic pain are then appraised. Since physical and emotional pain can affect these conditions, timely recognition and biopsychosocial management helps promote positive physical, mental and social health. A special focus is given to endometrial implants outside the uterine cavity (endometriosis). These can cause chronic pelvic pain, infertility, and pregnancy loss, but may be symptomless. Their aetiology remains unclear. Ovulation suppression relieves pain and treatment is tentative, with removal of the affected pelvic organs being an extreme option. Even after this, however, symptoms may persist. A pathway using the tailored psychosomatic approach is advocated to provide patient-centred care where indicated.
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Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0146.
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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly those that result in phosphate deficiency, hypophosphatasia, and vitamin D receptor or metabolizing enzyme mutations. Additionally, the pathogenesis of tumour-induced osteomalacia is becoming better understood. Osteomalacia may present as bone pain and tenderness, muscle pain and weakness, and skeletal deformity or fracture. Key investigations include biochemical assessment and plain radiographs. Radioisotope bone scans and bone biopsy may be considered in selected cases. Differential diagnoses include osteoporosis, seronegative arthritides, and localized soft tissue disorders. Treatment, guided by the underlying aetiology, aims to reduce symptoms, fracture risk, bone deformity and sequelae. Vitamin D deficient patients require vitamin D and calcium replacement.
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Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0146_update_001.
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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly those that result in phosphate deficiency, hypophosphatasia, and vitamin D receptor or metabolizing enzyme mutations. Additionally, the pathogenesis of tumour-induced osteomalacia is becoming better understood. Osteomalacia may present as bone pain and tenderness, muscle pain and weakness, and skeletal deformity or fracture. Key investigations include biochemical assessment and plain radiographs. Radioisotope bone scans and bone biopsy may be considered in selected cases. Differential diagnoses include osteoporosis, seronegative arthritides, and localized soft tissue disorders. Treatment, guided by the underlying aetiology, aims to reduce symptoms, fracture risk, bone deformity and sequelae. Vitamin D deficient patients require vitamin D and calcium replacement.
15
Henry, M. Stress fractures. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.012017.
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♦ Stress fractures are fractures occurring as the result of repetitive, submaximal loads, in the absence of a specific precipitating traumatic event.♦ These fractures can be subdivided into two groups on the basis of aetiology. Whereas ‘fatigue fractures’ result from the excessive repetitive (i.e. abnormal) loading of normal bone, ‘insufficiency fractures’ are fractures resulting from normal forces acting on abnormal bone.♦ Early diagnosis allows the initiation of effective treatment that can prevent prolonged pain and disability, as well as avoiding the progression to displacement or a non-union.♦ While management decisions are generally focused on activity modification, protection of weight bearing, and immobilization, there is a subset of fractures at high risk for progression to complete fracture, non-union, or delayed union. These high-risk stress fractures, including tension-side femoral neck fractures and anterior tibial cortex fractures, require aggressive treatment to prevent the sequelae of poor healing.
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Lee, Olivia T., Jennifer N. Wu, Frederick J. Meyers, and Christopher P. Evans. Genitourinary aspects of palliative care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0084.
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Genitourinary tract diseases in the palliative care setting most commonly involve urinary tract obstruction, intractable bleeding, fistulae, and bladder-associated pain. Sources of obstruction in the lower urinary tract include benign prostatic hyperplasia, invasive prostate or bladder cancer, urethral stricture, or bladder neck contracture. Upper tract obstruction includes intraluminal or extraluminal blockage of the renal collecting system and ureters, such as transitional cell carcinoma, fibroepithelial polyps, stricture, stones, pelvic or retroperitoneal malignancy, fibrosis, or prior radiation. Untreated, obstructive uropathy leads to elevated bladder, ureter, and kidney pressures, bladder dysfunction, urolithiasis, renal failure, pyelonephritis, or urosepsis. Intractable haematuria can cause problematic anaemia, frequent transfusions, clot retention, haemorrhagic shock, and death. In addition, urinary tract fistulae such as vesicovaginal and vesicoenteric fistulae are common in patients who have had prior pelvic surgery or radiation especially in the setting of immunocompromise, poor nutrition, and infection. Untreated, these symptoms lead to rash, skin breakdown, ulcers, chronic infection, and sepsis. Lastly, pelvic and bladder pain, depending on aetiology can be treated with oral medications, intravesical therapies, or surgical therapies such as palliative resection or urinary diversion. Selection of tests and treatment modalities in the palliative care setting should be based on using the least invasive means to achieve the most relief in suffering. Some genitourinary conditions are potentially fatal, and in the acute or subacute setting, require re-evaluation of the end-of-life goals and wishes of the patient and family.
17
Jayasumana, Channa, Carlos Orantes, and Marc E. De Broe. Chronic Interstitial Nephritis in Agricultural Communities. Edited by Neil Turner. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0366_update_001.
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Chronic Interstitial Nephritis in Agricultural Communities (CINAC) has been increasingly recognized since the early 1990s. It has been called epidemic chronic kidney disease unknown cause (CKDu) in Sri Lanka, and meso-American nephropathy in Central America. CINAC occurs regionally in the Tropics, predominantly in rural/agricultural zones. It is increasingly recognized, but also believed to be increasing in incidence. Men are affected up to three times more often than women. Its incidence increases with age, and a number of other epidemiological factors impact on it. In some areas, such as the North Central Province of Sri Lanka and regions of Central America, it drives extreme rates of CKD and end-stage renal failure. Clinically, it has the non-specific characteristics of other slowly-evolving chronic interstitial nephritis (Chapter 86). Perhaps distinctive is an inconsistent history of episodes of dysuria, sometimes loin pain, in earlier disease. Its aetiology remains unsolved. Maps of incidence commonly show a mosaic pattern, suggesting that exposure to local factors are implicated. It has been associated with working outdoors in high temperatures, but this seems inadequate as the sole explanation. Exposure to nephrotoxins, natural or possibly as agrochemicals, seems likely.
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Rajendram, Rajkumar. Management of acute pancreatitis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0191.
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The major causes of morbidity and mortality in acute pancreatitis are organ dysfunction and infection of necrotic tissue. Management should aim to prevent, or to diagnose and treat, the complications of pancreatic inflammation, and any predisposing factors to avoid recurrence. Medical management is essentially supportive with oxygen, intravenous fluids, analgesia, enteral or parenteral nutrition, and correction of metabolic abnormalities. Patients with severe acute pancreatitis are unlikely to resume prompt oral intake so nutritional support is also required. Post-pyloric feeding is not required if nasogastric feeding is tolerated. However, enteral nutrition, whether oral, gastric, or post-pyloric, can cause pain, recurrence of pancreatitis or an increase in fluid collections, so parenteral nutrition may be necessary. The necrotic pancreas becomes infected in a third of patients with severe acute pancreatitis. Treatment of infection includes systemic antimicrobials, enteral nutrition, percutaneous aspiration, and necrosectomy. However, compared with open necrosectomy, a minimally invasive step-up approach consisting of percutaneous drainage followed, if necessary, by open necrosectomy, reduces morbidity and mortality. The aetiology of the pancreatitis must also be treated to prevent recurrence and the complications of pancreatic failure. Gallstones are the most common cause of pancreatitis that requires specific treatment. Endoscopic or surgical removal of stones may reduce the severity of pancreatitis. Patients should also have cholecystectomy after recovery from gallstone pancreatitis. Effective management of acute pancreatitis requires multidisciplinary engagement. The mainstay of management involves supportive prevention and treatment of complications, infection, and organ failure to avoid or delay surgery.
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Fruhwald, Sonja, and Peter Holzer. Gastrointestinal motility drugs in critical illness. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0040.
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Gastrointestinal motility disturbances in critically-ill patients often require treatment with prokinetic drugs. The aetiology of motility disturbances is complex, and involves electrolyte imbalances, hypervolaemia, reduced intestinal secretion, adverse effects of drugs (catecholamines, opioids, or sedatives) and disease- or treatment-related changes of microflora. However, the choice of prokinetics is narrow, and the multiplicity of pathophysiological mechanisms often limits their efficacy. Gastroparesis can be managed with gastrokinetics such as domperidone, metoclopramide and erythromycin. Their choice depends not only on efficacy, but also on adverse effect profile. The arrhythmogenic potential of domperidone limits maximum daily dose and treatment duration. Metoclopramide and erythromycin induce tachyphylaxis, which restricts treatment duration. The combination of metoclopramide and erythromycin serves as rescue therapy in severe gastroparesis. Neostigmine and laxatives are used to manage colonic paralysis, and these treatment options may eventually be extended by drug candidates, such as prucalopride, lubiprostone, and linaclotide, whose utility in the ICU awaits to be evaluated. Neostigmine’s prokinetic efficacy in colonic paralysis is limited, but well documented in patients with acute colonic pseudo-obstruction (Ogilvie syndrome). Care is advocated in dosing because higher doses of neostigmine inhibit motility. Alternative options include osmotic and stimulant laxatives, especially for prophylactic use. The opioid receptor antagonist alvimopan is used for the short-term management of post-operative ileus, while methylnaltrexone is indicated in palliative care and chronic pain management. Since its efficacy in critically-ill patients remains to be proven, the use of methylnaltrexone in the ICU is off-label and requires proper documentation.
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Velsen, Cleo Van, and Kingsley Norton. Outpatient psychotherapeutic approaches with mentally disordered offenders. Edited by Alec Buchanan and Lisa Wootton. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198738664.003.0010.
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In the last 30 years, there has been an upsurge of interest in developing and refining psychological approaches to the treatment and management of offenders. This chapter focuses on outpatient interventions with those identified as suffering from forensic personality disorder. The potential range of treatments is vast; therefore, we examine general treatment principles. We describe the concept of forensic personality disorder and outline theoretical and evidence-based approaches to aetiology and therapy. Attention is paid to the establishment and maintenance of a therapeutic alliance, including the importance of boundaries, which can easily become distorted. Offender patients are usually seen in the context of the criminal justice system and risk, which means understanding the balance between confidentiality and information sharing. The effect on individuals and teams and the need to explore disagreements and conflicts in the treatment service are highlighted. Clinical vignettes are included to illustrate the concepts described.
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Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0068.
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Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.
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Gevaert, Sofie A., Eric Hoste, and John A. Kellum. Acute kidney injury. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0068_update_001.
Full textAbstract:
Acute kidney injury is a serious condition, occurring in up to two-thirds of intensive care unit patients, and 8.8-55% of patients with acute cardiac conditions. Renal replacement therapy is used in about 5-10% of intensive care unit patients. The term cardiorenal syndrome refers to combined heart and kidney failure; three types of acute cardiorenal syndrome have been described: acute cardiorenal syndrome or cardiorenal syndrome type 1, acute renocardiac syndrome or cardiorenal syndrome type 3, and acute cardiorenal syndrome type 5 (cardiac and renal injury secondary to a third entity such as sepsis). Acute kidney injury replaced the previously used term ‘acute renal failure’ and comprises the entire spectrum of the disease, from small changes in function to the requirement of renal replacement therapy. Not only failure, but also minor and less severe decreases, in kidney function are of clinical significance both in the short and long-term. The most recent definition for acute kidney injury is proposed by the Kidney Disease: Improving Global Outcomes clinical practice guidelines workgroup. This definition is a modification of the RIFLE and AKIN definitions and staging criteria, and it stages patients according to changes in the urine output and serum creatinine (see Tables 68.1 and 68.2). Acute kidney injury is a heterogeneous syndrome with different and multiple aetiologies, often with several insults occurring in the same individual. The underlying processes include nephrotoxicity, and neurohormonal, haemodynamic, autoimmune, and inflammatory abnormalities. The most frequent cause for acute kidney injury in intensive cardiac care patients are low cardiac output with an impaired kidney perfusion (cardiogenic shock) and/or a marked increase in venous pressure (acute decompensated heart failure). Predictors for acute kidney injury in these patients include: baseline renal dysfunction, diabetes, anaemia, and hypertension, as well as the administration of high doses of diuretics. In the intensive cardiac care unit, attention must be paid to the prevention of acute kidney injury: monitoring of high-risk patients, prompt resuscitation, maintenance of an adequate mean arterial pressure, cardiac output, and intravascular volume (avoidance of both fluid overload and hypovolaemia), as well as the avoidance or protection against nephrotoxic agents. The treatment of acute kidney injury focuses on the treatment of the underlying aetiology, supportive care, and avoiding further injury from nephrotoxic agents. More specific therapies have not yet demonstrated efficacy. Renal replacement therapy is indicated in life-threatening changes in fluid, electrolyte, and acid-base balance, but there are also arguments for more early initiation.