Early-morning nausea and vomiting can be commonly seen with metabolic causes. Up to 75% of cases of diabetic ketoacidosis are accompanied by nausea and vomiting. Emesis and nausea are found among as many as 90% of patients in Addisonian crisis. Uremia may be heralded by similar symptoms; nausea often improves with the correction of any associated hyponatremia, but it can be refractory. Binge drinkers experience early-morning nausea and dry heaves from excessive alcohol intake.

Early-morning nausea and vomiting are characteristic of early pregnancy, occurring in more than 50% of instances. The problem is severe in less than 1% of cases but can lead to electrolyte abnormalities, dehydration, and weight loss. Most cases are mild; symptoms begin after the first missed period and terminate by the 4th month. Women with severe cases often have a history of vomiting in response to psychosocial stress. Disturbed motility is also noted in many cases. The diagnosis of pregnancy is sometimes overlooked.

In the past, the term psychogenic vomiting was applied to patients with chronic, unexplained vomiting; however, this terminology has been largely replaced with the various functional nausea and vomiting disorders, which include idiopathic nausea, functional vomiting, cyclic vomiting syndrome (CVS), and rumination syndrome. Diagnoses are organized by the predominant symptom. CVS is characterized by discrete, limited episodes of nausea and vomiting, which occur cyclically with relatively normal intervening periods. Rumination syndrome is a rare condition, which is characterized by recurrent, effortless episodes of regurgitation with reswallowing of regurgitated material without emesis or preceding nausea or retching.

This of course is not to say that a psychological etiology of nausea and vomiting does not exist. In fact, the phenomenon of anticipatory nausea and vomiting has been documented in patients receiving multiple rounds of chemotherapy, whereby a proportion of patients reports nausea even before repeat administration of chemotherapeutic agents due to a conditioned response.

A pyloric channel ulcer or acute gastritis may be associated with marked postprandial emesis. The vomiting in ulcer disease is believed to be in part a consequence of irritation, edema, and spasm of the pyloric sphincter mechanism. Concurrent bleeding can lead to vomiting of “coffee grounds.” Patients who undergo surgery for peptic ulcer may be troubled by recurrent bilious vomiting, which is believed to be caused by reflux of bile into the stomach or gastric remnant. Patients vomit bile within 15 minutes of eating; little food is present. Nausea and a bad taste in the mouth are present on awakening in the morning.

Gastric retention results in vomiting of food eaten more than 6 hours previously. A succussion splash is detectable on examination, and food is seen in the stomach on upper gastrointestinal series. In chronic cases, gastric outflow obstruction or atony may be secondary to diabetic neuropathy, anticholinergic use, or gastric malignancy. Idiopathic delayed gastric emptying can also
be seen. Transient gastric dilation is a frequent concomitant of pancreatitis, peritonitis, gallbladder disease, and hypokalemia.

Gastroesophageal reflux disease usually does not present with nausea as the predominant symptom (see Chapter 61), but a subset of patients with otherwise unexplained intractable nausea may suffer from reflux. Reflux damage affects the vagus nerve, which mediates the sensation of nausea. Treatment of their reflux results in resolution of the nausea.

Acute episodes of vomiting accompany a host of conditions, which range from the self-limited to life threatening. The most common is viral gastroenteritis. After many years of attributing this illness to viral infection, investigators have finally isolated and identified the responsible viruses. Explosive bouts of nausea and vomiting in conjunction with watery diarrhea, cramping abdominal pain, myalgias, headache, and fever are typical. Recovery is rapid in most instances, but symptoms may linger for 7 to 10 days. Similarly, anorexia, nausea, and vomiting often dominate the prodromal stage of acute viral hepatitis (see Chapter 70).

Acute gastroenteritis that results from food poisoning secondary to Salmonella or Shigella infection has a similar clinical presentation and course; onset is 24 to 48 hours after exposure to the contaminated food. Domestic fowl and their eggs represent the largest single reservoir of Salmonella infection. Inadequate cooking is often responsible for human infection. Intake of pastries and similar items containing staphylococcal enterotoxin causes symptoms indistinguishable from those of viral gastroenteritis, except that onset is within 1 to 6 hours after ingestion of the spoiled food, fever is rare, and complete clearing takes place by 24 to 48 hours. Clostridial food poisoning rarely produces prominent nausea and vomiting.

Peritoneal irritation and acute obstruction may precipitate acute emesis, usually in the context of severe abdominal pain (see Chapter 58). In acute pancreatitis, emesis is seen in 85% of patients; however, upper abdominal pain radiating into the back is the cardinal symptom, occurring in 95% of patients (see Chapter 72). Anorexia, nausea, and vomiting are early symptoms in more than 90% of patients with acute appendicitis; usually, emesis clears early. As with pancreatitis, pain typically precedes other symptoms. Acute pyelonephritis may mimic a gastrointestinal etiology by causing nausea, vomiting, and abdominal pain. Acute cholecystitis sometimes triggers acute emesis, but it does so less regularly than does acute cholangitis resulting from sudden obstruction of the common duct. Intestinal obstruction, especially of the proximal small bowel, produces marked nausea and vomiting of bilious material. Distention may be lacking, but intermittent cramping abdominal pain is characteristic. Feculent emesis is found in distal small-bowel obstruction.

Angioedema, through its abnormal release of vasoactive peptides such as bradykinin, may trigger a host of gastrointestinal symptoms, including significant nausea and vomiting accompanied by abdominal discomfort that often mimics peritoneal irritation. Fluid shifts into the peritoneal cavity from increased vascular and peritoneal permeability may be substantial causing abdominal distention. In the hereditary form, onset of episodes begins in childhood and worsens with puberty. Typical attacks may be unprovoked and begin with tingling and swelling of the lips and other mucus membranes followed by swelling of the hands and feet and gastrointestinal upset. There is no urticaria.

Myocardial infarction may activate vagal afferents and produce nausea, vomiting, and epigastric discomfort, simulating intra-abdominal disease. A prospective series of 62 patients with acute infarction revealed nausea and vomiting at the outset in 69% of those with inferior infarctions and 27% of those with anterior infarctions.

Neurologic emergencies can provoke severe bouts of acute emesis. In midline cerebellar hemorrhage, nausea and vomiting are profuse, in association with severe gait ataxia; meningeal signs and headache are also seen. Within a few hours, the patient may become comatose and die unless the condition is promptly diagnosed and treated (see Chapter 165). One third of patients with increased intracranial pressure experience vomiting. When it is sudden, forceful, and not preceded by nausea, it is described as projectile, but this presentation is not specific. Concurrent bilateral frontal or occipital headache is the rule. Migraine headaches and vestibular disease are less worrisome neurologic causes of acute nausea and emesis (see Chapters 165 and 166). The former is suggested by photophobia and throbbing unilateral headache, the latter by vertigo.

Cancer chemotherapies and radiation therapy produce substantial nausea and vomiting, with cisplatin being among the most problematic of chemotherapy agents. The mechanism of nausea and vomiting is believed to involve drug-induced release of serotonin from enterochromaffin cells, which leads to the activation of serotonin receptors on visceral afferent fibers and the stimulation of the vomiting center and chemoreceptor trigger zone. Drugs that block such serotonin and substance P receptors have proved to be uniquely effective (see later discussion and Chapter 90).

Drug withdrawal and substance abuse may trigger emesis. Nausea, dry heaves, and retching beginning at about 36 hours are characteristic features of opiate withdrawal syndrome. Sweats, chills, and restlessness precede other symptoms; the vomiting peaks by 72 hours and then subsides (see Chapter 235).