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Where God's invitation to eat his flesh raises unexpected problems. What do we do with spiders and mice and where in the digestive system does the Eucharist turn back into flour and wine before things get really nasty.

This chapter examines how the cult of martyrs and saints promoted ideal responses to corporeal affliction. It examines the purging miracles recorded at the shrine of St. Martin of Tours, where health-giving violence experienced by the body in vomiting and intestinal purging was viewed as a template for divine power to purge the soul of sin. The chapter focuses on the purgatorial theology of Gregory of Tours, which identified the potion made of dust and water obtained at the tomb of St. Martin as a “celestial purgative.” It examines Gregory’s personal fears about his fate on judgement day.

This chapter notes that children with HIV/AIDS or cancer are very prone to mouth problems, particularly those who are malnourished. One of the most common causes of vomiting in children's palliative care is doctors' prescribing. While GI bleeding is very frightening for all concerned, one must anticipate and prepare for it, but not panic. It is quite rare for a child to bleed to death from a GI bleed. Meanwhile, diarrhoea is very common in children with HIV/AIDS and is the most common cause of illness and death during the first year of life.

Nausea and vomiting are reported to occur in up to 62% of terminally ill patients, with 40% experiencing these symptoms in the last six weeks of life. Most of the existing research on antiemetics involves chemotherapy-induced or radiation-induced nausea and vomiting and may not be relevant to the treatment of symptoms resulting from advanced disease. Prospective studies with symptomatology documented at entrance to a palliative care program or hospice care and careful reporting of symptoms and treatment thereafter are needed. There are numerous problems inherent in the study of people with advanced disease. Such patients have a myriad of symptoms interacting with each other and each requiring treatment. Treating one symptom may exacerbate or improve another or cause entirely new problems. Determining whether improvement or exacerbation is part of the disease process, the treatment, or another emerging problem is often very difficult.

This chapter contains a case study to display the desired skills, attitudes, and expertise required to manage nausea and vomiting in cancer patients. It considers several questions such as: What are the more common causes of nausea and vomiting in palliative care patients? How to decide on the appropriate treatment for the patient's nausea? Which anti-emetic to choose for the patient? How to manage the patient's hypercalcaemia of malignancy?

This chapter builds on a basic understanding of the central nervous system (CNS) as coordinator of regional gastrointestinal (GI) tract reflexes. The dorsal vagal complex in the CNS permissively governs the largely autonomous control by the enteric nervous system (ENS) of functions such as absorption, secretion and motility. The CNS actively coordinates voluntary and autonomic communication for complex behavioral functions, such as swallowing, emesis and defecation. The CNS and ENS communicate with inflammatory cells, endocrine cells and microbiota to maintain GI homeostasis and their dysfunction can give rise to clinical disorders. For example, stress or enteritis may predispose individuals to Irritable Bowel Syndrome in which altered bowel function is accompanied by visceral pain. Neural modulation of immune cells and release of inflammatory mediators may contribute to Inflammatory Bowel Diseases. Thus, the bi-directional brain-gut axis maintains GI health and its perturbation contributes to GI disorders.

From April to December, 1839, Charles Darwin often suffered from a malaise that depressed his capacities for socialization and work. In 1840, his illness worsened in two ways. At first, he had two new symptoms: periodic vomiting and flatulence, which continued for about two months. Then in the summer and fall of 1840, when he was with Emma in Maer during the first trimester of her second pregnancy, he had a second worsening of illness. His symptoms from the end of July through most of September, as recorded in Emma's diary, comprised “great flatulence”, languor, and vomiting in the day and night, which was more frequent than it had been previously. Mental stresses from Darwin's family life and his scientific work, as well as the infection with Chagas' disease along with mental stresses were the causes of his illness. The decline in physical vigor that he observed in himself at the age of thirty-three was the result of his experiencing frequent episodes of mental and physical fatigue, along with the discomforts and pains of daily and nightly episodes of flatulence.

Charles Darwin's 1842–45 letters to his Shrewsbury family reveal how he continued to depend on his father for advice, assistance, and medical treatment. During these years, Darwin's father remained in good health and spirits. However, he had periods of illness in 1846 and 1847. This caused Darwin to have accentuations of illness and to begin to realize that “Father's death [was] drawing slowly nearer & nearer”. From July 1848 through March 1849, he suffered from attacks of “violent vomiting”, that along with shivering, trembling, and languor were associated with a “swimming” head and black spots before his eyes. The apparent causes for these attacks were feelings of grief and loss over the loss of his father, and his work of classifying barnacles, which he found arduous, frustrating, time-consuming, and of questionable value. Darwin tried Dr. James Gully's hydropathy treatment. One reason for feeling stronger and less depressed, despite still vomiting, was that the Malvern treatments had “at once relieved” him of the nocturnal obsessions that interfered with sleep. As a result of the Malvern treatments, his health and mood improved in a variety of ways.

After reading how his enemy Richard Owen had mendaciously criticized the work of his friend Hugh Falconer, Charles Darwin had feelings of “burning...indignation” that interfered with sleep, and produced an episode of eczema which took “off the epidermis a dozen times clean off”. The eczema subsided, and he had no further complaints of illness in January of that year. His wellness was then sharply broken by the onset of an illness that would become prolonged and that resulted from his disturbed feelings on reading Charles Lyell's book, The Antiquity of Man. He also continued to be ill with vomiting and weakness. His treatment regimens under Drs. James Ayerst, James Gully, William Brinton, and William Jenner are described.

Charles Darwin went on to express frustrations over Dr. William Jenner's frequent changes of medication and with treatments by other doctors. He vomited almost every day from 21 April through 1 May. He then recalled that, several months earlier, Dr. John Chapman had sent him a book that he described as being “on the cure of Sea Sickness”, which at first he had not acknowledged receiving or read. Darwin now read Dr. Chapman's book, decided to try the ice treatment, and on 16 May asked Dr. Chapman to come to Down. At first, for two days, Darwin was free of flatulence and vomiting, but during the next few days the symptoms recurred. Darwin's prolonged vomiting may have been an immediate stimulus for him to consult with Dr. Henry Bence Jones. Over the next six weeks, as he continued to follow this treatment and restrict his daily intake of food, the number of entries in Emma's diary on his illness slowly decreased. Three episodes of illness that Darwin treated by himself, aided as always by Emma, were quite different in their causations and nature.

We have arranged the differential diagnosis in order of likelihood in a man of this age with more likely diagnoses in larger font and less likely diagnoses in smaller font in Figure 12.1. Pathologies that should be excluded at the earliest possible opportunity are shown in bold. Bear in mind that this differential diagnosis refers to epigastric pain as a presentation of ‘acute abdomen’ and thus differs markedly from epigastric pain presenting as outpatient dyspepsia. Note that although we have adopted a standard approach of history, examination, and investigations over the course of the following pages, you should use clinical judgement to deviate from this path if one of the ‘must exclude’ diagnoses is suspected, or if there is a need for urgent resuscitation. For example, if a 69-year-old male diabetic patient with known unstable angina presents with exercise-induced epigastric pain, you would be wise to perform an electrocardiogram (ECG) and obtain baseline observations at the earliest opportunity. Various characteristics of the pain will help to narrow our differential diagnosis of epigastric pain: Site: • Pain that has spread from the epigastrium to involve the rest of the abdomen may suggest peritonitis from a perforated GI tract (e.g. perforated gastric ulcer, which causes epigastric pain because the stomach is embryologically a foregut structure). • Pain that has spread from the epigastrium to involve the chest may be cardiac. • Biliary disease, although anatomically located in the right upper quadrant, may present with purely epigastric symptoms. Onset: • Pain that is of very sudden onset suggests perforation of a viscus (e.g. a perforated duodenal ulcer or Boerhaave’s perforation) or myocardial infarction. • Pain from acute pancreatitis and biliary colic develops maximal intensity over 10–20 minutes. • Inflammatory processes such as acute cholecystitis or pneumonia typically take hours to reach their peak. Character: • ‘Crushing’ or ‘tightness’ qualities are typical of cardiac pathology. • Sharp, ‘burning’ pain is typical of peptic ulcers, gastritis, and duodenitis. • Deep, ‘boring’ pain is typical of pancreatitis. Radiation: • Back pain is classically associated with pancreatitis, leaking abdominal aortic aneurysms, and sometimes seen with peptic ulcers.

The vomiting centre (mainly histamine and acetylcholine receptors) in the medulla oblongata can be activated by four main input systems shown in Figure 13.1: the vestibular system, the central nervous system, the chemoreceptor trigger zone (in the fourth ventricle of the brain), and cranial nerves IX and X. With these four inputs in mind, it becomes easier to understand some of the pathologies that can activate the vomiting centre and cause nausea and vomiting, as is shown in Figure 13.2. • Contents ■ Undigested: oesophageal disorders, e.g. achalasia, pharyngeal pouch ■ Partially digested: gastric outlet obstruction, gastroparesis (delayed stomach emptying, e.g. seen in diabetes mellitus) ■ Bile (green): small bowel obstruction (distal to the ampulla of Vater) ■ Faeculent: distal intestinal or colonic obstruction. Note: the only time you will see faecal (i.e. true faeces), as opposed to faeculent (i.e. foul looking), vomiting is in patients with a gastrocolonic fistula… or coprophagia ■ Blood/coffee-ground: haematemesis (see Chapter 5) ■ Large volume: less likely to be functional. • Timing ■ Early morning: classically in pregnancy and raised intracranial pressure. ■ Duration: this is useful in identifying the severity (patients with severe nausea and vomiting present early) and a longer time course makes acute pathologies such as bowel obstruction less likely, as untreated this will either deteriorate or resolve. • Association with eating? ■ Vomiting within an hour of eating suggests an obstruction high in the gastrointestinal (GI) tract proximal to the gastric outlet. If this is the case, you should ask about peptic ulcer disease (or a history of dyspepsia) as this can cause scarring and pyloric stenosis. ■ Vomiting after a longer postprandial delay is consistent with an obstruction lower in the GI tract, usually in the small bowel. ■ Early satiety, postprandial bloating, and abdominal discomfort together suggest gastroparesis or outlet obstruction. • Use the SOCRATES mnemonic to characterize the pain (see Chapter 12). • The site is indicative of certain pathologies (e.g. right upper quadrant suggests a hepatobiliary cause, epigastric suggests a pancreatic or gastroduodenal cause). However, localization of pain is far from accurate in abdominal pathology due to the neural wiring and embryology, and also anatomical variations.

Chapter 4 discusses training for extreme acceleration and, conversely, for microgravity. Trains travelers on how to deal with emergency situations. Examines everyday situations like going to the bathroom in space.

The perioperative period can be a life-changing event for many patients, the effects of which can be lifelong for better or worse. The anaesthetist’s communication at this time can have a profound impact on the care of their patients in the matter of both short-term cooperation and long-term perceptions of their hospital experience. Induction of anaesthesia is a stressful time for many patients, young and old. There is an inevitable loss of control when the patient hands this over temporarily to the anaesthetist. In order to enhance cooperation, anaesthetists will reap unexpected benefits by avoiding the use of negative language. Well-meaning staff may, however, sabotage an otherwise smooth induction by telling patients, ‘There is nothing to worry about’ with the implicit suggestion that there is ‘something to worry about’. Unfortunately such well-meaning statements, even when directed at children, tend to yield the opposite effect of what is intended. Patient stress at this time increases suggestibility such that comments frequently function as inadvertent suggestions—be they positive or negative. This can be utilized to enhance the anaesthetist’s ability to provide a smooth, safe and stress-free induction. A typical series of pre-induction communications may go something like, … ‘Don’t worry we won’t drop you’. As the patient is transferred from a trolley to the operating table. ‘The blood pressure cuff gets really tight and may hurt and try not to move while it’s pumping up’. ‘That noise over there is just the nurse checking the drill!’… Explaining what is happening in simple straightforward non-technical language, and at the same time communicating in a positive way, is invariably the more useful approach. For example, …‘Welcome to the operating room Mr P ’. ‘You can relax as we move you to this other bed—you are quite safe’. ‘We will place some monitoring leads on so we can keep you safe and comfortable. A pulse monitor gently placed on your finger, an ECG on your chest and a blood pressure cuff on your arm. As the blood pressure cuff tightens and we take its reading this often allows patients to relax knowing how closely we are looking after them’. …

The treatment of nausea has lagged behind the treatment of chemotherapy-induced vomiting, despite its prevalence. The first recognized medicinal benefit of THC after its discovery was for chemotherapy-induced nausea and vomiting. Since the discovery of the endocannabinoid system, our understanding of the mechanisms by which cannabinoids reduce nausea and vomiting has been greatly improved. CB₁ agonists reduce nausea in preclinical models. CBD and CBDA also show promise as non-psychoactive treatments. As well treatments that boost the endogenous cannabinoid system by inhibiting the degrading enzymes FAAH (elevating AEA) and MAGL (elevating 2-AG) or both have shown promise to treat nausea in preclinical models. New research identifies the interoceptive insular cortex as a region which may regulate the experience of nausea and its amelioration by 2-AG.

Among over 60 terpeno-phenols derived from the cannabis plant, delta-9-tetrahydrocannabinol (Δ‎⁹-THC) has by far been the most studied for its potential to reduce nausea and vomiting. Indeed, the first approved medical use of Δ‎⁹-THC was for nausea and vomiting. However, the remaining compounds in the plant have received relatively less investigation. This chapter reviews recent research on the potential of the phytocannabinoids, cannabidiol (CBD), cannabidiolic acid (CBDA), tetrahydrocannabinolic acid (THCA), tetrahydrocannabivarin (THCV), cannabivarin (CBDV), and cannabigerol (CBG) to reduce nausea and vomiting in animal models. CBD and CBDA attenuate nausea and vomiting via indirect agonism of the 5-HT_1A receptor, while CBG acts as a 5-HT_1A receptor antagonist, reversing the suppressive effect of CBD on nausea and vomiting. THCA potently reduces nausea and vomiting, possibly by a CB₁ receptor mechanism of action. Finally, CBDV, as well as a high dose of THCV, also attenuate nausea. These phytocannabinoids have therapeutic potential that merits further exploration.

With the expectation that innovation, insight, and discovery will come from researching neglected topics, this chapter explores human instincts, including yawning, laughing, vocal crying, emotional tearing, coughing, nausea and vomiting, itching and scratching, and changes in scleral color. The critical change approach is exploited to analyze recently evolved, uniquely human traits (e.g., human-type laughter and speech, emotional tearing, scleral color cues) and compare them with thir primate antecendents, seeking the specific neurological, glandular, and muscular processes responsible for their genesis. Particular attention is paid to contagious behaviors, with the anticipation that they may reveal the roots of sociality and empathy. Few of these curious behaviors are traditionally considered in the context of facial expression or emotion, but they deserve recognition for what they can contribute to behavioral neuroscience and social biology.

The psychology of the experience of air and fluids leaving the body, including our attempts to control their expulsion, is explored. The air removal senses of cough, sneeze, hiccup, belch, and flatulence are all reviewed, as are the fluid removal senses of micturition, defecation, vomiting, menstruation, and ejaculation. Two people help narrate the experiences of expulsion: a comedian discusses why flatulence is funny (it reminds us of our bestiality), and a student discusses the new version of an old behavior: voluntary vomiting.