Chapter 014. Abdominal Pain

Tham khảo bài viết bằng tiếng việt qua google  
Harrison's Internal Medicine > Chapter 14. Abdominal Pain
Abdominal Pain: IntroductionThe correct interpretation of acute abdominal pain is challenging. Since proper therapy may require urgent action, the unhurried approach suitable for the study of other conditions is sometimes denied. Few other clinical situations demand greater judgment, because the most catastrophic of events may be forecast by the subtlest of symptoms and signs. A meticulously executed, detailed history and physical examination are of great importance. The etiologic classification in Table 14-1, although not complete, forms a useful basis for the evaluation of patients with abdominal pain.Table 14-1 Some Important Causes of Abdominal Pain

Pain Originating in the Abdomen

Parietal peritoneal inflammation

Bacterial contamination

Perforated appendix or other perforated viscus

Pelvic inflammatory disease

Chemical irritation

Perforated ulcer

Pancreatitis

Mittelschmerz

Mechanical obstruction of hollow viscera

Obstruction of the small or large intestine

Obstruction of the biliary tree

Obstruction of the ureter

Vascular disturbances

Embolism or thrombosis

Vascular rupture

Pressure or torsional occlusion

Sickle cell anemia

Abdominal wall

Distortion or traction of mesentery

Trauma or infection of muscles

Distension of visceral surfaces, e.g. by hemorrhage

Hepatic or renal capsules

Inflammation of a viscus

Appendicitis

Typhoid fever

Typhlitis

Pain Referred from Extraabdominal Source

Cardiothoracic

Acute myocardial infarction

Myocarditis, endocarditis, pericarditis

Congestive heart failure

Pneumonia

Pulmonary embolus

Pleurodynia

Pneumothorax

Empyema

Esophageal disease, spasm, rupture, inflammation

Genitalia

Torsion of the testis

Metabolic Causes

Diabetes

Uremia

Hyperlipidemia

Hyperparathyroidism

Acute adrenal insufficiency

Familial Mediterranean fever

Porphyria

C'1 esterase inhibitor deficiency (angioneurotic edema)

Neurologic/Psychiatric Causes

Herpes zoster

Tabes dorsalis

Causalgia

Radiculitis from infection or arthritis

Spinal cord or nerve root compression

Functional disorders

Psychiatric disorders

Toxic Causes

Lead poisoning

Insect or animal envenomations

Black widow spiders

Snake bites

Uncertain Mechanisms

Narcotic withdrawal

Heat stroke

The diagnosis of "acute or surgical abdomen" is not an acceptable one because of its often misleading and erroneous connotation. The most obvious of "acute abdomens" may not require operative intervention, and the mildest of abdominal pains may herald an urgently correctable lesion. Any patient with abdominal pain of recent onset requires early and thorough evaluation and accurate diagnosis.Some Mechanisms of Pain Originating in the AbdomenInflammation of the Parietal PeritoneumThe pain of parietal peritoneal inflammation is steady and aching in character and is located directly over the inflamed area, its exact reference being possible because it is transmitted by somatic nerves supplying the parietal peritoneum. The intensity of the pain is dependent on the type and amount of material to which the peritoneal surfaces are exposed in a given time period. For example, the sudden release into the peritoneal cavity of a small quantity of sterile acid gastric juice causes much more pain than the same amount of grossly contaminated neutral feces. Enzymatically active pancreatic juice incites more pain and inflammation than does the same amount of sterile bile containing no potent enzymes. Blood and urine are often so bland as to go undetected if their contact with the peritoneum has not been sudden and massive. In the case of bacterial contamination, such as in pelvic inflammatory disease, the pain is frequently of low intensity early in the illness until bacterial multiplication has caused the elaboration of irritating substances.The rate at which the irritating material is applied to the peritoneum is important. Perforated peptic ulcer may be associated with entirely different clinical pictures dependent only on the rapidity with which the gastric juice enters the peritoneal cavity.The pain of peritoneal inflammation is invariably accentuated by pressure or changes in tension of the peritoneum, whether produced by palpation or by movement, as in coughing or sneezing. The patient with peritonitis lies quietly in bed, preferring to avoid motion, in contrast to the patient with colic, who may writhe incessantly.Another characteristic feature of peritoneal irritation is tonic reflex spasm of the abdominal musculature, localized to the involved body segment. The intensity of the tonic muscle spasm accompanying peritoneal inflammation is dependent on the location of the inflammatory process, the rate at which it develops, and the integrity of the nervous system. Spasm over a perforated retrocecal appendix or perforated ulcer into the lesser peritoneal sac may be minimal or absent because of the protective effect of overlying viscera. A slowly developing process often greatly attenuates the degree of muscle spasm. Catastrophic abdominal emergencies such as a perforated ulcer may be associated with minimal or no detectable pain or muscle spasm in obtunded, seriously ill, debilitated elderly patients or in psychotic patients.Obstruction of Hollow VisceraThe pain of obstruction of hollow abdominal viscera is classically described as intermittent, or colicky. Yet the lack of a truly cramping character should not be misleading, because distention of a hollow viscus may produce steady pain with only very occasional exacerbations. It is not nearly as well localized as the pain of parietal peritoneal inflammation.The colicky pain of obstruction of the small intestine is usually periumbilical or supraumbilical and is poorly localized. As the intestine becomes progressively dilated with loss of muscular tone, the colicky nature of the pain may diminish. With superimposed strangulating obstruction, pain may spread to the lower lumbar region if there is traction on the root of the mesentery. The colicky pain of colonic obstruction is of lesser intensity than that of the small intestine and is often located in the infraumbilical area. Lumbar radiation of pain is common in colonic obstruction.Sudden distention of the biliary tree produces a steady rather than colicky type of pain; hence the term biliary colic is misleading. Acute distention of the gallbladder usually causes pain in the right upper quadrant with radiation to the right posterior region of the thorax or to the tip of the right scapula, and distention of the common bile duct is often associated with pain in the epigastrium radiating to the upper part of the lumbar region. Considerable variation is common, however, so that differentiation between these may be impossible. The typical subscapular pain or lumbar radiation is frequently absent. Gradual dilatation of the biliary tree, as in carcinoma of the head of the pancreas, may cause no pain or only a mild aching sensation in the epigastrium or right upper quadrant. The pain of distention of the pancreatic ducts is similar to that described for distention of the common bile duct but, in addition, is very frequently accentuated by recumbency and relieved by the upright position.Obstruction of the urinary bladder results in dull suprapubic pain, usually low in intensity. Restlessness without specific complaint of pain may be the only sign of a distended bladder in an obtunded patient. In contrast, acute obstruction of the intravesicular portion of the ureter is characterized by severe suprapubic and flank pain that radiates to the penis, scrotum, or inner aspect of the upper thigh. Obstruction of the ureteropelvic junction is felt as pain in the costovertebral angle, whereas obstruction of the remainder of the ureter is associated with flank pain that often extends into the same side of the abdomen.Vascular DisturbancesA frequent misconception, despite abundant experience to the contrary, is that pain associated with intraabdominal vascular disturbances is sudden and catastrophic in nature. The pain of embolism or thrombosis of the superior mesenteric artery or that of impending rupture of an abdominal aortic aneurysm certainly may be severe and diffuse. Yet, just as frequently, the patient with occlusion of the superior mesenteric artery has only mild continuous diffuse pain for 2 or 3 days before vascular collapse or findings of peritoneal inflammation appear. The early, seemingly insignificant discomfort is caused by hyperperistalsis rather than peritoneal inflammation. Indeed, absence of tenderness and rigidity in the presence of continuous, diffuse pain in a patient likely to have vascular disease is quite characteristic of occlusion of the superior mesenteric artery. Abdominal pain with radiation to the sacral region, flank, or genitalia should always signal the possible presence of a rupturing abdominal aortic aneurysm. This pain may persist over a period of several days before rupture and collapse occur.Abdominal WallPain arising from the abdominal wall is usually constant and aching. Movement, prolonged standing, and pressure accentuate the discomfort and muscle spasm. In the case of hematoma of the rectus sheath, now most frequently encountered in association with anticoagulant therapy, a mass may be present in the lower quadrants of the abdomen. Simultaneous involvement of muscles in other parts of the body usually serves to differentiate myositis of the abdominal wall from an intraabdominal process that might cause pain in the same region.Referred Pain in Abdominal DiseasesPain referred to the abdomen from the thorax, spine, or genitalia may prove a vexing diagnostic problem, because diseases of the upper part of the abdominal cavity such as acute cholecystitis or perforated ulcer are frequently associated with intrathoracic complications. A most important, yet often forgotten, dictum is that the possibility of intrathoracic disease must be considered in every patient with abdominal pain, especially if the pain is in the upper part of the abdomen. Systematic questioning and examination directed toward detecting myocardial or pulmonary infarction, pneumonia, pericarditis, or esophageal disease (the intrathoracic diseases that most often masquerade as abdominal emergencies) will often provide sufficient clues to establish the proper diagnosis. Diaphragmatic pleuritis resulting from pneumonia or pulmonary infarction may cause pain in the right upper quadrant and pain in the supraclavicular area, the latter radiation to be distinguished from the referred subscapular pain caused by acute distention of the extrahepatic biliary tree. The ultimate decision as to the origin of abdominal pain may require deliberate and planned observation over a period of several hours, during which repeated questioning and examination will provide the diagnosis or suggest the appropriate studies.Referred pain of thoracic origin is often accompanied by splinting of the involved hemithorax with respiratory lag and decrease in excursion more marked than that seen in the presence of intraabdominal disease. In addition, apparent abdominal muscle spasm caused by referred pain will diminish during the inspiratory phase of respiration, whereas it is persistent throughout both respiratory phases if it is of abdominal origin. Palpation over the area of referred pain in the abdomen also does not usually accentuate the pain and in many instances actually seems to relieve it. Thoracic disease and abdominal disease frequently coexist and may be difficult or impossible to differentiate. For example, the patient with known biliary tract disease often has epigastric pain during myocardial infarction, or biliary colic may be referred to the precordium or left shoulder in a patient who has suffered previously from angina pectoris. For an explanation of the radiation of pain to a previously diseased area, see Chap. 12. Referred pain from the spine, which usually involves compression or irritation of nerve roots, is characteristically intensified by certain motions such as cough, sneeze, or strain and is associated with hyperesthesia over the involved dermatomes. Pain referred to the abdomen from the testes or seminal vesicles is generally accentuated by the slightest pressure on either of these organs. The abdominal discomfort is of dull aching character and is poorly localized.Metabolic Abdominal CrisesPain of metabolic origin may simulate almost any other type of intraabdominal disease. Several mechanisms may be at work. In certain instances, such as hyperlipidemia, the metabolic disease itself may be accompanied by an intraabdominal process such as pancreatitis, which can lead to unnecessary laparotomy unless recognized. C1 esterase deficiency associated with angioneurotic edema is often associated with episodes of severe abdominal pain. Whenever the cause of abdominal pain is obscure, a metabolic origin always must be considered. Abdominal pain is also the hallmark of familial Mediterranean fever (Chap. 323).The problem of differential diagnosis is often not readily resolved. The pain of porphyria and of lead colic is usually difficult to distinguish from that of intestinal obstruction, because severe hyperperistalsis is a prominent feature of both. The pain of uremia or diabetes is nonspecific, and the pain and tenderness frequently shift in location and intensity. Diabetic acidosis may be precipitated by acute appendicitis or intestinal obstruction, so if prompt resolution of the abdominal pain does not result from correction of the metabolic abnormalities, an underlying organic problem should be suspected. Black widow spider bites produce intense pain and rigidity of the abdominal muscles and back, an area infrequently involved in intraabdominal disease.Neurogenic CausesCausalgic pain may occur in diseases that injure sensory nerves. It has a burning character and is usually limited to the distribution of a given peripheral nerve. Normal stimuli such as touch or change in temperature may be transformed into this type of pain, which is frequently present in a patient at rest. The demonstration of irregularly spaced cutaneous pain spots may be the only indication of an old nerve lesion underlying causalgic pain. Even though the pain may be precipitated by gentle palpation, rigidity of the abdominal muscles is absent, and the respirations are not disturbed. Distention of the abdomen is uncommon, and the pain has no relationship to the intake of food.Pain arising from spinal nerves or roots comes and goes suddenly and is of a lancinating type (Chap. 16). It may be caused by herpes zoster, impingement by arthritis, tumors, herniated nucleus pulposus, diabetes, or syphilis. It is not associated with food intake, abdominal distention, or changes in respiration. Severe muscle spasm, as in the gastric crises of tabes dorsalis, is common but is either relieved or is not accentuated by abdominal palpation. The pain is made worse by movement of the spine and is usually confined to a few dermatomes. Hyperesthesia is very common.Pain due to functional causes conforms to none of the aforementioned patterns. Mechanism is hard to define. Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder characterized by abdominal pain and altered bowel habits. The diagnosis is made on the basis of clinical criteria (Chap. 290) and after exclusion of demonstrable structural abnormalities. The episodes of abdominal pain are often brought on by stress, and the pain varies considerably in type and location. Nausea and vomiting are rare. Localized tenderness and muscle spasm are inconsistent or absent. The causes of IBS or related functional disorders are not known.Approach to the Patient: Abdominal PainFew abdominal conditions require such urgent operative intervention that an orderly approach need be abandoned, no matter how ill the patient. Only those patients with exsanguinating intraabdominal hemorrhage (e.g., ruptured aneurysm) must be rushed to the operating room immediately, but in such instances only a few minutes are required to assess the critical nature of the problem. Under these circumstances, all obstacles must be swept aside, adequate venous access for fluid replacement obtained, and the operation begun. Many patients of this type have died in the radiology department or the emergency room while awaiting such unnecessary examinations as electrocardiograms or abdominal films. There are no contraindications to operation when massive intraabdominal hemorrhage is present. Fortunately, this situation is relatively rare. These comments do not pertain to gastrointestinal hemorrhage, which can often be managed by other means (Chap. 42).Nothing will supplant an orderly, painstakingly detailed history, which is far more valuable than any laboratory or radiographic examination. This kind of history is laborious and time-consuming, making it not especially popular, even though a reasonably accurate diagnosis can be made on the basis of the history alone in the majority of cases. Computer-aided diagnosis of abdominal pain provides no advantage over clinical assessment alone. In cases of acute abdominal pain, a diagnosis is readily established in most instances, whereas success is not so frequent in patients with chronic pain. IBS is one of the most common causes of abdominal pain and must always be kept in mind (Chap. 290). The location of the pain can assist in narrowing the differential diagnosis (see Table 14-2); however, the chronological sequence of events in the patient's history is often more important than emphasis on the location of pain. If the examiner is sufficiently open-minded and unhurried, asks the proper questions, and listens, the patient will usually provide the diagnosis. Careful attention should be paid to the extraabdominal regions that may be responsible for abdominal pain. An accurate menstrual history in a female patient is essential. Narcotics or analgesics should not be withheld until a definitive diagnosis or a definitive plan has been formulated; obfuscation of the diagnosis by adequate analgesia is unlikely.
 Table 14-2 Differential Diagnoses of Abdominal Pain by Location

Right Upper Quadrant	Epigastric	Left Upper Quadrant
Cholecystitis	Peptic ulcer disease	Splenic infarct
Cholangitis	Gastritis	Splenic rupture
Pancreatitis	GERD	Splenic abscess
Pneumonia/empyema	Pancreatitis	Gastritis
Pleurisy/pleurodynia	Myocardial infarction	Gastric ulcer
Subdiaphragmatic abscess	Pericarditis	Pancreatitis
Hepatitis	Ruptured aortic aneurysm	Subdiaphragmatic abscess
Budd-Chiari syndrome	Esophagitis
Right Lower Quadrant	Periumbilical	Left Lower Quadrant
Appendicitis	Early appendicitis	Diverticulitis
Salpingitis	Gastroenteritis	Salpingitis
Inguinal hernia	Bowel obstruction	Inguinal hernia
Ectopic pregnancy	Ruptured aortic aneurysm	Ectopic pregnancy
Nephrolithiasis		Nephrolithiasis
Inflammatory bowel disease		Irritable bowel syndrome
Mesenteric lymphadenitis		Inflammatory bowel disease
Typhlitis
Diffuse Nonlocalized Pain
Gastroenteritis	Diabetes
Mesenteric ischemia	Malaria
Bowel obstruction	Familial Mediterranean fever
Irritable bowel syndrome	Metabolic diseases
Peritonitis	Psychiatric disease

In the examination, simple critical inspection of the patient, e.g., of facies, position in bed, and respiratory activity, may provide valuable clues. The amount of information to be gleaned is directly proportional to the gentleness and thoroughness of the examiner. Once a patient with peritoneal inflammation has been examined brusquely, accurate assessment by the next examiner becomes almost impossible. Eliciting rebound tenderness by sudden release of a deeply palpating hand in a patient with suspected peritonitis is cruel and unnecessary. The same information can be obtained by gentle percussion of the abdomen (rebound tenderness on a miniature scale), a maneuver that can be far more precise and localizing. Asking the patient to cough will elicit true rebound tenderness without the need for placing a hand on the abdomen. Furthermore, the forceful demonstration of rebound tenderness will startle and induce protective spasm in a nervous or worried patient in whom true rebound tenderness is not present. A palpable gallbladder will be missed if palpation is so brusque that voluntary muscle spasm becomes superimposed on involuntary muscular rigidity.As in history taking, sufficient time should be spent in the examination. Abdominal signs may be minimal but nevertheless, if accompanied by consistent symptoms, may be exceptionally meaningful. Abdominal signs may be virtually or totally absent in cases of pelvic peritonitis, so careful pelvic and rectal examinations are mandatory in every patient with abdominal pain. Tenderness on pelvic or rectal examination in the absence of other abdominal signs can be caused by operative indications such as perforated appendicitis, diverticulitis, twisted ovarian cyst, and many others.Much attention has been paid to the presence or absence of peristaltic sounds, their quality, and their frequency. Auscultation of the abdomen is one of the least revealing aspects of the physical examination of a patient with abdominal pain. Catastrophes such as strangulating small intestinal obstruction or perforated appendicitis may occur in the presence of normal peristaltic sounds. Conversely, when the proximal part of the intestine above an obstruction becomes markedly distended and edematous, peristaltic sounds may lose the characteristics of borborygmi and become weak or absent, even when peritonitis is not present. It is usually the severe chemical peritonitis of sudden onset that is associated with the truly silent abdomen. Assessment of the patient's state of hydration is important.Laboratory examinations may be of great value in assessment of the patient with abdominal pain, yet with few exceptions they rarely establish a diagnosis. Leukocytosis should never be the single deciding factor as to whether or not operation is indicated. A white blood cell count >20,000/µL may be observed with perforation of a viscus, but pancreatitis, acute cholecystitis, pelvic inflammatory disease, and intestinal infarction may be associated with marked leukocytosis. A normal white blood cell count is not rare in cases of perforation of abdominal viscera. The diagnosis of anemia may be more helpful than the white blood cell count, especially when combined with the history.The urinalysis may reveal the state of hydration or rule out severe renal disease, diabetes, or urinary infection. Blood urea nitrogen, glucose, and serum bilirubin levels may be helpful. Serum amylase levels may be increased by many diseases other than pancreatitis, e.g., perforated ulcer, strangulating intestinal obstruction, and acute cholecystitis; thus, elevations of serum amylase do not rule out the need for an operation. The determination of the serum lipase may have greater accuracy than that of the serum amylase.Plain and upright or lateral decubitus radiographs of the abdomen may be of value in cases of intestinal obstruction, perforated ulcer, and a variety of other conditions. They are usually unnecessary in patients with acute appendicitis or strangulated external hernias. In rare instances, barium or water-soluble contrast study of the upper part of the gastrointestinal tract may demonstrate partial intestinal obstruction that may elude diagnosis by other means. If there is any question of obstruction of the colon, oral administration of barium sulfate should be avoided. On the other hand, in cases of suspected colonic obstruction (without perforation), contrast enema may be diagnostic.In the absence of trauma, peritoneal lavage has been replaced as a diagnostic tool by ultrasound, CT, and laparoscopy. Ultrasonography has proved to be useful in detecting an enlarged gallbladder or pancreas, the presence of gallstones, an enlarged ovary, or a tubal pregnancy. Laparoscopy is especially helpful in diagnosing pelvic conditions, such as ovarian cysts, tubal pregnancies, salpingitis, and acute appendicitis. Radioisotopic scans (HIDA) may help differentiate acute cholecystitis from acute pancreatitis. A CT scan may demonstrate an enlarged pancreas, ruptured spleen, or thickened colonic or appendiceal wall and streaking of the mesocolon or mesoappendix characteristic of diverticulitis or appendicitis.Sometimes, even under the best circumstances with all available aids and with the greatest of clinical skill, a definitive diagnosis cannot be established at the time of the initial examination. Nevertheless, despite lack of a clear anatomic diagnosis, it may be abundantly clear to an experienced and thoughtful physician and surgeon that on clinical grounds alone operation is indicated. Should that decision be questionable, watchful waiting with repeated questioning and examination will often elucidate the true nature of the illness and indicate the proper course of action.Further Readings

Cervero F, Laird JM: Visceral pain. Lancet 353:2145, 1999 [PMID: 10382712]

Jones PF: Suspected acute appendicitis: Trends in management over 30 years. Br J Surg 88:1570, 2001 [PMID: 11736966]

Lyon C, Clark DC: Diagnosis of acute abdominal pain in older patients. Am Fam Physician 74:1537, 2006 [PMID: 17111893]

Silen W: Cope's Early Diagnosis of the Acute Abdomen, 21st ed, New York and Oxford: Oxford University Press, 2005

Tait IS et al: Do patients with abdominal pain wait unduly long for analgesia? J R Coll Surg Edinb 44:181, 1999 [PMID: 10372490]

Bibliography

Attard AR et al: Safety of early pain relief for acute abdominal pain. BMJ 305:554, 1992 [PMID: 1393034]

Bugliosi TF et al: Acute abdominal pain in the elderly. Ann Emerg Med 19:1383, 1990 [PMID: 2240749]

Gatzen C et al: Management of acute abdominal pain: Decision making in the accident and emergency department. J R Coll Surg Edinb 36:121, 1991 [PMID: 2051408]

Scott HJ, Rosin RD: The influence of diagnostic and therapeutic laparoscopy on patients presenting with an acute abdomen. J R Soc Med 86:699, 1993 [PMID: 8308808]

Taourel P et al: Acute abdomen of unknown origin: Impact of CT on diagnosis and management. Gastrointest Radiol 17:287, 1992 [PMID: 1426841]

Weyant MJ et al: Interpretation of computed tomography does not correlate with laboratory or pathologic findings in surgically confirmed acute appendicitis. Surgery 128:145, 2000 [PMID: 10922984]

Chapter 013. Chest Discomfort

Tham khảo bài viết bằng tiếng việt qua google  
Chest Discomfort: IntroductionChest discomfort is one of the most common challenges for clinicians in the office or emergency department. The differential diagnosis includes conditions affecting organs throughout the thorax and abdomen, with prognostic implications that vary from benign to life-threatening (Table 13-1). Failure to recognize potentially serious conditions such as acute ischemic heart disease, aortic dissection, tension pneumothorax, or pulmonary embolism can lead to serious complications, including death. Conversely, overly conservative management of low-risk patients leads to unnecessary hospital admissions, tests, procedures, and anxiety.Table 13-1 Differential Diagnoses of Patients Admitted to Hospital with Acute Chest Discomfort Ruled Not Myocardial Infarction

Diagnosis	Percent
Gastroesophageal diseasea	42
Gastroesophageal reflux
Esophageal motility disorders
Peptic ulcer
Gallstones
Ischemic heart disease	31
Chest wall syndromes	28
Pericarditis	4
Pleuritis/pneumonia	2
Pulmonary embolism	2
Lung cancer	1.5
Aortic aneurysm	1
Aortic stenosis	1
Herpes zoster	1

^aIn order of frequency.Source: P Fruergaard et al: Eur Heart J 17:1028, 1996.

Causes of Chest DiscomfortMyocardial Ischemia and InjuryMyocardial ischemia occurs when the oxygen supply to the heart is not sufficient to meet metabolic needs. This mismatch can result from a decrease in oxygen supply, a rise in demand, or both. The most common underlying cause of myocardial ischemia is obstruction of coronary arteries by atherosclerosis; in the presence of such obstruction, transient ischemic episodes are usually precipitated by an increase in oxygen demand as a result of physical exertion. However, ischemia can also result from psychological stress, fever, or large meals or from compromised oxygen delivery due to anemia, hypoxia, or hypotension. Ventricular hypertrophy due to valvular heart disease, hypertrophic cardiomyopathy, or hypertension can predispose the myocardium to ischemia because of impaired penetration of blood flow from epicardial coronary arteries to the endocardium.Angina Pectoris(See also Chap. 237) The chest discomfort of myocardial ischemia is a visceral discomfort that is usually described as a heaviness, pressure, or squeezing (Table 13-2). Other common adjectives for anginal pain are burning and aching. Some patients deny any "pain" but may admit to dyspnea or a vague sense of anxiety. The word "sharp" is sometimes used by patients to describe intensity rather than quality.Table 13-2 Typical Clinical Features of Major Causes of Acute Chest Discomfort

Condition	Duration	Quality	Location	Associated Features
Angina	More than 2 and less than 10 min	Pressure, tightness, squeezing, heaviness, burning	Retrosternal, often with radiation to or isolated discomfort in neck, jaw, shoulders, or arms—frequently on left	Precipitated by exertion, exposure to cold, psychologic stressS4 gallop or mitral regurgitation murmur during pain
Unstable angina	10–20 min	Similar to angina but often more severe	Similar to angina	Similar to angina, but occurs with low levels of exertion or even at rest
Acute myocardial infarction	Variable; often more than 30 min	Similar to angina but often more severe	Similar to angina	Unrelieved by nitroglycerinMay be associated with evidence of heart failure or arrhythmia
Aortic stenosis	Recurrent episodes as described for angina	As described for angina	As described for angina	Late-peaking systolic murmur radiating to carotid arteries
Pericarditis	Hours to days; may be episodic	Sharp	Retrosternal or toward cardiac apex; may radiate to left shoulder	May be relieved by sitting up and leaning forwardPericardial friction rub
Aortic dissection	Abrupt onset of unrelenting pain	Tearing or ripping sensation; knifelike	Anterior chest, often radiating to back, between shoulder blades	Associated with hypertension and/or underlying connective tissue disorder, e.g., Marfan syndromeMurmur of aortic insufficiency, pericardial rub, pericardial tamponade, or loss of peripheral pulses
Pulmonary embolism	Abrupt onset; several minutes to a few hours	Pleuritic	Often lateral, on the side of the embolism	Dyspnea, tachypnea, tachycardia, and hypotension
Pulmonary hypertension	Variable	Pressure	Substernal	Dyspnea, signs of increased venous pressure including edema and jugular venous distention
Pneumonia or pleuritis	Variable	Pleuritic	Unilateral, often localized	Dyspnea, cough, fever, rales, occasional rub
Spontaneous pneumothorax	Sudden onset; several hours	Pleuritic	Lateral to side of pneumothorax	Dyspnea, decreased breath sounds on side of pneumothorax
Esophageal reflux	10–60 min	Burning	Substernal, epigastric	Worsened by postprandial recumbencyRelieved by antacids
Esophageal spasm	2–30 min	Pressure, tightness, burning	Retrosternal	Can closely mimic angina
Peptic ulcer	Prolonged	Burning	Epigastric, substernal	Relieved with food or antacids
Gallbladder disease	Prolonged	Burning, pressure	Epigastric, right upper quadrant, substernal	May follow meal
Musculoskeletal disease	Variable	Aching	Variable	Aggravated by movementMay be reproduced by localized pressure on examination
Herpes zoster	Variable	Sharp or burning	Dermatomal distribution	Vesicular rash in area of discomfort
Emotional and psychiatric conditions	Variable; may be fleeting	Variable	Variable; may be retrosternal	Situational factors may precipitate symptomsAnxiety or depression often detectable with careful history

 The location of angina pectoris is usually retrosternal; most patients do not localize the pain to any small area. The discomfort may radiate to the neck, jaw, teeth, arms, or shoulders, reflecting the common origin in the posterior horn of the spinal cord of sensory neurons supplying the heart and these areas. Some patients present with aching in sites of radiated pain as their only symptoms of ischemia. Occasional patients report epigastric distress with ischemic episodes. Less common is radiation to below the umbilicus or to the back.Stable angina pectoris usually develops gradually with exertion, emotional excitement, or after heavy meals. Rest or treatment with sublingual nitroglycerin typically leads to relief within several minutes. In contrast, pain that is fleeting (lasting only a few seconds) is rarely ischemic in origin. Similarly, pain that lasts for several hours is unlikely to represent angina, particularly if the patient's electrocardiogram (ECG) does not show evidence of ischemia.Anginal episodes can be precipitated by any physiologic or psychological stress that induces tachycardia. Most myocardial perfusion occurs during diastole, when there is minimal pressure opposing coronary artery flow from within the left ventricle. Since tachycardia decreases the percentage of the time in which the heart is in diastole, it decreases myocardial perfusion.Unstable Angina and Myocardial Infarction(See also Chaps. 238 and 239) Patients with these acute ischemic syndromes usually complain of symptoms similar in quality to angina pectoris, but more prolonged and severe. The onset of these syndromes may occur with the patient at rest, or awakened from sleep, and sublingual nitroglycerin may lead to transient or no relief. Accompanying symptoms may include diaphoresis, dyspnea, nausea, and light-headedness.The physical examination may be completely normal in patients with chest discomfort due to ischemic heart disease. Careful auscultation during ischemic episodes may reveal a third or fourth heart sound, reflecting myocardial systolic or diastolic dysfunction. A transient murmur of mitral regurgitation suggests ischemic papillary muscle dysfunction. Severe episodes of ischemia can lead to pulmonary congestion and even pulmonary edema.Other Cardiac CausesMyocardial ischemia caused by hypertrophic cardiomyopathy or aortic stenosis leads to angina pectoris similar to that caused by coronary atherosclerosis. In such cases, a loud systolic murmur or other findings usually suggest that abnormalities other than coronary atherosclerosis may be contributing to the patient's symptoms. Some patients with chest pain and normal coronary angiograms have functional abnormalities of the coronary circulation, ranging from coronary spasm visible on coronary angiography to abnormal vasodilator responses and heightened vasoconstrictor responses. The term "cardiac syndrome X" is used to describe patients with angina-like chest pain and ischemic-appearing ST-segment depression during stress despite normal coronary arteriograms. Some data indicate that many such patients have limited changes in coronary flow in response to pacing stress or coronary vasodilators. Despite the possibility that chest pain may be due to myocardial ischemia in such patients, their prognosis is excellent.Pericarditis(See also Chap. 232) The pain in pericarditis is believed to be due to inflammation of the adjacent parietal pleura, since most of the pericardium is believed to be insensitive to pain. Thus, infectious pericarditis, which usually involves adjoining pleural surfaces, tends to be associated with pain, while conditions that cause only local inflammation (e.g., myocardial infarction or uremia) and cardiac tamponade tend to result in mild or no chest pain.The adjacent parietal pleura receives its sensory supply from several sources, so the pain of pericarditis can be experienced in areas ranging from the shoulder and neck to the abdomen and back. Most typically, the pain is retrosternal and is aggravated by coughing, deep breaths, or changes in position—all of which lead to movements of pleural surfaces. The pain is often worse in the supine position and relieved by sitting upright and leaning forward. Less common is a steady aching discomfort that mimics acute myocardial infarction. Diseases of the Aorta(See also Chap. 242) Aortic dissection is a potentially catastrophic condition that is due to spread of a subintimal hematoma within the wall of the aorta. The hematoma may begin with a tear in the intima of the aorta or with rupture of the vasa vasorum within the aortic media. This syndrome can occur with trauma to the aorta, including motor vehicle accidents or medical procedures in which catheters or intraaortic balloon pumps damage the intima of the aorta. Nontraumatic aortic dissections are rare in the absence of hypertension and/or conditions associated with deterioration of the elastic or muscular components of the media within the aorta's wall. Cystic medial degeneration is a feature of several inherited connective tissue diseases, including Marfan and Ehlers-Danlos syndromes. About half of all aortic dissections in women under 40 years of age occur during pregnancy.Almost all patients with acute dissections present with severe chest pain, although some patients with chronic dissections are identified without associated symptoms. Unlike the pain of ischemic heart disease, symptoms of aortic dissection tend to reach peak severity immediately, often causing the patient to collapse from its intensity. The classic teaching is that the adjectives used to describe the pain reflect the process occurring within the wall of the aorta—"ripping" and "tearing"—but more recent data suggest that the most common presenting complaint is sudden onset of severe, sharp pain. The location often correlates with the site and extent of the dissection. Thus, dissections that begin in the ascending aorta and extend to the descending aorta tend to cause pain in the front of the chest that extends into the back, between the shoulder blades.Physical findings may also reflect extension of the aortic dissection that compromises flow into arteries branching off the aorta. Thus, loss of a pulse in one or both arms, cerebrovascular accident, or paraplegia can all be catastrophic consequences of aortic dissection. Hematomas that extend proximally and undermine the coronary arteries or aortic valve apparatus may lead to acute myocardial infarction or acute aortic insufficiency. Rupture of the hematoma into the pericardial space leads to pericardial tamponade.Another abnormality of the aorta that can cause chest pain is a thoracic aortic aneurysm. Aortic aneurysms are frequently asymptomatic but can cause chest pain and other symptoms by compressing adjacent structures. This pain tends to be steady, deep, and sometimes severe.Pulmonary Embolism (See also Chap. 256) Chest pain due to pulmonary embolism is believed to be due to distention of the pulmonary artery or infarction of a segment of the lung adjacent to the pleura. Massive pulmonary emboli may lead to substernal pain that is suggestive of acute myocardial infarction. More commonly, smaller emboli lead to focal pulmonary infarctions that cause pain that is lateral and pleuritic. Associated symptoms include dyspnea and, occasionally, hemoptysis. Tachycardia is usually present. Although not always present, certain characteristic ECG changes can support the diagnosis.Pneumothorax (See also Chap. 257) Sudden onset of pleuritic chest pain and respiratory distress should lead to consideration of spontaneous pneumothorax, as well as pulmonary embolism. Such events may occur without a precipitating event in persons without lung disease, or as a consequence of underlying lung disorders.Pneumonia or Pleuritis (See also Chaps. 251 and 257) Lung diseases that damage and cause inflammation of the pleura of the lung usually cause a sharp, knifelike pain that is aggravated by inspiration or coughing.Gastrointestinal Conditions(See also Chap. 286) Esophageal pain from acid reflux from the stomach, spasm, obstruction, or injury can be difficult to discern from myocardial syndromes. Acid reflux typically causes a deep burning discomfort that may be exacerbated by alcohol, aspirin, or some foods; this discomfort is often relieved by antacid or other acid-reducing therapies. Acid reflux tends to be exacerbated by lying down and may be worse in early morning when the stomach is empty of food that might otherwise absorb gastric acid.Esophageal spasm may occur in the presence or absence of acid reflux and leads to a squeezing pain indistinguishable from angina. Prompt relief of esophageal spasm is often provided by antianginal therapies such as sublingual nifedipine, further promoting confusion between these syndromes. Chest pain can also result from injury to the esophagus, such as a Mallory-Weiss tear caused by severe vomiting.Chest pain can result from diseases of the gastrointestinal tract below the diaphragm, including peptic ulcer disease, biliary disease, and pancreatitis. These conditions usually cause abdominal pain as well as chest discomfort; symptoms are not likely to be associated with exertion. The pain of ulcer disease typically occurs 60 to 90 min after meals, when postprandial acid production is no longer neutralized by food in the stomach. Cholecystitis usually causes a pain that is described as aching, occurring an hour or more after meals.Neuromusculoskeletal ConditionsCervical disk disease can cause chest pain by compression of nerve roots. Pain in a dermatomal distribution can also be caused by intercostal muscle cramps or by herpes zoster. Chest pain symptoms due to herpes zoster may occur before skin lesions are apparent.Costochondral and chondrosternal syndromes are the most common causes of anterior chest musculoskeletal pain. Only occasionally are physical signs of costochondritis such as swelling, redness, and warmth (Tietze's syndrome) present. The pain of such syndromes is usually fleeting and sharp, but some patients experience a dull ache that lasts for hours. Direct pressure on the chondrosternal and costochondral junctions may reproduce the pain from these and other musculoskeletal syndromes. Arthritis of the shoulder and spine and bursitis may also cause chest pain. Some patients who have these conditions and myocardial ischemia blur and confuse symptoms of these syndromes.Emotional and Psychiatric ConditionsAs many as 10% of patients who present to emergency departments with acute chest discomfort have panic disorder or other emotional conditions. The symptoms in these populations are highly variable, but frequently the discomfort is described as visceral tightness or aching that lasts more than 30 min. Some patients offer other atypical descriptions, such as pain that is fleeting, sharp, and/or localized to a small region. The ECG in patients with emotional conditions may be difficult to interpret if hyperventilation causes ST-T-wave abnormalities. A careful history may elicit clues of depression, prior panic attacks, somatization, agoraphobia, or other phobias.Approach to the Patient: Chest Discomfort The evaluation of the patient with chest discomfort must accommodate two goals—determining the diagnosis and assessing the safety of the immediate management plan. The latter issue is often dominant when the patient has acute chest discomfort, such as patients seen in the emergency department. In such settings, the clinician must focus first on identifying patients who require aggressive interventions to diagnose or manage potentially life-threatening conditions, including acute ischemic heart disease, acute aortic dissection, pulmonary embolism, and tension pneumothorax. If such conditions are unlikely, the clinician must address questions such as the safety of discharge to home, admission to a non-coronary care unit facility, or immediate exercise testing. Table 13-3 displays a sequence of questions that can be used in the evaluation of the patient with chest discomfort, with the diagnostic entities that are most important for consideration at each stage of the evaluation.Table 13-3 Considerations in the Assessment of the Patient with Chest Discomfort

1. Could the chest discomfort be due to an acute, potentially life-threatening condition that warrants immediate hospitalization and aggressive evaluation?
Acute ischemic heart disease	Pulmonary embolism
Aortic dissection	Spontaneous pneumothorax
2. If not, could the discomfort be due to a chronic condition likely to lead to serious complications?
Stable angina
Aortic stenosis
Pulmonary hypertension
3. If not, could the discomfort be due to an acute condition that warrants specific treatment?
Pericarditis
Pneumonia/pleuritis
Herpes zoster
4. If not, could the discomfort be due to another treatable chronic condition?
Esophageal reflux	Cervical disk disease
Esophageal spasm	Arthritis of the shoulder or spine
Peptic ulcer disease	Costochondritis
Gallbladder disease	Other musculoskeletal disorders
Other gastrointestinal conditions	Anxiety state

 Acute Chest DiscomfortIn patients with acute chest discomfort, the clinician must first assess the patient's respiratory and hemodynamic status. If either is compromised, initial management should focus on stabilizing the patient before the diagnostic evaluation is pursued. If, however, the patient does not require emergent interventions, then a focused history, physical examination, and laboratory evaluation should be performed to assess the patient's risk of life-threatening conditions. Clinicians who are seeing patients in the office setting should not assume that they do not have acute ischemic heart disease, even if the prevalence may be lower. Malpractice litigation related to myocardial infarctions that were missed during office evaluations is becoming increasingly common, and ECGs were not performed in many such cases. The prevalence of high-risk patients seen in office settings may be increasing due to congestion in emergency departments.In either setting, the history should include questions about the quality and location of the chest discomfort (Table 13-2). The patient should also be asked about the nature of onset of the pain and its duration. Myocardial ischemia is usually associated with a gradual intensification of symptoms over a period of minutes. Pain that is fleeting or that lasts hours without being associated with electrocardiographic changes is not likely to be ischemic in origin. Although the presence of risk factors for coronary artery disease may heighten concern for this diagnosis, the absence of such risk factors does not lower the risk for myocardial ischemia enough to be used to justify a decision to discharge a patient.Wide radiation of chest pain increases probability that pain is due to myocardial infarction. Radiation of chest pain to the left arm is common with acute ischemic heart disease, but radiation to the right arm is also highly consistent with this diagnosis. Figure 13-1 shows estimates derived from several studies of the impact of various clinical features from the history on the probability that a patient has an acute myocardial infarction.

Impact of chest pain characteristics on odds of acute myocardial infarction (AMI). (Figure prepared from data in Swap and Nagurney.)Right shoulder pain is also common with acute cholecystitis, but this syndrome is usually accompanied by pain that is located in the abdomen rather than chest. Chest pain that radiates between the scapulae raises the question of aortic dissection.The physical examination should include evaluation of blood pressure in both arms and of pulses in both legs. Poor perfusion of a limb may be due to an aortic dissection that has compromised flow to an artery branching from the aorta. Chest auscultation may reveal diminished breath sounds; a pleural rub; or evidence of pneumothorax, pulmonary embolism, pneumonia, or pleurisy. Tension pneumothorax may lead to a shift in the trachea from the midline, away from the side of the pneumothorax. The cardiac examination should seek pericardial rubs, systolic and diastolic murmurs, and third or fourth heart sounds. Pressure on the chest wall may reproduce symptoms in patients with musculoskeletal causes of chest pain; it is important that the clinician ask the patient if the chest pain syndrome is being completely reproduced before drawing too much reassurance that more serious underlying conditions are not present.An ECG is an essential test for adults with chest discomfort that is not due to an obvious traumatic cause. In such patients, the presence of electrocardiographic changes consistent with ischemia or infarction (Chap. 221) is associated with high risks of acute myocardial infarction or unstable angina (Table 13-4); such patients should be admitted to a unit with electrocardiographic monitoring and the capacity to respond to a cardiac arrest. The absence of such changes does not exclude acute ischemic heart disease, but the risk of life-threatening complications is low for patients with normal electrocardiograms or only nonspecific ST-T-wave changes. If these patients are not considered appropriate for immediate discharge, they are often candidates for early or immediate exercise testing.

Finding	Prevalence
	Myocardial Infarction, %	Unstable Angina, %
ST elevation ( 1 mm) or Q waves on ECG not known to be old	79	12
Ischemia or strain on ECG not known to be old (ST depression 1 mm or ischemic T waves)	20	41
None of the preceding ECG changes but a prior history of angina or myocardial infarction (history of heart attack or nitroglycerin use)	4	51
None of the preceding ECG changes and no prior history of angina or myocardial infarction (history of heart attack or nitroglycerin use)	2	14

 Note: ECG, electrocardiogram.Unpublished data from Brigham and Women's Hospital Chest Pain Study, 1997–1999Markers of myocardial injury are often obtained in the emergency department evaluation of acute chest discomfort. The most commonly used markers are creatine kinase (CK), CK-MB, and the cardiac troponins (I and T). Rapid bedside assays of the cardiac troponins have been developed and shown to be sufficiently accurate to predict prognosis and guide management. Some data support the use of other markers, such as serum myoglobin, C-reactive protein (CRP), placental growth factor, myeloperoxidase, and B-type natriuretic peptide (BNP); their roles are the subject of ongoing research. Single values of any of these markers do not have high sensitivity for acute myocardial infarction or for prediction of complications. Hence, decisions to discharge patients home should not be made on the basis of single negative values of these tests.Provocative tests for coronary artery disease are not appropriate for patients with ongoing chest pain. In such patients, rest myocardial perfusion scans can be considered; a normal scan reduces the likelihood of coronary artery disease and can help avoid admission of low-risk patients to the hospital. Promising early results suggest that 64-slice CT and cardiac MRI may be of sufficient accuracy for diagnosis of coronary disease that these technologies may become widely used for patients with acute chest pain in whom the diagnosis is not clear. Clinicians frequently employ therapeutic trials with sublingual nitroglycerin or antacids or, in the stable patient seen in the office setting, a proton pump inhibitor. A common error is to assume that a response to any of these interventions clarifies the diagnosis. While such information is often helpful, the patient's response may be due to the placebo effect. Hence, myocardial ischemia should never be considered excluded solely because of a response to antacid therapy. Similarly, failure of nitroglycerin to relieve pain does not exclude the diagnosis of coronary disease.If the patient's history or examination is consistent with aortic dissection, imaging studies to evaluate the aorta must be pursued promptly because of the high risk of catastrophic complications with this condition. Appropriate tests include a chest CT scan with contrast, MRI, or transesophageal echocardiography.Acute pulmonary embolism should be considered in patients with respiratory symptoms, pleuritic chest pain, hemoptysis, or a history of venous thromboembolism or coagulation abnormalities. Initial tests usually include CT angiography or a lung scan, which are sometimes combined with lower extremity venous ultrasound or D-dimer testing.If patients with acute chest discomfort show no evidence of life-threatening conditions, the clinician should then focus on serious chronic conditions with the potential to cause major complications, the most common of which is stable angina. Early use of exercise electrocardiography, stress echocardiography, or stress perfusion imaging for such patients, whether in the office or the emergency department, is now an accepted management strategy for low-risk patients. Exercise testing is not appropriate, however, for patients who (1) report pain that is believed to be ischemic occurring at rest or (2) have electrocardiographic changes not known to be old that are consistent with ischemia.Patients with sustained chest discomfort who do not have evidence for life-threatening conditions should be evaluated for evidence of conditions likely to benefit from acute treatment (Table 13-3). Pericarditis may be suggested by the history, physical examination, and ECG (Table 13-2). Clinicians should carefully assess blood pressure patterns and consider echocardiography in such patients to detect evidence of impending pericardial tamponade. Chest x-rays can be used to evaluate the possibility of pulmonary disease.Guidelines and Critical Pathways for Acute Chest DiscomfortGuidelines for the initial evaluation for patients with acute chest pain have been developed by the American College of Cardiology, American Heart Association, and other organizations. These guidelines recommend performance of an ECG for virtually all patients with chest pain who do not have an obvious noncardiac cause of their pain, and performance of a chest x-ray for patients with signs or symptoms consistent with congestive heart failure, valvular heart disease, pericardial disease, or aortic dissection or aneurysm.The American College of Cardiology/American Heart Association guidelines on exercise testing support its use in low-risk patients presenting to the emergency department, as well as in selected intermediate-risk patients. However, these guidelines emphasize that exercise tests should be performed only after patients have been screened for high-risk features or other indicators for hospital admission. Many medical centers have adopted critical pathways and other forms of guidelines to increase efficiency and to expedite the treatment of patients with high-risk acute ischemic heart disease syndromes. These guidelines emphasize the following strategies:       Rapid identification and treatment of patients for whom emergent reperfusion therapy, either via percutaneous coronary interventions or thrombolytic agents, is likely to lead to improved outcomes.        Triage to non-coronary care unit monitored facilities such as intermediate-care units or chest pain units of patients with a low risk for complications, such as patients without new ischemic changes on their ECGs and without ongoing chest pain. Such patients can usually be safely observed in non-coronary care unit settings, undergo early exercise testing, or be discharged home. Risk stratification can be assisted through use of prospectively validated multivariate algorithms that have been published for acute ischemic heart disease and its complications.        Shortening lengths of stay in the coronary care unit and hospital. Recommendations regarding the minimum length of stay in a monitored bed for a patient who has no further symptoms have decreased in recent years to 12 h or less if exercise testing or other risk stratification technologies are available.Nonacute Chest DiscomfortThe management of patients who do not require admission to the hospital or who no longer require inpatient observation should seek to identify the cause of the symptoms and the likelihood of major complications. Noninvasive tests for coronary disease serve both to diagnose this condition and to identify patients with high-risk forms of coronary disease who may benefit from revascularization. Gastrointestinal causes of chest pain can be evaluated via endoscopy or radiology studies, or with trials of medical therapy. Emotional and psychiatric conditions warrant appropriate evaluation and treatment; randomized trial data indicate that cognitive therapy and group interventions lead to decreases in symptoms for such patients.Further Readings

Brennan M-L et al: Prognostic value of myeloperoxidase in patients with chest pain. N Engl J Med 349:1595, 2003 [PMID: 14573731]

Gibbons RJ et al: ACC/AHA 2002 guideline update for exercise testing. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Exercise Testing). Available at http://www.acc.org/qualityandscience/clinical/guidelines/exercise/dirindex.htm. Accessed on January 22, 2006

Gibson PB et al: Low event rate for stress-only perfusion imaging in patients evaluated for chest pain. J Am Coll Cardiol 39:999, 2002 [PMID: 11897442]

Heeschem C et al: Prognostic value of placental growth factor in patients with chest pain. JAMA 291:435, 2004

Kwong RY et al: Detecting acute coronary syndrome in the emergency department with cardiac magnetic resonance imaging. Circulation 197:531, 2003

Leber AW et al: Quantification of obstructive and nonobstructive coronary lesions of 64-slice computed tomography. J Am Coll Cardiol 46:147, 2005 [PMID: 15992649]

Swap CJ, Nagurney JT: Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA 294:2623, 2005 [PMID: 16304077]

Tong KL et al: Myocardial contrast echocardiography versus Thrombolysis in Myocardial Infarction score in patients presenting to the emergency department with chest pain and a nondiagnostic electrocardiogram. J Am Coll Cardiol 46:928, 2005

Tsai TT et al: Acute aortic syndromes. Circulation 205:3802, 2005