bluuebunny/crossref_metadata_2025 huggingface dataset:
Heart muscle disease (cardiomyopathy)
Authors: Rahimi Kazem
Published: August 2018

Cardiomyopathy is defined as disease of heart muscle, and typically refers to diseases of ventricular myocardium. A consensus statement of the European Society of Cardiology (ESC) working group on myocardial and pericardial diseases, published in 2007, abandoned the inconsistent and rather arbitrary classification into primary and secondary causes and based its classification on ventricular morphology and function only. This classification distinguishes five types of cardiomyopathy: dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, and unclassified cardiomyopathies (such as takotsubo cardiomyopathy and left ventricular non-compaction). Each category is further subdivided into familial and non-familial causes. In a departure from the 1995 WHO classification, the ESC consensus statement excludes myocardial dysfunction caused by coronary artery disease, hypertension, valvular disease, and congenital heart disease from the definition of cardiomyopathy. The rationale for this was to highlight the differences in diagnostic and therapeutic approaches of these common diseases, and to make the new classification system more acceptable for the routine clinical use. In contrast to the American Heart Association scientific statement, the ESC definition does not consider channelopathies as cardiomyopathies. The sections on cardiomyopathy in this chapter are based on the ESC definition, with a brief reference to channelopathies.
Tumours and the heart
Authors: Rahimi Kazem
Published: August 2018

This chapter discusses myxoma, pericardial malignancy, and myocardial malignancy, including definitions of the disease, etiology, typical symptoms, uncommon symptoms, demographics, natural history, complications, diagnostic approaches, other diagnoses that should be considered, prognosis, and treatment. It also discusses cancer treatment and the heart.
Cardiac infection
Authors: Shirodaria Cheerag , Newton Jim
Published: August 2018

This chapter discusses endocarditis and acute rheumatic fever, including definitions of the disease, etiology, typical symptoms, uncommon symptoms, demographics, natural history, complications, diagnostic approaches, other diagnoses that should be considered, prognosis, and treatment.
Pericardial disease
Authors: Adlam David
Published: August 2018

The pericardium forms a continuous sac around the heart, analogous to the pleura surrounding the lungs, and the peritoneum surrounding the abdominal viscera. Between the parietal and visceral layers of the serous pericardium is the pericardial space, which normally contains a small volume of pericardial fluid. The clinical spectrum of pericardial diseases can be divided into: pericarditis, caused by acute inflammation; pericardial effusion, or fluid accumulation in the pericardial space, leading to tamponade; and constrictive pericarditis, caused by chronic infiltration or inflammation leading to pericardial constriction.
Extrasystoles
Authors: El-Kadri Moutaz , Hart George
Published: August 2018

An extrasystole is a cardiac electrical impulse (often premature) which is not part of the normal heart rhythm. Extrasystoles most frequently arise from the ventricles and are then called ventricular extrasystoles, or premature ventricular complexes. Less often, they originate from the atria, the atrioventricular junction or, rarely, from the sinus node—these are termed supraventricular extrasystoles. The term ‘bigeminy’ refers to an extrasystole every second beat, and ‘trigeminy’, every third beat. Two successive extrasystoles are called a ‘couplet’; three are called a ‘triplet’. Extrasystoles with varying morphology are described as ‘polymorphic’ or ‘multifocal’, whereas those maintaining the same morphology are termed ‘unifocal’.
Sinus tachycardia
Authors: Jones Michael , Qureshi Norman , Rajappan Kim
Published: August 2018

Sinus tachycardia is a condition of multiple different potential etiologies, characterized by an elevated rate of automaticity of the sinoatrial node, such that the heart rate is elevated. The exact point at which sinus tachycardia meets sinus rhythm is debatable; however, by convention, an upper rate of 100 min−1 is accepted for sinus rhythm; >100 min−1 denotes sinus tachycardia.
Focal (ectopic) atrial tachycardia
Authors: Jones Michael , Qureshi Norman , Rajappan Kim
Published: August 2018

Focal atrial tachycardia is an atrial arrhythmia arising in either the left or the right atrium, usually faster than 100 min−1 and regular, with a P-wave morphology that is different from the normal P-wave morphology associated with sinus rhythm—the difference in morphology being more pronounced the further away the focus lies from the sinus node. The ventricular rate is generally fast also, dependent on the nature of the atrioventricular conduction (AV); 1:1 conduction may be seen, especially in younger patients or patients with accessory pathways capable of very rapid antegrade conduction; alternatively, 2:1, Wenckebach-type, or higher-grade AV block may be seen.
Multifocal atrial tachycardia
Authors: Jones Michael , Qureshi Norman , Rajappan Kim
Published: August 2018

Multifocal atrial tachycardia (MAT) is an atrial arrhythmia arising in the left or right atrium, or both, with multiple different P wave morphologies (at least three), with an atrial rate usually faster than 100 min−1. The atrial rhythm may be irregular; however, the defining difference between MAT and atrial fibrillation is the presence of a P wave prior to each QRS complex in MAT (but the absence of P waves in atrial fibrillation). MAT may be compared to sinus rhythm with very frequent polymorphic atrial ectopic beats, and in fact similar pathophysiologic mechanisms underlie both conditions; thus, differentiating one from the other may be difficult—the principle difference is the lack of a single dominant sinus pacemaker in MAT.
Atrioventricular nodal re-entrant tachycardia
Authors: Jones Michael , Qureshi Norman , Rajappan Kim
Published: August 2018

Atrioventricular nodal re-entrant tachycardia (abbreviated as AVNRT) is one of the five subtypes of supraventricular tachycardia, manifesting most commonly as a regular, narrow QRS complex tachycardia, rate 150–250 min−1 (usually 160–180 min−1), occurring paroxysmally, with P waves either not apparent, or seen to follow the QRS complexes.
Atrioventricular re-entrant tachycardia
Authors: Jones Michael , Qureshi Norman , Rajappan Kim
Published: August 2018

Atrioventricular (AV) re-entrant tachycardia (AVRT) is a type of supraventricular tachycardia, manifesting most commonly as a regular, narrow-QRS-complex tachycardia. It is usually a paroxysmal tachycardia, and is dependent upon the presence of an accessory electrical connection located between the atria and the ventricles (distinct and separate from the AV node–His–Purkinje system) and which is capable of atrioventricular (antegrade) or ventriculoatrial (retrograde) electrical conduction (or both). This pathway, together with the AV node–His–Purkinje system and the atrial and ventricular myocardia, forms a macro-re-entrant circuit which enables AVRT to occur.
Atrial fibrillation
Authors: Jones Michael , Qureshi Norman , Rajappan Kim
Published: August 2018

Atrial fibrillation is a tachycardia arising in the atria, with atrial electrical activity occurring chaotically and continuously, without any effective atrial contraction occurring. The effects of this are an irregular ventricular rate, loss of the atrial contribution to ventricular filling, and the pooling of blood in the atria, thus increasing the risk of thrombus formation. The ventricular rate may be fast, slow, or of normal speed, depending on the state of the patient’s atrioventricular conduction. Atrial fibrillation is classified as paroxysmal (self-terminating within 7 days), persistent (lasting longer than 1 week, or requiring cardioversion to terminate) or permanent (cardioversion unable to terminate durably to sinus rhythm).
Atrial flutter
Authors: Jones Michael , Qureshi Norman , Rajappan Kim
Published: August 2018

Atrial flutter is the term given to one of the four types of supraventricular tachycardia; in it, atrial activation occurs as a consequence of a continuous ‘short circuit’: a defined and fixed anatomical route, resulting in a fairly uniform atrial rate, and uniform atrial flutter waves on the ECG. The ventricles are not a part of this arrhythmia circuit, and ventricular activation is variable, dependent on atrioventricular (AV) nodal conduction. Given that the atrial rate is essentially uniform (e.g. 300 min−1), ventricular activation tends to be regular (i.e. 150 min−1, 100 min−1, 75 min−1, etc., if the atrial rate is 300 mins−1), or regularly irregular if changes are occurring in the fraction of conducted impulses to the ventricles. When AV nodal conduction permits only 4:1 conduction or less, atrial flutter is usually obvious, but when ventricular rates are higher (150 min−1 or more) the flutter waves can be obscured by the QRS complexes, making diagnosis more difficult. Atrial flutter is of two types, typical and atypical. Typical atrial flutter is a right atrial tachycardia, with electrical activation proceeding around the tricuspid valve annulus. This arrhythmia is dependent on a zone of slow electrical conduction through the cavotricuspid isthmus (the tissue lying between the origin of the inferior vena cava and the posterior tricuspid valve). The resulting circuit can be either anticlockwise (activation proceeds up the inter-atrial septum, across the atrial roof, down the free wall, and then through the cavotricuspid isthmus to the basal septum) or clockwise (down the inter-atrial septum and around the circuit in the opposite direction). Anticlockwise typical atrial flutter is more common. Atypical atrial flutter refers to all other atrial flutters, and this includes other right atrial flutters (e.g. pericristal flutter), left atrial flutters, post-ablation or post-surgical flutters, and pulmonary vein flutters. The feature common to all types of flutter and which differentiates flutter from other types of supraventricular tachycardia is the presence of a macro-re-entrant anatomical circuit around which the electrical impulse travels continuously and repeatedly, thereby generating the flutter. Even though typical atrial flutter has a fairly obvious and specific appearance on the ECG, atypical flutters do not, and often it is only possible to differentiate atypical flutter from atrial tachycardias by invasive electrophysiology studies, as the ECG alone may be insufficient.
Ventricular tachyarrhythmias: Ventricular tachycardia and ventricular fibrillation
Authors: Jones Michael , Qureshi Norman , Rajappan Kim
Published: August 2018

Ventricular tachyarrhythmias are abnormal patterns of electrical activity arising from the ventricular tissue (myocardium and conduction tissue). Ventricular tachycardia (VT) is an abnormal rapid heart rhythm originating from the ventricles. The rhythm may arise from the ventricular myocardium and/or from the distal conduction system. The normal heart rate is usually regular, between 60 and 100 bpm, and there is synchronized atrial and ventricular contraction. In VT, the ventricles contract at a rate greater than 120 bpm and typically from 150 to 300 bpm, and are no longer coordinated with the atria. There is still organized contraction of the ventricles in VT, with discrete QRS complexes. It is a potentially life-threatening arrhythmia, with the risk of degenerating into ventricular fibrillation and resulting in sudden cardiac death. It is characterized by a broad-complex tachycardia on ECG.
Bradyarrhythmias
Authors: Rajappan Kim
Published: August 2018

A bradyarrhythmia is defined as a rhythm disturbance that results in a heart rate of less than 60 bpm. It is important to note that many healthy people have a resting heart rate that is less than 60 bpm, most commonly due to sinus bradycardia (i.e. a rhythm arising from the sinus node but with a ventricular rate less than 60 bpm). Other forms of bradyarrhythmia are sinus node disease, sick sinus syndrome, first-degree atrioventricular (AV) block, second-degree AV block (which can be characterized as Möbitz type I (Wenckebach phenomenon) or Möbitz type II), and third-degree AV block (also known as complete heart block). This chapter discusses the bradyarrhythmias, focusing on their etiology, symptoms, demographics, diagnosis, prognosis, and treatment.
Sudden cardiac death
Authors: Qureshi Norman , Rajappan Kim
Published: August 2018

Sudden cardiac death (SCD) is defined as unexpected death due to a cardiac disease, in a patient with or without known cardiac disease and which occurs within 1 hour from the appearance of the first clinical symptoms. The sudden cessation of cardiac activity leads to haemodynamic collapse, typically due to sustained ventricular tachyarrhythmias. The event is described as an aborted SCD (or sudden cardiac arrest) when an intervention (e.g. defibrillation) or spontaneous reversion restores circulation. The lack of uniformity with this definition complicates SCD statistics. By convention, the use of SCD to describe both fatal and non-fatal cardiac arrests persists. SCD continues to be a leading cause of death in Western countries, and accounts for 15%–20% of all natural deaths in adults in the US and Western Europe, and up to 50% of all cardiovascular deaths. In the US, estimates of SCDs from retrospective death certificate analyses range from 300 000 to 350 000 annually, giving an incidence of 0.1%–0.2% per year amongst the population above the age of 35 years. Event rates are said to be similar in Europe, although worldwide incidence is difficult to estimate and varies in accordance to the prevalence of CHD. The incidence of SCD increases with age and underlying cardiac disease. There is also a male preponderance, with men 2–3 times more likely to experience SCD than women, and this reflects the higher incidence of CHD in men.
Cardiac device therapy
Authors: Rajappan Kim
Published: August 2018

The term ‘device therapy’ is used in cardiology to refer to three different types of implantable cardiac-rhythm-management devices: pacemakers, implantable cardioverter defibrillators (also known as ICDs), and cardiac resynchronization therapy devices (also known as CRT devices). There has been a steady increase in the number of patients receiving these cardiac devices; in relation to CRT devices, the increase has been almost exponential.
Drug-induced cardiovascular disease
Authors: Loke Yoon
Published: August 2018

Many drugs can cause or exacerbate cardiovascular disease, and clinicians should be vigilant when prescribing potentially cardiotoxic medication to patients at risk, so that preventive measures and close monitoring can be implemented. Conversely, the possibility of drug-related disease should always be considered in patients with cardiovascular symptoms, so that culprit drugs can be identified and alternative therapies considered.
Psychological management of coronary heart disease
Authors: Morris Rhiain
Published: August 2018

Both anxiety and depression have been found to increase the risk of developing coronary heart disease (CHD) and lead to exacerbation of cardiac symptoms, with the latter subsequently impacting recovery/rehabilitation (e.g. leading to an increased number of readmissions to hospital, and an increased mortality risk following myocardial infarction (MI)). This may be due to pathophysiologic effects, such as vascular inflammation and autonomic dysfunction, and poor lifestyle/behavioural patterns, including non-attendance at cardiac rehabilitation classes; and/or poor treatment adherence. Psychosocial factors such as stress, hostility, social isolation, socio-economic status, and psychological defensiveness can also affect the course of cardiac illness.
Treatment of terminal cardiovascular disease
Authors: Riley Dave
Published: August 2018

This chapter is an introduction to the key components of the palliative treatment of terminal cardiovascular disease. While definitions of the term ‘terminal’ may vary, a person who may die within 6–12 months could be considered to be approaching the terminal stage of their illness, while those expected to die within a number of days or hours would be considered to be at the terminal stage. Either situation is a valid time to implement palliative treatment, but considering end-of-life care earlier provides opportunities that may otherwise be missed.
Normal respiratory function
Authors: Nasimudeen Abdul
Published: August 2018

Respiration has two components: external respiration, which enables the absorption of O2 and the removal of CO2, and internal respiration, which enables the utilization of O2 and production of CO2 and mediates gas exchange between the cells and their fluid medium. This chapter addresses the mechanics of respiration; gas exchange in the lungs; the pulmonary circulation; lung defence mechanisms; and the metabolic and endocrine functions of the lungs.
Diagnosis in suspected respiratory disease
Authors: Bonnington James
Published: August 2018

When there is suspicion of respiratory pathology, the clinician’s role is to obtain a diagnosis accurately and, where possible, swiftly while subjecting the patient to the minimum of anxiety and invasive or potentially harmful tests. It is not only in rapidly progressive disease and malignancy where speed is of the essence. Potentially reversible airways disease often becomes irreversible once established and conditions that erode into lung reserve lead to increasing levels of disability if unchecked. Furthermore, in the case of respiratory-borne infections, there may be a public health risk.
Upper respiratory tract infections, including influenza
Authors: Newton Pippa
Published: August 2018

Infections of the nasal cavity, sinuses, pharynx, epiglottis, and larynx are termed upper respiratory tracts infections. These include acute coryza, pertussis, sinusitis, pharyngitis, tonsillitis, epiglottitis, laryngitis, laryngotracheobronchitis, and influenza. Rhinoviruses and coronaviruses account for the majority of acute coryzal illnesses. Acute sinusitis (<4 weeks duration) is also usually viral in origin. About 70% of pharyngitis and tonsillitis cases are viral in etiology. Haemophilus influenzae (Type B) is responsible for most cases of epiglottitis. Acute laryngitis and laryngotracheobronchitis are usually caused by human parainfluenza viruses. This chapter focuses on upper respiratory tract infections, including their etiology, symptoms, demographics, natural history, complications, diagnosis, prognosis, and treatment.
Pneumonia
Authors: Newton Pippa
Published: August 2018

Pneumonia is defined as acute infection of the pulmonary parenchyma, presenting with consistent symptoms and signs and associated with new radiographic shadowing. It may be acute or chronic in onset and involve either one area of a lung (e.g. lobar pneumonia) or be multifocal in nature. It may be community acquired or hospital acquired. Community- acquired pneumonia is defined as pneumonia occurring in an individual with no recent contact with a healthcare setting, or in a patient admitted to hospital with development of symptoms and/or signs of pneumonia within 48 hours of admission. Hospital-acquired pneumonia or nosocomial pneumonia occurs when a patient develops symptoms or signs of pneumonia after 48 hours of admission to a healthcare setting or in the context of a long-term nursing home resident. A subtype of nosocomial pneumonia is ventilator-associated pneumonia, defined as pneumonia occurring at least 48–72 hours post intubation.
Pneumothorax
Authors: Khalid Saifudin , Bright-Thomas Rowland J. , Grundy Seamus
Published: August 2018

Pneumothorax is defined as the presence of air within the pleural space. Pneumothoraces are divided into spontaneous and traumatic categories, depending on the presence or absence of preceding trauma. Spontaneous pneumothoraces are subclassified as primary or secondary: a primary spontaneous pneumothorax (PSP) occurs in a person without underlying lung disease, whereas a secondary spontaneous pneumothorax (SSP) takes place in a person who has an underlying lung condition such as COPD or asthma. Tension pneumothorax is a medical emergency where air entering the pleural space on inspiration is unable to escape on expiration, causing mediastinal shift and cardiovascular compromise.
Cystic fibrosis
Authors: Bright-Thomas Rowland J. , Jones Andrew M.
Published: August 2018

Cystic fibrosis is the most common lethal autosomal recessive disorder in Caucasians. There is no known survival advantage of the heterozygote carrier state. Chronic progressive pulmonary infection and bronchiectasis are the major causes of morbidity and mortality. The disease affects all ductal systems where the basic defect is manifest, including the pancreas, gastrointestinal tract, sinuses, hepatobiliary system, and male reproductive system, and has significant effects on nutrition and growth.
Asthma
Authors: Jeffrey Andrew , Nasimudeen Abdul , Agbetile Joshua
Published: August 2018

Asthma is a disorder of airway smooth muscle and airway inflammation, manifested by variable airflow limitation. This definition continues to be refined in light of developments in the understanding of asthma’s pathophysiology, immunology, and treatment.
Chronic obstructive pulmonary disease
Authors: Davey Patrick , Gonem Sherif , Siddiqui Salman , Sprigings David
Published: August 2018

The Global Initiative for Chronic Lung Disease (GOLD) states that ‘chronic obstructive pulmonary disease (COPD), a common preventable and treatable disease, is characterised by persistent airflow limitation that is usually progressive and is associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles and gases. Exacerbations and comorbidities contribute to the overall severity in individual patients.’
Obstructive sleep apnoea
Authors: Craig Sonya , West Sophie
Published: August 2018

Obstructive sleep apnoea (OSA) is caused by the repetitive closure of the pharynx during sleep, leading to sleep fragmentation and, often, daytime somnolence. Traditionally, it is defined as either the number of apnoeas (complete cessation of breathing for longer than 10 seconds) or hyponoeas (reduction in air flow by >50%) per hour in an overnight sleep study. However, it must be remembered that this definition is arbitrary, and OSA is better viewed as a spectrum with trivial snoring at one end and severe, almost continuous obstruction at the other. In addition to the sleep-study findings, if the patient is sleepy during the day, as defined by the Epworth Sleepiness Scale, then this condition is termed ‘obstructive sleep apnoea syndrome’. This distinction is important, as patients with this syndrome usually warrant treatment.
Bronchiectasis
Authors: Jones Andrew M. , Bright-Thomas Rowland J.
Published: August 2018

Bronchiectasis may be defined clinically as the chronic daily production of copious mucopurulent sputum. Pathologically, the disease is characterized by inflamed, thick-walled, dilated bronchi. Bronchiectasis has many potential underlying causes and associations with other diseases but in individual cases the underlying cause is often unknown. The typical symptom is cough with sputum. Bronchiectasis is a chronic condition; systemic complications are common and include tiredness, malaise, and weight loss. The aim of therapy should be to control symptoms, prevent complications and disease progression, while minimizing treatment burden. This chapter discusses bronchiectasis, including its etiology, symptoms, demographics, natural history, complications, diagnosis, prognosis, and treatment.
Sarcoidosis and other granulomatous lung disease
Authors: Crawshaw Anjali
Published: August 2018

Sarcoidosis is a multisystem disorder characterized by the formation of non-caseating granulomas in many tissues. A granuloma is an organized aggregate of immune cells; it forms in response to an antigenic stimulus. It contains abnormal macrophages (epithelioid histiocytes, which often fuse to form multinucleated giant cells), lymphocytes, neutrophils, eosinophils, fibroblasts, and collagen.
Interstitial lung disease
Authors: Davey Patrick , Gonem Sherif , Sprigings David
Published: August 2018

The interstitial lung diseases, also known as the diffuse or diffuse parenchymal lung diseases, are a broad group of pulmonary disorders which mainly affect the lung parenchyma as opposed to the airways. By convention, infectious and malignant conditions are excluded from this definition. Thus, the interstitial lung diseases comprise a group of conditions characterized by variable degrees of inflammation and fibrosis, centred on the lung interstitium and alveolar airspaces.
Lung cancer (including management of an isolated lung lesion)
Authors: Verma Raman , Deacon Sarah
Published: August 2018

Lung cancer is the second most common type of cancer in the UK. It is termed ‘primary’ if it originates in the lungs. and ‘secondary’ if it manifests elsewhere in the body but then spreads to the lungs. The main types of primary lung cancer are small cell lung carcinoma and non-small cell lung carcinoma. Bronchial carcinoids account for up to 5% of lung cancer. These are generally small when diagnosed and occur most commonly in people under 40 years of age. Unrelated to cigarette smoking, carcinoid tumours can metastasize and a small proportion of these tumours secrete hormone-like substances that may cause specific symptoms related to the hormone being produced. Carcinoids generally grow and spread more slowly than bronchogenic cancers, and many are detected early enough to be amenable to surgical resection. Mesothelioma is a rare type of cancer that affects the pleura.
Occupational lung disease
Authors: Cullinan Paul , Szram Joanna
Published: August 2018

Some occupational lung diseases are defined by their clinical or pathological nature (e.g. occupational asthma or mesothelioma), while others are defined by their specific etiology (e.g. silicosis, farmer’s lung). Most fall into one of three categories. The first is airways disease, including occupational asthma (induced by a workplace agent), work-exacerbated asthma (preexisting asthma provoked by one or more agents at work), and irritant-induced asthma (initiated by a single, toxic exposure to a respiratory irritant); COPD and obliterative bronchiolitis may arise from workplace exposures, and around 10% of lung cancers have an occupational etiology. The second is parenchymal diseases, incorporating the many types of pneumoconiosis, differentiated by the dust that caused them, and the many types of extrinsic allergic alveolitis (or hypersensitivity pneumonia) categorized by the occupations in which they arise. The third is pleural diseases comprising pleural plaques, diffuse pleural thickening, and mesothelioma.
Pleural infection and malignancy
Authors: Grundy Seamus
Published: August 2018

Pleural infection transitions from simple parapneumonic effusion, to complex parapneumonic effusion, to empyema. Primary empyema occurs without an underlying pneumonic process. Pleural infection commonly presents identically to pneumonia with dyspnoea, purulent sputum, and fevers. It may be associated with pleuritic chest pain. Empyema can cause systemic sepsis, leading to cardiovascular instability and multi-organ failure. A malignant pleural effusion arises when malignant cells infiltrate the pleura, resulting in increased production and decreased lymphatic drainage of pleural fluid. Malignant pleural effusions are either metastatic or primary mesothelioma. This chapter discusses pleural infection, malignant pleural effusion, and mesothelioma, focusing on etiology, symptoms, demographics, diagnosis, prognosis, and treatment.
Drug-induced lung disease
Authors: Siddiqui Salman , Desai Dhananjay
Published: August 2018

Pulmonary drug toxicity is being increasingly recognized as a cause of various forms of lung disease. The spectrum of disease can range from transient, minor reactions to rapidly progressive disease with fatal consequences. A large number of drugs are linked to pulmonary disease; however, causality is often difficult to establish, because the length of the latency period between exposure and the onset of disease can vary and because there can be discordance between symptom development and the appearance of radiological changes, which may not be present at all (e.g. angiotensin-converting enzyme inhibitors can cause cough-related airways disease in the absence of radiological change).
Psychology in respiratory disease, including dysfunctional breathing
Authors: Jeffrey Andrew
Published: August 2018

The real burden to any sufferer of respiratory disease is shown in the human suffering of the individual. It is increasingly understood that there is a link between the psychological aspects of respiratory disease and morbidity and that patients’ attitudes to illness can affect their ways of coping and, indeed, impact upon their compliance with treatment. Breathlessness is a symptom of many psychological states, both positive and negative; indeed, it is embedded within the English language: ‘It took my breath away! I was breathless with anticipation!’ An understanding of the links between psychological factors and physical symptoms and behaviours is essential to achieve the best possible outcomes for many patients.
Terminal care in respiratory illness
Authors: Scadding Alys
Published: August 2018

The terminal phase is the period of time between living with a reasonable quality of life, and the process of dying. While lung cancer and pulmonary fibrosis have the potential to deteriorate rapidly, the majority of lung diseases worsen over years. Every exacerbation of the condition leads to a decline in both lung function and performance status, and often the pre-exacerbation level of functioning is never regained. There is not a defining point to indicate whether a patient is entering the terminal stages of their illness, but practice shows that the following signs are suggestive: increasing breathlessness and thus becoming increasingly housebound; increasing oxygen requirements; declining pulmonary function test results; increasingly frequent exacerbations requiring hospital admission and/or non-invasive ventilation; developing cor pulmonale; weight loss and difficulty maintaining weight; anxiety and depression; if the death of the patient within the next year would not be a surprise.
Critical illness
Authors: Wise Matt , Frost Paul
Published: August 2018

Critical illness can be considered to be any disease process which causes physiological instability that leads to disability or death within minutes or hours. Fortunately, physiological instability associated with critical illness is easily detected by perturbations of simple clinical observations such as blood pressure, heart rate, respiratory rate, oxygen saturations, level of consciousness, and urine output. Individual abnormalities in these observations are sensitive for the presence of critical illness but non-specific. Specificity for critical illness improves as the number of abnormal clinical observations increases. Over recent years, a greater appreciation of the importance of deviations in simple clinical observations as a method of detecting critical illness has led to the development of a number of ‘early warning’ or ‘track and trigger’ systems. These systems attribute a score according to the magnitude and number of abnormal observations that are present, and a high score prompts immediate medical review. Although intuitively sensible, the evidence that these systems are effective in ameliorating or preventing critical illness is currently lacking. This chapter looks at the approach to diagnosis of critical illness, including the pitfalls in diagnosis.
Role of the intensive care unit
Authors: Wise Matt , Frost Paul
Published: August 2018

The intensive care unit (ICU) can be defined as an area reserved for patients with potential or established organ failure and has the facilities for the diagnosis, prevention, and treatment of multi-organ failure. Usually, the ICU is located in close proximity to A & E, the radiology department, and the operating theatres, as it is between these areas that patient flows are greatest. In large urban hospitals, there may be more than one ICU, some of which serve specific patient populations, such as paediatrics, neurosurgery, cardiothoracic surgery, liver failure, and burns. Many hospitals also have high-dependency units (HDUs) that offer higher nurse-to-patient ratios and more advanced monitoring than a general wards does, as well as limited organ support. In the UK, the distinctions between ICU, HDU, and general ward have been abandoned in favour of a classification based on the patient’s needs rather than their location.
ICU treatment of cardiovascular failure
Authors: Wise Matt , Frost Paul
Published: August 2018

Cardiovascular failure or shock is best defined as inadequate delivery or utilization of oxygen for cellular metabolic needs. The majority of shock states are characterized by limitations in perfusion rather than extraction of oxygen by tissues. It is important to recognize that ineffectual tissue perfusion may occur in the absence of hypotension and, therefore, a normal blood pressure does not exclude shock. This chapter covers the etiology of shock, as well as symptoms, complications, diagnosis, prognosis, and treatment.
ICU treatment of acute kidney injury
Authors: Wise Matt , Frost Paul
Published: August 2018

Traditionally, the etiology of acute kidney injury (AKI) is considered in terms of prerenal, renal, and obstructive causes. However, this categorization is less useful in the ICU, where the etiology of AKI is usually multifactorial and often occurs in the context of multi-organ failure. Hypotension, nephrotoxic drugs, and severe sepsis or septic shock are the most important identifiable factors. Less frequently encountered causes include pancreatitis, abdominal compartment syndrome, and rhabdomyolysis. Primary intrinsic renal disease such as glomerulonephritis is extremely uncommon. A previous history of cirrhosis, cardiac failure, or haematological malignancy, and age >65 years, are important risk factors. This chapter covers symptoms, complications, diagnosis, investigations, prognosis, and treatment of renal failure in the ITU.
ICU treatment of sepsis and septic shock
Authors: Wise Matt , Frost Paul
Published: August 2018

Bacteria are the most frequent causes of severe sepsis and septic shock, while viruses, fungi, and parasites are implicated less often. Positive cultures are found in only 60% of cases; this may be the result of previous antibiotic therapy or inadequate sampling or testing. The etiology of sepsis is constantly changing; whereas Gram-negative organisms used to make up the majority of cases, Gram-positive bacteria now predominate. Sepsis due to fungal disease has also seen a dramatic rise. These changes may be explained by alterations in patient demographics, such as an increasingly elderly population with multiple comorbidities; an increased frequency of indwelling catheters or devices; and greater numbers of patients with immunosuppression as a result of disease or drug therapy. This chapter covers symptoms, demographics, diagnosis, investigation, prognosis, and treatment within the ITU environment.
Terminal care in the intensive care unit
Authors: Wise Matt , Frost Paul
Published: August 2018

In the UK, around 10%–20% of all patients admitted to the intensive care unit (ICU) do not survive while, in the United States, it has been estimated that 22% of all deaths occur in an ICU. Therefore, terminal or palliative care is as important as any of the life-saving interventions that occur in the ICU. The goal of palliative care is to achieve a good death. In the ICU, the switch from care with curative intent to palliation occurs when it becomes obvious that the patient is not responding to treatment. Typically, this is manifest by deteriorating physiology and escalating organ support in the setting of overwhelming disease or injury. It is predominantly expert opinion (consensus amongst treating medical and nursing teams) that determines the point at which the patient is recognized as not responding to treatment and, in fact, dying. This chapter covers the ethical considerations, communication, family disagreement, organ donation, withdrawal of therapies, care after death, and diagnosing death.
Brain death
Authors: Wise Matt , Frost Paul
Published: August 2018

Mechanical ventilation has made it possible for the heart to continue to beat and perfuse other organs even when the brain is dead. This means that death can be diagnosed in two distinct ways: first, in the traditional manner, as permanent cessation of cardiorespiratory function; and, second, while the patient is ventilated, as brain death (BD). In 1976 the Conference of Medical Royal Colleges and their Faculties in the United Kingdom, in a statement on the diagnosis of BD, recognized the brainstem as the centre of brain activity, without which life was not possible. Brainstem death (BSD) occurs when there is complete, irreversible loss of brainstem function, that is, irreversible loss of the capacity for consciousness, coupled with irreversible loss of the capacity to breathe. In the UK, the terms BD and BSD are used interchangeably and are legally synonymous with somatic death. This chapter covers examination for BSD, complications, diagnosis, investigation, and actions arising after BSD, as well as a definition of BD.
Normal renal function
Authors: Chakera Aron , Herrington William G. , O’Callaghan Christopher A.
Published: August 2018

The kidney is a vital organ with multiple functions. Without kidney function, death will occur in a matter of days. Fortunately, several forms of effective renal replacement therapy are available. This chapter gives a concise introduction to basic urinary tract structure, kidney/glomerulus/tubular function and assessment of kidney function.
Diagnosis in suspected renal disease
Authors: Herrington William G. , Chakera Aron , O’Callaghan Christopher A.
Published: August 2018

Renal dysfunction can be easily and, in most cases, unambiguously diagnosed from an elevation in serum creatinine and/or abnormal urinalysis. The clinical challenges lie in first suspecting that renal dysfunction is present and therefore requesting the appropriate test (e.g. serum creatinine/urine analysis), and then identifying the underlying etiology. A major clue to renal dysfunction in the hospitalized patient can be a reduction in urine output. Therefore, urine output should be carefully monitored in those patients who are at risk, which includes most significantly ill hospitalized patients.
Investigation in renal disease
Authors: Herrington William G. , Chakera Aron , O’Callaghan Christopher A.
Published: August 2018

Renal physicians use a combination of tests to diagnose and monitor renal disease. These include urine, blood, and imaging investigations. This chapter looks at the main diagnostic tests and imaging that are routinely used, and describes their use in the primary and secondary care environment.
Urinary tract infection
Authors: Herrington William G. , Chakera Aron , O’Callaghan Christopher A.
Published: August 2018

A urinary tract infection (UTI) is defined as present when urine culture results in the growth of a single organism at greater than 105 colony-forming units/ml of urine. Bowel flora are the commonest cause of UTIs. Escherichia coli accounts for 80% of infections. Klebsiella spp., Proteus mirabilis, Enterococcus faecalis, and Staphylococcal saprophyticus account for most of the remaining 20%. Staphylcoccus aureus culture is usually catheter related or secondary to haematogenous spread. This chapter looks at the symptoms of a UTI, as well as its demographics, complications, diagnosis (including investigations), and treatment. It also discusses prognosis.
Glomerulonephritis
Authors: Herrington William G. , Chakera Aron , O’Callaghan Christopher A.
Published: August 2018

Glomerulonephritis (GN) is inflammation of the glomerulus. It can be caused by many different underlying conditions and can present in a range of ways. The key features, however, are evidence of renal dysfunction (clinical and investigative) with associated glomerular disease—the latter is often initially suspected from urine dipstick examination (Chapter 157), and may then be confirmed by a renal biopsy. This chapter looks at the etiology of GN, as well as its symptoms, clinical features, demographics, complications, diagnosis, and treatment.
Interstitial renal disease
Authors: Herrington William G. , Chakera Aron , O’Callaghan Christopher A.
Published: August 2018

Tubulointerstitial renal diseases affect the renal tubules and/or the supporting interstitial tissue around them. The glomeruli are typically spared in early disease. Acute interstitial nephritis is characterized by an inflammatory infiltrate (often containing eosinophils). Chronic tubulointerstitial nephritis (TIN) is characterized by extensive tubular atrophy and interstitial fibrosis. The processes are clinically distinct but a prolonged acute interstitial nephritis will develop into chronic disease. This chapter looks at the etiology of interstitial renal disease, as well as its symptoms and clinical features, demographics, complications, diagnosis, and treatment.
Nephrotic syndrome
Authors: Herrington William G. , Chakera Aron , O’Callaghan Christopher A.
Published: August 2018

Nephrotic syndrome is a clinical syndrome of heavy proteinuria (greater than 3.5 g per 24 hours), oedema, and hypoalbuminaemia, which is associated with hyperlipidaemia and a procoagulant state. Causes of nephrotic syndrome are traditionally classified by their histopathological descriptions. In most cases, the histological picture can have a primary (idiopathic) or secondary cause. Minimal change, membranous nephropathy, and focal segmental glomerulosclerosis account for over 60% of cases. Diabetic nephropathy and renal amyloidosis are common secondary causes of nephrotic syndrome. Nephrotic-range proteinuria will show up as at least 3+ protein on urinalysis. The diagnosis is confirmed by a urinary protein-to-creatinine ratio over 300 mg/mmol, and hypalbuminaemia. In adults, renal biopsy is the diagnostic test. This chapter addresses the causes, diagnosis, and management of nephrotic syndrome in adults.
Acute kidney injury
Authors: Chakera Aron , Herrington William G. , O’Callaghan Christopher A.
Published: August 2018

Acute renal failure (also referred to as acute kidney injury) refers to a rapid decrease in renal function; it is reflected by an increase in blood urea and creatinine and is often associated with oliguria (a urine volume of less than 400 ml/24 hours). It usually develops over days to weeks. Acute kidney injury has been variously classified, but the current classifications are based on the glomerular filtration rate (or creatinine), looking at changes from baseline, and the presence of oliguria or anuria. The potential etiologies of acute kidney injury are usually considered anatomically under the headings prerenal, renal (intrinsic), and postrenal. This chapter looks at the etiology, symptoms, clinical features, demographics, complications, diagnosis, and treatment of acute kidney injury.
Chronic kidney disease
Authors: Herrington William G. , Chakera Aron , O’Callaghan Christopher A.
Published: August 2018

Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function, where the abnormalities have been present for >3 months and have implications for health. It is characterized by a reduced estimated glomerular filtration rate (eGFR) or other renal abnormalities. CKD is staged according to the eGFR or the degree of albuminuria. The KDIGO (Kidney Disease: Improving Global Outcomes) criteria for CKD is either an eGFR that is <60 ml/min 1.73 m−2 and has been present for >3 months, or one or more markers of kidney damage, when these have been present for >3 months.
Diabetic renal disease
Authors: Herrington William G. , Chakera Aron , O’Callaghan Christopher A.
Published: August 2018

Diabetic nephropathy is kidney damage occurring as a result of diabetes mellitus. Overt diabetic nephropathy is defined as proteinuria greater than 0.5 g/day. Diabetic nephropathy has a complicated pathogenesis including glomerular hypertension with hyperfiltration and advanced glycation end products. Poor glycaemic control is associated with progression to microalbuminuria and overt diabetic nephropathy. The lifetime risk is fairly equivalent for type 1 and type 2 diabetes mellitus. Early disease is usually asymptomatic. Hyperglycaemia causes an osmotic diuresis and, thus, diabetes can present with polyuria. Hypertension develops with microalbuminuria; oedema indicates abnormal sodium and water retention and, occasionally, the development of nephrotic syndrome. Patients with diabetes, perhaps due to accompanying cardiac disease, are particularly susceptible to fluid overload and uraemic symptoms. End-stage renal disease can occur as early as when the estimated glomerular filtration rate is 15 ml/min 1.73 m−2.
Renal calculi
Authors: Herrington William G. , Chakera Aron , O’Callaghan Christopher A.
Published: August 2018

Nephrolithiasis is the presence of kidney stones, which are also known as ‘renal calculi’. Renal calculi arise when urine becomes supersaturated with insoluble components. This may occur when there is excessive production of these components, a decrease in factors maintaining their solubility (e.g. citrate), or a reduction in urine volume (leading to increased concentration). Infection may play a significant role in the initiation of renal calculus formation, by creating a nidus for further crystal growth. Renal calculi are usually classified into two categories: those containing calcium (80%), and non-calcareous calculi (20%).
Renal and bladder cancer
Authors: Chapman Hannah , Elwell Christine
Published: August 2018

This chapter addresses the diagnosis and management of bladder and renal cancers. In the UK, bladder cancer is the fourth most common cancer in men, and the eighth most common cancer in women. Bladder cancer arises from the bladder urothelium, and is typically a papillary transitional cell carcinoma. Chronic infection with the parasite Schistosoma haematobium is associated with squamous cell carcinoma of the bladder, and is most prevalent in Egypt and sub-Saharan Africa. Renal cancer accounts for 3% of cancers in adults in the UK and, in most cases, is a renal cell carcinoma arising from proximal renal tubule epithelium. A further 5%–10% of renal cancers are transitional cell (urothelial) carcinomas of the renal pelvis. Benign kidney tumours, such as cysts, are also common.
Inherited renal diseases
Authors: Herrington William G. , Chakera Aron , O’Callaghan Christopher A.
Published: August 2018

The causes of inherited renal diseases can be divided into cystic, glomerular, tubular, and systemic diseases. By far, the most common of these in clinical practice is adult polycystic kidney disease (APKD). This chapter reviews APKD, other inherited cystic renal diseases, inherited glomerular and tubular diseases, and inherited systemic diseases with renal involvement.
The kidney in systemic disease
Authors: Herrington William G. , Chakera Aron , O’Callaghan Christopher A.
Published: August 2018

Many systemic diseases can affect the kidney, including autoimmune conditions, malignancies, infections, and vascular diseases. Autoimmune conditions can cause inflammation of the glomeruli or tubules, or deposition of inflammatory proteins (AA amyloidosis). Malignancy can cause infiltration of normal renal tissue, immunoglobulin deposition in the renal vessels, glomeruli or tubules, or paraneoplastic renal dysfunction as occurs in secondary focal segmental glomerulosclerosis. Infections can cause inflammation in glomeruli, in association with immune complex deposition. Vascular disease and vasculitis reduce kidney blood supply and cause renal ischaemia. This chapter provides an overview of these diseases.