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CHAPTER 72: Nausea and Vomiting 481 The clinical differentiation of adynamic ileus and mechanical small bowel obstruction can be difficult. Patients with obstruction may report a temporary return of GI function postoperatively. The symptoms of obstruction are similar to those of adynamic ileus, but vary depending on the location and extent of the obstruction. Proximal obstruction is usually associated with early emesis and less abdominal distention, distal obstruction with later (sometimes bilious or feculent) emesis, and significant abdominal distention. High-pitched bowel sounds suggest mechanical obstruction. Plain abdominal radiographs show air-fluid levels (which suggest but are not pathognomonic for obstruction), thickened valvulae conniventes proximal to the obstruction, and little air in the bowel distal to the obstruction. The amount of dilated bowel is variable. Abdominal CT can reliably identify the transition point of normal to abnormal bowel, the degree of mechanical obstruction, and the presence of complications (perforation, abscess). In the absence of complications, partial small bowel obstruction is managed with observation. Surgery is generally required for high-grade obstruction or peritonitis. Mechanical small bowel obstruction is most often caused by adhesions.  ACUTE URINARY RETENTION Acute urinary retention after ambulatory surgery should be an obvious diagnosis based on the patient’s report of inability to urinate. Bedside bladder US confirms the diagnosis. Treatment is urinary bladder drainage.  ABDOMINAL COMPARTMENT SYNDROME Abdominal compartment syndrome is a serious condition seen in criti cally ill patients. Intra-abdominal hypertension is defined as persistent intra-abdominal pressure above 12 mm Hg. Abdominal compartment syndrome occurs as increased intra-abdominal pressure, often above 20 mm Hg, causes associated organ dysfunction. It is most often seen in critically ill septic, trauma, burn, and postoperative patients who receive aggressive fluid resuscitation. The diagnosis of abdominal compartment syndrome should be considered in the critically ill unstable patient with a tense abdomen, although a tense abdomen is not required to make the diagnosis. Abdominal compartment syndrome is confirmed by assessing intra-abdominal pressure, which is most often measured via urinary bladder pressure monitoring. Medical management involves identification and treatment of the contributing factors of abdominal compartment syndrome, evacuating intraluminal contents, improving abdominal wall compliance, and optimizing fluid administration and perfusion. 38,39 Surgical decompression is required in patients with severe or refractory abdominal compartment syndrome. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Nausea and Vomiting Bophal Sarha Hang Jeffrey S. Ditkoff Alex Koyfman Brit Long INTRODUCTION AND EPIDEMIOLOGY Nausea and vomiting accompany a variety of illnesses. Symptoms may be due to primary GI disorders such as bowel obstruction or gastroen teritis. However, symptoms may also represent pathology of the CNS (increased intracranial pressure, tumor), psychiatric conditions (bulimia nervosa, anxiety), endocrine or metabolic abnormalities (DKA, CHAPTER hyponatremia), or iatrogenic causes (medications, toxins). Also, nausea and vomiting may be the result of severe pain, myocardial infarction, sepsis, or other systemic illnesses.

ncreased intracranial pressure, tumor), psychiatric conditions (bulimia nervosa, anxiety), endocrine or metabolic abnormalities (DKA, CHAPTER hyponatremia), or iatrogenic causes (medications, toxins). Also, nausea and vomiting may be the result of severe pain, myocardial infarction, sepsis, or other systemic illnesses. A comprehensive history and physical examination, as well as the use of various diagnostic modalities, are needed to determine the cause and its complications. In the United States, the most common cause of acute nausea and vomiting is viral gastroenteritis. Other important considerations are side effects from medication and, in young women, pregnancy. PATHOPHYSIOLOGY Multiple neurons in the medulla oblongata are activated in a sequential fashion to induce vomiting. The vomiting center is the chemorecep tor trigger zone, located in the area postrema of the fourth ventricle. Chemoreceptors in this area are outside the blood–brain barrier and are stimulated by circulating medications and toxins, including dopa minergic antagonists (levodopa, bromocriptine), nicotine, digoxin, and opiate analgesics. Another important peripheral pathway for emesis is mediated through vagal afferents. Vagal activation is triggered by direct gastric mucosal irritants (such as NSAIDs) or increased luminal distention (gastric outlet obstruction, gastroparesis). Vagus activation stimulates neurons in the area postrema and nucleus tractus solitarius. These areas are rich in serotonin receptors and are a major site of action of antiemetic drugs, such as granisetron and odansetron. 2 Similar receptors are found throughout the GI tract, as well as the cortex and limbic system, vestibular system, heart, and genitalia. CLINICAL FEATURES The differential diagnosis of nausea and vomiting is exhaustive, as pathology of almost every organ system may lead to nausea and vomiting (Table 72-1). A thorough history and physical examination will help guide the diagnostic approach to the patient presenting with nausea and vomiting.  HISTORY Identify the onset and duration of the symptoms. The evaluation of acute conditions differs from a more chronic condition. For chronic conditions, understanding the scope of prior testing and treatment may help narrow the diagnostic possibilities. Chronic symptoms are defined as those symptoms present for >1 month. Frequency of the episodes and interval between episodes are help ful to gauge the severity of illness. Timing, such as increased number of episodes in the morning, may suggest pregnancy or a CNS cause, whereas postprandial vomiting suggests a GI cause such as gastroparesis or gastric outlet obstruction. The content of the vomitus may be helpful to determine whether an obstruction is present and its location. Esophageal disorders produce vomitus with undigested food particles. Bile is often associated with a small bowel obstruction, whereas vomitus composed of food particles and devoid of bile often represents a gastric outlet obstruction. Large bowel obstruction often is composed of feculent material and has a foul odor. Because of the number of organ systems that are the potential cause of pathology, it is important to ask the patient about associated symptoms. The presence or absence of abdominal pain is a focal starting point. If pain is present, elicit its location and quality. Pain preceding the nausea and vomiting is most particularly associated with an obstructive process. Fever or, possibly, diarrhea suggests gastroenteritis. Ask about sick contacts or ingestion of food suspicious for a foodborne illness. A his tory of recent weight loss is associated with a malignancy or psychiatric component.

receding the nausea and vomiting is most particularly associated with an obstructive process. Fever or, possibly, diarrhea suggests gastroenteritis. Ask about sick contacts or ingestion of food suspicious for a foodborne illness. A his tory of recent weight loss is associated with a malignancy or psychiatric component. Any CNS sign, such as headache, visual changes, vertigo, or neurologic deficits, may suggest a central cause for the nausea and vomiting. Obtain a thorough past medical and travel history. Prior abdominal surgery is a major risk factor for bowel obstruction from adhesions. Review the patient’s medication list to identify a medication with a common side effect of nausea and vomiting, such as NSAIDs, chemotherapeutic agents, antibiotics, various antihypertensives and antiarrhythmics, and oral contraceptives. Other medications at toxic Tintinalli_Sec09_p0473-0562.indd 481 8/2/19 6:49 PM

ns. Review the patient’s medication list to identify a medication with a common side effect of nausea and vomiting, such as NSAIDs, chemotherapeutic agents, antibiotics, various antihypertensives and antiarrhythmics, and oral contraceptives. Other medications at toxic Tintinalli_Sec09_p0473-0562.indd 481 8/2/19 6:49 PM 482 SECTION 9: Gastrointestinal Disorders TABLE 72-1 Differential Diagnosis of Nausea and Vomiting GI Neurologic Infectious Drugs/Toxins Endocrine Miscellaneous Functional disorders Head injury Bacterial toxins Digoxin Pregnancy Myocardial infarction Psychogenic Stroke Pneumonia Aspirin Adrenal insufficiency Acute glaucoma Irritable bowel syndrome Pseudotumor Spontaneous bacterial peritonitis NSAIDs DKA Nephrolithiasis Obstruction Hydrocephalus Urinary tract infection Acetaminophen Parathyroid disorders Pain Adhesions Mass lesion Viruses Opiates Thyroid disorders Psychiatric disorders Esophageal disorders Meningitis Adenovirus Alcohol Uremia Anorexia nervosa Achalasia Migraines Norwalk virus Theophylline Electrolyte disorders, especially hyponatremia Bulimia Intussusception Labyrinthitis Rotavirus Chemotherapeutics   Conversion disorder Tumor Ménière’s disease   Anticonvulsants   Depression Pyloric stenosis Motion sickness   Antibiotics Strangulated hernia     Antiarrhythmics Volvulus     Hormones Organic disorders     Illicit drugs Appendicitis     Radiation therapy Cholecystitis     Toxins Cholangitis     Arsenic Hepatitis     Organophosphates Irritable bowel disease     Carbon monoxide Mesenteric ischemia     Ricin Pancreatitis Peptic ulcer disease Peritonitis levels are known to cause nausea and vomiting. Examples include acetaminophen, salicylates, and digoxin.  PHYSICAL EXAMINATION Assess vital signs for hypotension and tachycardia. Observe skin turgor, mucous membrane hydration, and capillary refill to assess for dehydra tion. In children, the most useful predictors of significant dehydration (>5% loss of body weight) are abnormal capillary refill, abnormal skin turgor, absent tears, and abnormal respiratory pattern. 3 The abdominal examination is particularly important to assess for an emergent problem, as well as to help narrow the differential diagnosis to a possible GI cause. Inspect, auscultate, and palpate the abdomen. (For further discussion of abdominal evaluation, see Chapter 71, “ Acute Abdominal Pain. ”) Investigate any other important examination findings particular to various organ systems, as findings may provide valuable information regarding the cause of the nausea and vomiting (Table 72-2).  IMAGING AND ANCILLARY TESTING Diagnostic testing in the ED depends on differential diagnosis raised by a detailed history and physical exam. Often, CBC and basic metabolic panel are part of the initial evaluation. However, liver function tests and lipase may be considered if the patient is presenting with signs of biliary obstruction or upper abdominal pain. A pregnancy test should be considered for all woman of childbearing age. Further imaging with abdominal radiographs, CT scan, or US depends on the presentation and concern for acute intra-abdominal pathology. Head CT or brain MRI is ordered to evaluate for an intracranial mass or lesion. TREATMENT After initial evaluation of airway, breathing and circulation, focus on providing symptomatic relief (Table 72-3). Definitive management will often require disease-specific treatment. First-line supportive treatment should include fluid hydration with normal saline or lactated Ringer’s and may be sufficient for most patients. H 1 histaminergic agents such as promethazine or a serotonin receptor antagonist such as ondansetron may also be helpful for initial treatment.

uire disease-specific treatment. First-line supportive treatment should include fluid hydration with normal saline or lactated Ringer’s and may be sufficient for most patients. H 1 histaminergic agents such as promethazine or a serotonin receptor antagonist such as ondansetron may also be helpful for initial treatment. 5 However, promethazine is more sedating, with the potential side effect of vascular damage during IV administration. Metoclopramide and prochlorperazine are also commonly used drugs in the ED. Patients given these drugs may develop akathisia up to 48 hours after administration. 6 Studies comparing the efficacy of different drugs for treatment of nausea and vomiting in the ED report no definitive evidence to support the superiority of one drug over another or over placebo. 7,8  ONDANSETRON In the ED, serotonin receptor antagonists such as ondansetron have been first-line therapy for undifferentiated nausea and vomiting for all age groups. In 2011, the U.S. Food and Drug Administration issued a safety advisory for ondansetron due to concern for QT prolongation. Despite this warning, the clinical impact of QT prolongation associated with ondansetron use in the ED is unclear. 10 There are a few pediatric case reports of cardiac death possibly associated with ondansetron use.11 In a recent pediatric study, the risk of ventricular arrhythmia was three in 100,000 patients and increased with underlying cardiac conditions. Thus, patients with congenital long QT syndrome, congestive heart failure, or bradyarrhythmias or taking concomitant medications that pro long QT interval are at risk, and cardiac monitoring should be instituted for this population. In addition, electrolyte abnormalities (e.g., hypo kalemia or hypomagnesemia) should be corrected prior to administra tion of ondansetron. Consider ordering an ECG prior to ondansetron administration for a patient with a history of cardiac disease. GASTROPARESIS  PATHOPHYSIOLOGY Gastroparesis is delayed gastric emptying in the absence of an obstructing lesion. This condition, which is typically chronic, is associated with decreased quality of life and increased healthcare utilization, although it is not typically associated with significant mortality. 13-15 The most common cause is idiopathic, but other causes include diabetes, bariatric Tintinalli_Sec09_p0473-0562.indd 482 8/2/19 6:49 PM

, which is typically chronic, is associated with decreased quality of life and increased healthcare utilization, although it is not typically associated with significant mortality. 13-15 The most common cause is idiopathic, but other causes include diabetes, bariatric Tintinalli_Sec09_p0473-0562.indd 482 8/2/19 6:49 PM CHAPTER 72: Nausea and Vomiting 483 and gastric surgery, viral illness, gastroesophageal reflux disease, and nonulcer dyspepsia. 13-16 Connective tissue or neurologic disease, and even pregnancy, can also be associated with gastroparesis. The incidence appears to be increasing, especially in diabetics. 16-18  DIAGNOSIS Symptoms of gastroparesis typically include early satiety, bloating, postprandial nausea, gastroesophageal reflux, vomiting, and abdomi nal pain. 13-15 If severe and chronic, patients may develop weight loss, electrolyte abnormalities, and nutritional or vitamin deficiencies. Physical examination may reveal a succussion splash, which indicates excessive gastric fluid from delayed emptying or mechanical outlet obstruction. 13-15,19 Significant abdominal tenderness and peritoneal findings should be absent.13-15,19 Initial investigations include serum electrolytes, liver function studies, serum lipase, and pregnancy test. If concern for mechanical obstruc tion is present, image with abdominal/pelvic CT. US has been used to diagnose gastroparesis and determine effectiveness of treatment. Outpatient diagnostics include endoscopy, scintigraphy, electrogastrography, and assessment with the wireless motility capsule.13-15  TREATMENT Management includes volume resuscitation with electrolyte repletion. Several medications may be used for symptomatic treatment. Pro kinetic agents include metoclopramide (dopamine antagonist, 5 to 20 milligrams) and erythromycin (motilin receptor agonist, 40 to 250 milligrams). Both agents may decrease symptoms and increase gas tric emptying. Metoclopramide can decrease nausea, provide analgesia, and act as a prokinetic and is a first-line agent. Erythromycin may demonstrate tachyphylaxis and should be a second-line medication. Other medications include domperidone (a peripherally selective dopamine 2 receptor antagonist that is approved in Canada but, as of January 2018, not in the United States), diphenhydramine, prochlorperazine, and ondansetron. Opioids can treat pain; however, they may result in delayed gastric emptying and are not recommended for first-line therapy. 13-15 Haloperidol can treat symptoms of nausea, vomiting, and pain. Haloperidol may be administered IV or IM. One study demonstrated a significant decrease in ED and hospital length of stay, hospital admis sion, and opioid administration, with no adverse events. 21 A randomized controlled trial reported that haloperidol 5 milligrams IV significantly reduces pain and nausea. 22 Patients whose symptoms improve are appropriate for discharge and follow-up with a primary care provider or gastroenterologist for further management. CYCLIC VOMITING SYNDROME  PATHOPHYSIOLOGY Cyclic vomiting syndrome usually presents in childhood, with more than half of cases resolving by the teenage years. The condition is rare in adults. Predisposing mitochondrial DNA mutations (15519T and 3010A) have been found in many patients with cyclic vomiting syndrome. It is more common in females than males. In adults, there is a higher incidence of opiate and tobacco use. The cause is unknown, but it is thought to be related to dysregulation of the neuroendocrine system. Accompanying symptoms of lethargy, anorexia, pallor, abdominal pain, or autonomic symptoms such as sweating and salivation implicate abnormal vagal tone. It has also been suggested that cyclic vomiting syndrome is a functional disorder associated with migraines.

be related to dysregulation of the neuroendocrine system. Accompanying symptoms of lethargy, anorexia, pallor, abdominal pain, or autonomic symptoms such as sweating and salivation implicate abnormal vagal tone. It has also been suggested that cyclic vomiting syndrome is a functional disorder associated with migraines. Patients commonly have a history of migraines and report a prodrome with nausea and photophobia prior to attacks.  DIAGNOSIS Cyclic vomiting syndrome is characterized by recurrent nausea and vomiting separated by symptom-free periods. Since there is no specific confirmatory test for cyclic vomiting syndrome, diagnosis is clinical and involves excluding other common causes of symptoms. The diagnosis is often delayed for years after multiple ED visits and hospitalizations. Patients may be given the label of “drug-seeking. ” Comorbid conditions may include anxiety, depression, and irritable bowel. Cyclic vomiting syndrome has been well described with four phases: (1) asymptomatic periods of several or many months; (2) prodrome phase lasting minutes to hours, with lethargy, photophobia, anorexia, sweating, or salivation; (3) hyperemesis phase, which usually starts in the morning with severe nausea and vomiting, lasting for days to a week, with the mean duration being 3.4 days; and (4) finally, recovery phase with improvement in symptoms and energy levels. The Rome III diagnosis criteria include recurrent episodes of intrac table vomiting that are self-limiting, last less than 7 days, and do not have an organic cause. Typically, patients have more than two episodes of vomiting in the past year with symptom-free intervals in between.  TREATMENT Management in the ED is symptomatic, with antiemetics (ondansetron), sedatives (lorazepam), analgesics, and IV fluids. For prophylaxis, patients can try to avoid triggers such as sleep deprivation, diet, and physical or emotional stress. Amitriptyline is the standard for medi cal prophylaxis and has shown response rates as high as 86%. Other therapies include migraine prophylaxis drugs such as sumatriptan, TABLE 72-2 Differential Diagnosis Based on Physical Examination Findings Physical Examination Abnormal Signs or Symptoms Some Diagnostic Considerations General Toxic appearing Dehydration Generalized weakness Chronic malnutrition Weight loss Malignancy Vital signs Fever  Infection (gastroenteritis, appendicitis, cholecystitis) Tachycardia  Bowel perforation secondary to peritonitis Hypotension Severe volume depletion Hypertension Intracranial hemorrhage or stroke Head, eyes, ears, nose, throat Nystagmus Peripheral vs. central causes (benign positional vertigo, cerebellar infarct) Exophthalmos Graves’ disease Pinpoint pupils Opiate abuse Fixed-dilated pupil, eye pain Acute glaucoma Dry mucous membranes Dehydration Bulimia Poor dental enamel, parotid gland enlargement Bulimia Abdomen Distention, decreased bowel sounds, surgical scars Small bowel obstruction, gastroparesis, gastric outlet obstruction, ileus Hernias or palpable masses Incarcerated hernia, tumors Abdominal rigidity Peritonitis Neurologic Mental status Cranial nerve findings or neurologic deficits Papilledema Dehydration, intracranial lesion or pathology, brainstem tumor, elevated intracranial pressure Extremities Scarring on dorsal surface of the hands Bulimia Skin Jaundice  Hepatobiliary disease (hepatitis, choledocholithiasis) Poor skin turgor Dehydration Hyperpigmentation Addison’s disease Decreased elasticity Scleroderma Skin track marks Drug abuse/withdrawal Tintinalli_Sec09_p0473-0562.indd 483 8/2/19 6:49 PM