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Nausea, Vomiting, and Indigestion

Chapter 48 | Part 2: Cardinal Manifestations and Presentation of Diseases

KEY CLINICAL POINTS

  • Nausea and vomiting are caused by intracranial, gastrointestinal, metabolic, and medication-related factors.
  • GERD is the most common cause of chronic heartburn and regurgitation, with 18–28% of the population experiencing weekly symptoms.
  • Functional dyspepsia affects 7.2% of the population and is characterized by postprandial fullness, early satiety, or epigastric pain without organic disease.
  • Eosinophilic esophagitis is an increasingly recognized cause of dysphagia requiring dietary allergen elimination and proton pump inhibitors.
  • PPIs are first-line therapy for GERD and functional dyspepsia, with long-term use associated with risks like nutrient deficiencies and Clostridioides difficile infection.

1. DEFINITION & OVERVIEW

Nausea is the feeling of needing to vomit; vomiting is the forceful expulsion of gastric contents. Indigestion encompasses symptoms like nausea, vomiting, heartburn, and dyspepsia. Dysphagia refers to difficulty swallowing, which may involve oral, pharyngeal, or esophageal dysfunction.

Table 48-1 Causes of Nausea and Vomiting

INTRAPERITONEAL EXTRAPERITONEAL MEDICATIONS/METABOLIC DISORDERS
Pyloric obstruction Cardiomyopathy Cancer chemotherapy
Small-bowel obstruction Myocardial infarction Opioids
Colonic obstruction Labyrinthine disease Analgesics
Superior mesenteric artery syndrome Motion sickness Glucagon-like peptide-1 (GLP-1) receptor agonists
Enteric infections Labyrinthitis Oral hypoglycemics
Inflammatory diseases Malignancy Parkinson’s disease/restless legs therapies
Gastroparesis Psychiatric illness Antidepressants
Intestinal pseudoobstruction Anorexia and bulimia nervosa Smoking cessation agents
Gastroesophageal reflux Depression Antibiotics
Chronic nausea vomiting syndrome Postoperative vomiting Cardiac antiarrhythmics/antihypertensives
Gastroparesis-like symptoms Pregnancy Oral contraceptives
INTRAPERITONEAL EXTRAPERITONEAL MEDICATIONS/METABOLIC DISORDERS
Cyclic vomiting syndrome Uremia Endocrine/metabolic disease
Cannabinoid hyperemesis syndrome Ketoacidosis Toxins
Rumination syndrome Thyroid and parathyroid disease Liver failure
Mesenteric insufficiency Adrenal insufficiency Ethanol

1.1 Neurotransmitter Pathways

Vomiting is coordinated by the brainstem and involves pathways including 5-HT3, NK1, dopamine D2, and muscarinic receptors. The area postrema acts as a chemoreceptor trigger zone for bloodborne toxins.

1.2 Mechanisms of Vomiting

Vomiting is triggered by central (CNS), peripheral (gastrointestinal), and chemoreceptor pathways. Neurotransmitters like 5-HT3, NK1, and dopamine mediate vomiting, while anticholinergics and dopamine antagonists are key therapeutic targets.

2. EPIDEMIOLOGY

Nausea alone occurs in 1.9% of the population weekly, with nausea plus vomiting in 1.1%. GERD affects 18–28% with weekly symptoms. Functional dyspepsia has a prevalence of 7.2%. Cyclic vomiting syndrome (CVS) occurs in 1.4% of the population.

2.1 Risk Factors

Risk factors include obesity, NSAID use, H. pylori infection, pregnancy, and metabolic disorders like diabetes. Smoking, caffeine, and alcohol exacerbate GERD.

2.2 Demographics

GERD and functional dyspepsia are more common in adults, with increased prevalence in older age. CVS and CHS are more prevalent in adolescents and young adults.

3. ETIOLOGY & PATHOPHYSIOLOGY

Nausea/vomiting arise from CNS, gastrointestinal, metabolic, or medication-induced causes. GERD results from LES dysfunction and acid reflux. Functional dyspepsia involves altered motility, hypersensitivity, or microbiome dysbiosis.

3.1 Neurotransmitter Pathways

Vomiting is mediated by 5-HT3, NK1, dopamine D2, and muscarinic receptors. The area postrema responds to bloodborne toxins, while the vestibular system mediates motion sickness.

3.2 Mechanisms of GERD

Reduced LES tone, transient LES relaxations (TLESRs), and delayed gastric emptying contribute to reflux. Hiatal hernias and obesity exacerbate symptoms.

4. CLINICAL FEATURES

Symptoms include heartburn, regurgitation, epigastric pain, bloating, and early satiety. Alarm features (Table 48-3) indicate serious pathology like malignancy or ischemia.

Table 48-3 Alarm Symptoms in Gastroesophageal Reflux Disease

Symptoms
Odynophagia or dysphagia
Unexplained weight loss
Recurrent vomiting
Occult or gross gastrointestinal bleeding
Jaundice
Palpable mass or adenopathy
Family history of gastroesophageal malignancy

4.1 GERD Presentation

Heartburn (substernal warmth), regurgitation, and water brash. Atypical symptoms include asthma, cough, and chest pain.

4.2 Functional Dyspepsia

Postprandial fullness, early satiety, or epigastric pain without organic cause. Subtypes include postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS).

5. DIFFERENTIAL DIAGNOSIS

Differential diagnoses include GERD, functional dyspepsia, peptic ulcer disease, esophageal strictures, cyclic vomiting syndrome (CVS), cannabinoid hyperemesis syndrome (CHS), and malignancy.

5.1 Esophageal Disorders

Esophageal strictures, achalasia, Zenker’s diverticulum, and eosinophilic esophagitis. Symptoms include dysphagia, odynophagia, and regurgitation.

5.2 Gastrointestinal Obstruction

Small-bowel or colonic obstruction, intestinal pseudoobstruction, and mesenteric ischemia present with vomiting, abdominal pain, and distension.

6. INVESTIGATIONS & DIAGNOSIS

Diagnostic tests include upper endoscopy, esophageal pH/impedance monitoring, gastric emptying studies, and imaging. Endoscopy is critical for ruling out malignancy or structural causes.

6.1 Diagnostic Algorithms

For uninvestigated dyspepsia: Test for H. pylori (urea breath/fecal antigen). Endoscopy is indicated for patients >60 years, with alarm symptoms, or refractory to PPI therapy.

6.2 Imaging and Functional Tests

CT/MRI for bowel obstruction, esophageal manometry for motility disorders, and FLIP (functional lumen imaging probe) for esophagogastric junction dysfunction.

7. MANAGEMENT & TREATMENT

Treatment includes lifestyle modifications, acid suppression, prokinetics, and targeted therapies. PPIs are first-line for GERD, while H2 blockers are used for mild cases.

Table 48-2 Treatment of Nausea and Vomiting

TREATMENT MECHANISM CLINICAL INDICATIONS
Antiemetic agents Antihistaminergic Motion sickness, inner ear disease
Antiemetic agents Anticholinergic Motion sickness, inner ear disease
Antiemetic agents Antidopaminergic Medication-, toxin-, or metabolic-induced emesis
Antiemetic agents 5-HT antagonist Chemotherapy- and radiation-induced emesis
Antiemetic agents Cannabinoids Chemotherapy-induced emesis, gastroparesis
Antiemetic agents Tricyclic antidepressant Chronic nausea vomiting syndrome
Antiemetic agents Other antidepressant/atypical antipsychotic Functional dyspepsia
Antiemetic agents Neuropathic modulator Chemotherapy-induced emesis
Antiemetic agents Neurokinin (NK) receptor antagonists Chemotherapy-induced emesis
Antiemetic agents 5-HT agonist and antidopaminergic Gastroparesis
Antiemetic agents Motilin agonist Gastroparesis
Antiemetic agents Peripheral antidopaminergic Gastroparesis
Antiemetic agents Pure 5-HT agonist Idiopathic gastroparesis
Antiemetic agents Somatostatin analogue Intestinal pseudoobstruction
Antiemetic agents Acetylcholinesterase inhibitor Small-intestinal dysmotility/pseudoobstruction
Special settings Benzodiazepines Anticipatory nausea and vomiting with chemotherapy
Special settings 5-HT agonist Functional dyspepsia
Special settings Glucocorticoids Chemotherapy-induced emesis
Special settings Anticonvulsants Cyclic vomiting syndrome
Special settings Antimigraine agents Cyclic vomiting syndrome
Special settings Topical analgesic Cannabinoid hyperemesis syndrome

7.1 Pharmacologic Therapy

PPIs (omeprazole, esomeprazole) for GERD; prokinetics (metoclopramide, domperidone) for gastroparesis; and antiemetics (ondansetron, aprepitant) for chemotherapy-induced vomiting.

7.2 Nonpharmacologic Interventions

Dietary modifications (low-fat meals, avoidance of caffeine/alcohol), weight management, and elevating the head of the bed for GERD.

8. PROGNOSIS & COMPLICATIONS

GERD may progress to Barrett’s esophagus and esophageal adenocarcinoma. Prolonged vomiting can lead to dehydration, electrolyte imbalances, and aspiration pneumonia. Gastroparesis may result in malnutrition and weight loss.

8.1 Complications of GERD

Barrett’s esophagus (10–15% of GERD patients), esophageal strictures, and aspiration pneumonia. Long-term PPI use increases risk of nutrient deficiencies.

8.2 Gastroparesis Outcomes

Chronic nausea, weight loss, and malnutrition. Surgical options like gastric electrical stimulation may improve symptoms in refractory cases.

9. SPECIAL CONSIDERATIONS

Pregnancy-related nausea (hyperemesis gravidarum) requires hydration and thiamine. Elderly patients are at higher risk for aspiration and drug interactions. Cyclic vomiting syndrome (CVS) may require prophylactic anticonvulsants.

9.1 Pregnancy

Nausea of pregnancy is common; hyperemesis gravidarum may require intravenous fluids and corticosteroids. Avoid NSAIDs and antihistamines in early pregnancy.

9.2 Elderly Patients

Increased risk of aspiration and drug interactions. Use caution with prokinetics (e.g., metoclopramide) due to risk of extrapyramidal symptoms.

10. KEY POINTS & CLINICAL PEARLS

  1. PPIs are first-line for GERD and functional dyspepsia. 2. Rule out malignancy in patients >60 years or with alarm symptoms. 3. Avoid NSAIDs and anticholinergics in patients with gastroparesis. 4. Use gastric emptying tests for suspected intestinal pseudoobstruction. 5. Monitor for complications of long-term PPI use (e.g., vitamin deficiencies).