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446
C. J. Rees et al.
Time-Dependent Interventions
• The only time-dependent intervention is to exclude more serious causes of
pain.
Overall Principles ofTreatment
• Patients with a suggestive history, as well as those in whom more serious
causes of the symptoms have been excluded, often are treated empirically
with acid suppression and lifestyle changes.
• Lifestyle changes include decreasing or stopping known exacerbating substances, weight loss, and elevating the head of the bed.
• Acid suppression usually is attempted with either H2-blockers or protonpump inhibitors (PPIs). H2-blockers have been shown to promote esophageal
healing in mild esophagitis. PPIs suppress acid more effectively than
H2-blockers and are more efcacious both in relieving symptoms and in promoting esophageal mucosal healing. However, PPIs are much more expensive
than H2-blockers.
• Anywhere from 40–90 % of patients will report symptom improvement from
PPIs.
• However, symptom improvement is not a diagnostic criterion for GERD.
• Patients whose symptoms are refractory to treatment may need further evaluation, although this group of patients usually constitutes a small minority.
This is especially true for patients with worrisome symptoms such as dysphagia and odynophagia.
• Further evaluation may include esophagogastroduodenoscopy (EGD), esophageal manometry, and ambulatory pH monitoring.
• It is worth remembering that EGD may be normal in GERD, and this study
usually is performed to exclude other diagnoses.
• Esophageal manometry and ambulatory pH monitoring are invasive tests;
patients should be evaluated by a specialist before undergoing these studies.
Disease Course
• GERD is a chronic condition. It often requires long-term medical therapy for
control.
• A minority of patients have long-term relief from lifestyle changes.
• GERD may be associated with several long-term complications, many of
them serious.
30 Gastroesophageal Reux Disease
• GERD may be associated with chronic esophageal mucosal changes, starting with
thinning and inammation and then scarring. These events may lead to esophageal strictures, which may cause dysphagia, odynophagia, food impactions, etc.
• The most serious complication of GERD is damage to the normal esophageal
stratied squamous epithelium by acid, leading to replacement with metaplastic columnar epithelium. This condition, known as Barrett’s esophagus, is
associated with a higher incidence of esophageal adenocarcinoma. Currently,
it is believed that 1–10 % of people with Barrett’s esophagus will develop
esophageal adenocarcinoma. Patients with Barrett’s esophagus require endoscopic surveillance with biopsies to look for cancerous changes.
447
Endoscopic photograph of long-segment Barrett’s esophagus. The arrows mark the
proximal extent of the gastric folds, which is the location of the gastroesophageal
junction. Note that Barrett’s metaplasia extends well above the GEJ to line the distal
esophagus. The reddish-pink (salmon) color and velvet-like texture of Barrett’s epithelium contrasts sharply with the pale and glossy appearance of the esophageal
squamous epithelium. [Spechler SJ.Barrett’s Esophagus. In: Shaker R, Belafsky PC,
Postma GN, Easterling C, editors. Principles of Deglutition [Internet]. NewYork,
NY: Springer New York; 2013 [cited 2015 May 14]. p. 723–38. Available from:
http://link.springer.com/10.1007/978-1-4614-3794-9_49] Caption from original
Related Evidence
Papers of particular interest have been highlighted as:
** Of key importance
448
C. J. Rees et al.
Practice Guideline
Davies I, Burman-Roy S, Murphy MS; Guideline Development Group. Gastro-
oesophageal reux disease in children: NICE guidance. BMJ. 2015 Jan
14;350:g7703. https://doi.org/10.1136/bmj.g7703. PMID: 25591811. http://
www.ncbi.nlm.nih.gov/pubmed/25591811 **
Katz PO, Gerson LB, Vela MF.Guidelines for the diagnosis and management of
gastroesophageal reux disease. Am J Gastroenterol. 2013 Mar;108(3):308-28;
quiz 329. https://doi.org/10.1038/ajg.2012.444. PMID: 2341938. http://www.
ncbi.nlm.nih.gov/pubmed/23419381 **
Shaheen NJ, Weinberg DS, Denberg TD, Chou R, Qaseem A, Shekelle P; Clinical
Guidelines Committee of the American College of Physicians. Upper endoscopy
for gastroesophageal reux disease: best practice advice from the clinical guidelines committee of the American College of Physicians. Ann Intern Med. 2012
Dec 4;157(11):808-16. https://doi.org/10.7326/0003-4819-157-11-201212040-
00008. PMID: 23208168. http://www.ncbi.nlm.nih.gov/pubmed/23208168 **
Vandenplas Y, Rudolph CD, Di Lorenzo C, Hassall E, Liptak G, Mazur L,
Sondheimer J, Staiano A, Thomson M, Veereman-Wauters G, Wenzl TG, North
American Society for Pediatric Gastroenterology Hepatology and Nutrition,
European Society for Pediatric Gastroenterology Hepatology and Nutrition.
Pediatric gastroesophageal reux clinical practice guidelines: joint recommendations of the North American Society for Pediatric Gastroenterology,
Hepatology, and Nutrition (NASPGHAN) and the European Society for Pediatric
Gastroenterology, Hepatology, and Nutrition (ESPGHAN). J Pediatr
Gastroenterol Nutr. 2009 Oct;49(4):498-547. https://doi.org/10.1097/
MPG.0b013e3181b7f563. PMID: 19745761. http://www.ncbi.nlm.nih.gov/
pubmed/19745761 **
Review
Spechler SJ. Barrett esophagus and risk of esophageal cancer: a clinical review.
JAMA. 2013 Aug 14;310(6):627-36. https://doi.org/10.1001/jama.2013.226450.
PMID: 23942681.
Lee YY, McColl KE. Pathophysiology of gastroesophageal reux disease. Best
Pract Res Clin Gastroenterol. 2013 Jun;27(3):339-51. https://doi.org/10.1016/j.
bpg.2013.06.002. PMID: 23998973. http://www.ncbi.nlm.nih.gov/
pubmed/23998973 **
Chandra S, Gorospe EC, Leggett CL, Wang KK. Barrett's esophagus in 2012:
updates in pathogenesis, treatment, and surveillance. Curr Gastroenterol Rep.
2013 May;15(5):322.
23605564. http://www.ncbi.nlm.nih.gov/pubmed/23605564
http://www.ncbi.nlm.nih.gov/pubmed/23942681
https://doi.org/10.1007/s11894-013-0322-8. PMID:
30 Gastroesophageal Reux Disease
449
McConaghy JR, Oza RS.Outpatient diagnosis of acute chest pain in adults. Am
Fam Physician. 2013 Feb 1;87(3):177-82. PMID: 23418761. http://www.ncbi.
nlm.nih.gov/pubmed/23418761 **
Gill RS, Collins JS, Talley NJ.Management of noncardiac chest pain in women.
Womens Health (Lond Engl). 2012 Mar;8(2):131-43; quiz 144-5.
https://doi.
org/10.2217/whe.12.3. PMID: 22375717. http://www.ncbi.nlm.nih.gov/
pubmed/22375717
Smith JA, Abdulqawi R, Houghton LA.GERD-related cough: pathophysiology and
diagnostic approach. Curr Gastroenterol Rep. 2011 Jun;13(3):247-56. https://
doi.org/10.1007/s11894-011-0192-x. PMID: 21465223. http://www.ncbi.nlm.
nih.gov/pubmed/21465223 **
Lacy BE, Weiser K, Chertoff J, Fass R, Pandolno JE, Richter JE, Rothstein RI,
Spangler C, Vaezi MF.The diagnosis of gastroesophageal reux disease. Am J
Med. 2010 Jul;123(7):583-92.
https://doi.org/10.1016/j.amjmed.2010.01.007.
PMID: 20493461. http://www.ncbi.nlm.nih.gov/pubmed/20493461
Oranu AC, Vaezi MF.Noncardiac chest pain: gastroesophageal reux disease. Med
Clin North Am. 2010 Mar;94(2):233-42. https://doi.org/10.1016/j.
mcna.2010.01.001. PMID: 20380953. http://www.ncbi.nlm.nih.gov/
pubmed/20380953 **
Use PubMed Clinical Queries to nd the most recent evidence. Use this search
strategy:
“Gastroesophageal Reux”[Mesh] OR “Gastroesophageal Reex” OR “GERD”
Chapter 31
Goiter
ChristopherJ.Rees, CharlesV.Pollack,Jr., andJaimeFrielBlanck
Name andSynonyms
Goiter
Incidence/Epidemiology
• Dietary deciency of iodine is the most common cause of goiter worldwide.
There are estimated to be about 200 million cases of iodine-decient goiter
worldwide.
• In the United States (where signicant dietary deciency of iodine only
occurs in new immigrants), the most common cause of goiter is multinodular
goiter.
• The female: male ratio is 4:1.
• Goiter is distributed equally among races.
• The incidence of goiter increases with age.
C. J. Rees
Emergency Department, Pennsylvania Hospital, Philadelphia, PA, USA
C. V. Pollack,
Department of Emergency Medicine, Thomas Jefferson University,
Philadelphia, PA, USA
J. F. Blanck
Welch Medical Library, Johns Hopkins University, Baltimore, MD, USA
C. V. Pollack, Jr. (ed.), Differential Diagnosis of Cardiopulmonary Disease,
https://doi.org/10.1007/978-3-319-63895-9_31
Jr. ()
451© Springer Nature Switzerland AG 2019
452
C. J. Rees et al.
Differential Diagnosis
• Goiters often present as an anterior neck mass on physical examination. The
differential diagnosis of anterior neck masses is broad, but generally falls into
several categories:
• Inammatory masses (such as lymphadenopathy)
• Neoplastic masses (both primary and metastatic)
• Congenital (vascular anomalies, thyroglossal duct cysts)
• Some goiters extend into the thoracic cavity (substernal goiters) and present
as mediastinal masses (most often anterior mediastinal masses) found on an
imaging study (CXR, CT chest) performed for other reasons. The most common causes of a mediastinal mass (in decreasing order of frequency) are:
• Substernal goiter
• Neurogenic tumors
• Thymoma
• Pericardial or bronchogenic cysts
• Lymphoma
• Teratoma
Pathophysiology andEtiology
• A goiter refers to an abnormally enlarged thyroid gland.
• Goiters can be classied as diffuse or nodular, toxic or non-toxic, and either
benign or malignant. A toxic goiter overproduces thyroid hormone.
• The most common pathophysiologic reason for goiter formation is increased
secretion of thyroid stimulating hormone (TSH) by the anterior pituitary
gland. This occurs as the thyroid becomes unable to synthesize adequate
amounts of T3 and T4. This can have multiple causes, such as iodine deciency and thyroid cell inammation and destruction from autoimmune thyroiditis (Hashimoto’s Thyroiditis).
• Goiters can also form when TSH secretion is normal. This can result from the
action of multiple growth factors acting on thyroid cells over a long period of
time, usually in the presence of a genetic predisposition to goiter formation.
This leads to nontoxic, multinodular goiters.
• Patients with Graves’ disease produce TSH receptor antibodies. These auto-
antibodies stimulate the TSH receptor and lead to thyroid growth and overproduction of thyroid hormones.
• As stated in the Incidence/Epidemiology section, iodine deciency is the
leading cause of goiter worldwide. However, iodine deciency is mostly
unheard of in the United States and Western Europe. In these areas iodine
deciency is usually only found among recent immigrants.
31 G oiter
• In most Western countries, multinodular goiter, Hashimoto’s disease
(autoimmune thyroiditis), and Graves’ disease are the most common
causes of goiter.
• Less common causes of goiter include thyroiditis (of any cause), thyroid
tumors, and inltrative diseases of the thyroid.
Presentation
Typical/“Classic”
• It is important to review the anatomy of the thyroid gland, as the presenting
symptoms of goiter can be related to compression of neighboring structures.
• The thyroid sits just below the larynx; it has 2 lobes connected by a small
bridge of thyroid tissue termed the isthmus. The thyroid partially encircles
the anterolateral aspects of the trachea. It is bordered posteriorly by the
trachea and esophagus, and laterally by the carotid sheaths. Anteriorly, the
thyroid is covered only by the thin strap muscles anterolaterally, and then
connective tissue, subcutaneous tissue, and skin. As a result of this minimal anterior anatomic coverage, the thyroid mostly enlarges outward and
does not usually compress any lateral or posterior structures.
453
Position and anatomy of the thyroid gland. (a) Normal position of the thyroid
gland, (b) anatomy of the thyroid gland. [Youn Y-K, Lee KE, Choi JY.Surgical
Anatomy of the Thyroid Gland. Color Atlas of Thyroid Surgery [Internet]. Berlin,
Heidelberg: Springer Berlin Heidelberg; 2014 [cited 2015 Dec 4]. p. 1–10.
Available from: http://link.springer.com/10.1007/978-3-642-37262-9_1] Caption
from original
454
C. J. Rees et al.
Surgical anatomy during thyroidectomy: trachea, esophagus, common carotid
artery, superior thyroid artery, superior thyroid vein, middle thyroid vein, inferior
thyroid artery, inferior thyroid vein, and recurrent laryngeal nerve [Sarpel
U.Thyroidectomy. Surgery [Internet]. NewYork, NY: Springer New York; 2014
[cited 2015 Dec 4]. p. 195–205. Available from: http://link.springer.
com/10.1007/978-1-4939-0903-2_18] Caption from original
31 G oiter
455
Thyroid gland anatomy and blood supply [Porter S, Schwartz A, DeMaria S, Genden
EM. Thyroid, Parathyroid, and Parotid Surgery. In: Levine AI, Govindaraj S,
DeMaria, S, editors. Anesthesiology and Otolaryngology [Internet]. NewYork, NY:
Springer NewYork; 2013 [cited 2015 Dec 4]. p.217–40. Available from:
http://link.
springer.com/10.1007/978-1-4614-4184-7_14] Caption from original
• In goiters that grow asymmetrically, however, enlargement of one lobe is predominant. Asymmetrical goiters can also enlarge circumferentially around
the trachea, which can cause compression of the jugular veins, tracheal narrowing, and/or impingement of the esophagus.
• Goiters can also extend caudally into the thoracic inlet. The thoracic inlet is an
oval-shaped area about 5cm (anteroposteriorly) by 10 cm (laterally). It is bordered anteriorly by the sternum, laterally by the rst ribs, and posteriorly by the
rst thoracic vertebra. Structures within the thoracic include the trachea, esophagus, and major vascular structures. As the borders of the thoracic inlet are all bony,
there is no room for expansion. If a goiter extends caudad through the thoracic
inlet, the goiter is referred to as substernal (or retrosternal). Substernal goiters are
more likely to cause compression than purely cervical goiters. Substernal goiters
are thought to account for anywhere from 2–20 % of all goiters.
• Most goiters grow very slowly, do not cause thyroid dysfunction, and are
asymptomatic. They are usually found on routine physical examination, and
on imaging studies being performed for other reasons.
• Most goiters are painless.
• Once a goiter is detected, an evaluation should be performed with three major
goals:
• Identify the underlying cause.
• Evaluate for the presence of obstructive symptoms.
• Evaluate for the presence of features suspicious for malignancy.
Atypical
• As most goiters are asymptomatic, any symptomatic goiter can be considered
the “atypical” presentation of goiter.
• However, goiters may be associated with either hypo- or hyperthyroidism,
and patients can present with symptoms of those disorders.
• Hypothyroidism. A goiter due to long-standing, burned-out Hashimoto’s
(autoimmune) thyroiditis, and severe iodine deciency, can be associated
with hypothyroidism. Those symptoms are protean and can include profound
fatigue, unintentional weight gain, constipation, and cold intolerance.
• Hyperthyroidism. Some causes of goiter can be associated with hyperfunc-
tioning thyroid tissue (multinodular goiter with autonomously functioning
nodules), and Graves’ disease. Patients with goiter from these conditions
may present with symptoms of hyperthyroidism, such as unexplained
weight loss, palpitations, and dyspnea on exertion.
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C. J. Rees et al.
• Goiters may present with symptoms of obstruction or compression of neighboring structures. This occurs most commonly from substernal goiters, but
can also occur from large cervical goiters. It can also happen acutely, if there
is acute enlargement of the thyroid. This can happen from acute thyroiditis,
and also, rarely, from hemorrhage into a thyroid nodule (these situations are
also associated with pain in the thyroid.)
• Exertional dyspnea is the most common compressive symptom from goi-
ters, present in 30–60 % that have compressive symptoms. The development of exertional dyspnea usually indicates that the tracheal diameter
has been reduced to less than 8mm. When the tracheal diameter is reduced
below 5 mm, patients will typically have wheezing or stridor.
• In the early stages, the dyspnea may be intermittent and positional,
occurring when lying down, or when reaching or bending (reaching and
bending force the thyroid further into the thoracic inlet.)
• Cough is also a common symptom of obstruction, present in 10–30 % of
patients with compressive symptoms.
• Other, less common obstructive/compressive symptoms include:
• Dysphagia from extrinsic narrowing of the esophagus.
• Hoarseness from compression of the recurrent laryngeal nerve with
vocal cord paralysis (can be transient or permanent).
• Venous engorgement of the face, neck, and upper anterior chest from
jugular vein compression. This can also lead to thrombosis of the
jugular vein.
Photograph of a woman who has a large retrosternal goiter with signs of compression of the venous system. She has engorged supercial veins on her anterior neck