Vomiting

Done by:Moahmmed Qazzaz

TerminologyNausea: is an unpleasant subjective sensation that most people have experienced at some point in their lives and usually recognize as a feeling of impending vomiting in the epigastrium or throat.

Retching: muscular activity of the abdomen and thorax, often voluntary, leading to forced inspiration against a closed mouth and glottis without oral discharge of gastric contents (“dry heaves”)

Vomiting: Vomiting is a partially voluntary act of forcefully expelling gastric or intestinal content through the mouth.

Regurgitation: effortless return of esophageal or gastric contents into the mouth unassociated with nausea or involuntary muscle contractions.

Rumination: food that is regurgitated in the postprandial period, re-chewed and then re-swallowed.

PATHOPHYSIOLOGYNeurologic coordination of the various components of vomiting is provided by the emetic center (or vomiting center) located in the medulla, specifically in the dorsal portion of the lateral reticular formation in the vicinity of the fasciculus solitarius

The afferent neural pathways that carry activating signals to the emetic center arise from many locations in the body.

Afferent neural pathways arise from various sites along the digestive tract—the pharynx, stomach, and small intestine.

Afferent impulses from these organs are relayed at the solitary nucleus (nucleus tractus solitarius) to the emetic center.

Afferent pathways also arise from nondigestive organs such as the heart.

Pathways from the chemoreceptor trigger zone (CTZ) located in the area postrema on the floor of the fourth ventricle activate the emetic center.

Despite its central location, the CTZ is outside, at least in part, the blood-brain barrier and serves primarily as a sensitive detection apparatus for circulating endogenous and exogenous molecules that may activate emesis. The vomit center receives input from four major areas the GI tract, the chemoreceptor trigger zone, the vestibular apparatus, and the cerebral cortex.

When activated, the emetic center sets into motion, through neural efferents, the various components of the emetic sequence.

First, nausea develops as a result of activation of the cerebral cortex; the stomach relaxes concomitantly, and antral and intestinal peristalsis are inhibited.

Second, retching occurs as a result of activation of spasmodic contractions of the diaphragm and intercostal muscles combined with closure of the glottis.

Third, the act of vomiting occurs when somatic and visceral components are activated simultaneously.

The components include brisk contraction of the diaphragm and abdominal muscles, relaxation of the lower esophageal sphincter, and a forceful retrograde peristaltic contraction in the jejunum that pushes enteric content into the stomach and from there toward the mouth.

Simultaneously, protective reflexes are activated. The soft palate is raised to prevent gastric content from entering the nasopharynx, respiration is inhibited momentarily, and the glottis is closed to prevent pulmonary aspiration, which is a potentially serious complication of vomiting.

CLINICAL CHARACTERISTICS OF VOMITING;

• Certain clinical features may be characteristic of specific causes of vomiting.

• Nausea and vomiting that occur in the morning or with an empty stomach are characteristic of vomiting produced by direct activation of the emetic center or CTZ.

• This type of emesis is most typical of pregnancy, drugs, toxins (e.g., alcohol abuse), or metabolic disorders (diabetes mellitus, uremia).

• Pseudovomitus, in which totally undigested food that has not been exposed to gastric juice is expelled, may occur in long-standing achalasia or with a large Zenker's diverticulum.

• Bilious vomiting is commonly seen after multiple vomiting episodes occur in close succession because of retrograde entry of intestinal material into the stomach. It is also characteristic of patients with a surgical enterogastric anastomosis, in whom the gastric contents normally include bile-stained enteric refluxate.

Vomitus with a feculent odor suggests intestinal obstruction, ileus associated with peritonitis. Vomiting that develops abruptly without preceding nausea or retching (projectile vomiting) is characteristic of, but not specific for, direct stimulation of the emetic center, as may occur with intracerebral lesions (tumor, abscess) or increased intracranial pressure.

• Vomiting that occurs outside the immediate postprandial period and that is characterized by evacuation of retained and partially digested food is typical of slowly developing gastric outlet obstruction or gastroparesis.

Common etiologies of nausea and vomiting;

Abdominal Causes;

• Mechanical obstruction • Gastric outlet obstruction • Small bowel obstruction• Motility disorders.• Chronic intestinal pseudo-obstruction.• Gastroparesis.

Other intra-abdominal causes;• Acute appendicitis• Acute cholecystitis• Acute hepatitis.• Acute mesenteric ischemia.• Crohn's disease.• Gastric and duodenal ulcer disease.• Pancreatitis and pancreatic neoplasms.• Peritonitis and peritoneal carcinomatosis.• Retroperitoneal and mesenteric pathology.• SUPERIOR MESENTERIC ARTERY SYNDROME.

Infectious Causes;

• Acute gastroenteritis.• Viral• Bacterial• Nongastrointestinal (systemic) infections

Metabolic and Endocrine Causes;

• Acute intermittent porphyria• Addison's disease• Diabetic ketoacidosis• Diabetes mellitus• Hyperparathyroidism/hypercalcemia.• Hyperthyroidism• Hyponatremia• Hypoparathyroidism• Pregnancy.

Nervous System Causes;• Demyelinating disorders• Disorders of the autonomic system• Hydrocephalus• Intracerebral lesions with edema Abscess• Hemorrhage• Infarction• Neoplasm• Labyrinthine disorders • Meningitis• Migraine headaches• Otitis media• Seizure disorders

Other Causes;• Anxiety and depression• Cardiac disease• Congestive heart failure• Myocardial infarction, ischemia• Collagen vascular disorders Scleroderma• Systemic lupus erythematosus• Eating disorders• Ethanol abuse• Hypervitaminosis A• Intense pain• Paraneoplastic syndrome• Postoperative state• Postvagotomy• Radiation therapy• Starvation

Medications that often cause nausea and vomiting;

• Cancer chemotherapy– e.g. cisplatin

• Analgesics– e.g. opiates, NSAIDs

• Anti-arrythmics– e.g., digoxin, quinidine

• Antibiotics– e.g., erythromycin

• Oral contraceptives

• Metformin• Anti-parkinsonians

– e.g., bromcryptine, L-DOPA

• Anti-convulsants– e.g., phenytoin, carbamazepine

• Anti-hypertensives • Theophylline• Anesthetic agents

Complications of Vomiting;

• Nutritional – adults: weight loss; kids: failure to gain weight.

• Cutaneous (petechia, purpura)• Orophayngeal (dental, sore throat)• Esophagitis/ esophageal hematoma• GE Junctional: M-W tears; rupture (Boorhaave’s)

• Metabolic: electrolyte, acid-base, water • Renal: prerenal azotemia; ATN;

hypokalemic nephropathy

Metabolic alkalosisretention of HCO3

- + volume-contraction

Hypokalemiarenal K+ losses + GI K+ loss + oral K+ intake

Hypochloremiagastric chloride losses

Hyponatremiafree water retention due to volume contraction

Note: Patients with uremia or Addison’s disease may have normal or even high serum K+ despite vomiting

Mallory-Weiss tear

Mallory-Weiss tear with clot;

Post-emetic purpura ;

History and Examination

How long?Relationship to meals?Contents of vomitus?Associated symptoms

pain in the chest or abdomen, fever, myalgias, diarrhea, vertigo, dizziness, headache, focal neurological symptoms, jaundice, weight loss

Diabetes?When was last menstrual period?

Vital signsBP and pulse tilt testCardiopulmonary examAbdominal examRectal examNeurological exam including funduscopic exam (papilledema)

Laboratory studies: guided by history and physical;

• Electrolytes, glucose, BUN/creatinine • Calcium, albumin, total serum proteins• CBC• LFTs• Pregnancy test• Urinalysis• Serum lipase amylase

Radiology studies: guided by history and physical;

• Plain abdominal films• Abdominal sono or CT.• Head CT or MRI if severe headache, papill-

edema, marked hypertension, altered mental status, or focal neurological findings

• EGD or upper GI to separate GOO or high duodenal obstruction from gastroparesis

• Radiopaque marker emptying studies or radionuclide scintigraphy, esp. if diabetic.

Treatment of nausea and vomiting;

1. Treat complications regardless of causee.g., replace salt, water, potassium losses

2. Identify and treat underlying cause, whenever possible

3. Provide temporary symptomatic relief of the symptoms

4. Use preventive measures when vomiting is likely to occur (e.g., cancer chemotherapy, parenteral opiate administration)

Drugs with anti- emetic prop-erties and known mechanisms;

• Antihistamines, e.g., meclizine.– esp. for vestibular disorders

• Anticholinergics, e.g., scopolamine.– esp. for vestibular and GI disorders

• Dopamine antagonists, e.g.,metoclopramide or prochlorperazine.– esp. for GI disorders

• Selective serotonin-3 (5HT3) RAs, e.g., odansetron, granisetron, dolasetron– esp. to prevent chemotherapy-induced

nausea/vomiting

Drugs with anti-emetic properties;

Multiple mechanisms of action:• Promethazine (Phenergan)

– dopamine antagonist– H1 antihistamine– anticholinergic– CNS sedative– prevention of opiate-induced nausea and vomiting

• Hydroxyzine.– H1 antihistamine– anticholinergic– CNS sedation– prevention of opiate-induced nausea and vomiting

Adjunctive antiemetic agents;

• Dexamethasone.– along with other anti-emetics for prevention

of cancer chemotherapy-induced emesis.

Summary;

• Nausea and vomiting are features of many GI and non-GI diseases and disorders.

• Regardless of its cause, treatment of nausea and vomiting should initially focus on replacing volume and electrolyte deficits. Later on, nutritional deficits must be addressed.

• Regardless of its cause, nausea and vomiting can cause several life-threatening GI and non-GI complications.

• Elucidation of the cause is often possible, and treatment of the underlying cause will usually be successful.

• Effective symptomatic therapies for nausea and vomiting are available when the cause is unclear or when the treatment of the underlying cause takes time to work.

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