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Chapter 11 FEVER78
15. What is a fever of unknown origin (FUO)?
The classic 1961 definition by Petersdorf, et al., defines FUO as a fever greater than 38.3°C
(100.9°F) documented on several occasions during a period longer than 3 weeks, with an
uncertain diagnosis after 1 week of evaluation in the hospital. The most common cause of
FUO is occult infection (particularly tuberculosis) and malignancy, each accounting for
approximately 30% of cases.
16. For how long do typical febrile illnesses last?
In most cases, the fever resolves within 3 to 7 days.
17. How do I approach a child younger than 3 years with a fever?
See Chapter 60.
CONTROVERSY
18. Is a fever a friend or foe?
This question has been controversial for centuries. Although fever per se is self-limiting and
rarely serious, it is often considered by patients and doctors to be a major and harmful sign of
illness, and parents and medical practitioners may develop what has been termed fever
phobia, treating the fever almost as an illness in itself rather than a symptom. More and more
research is proving, however, that fever may be beneficial in fighting some infections. Higher
temperatures increase the activity of neutrophils and lymphocytes and decrease the levels of
serum iron, a substrate that many bacteria need to reproduce. It enhances immunological
processes, including the activity of IL-1, T helper cells and cytolytic T cells, and B cell and
immunoglobulin synthesis. A study of children with meningitis observed those with a fever
had mortality benefit over those who were afebrile or hypothermic. A Finnish study of children
with salmonella gastroenteritis demonstrated a significant negative correlation between the
degree of fever and the duration of excretion of organisms.
19. Many physicians recommend alternating acetaminophen and ibuprofen for
fevers. Is this effective?
This is not an evidence-based practice. There is presently no scientific evidence that this
combination is safe or achieves faster antipyresis than an adequate dose of either agent alone.
The observed fever reduction of 0.5°C when combining antipyretics, compared with a single
antipyretic, is insufficient to warrant routine use. Additionally, alternating antipyretics can be
confusing for caregivers, potentially leading to incorrect dosing of either product. The practice
can also increase parents’ fever phobia because it increases parental preoccupation with the
height of the fever.
KEY POINTS: FEVER
1. Increased temperature may be indicative of either a fever or hyperthermia due to another
cause, such as heat illness, particularly in times of increased ambient temperatures.
2. Response to antipyretics does not differentiate serious from more benign causes of fever.
3. The degree of temperature elevation is not predictive of serious illness.
Chapter 11 FEVER 79
BIBLIOGRAPHY
1. Baraff LJ: Management of fever without source in infants and children. Ann Emerg Med 36:602, 2000.
2. Craig JV, Lancaster GA, Taylor S, et al: Infrared ear thermometry compared with rectal thermometry in
children: a systemic review. Lancet 360:603–609, 2002.
3. Craig JV, Lancaster GA, PR Williamson, et al: Temperature measured at the axilla compared with rectum in
children and young people: a systematic review. BMJ 320:1174, 2000.
4. El-Radhi AS: Why is the evidence not affecting the practice of fever management? Arch Dis Child 93(11):
918–920, 2008.
5. El-Radhi AS, Barry W: Do antipyretics prevent febrile convulsions? Arch Dis Child 88:641–642, 2003.
6. El-Radhi AS, Rostila T, Vesikari T: Association of high fever and short bacterial excretion after salmonellosis.
Arch Dis Child 67:81, 1992.
7. Erlewyn-Lajeunesse MDS, Coppins K, Hunt LP, et al: Randomized controlled trial of combined paracetamol
and ibuprofen for fever. Arch Dis Child 91:414–416, 2006.
8. Katz-Sidlow RJ, Rowberry JP, Ho M: Fever determination in young infants: prevalence and accuracy of
parental palpation. Ped Emerg Care 25(1):12, 2009.
9. Mayoral CE, Marino RV, Rosenfeld W, et al: Alternating antipyretics: is this an alternative? Pediatrics
105:1009–1012, 2000.
10. Meremikwu M, Oyo-Ita A: Paracetamol for treating fever in children. Cochrane Database Syst Rev
2:CD003676, 2002.
11. Petersdorf RG, Beeson PB: Fever of unexplained origin: report on 100 cases. Medicine 40:1–30, 1961.
12. Purssell E: Physical treatment of fever. Arch Dis Child 82:238–239, 2000.
13. Stoll ML, Rubin LG: Incidence of occult bacteremia among highly febrile young children in the era of the
pneumococcal conjugate vaccine. Arch Ped Adol Med 158;671:2004.
14. Wong VK, Hitchcock W, Mason WH: Meningococcal infections in children: a review of 100 cases. Pediatr
Infect Dis J 8:224–227, 1998.
15. Wright AD, Liebelt EL: Alternating antipyretics for fever reduction in children: an unfounded practice passed
down to parents from pediatricians. Clin Pediatr 46:146–150, 2007.
80
CHEST PAIN
CHAPTER 12
Eric A. Wong, MD, and Shamai A. Grossman, MD, MS
1. Why is the cause of chest pain often difficult to determine in the ED?
n
Numerous disease processes in a variety of organs may result in chest pain.
n
The severity of the pain is often unrelated to its life-threatening potential.
n
The location of the pain as perceived by the patient frequently does not correspond
with its source.
n
Reproducible chest pain can have a cardiac etiology.
n
Physical findings, laboratory assays, and radiologic studies are often non-diagnostic
in the ED.
n
More than one disease process may be present.
n
The causes of acute chest pain often can be dynamic processes.
2. Why is the location of chest pain not diagnostic of its cause?
Somatic fibers from the dermis are numerous and enter the spinal cord at a single level,
resulting in sharp, localized pain. Visceral afferent fibers from the thorax and upper
abdomen are less numerous. They enter the spinal cord at multiple levels, resulting in a
pain that is dull, aching, and poorly localized. Connections between the visceral and
somatic fibers may result in the visceral pain being perceived as originating from
somatic locations, such as the shoulder, arm, neck, or jaw.
3. List life-threatening causes of acute chest pain that must be considered
first when evaluating a patient in the ED.
n
Myocardial infarction
n
Aortic dissection
n
Unstable angina
n
Pulmonary embolism (PE)
4. List some other conditions that may present with chest pain.
n
Stable angina
n
Valvular heart disease
n
Pneumonia
n
Gastroesophageal reflux disease
(GERD)
n
Esophageal spasm
n
Thoracic outlet syndrome
n
Mediastinitis
n
Musculoskeletal pain
n
Peptic ulcer disease
n
Cholecystitis
n
Pancreatitis
n
Herpes zoster
n
Sickle cell anemia
n
Anxiety
n
Pneumothorax
n
Acute pericarditis
n
Esophageal rupture
n
Myocarditis
5. What is the best initial approach to patients presenting with chest
pain?
All patients with acute chest pain should be approached with the assumption that a
life-threatening cause is present. Once patient stability is established, with few
exceptions, supplemental oxygen, intravenous access, and cardiac monitoring should be
initiated (Fig. 12-1) before any diagnostic studies are started.
Chapter 12 CHEST PAIN 81
6. How do I evaluate the patient with chest pain?
An accurate history is the most important component of the evaluation. Factors to be
considered include onset, character and quality, severity, location, pattern of radiation,
duration of pain, and associated symptoms. Precipitating factors, such as exertion, movement,
or inspiration, and relieving factors, such as rest or body position, may provide clues to the
origin of the pain (Table 12-1). Relief of chest pain with nitroglycerin is not useful in
distinguishing between cardiac and noncardiac causes of chest pain.
7. What are the major risk factors associated with ischemic heart disease, PE,
and aortic dissection?
See Chapters 27, 29, and 31.
Figure. 12-1. Evaluation of chest pain. ACS, acute coronary syndrome; CAD, coronary artery
disease; CCU, coronary care unit; CPU, chest pain observation unit; ICU, intensive care unit; NSTEMI,
non-ST segment elevation myocardial infarction; STEMI, ST segment elevation myocardial infarction,
UA, unstable angina.
8. Are risk factors for cardiac ischemia useful in the ED?
Although the classic risk factors for cardiac ischemia are useful in determining long-term risk
of a patient developing coronary artery disease, risk factors have very limited utility in the ED
setting when trying to determine the acute risk of acute coronary syndrome (ACS). Recent
American College of Cardiology/American Heart Association (ACC/AHA) guidelines suggest
that the most important factor in predicting ACS in a patient presenting with chest pain is the
history of present illness, rather than cardiac risk factors.
9. Are there any useful clinical prediction rules for risk stratifying patients with
suspected PE?
Yes. See Chapter 27.
10. Is radiation of chest pain significant?
Radiating chest pain is suggestive but not diagnostic of cardiac ischemia. Visceral pain,
including aortic, esophageal, gastric, and pulmonary processes, may present with radiation
of pain to the neck, shoulder, or arm. Chest pain that radiates to the arms increases the
likelihood of acute myocardial infarction, with radiation only to the right arm having a higher
likelihood than radiation to both arms, which interestingly has a higher likelihood than
radiation to only the left arm.
11. How does the patient’s appearance correlate with the origin of chest pain?
Catastrophic illnesses often result in anxiety, diaphoresis, and an ill appearance. Splinting may
be caused by PE, pleurisy, pneumothorax, pneumonia, or musculoskeletal chest pain. Levine’s
sign, which consists of a patient placing a clenched fist over the sternum to describe the pain,
is frequently associated with ischemic heart disease. Kussmaul’s sign is a paradoxical filling of
Chapter 12 CHEST PAIN82
Etiology Quality Location Radiation Duration Associated Symptoms Onset
Myocardial
infarction
Visceral Retrosternal Neck, jaw, shoulder, arm .15 min Nausea, vomiting, diaphoresis,
dyspnea
Variable
Angina Visceral Retrosternal Neck, jaw, shoulder, arm 5–15 min Nausea, diaphoresis, dyspnea Gradual
Aortic
dissection
Severe, tearing Retrosternal Interscapular Constant Nausea, dyspnea, diaphoresis Sudden
Pulmonary
embolism
Pleuritic Lateral Constant Dyspnea, apprehension Sudden
Pneumothorax Pleuritic Lateral Neck, back Constant Dyspnea Sudden
Pericarditis Sharp, stabbing Retrosternal Neck, back shoulder, arm Constant Dyspnea, dysphagia Variable
Esophageal
rupture
Boring Retrosternal, epigastric Posterior thorax Constant Diaphoresis, dyspnea (late) Sudden
Esophagitis Aching, boring Retrosternal Interscapular Minutes to hours Dysphagia Variable
Esophageal
spasm
Visceral Retrosternal Interscapular Minutes to hours Dysphagia Variable
Musculoskeletal Sharp, aching,
superficial
Localized Variable Dyspnea Variable
TABLE 12–1. CLASSIC PATTERNS OF CHEST PAIN
Chapter 12 CHEST PAIN 83
the neck veins during inspiration, suggesting a right ventricular infarction, PE, or pericarditis
with associated cardiac tamponade.
12. How are vital signs helpful?
A blood pressure difference of more than 20 mm Hg between the upper extremities or a loss
or reduction of lower extremity pulses is suggestive of an aortic dissection. The presence of
tachycardia should raise the suspicion of serious pathology with severe pain or anxiety as
diagnoses of exclusion. Tachypnea may be caused by a PE, pneumonia, or pneumothorax, or
may be secondary to pain. An elevated temperature usually indicates an inflammatory or
infectious process, such as pericarditis or pneumonia. However, fever can also be associated
with an acute myocardial infarction or PE.
13. Which physical examination findings may help differentiate the causes of
acute chest pain?
Isolated physical findings are rarely diagnostic of the origin of chest pain, but when used in
context with the history, they may be extremely valuable. Palpation may reveal localized
tenderness and reproduce musculoskeletal pain, but 5% to 10% of patients with ACS have
chest pain and associated palpable chest tenderness. Cardiac auscultation may reveal a new
murmur of aortic insufficiency suggestive of aortic dissection or a new murmur of mitral
regurgitation secondary to papillary muscle dysfunction from ACS. A third or fourth heart
sound increases the likelihood of ACS. A pericardial friction rub is associated with pericarditis.
Mediastinal air from an esophageal or bronchial rupture results in a crunching sound called
Hamman’s sign. Decreased breath sounds, localized subcutaneous emphysema, or hyper-
resonance may indicate a pneumothorax. Localized rales suggest pulmonary pathology as the
cause of the chest pain. Patients with unilateral leg swelling, pitting edema of one leg,
tenderness over the deep venous system, or calf swelling may have PE as the cause of their
chest pain.
14. How is the electrocardiogram (ECG) helpful in the evaluation of chest pain?
The ECG findings most often associated with ACS are ST segment elevation, ST segment
depression, inverted T waves, and new bundle branch blocks. However, the initial ECG may be
normal in 20% to 50% of ED patients who are later diagnosed as having had an acute
myocardial infarction. Furthermore, there is no difference in the frequency of ACS between
patients with chest pain at the time of acquisition of a normal ECG and those without chest
pain during acquisition of a normal ECG. Comparison with previous ECGs is critical when
possible. In pericarditis, the initial ECG changes may consist of diffuse ST elevation with
depression of the PR segment. The ECG associated with a PE most often demonstrates a
normal sinus rhythm. Common ECG findings associated with acute PE are sinus tachycardia
or nonspecific ST-T wave abnormalities in the right precordial leads. Right heart strain
secondary to a PE will result in a peaked P wave, right axis deviation, or a prominent S wave
in lead I; a Q wave in lead III; and a new T-wave inversion in lead III (S1 Q3 T3 pattern);
however, the S1 Q3 T3 pattern associated with PE occurs infrequently.
15. What abnormalities may appear on the chest radiograph in diseases causing
chest pain?
The chest X-ray films of patients presenting with chest pain are frequently normal but may
be diagnostic, as in a pneumothorax. The mediastinum will be shifted away from the side of
a tension pneumothorax. Aortic dissection may show a widened mediastinum, depression of
the left main stem bronchus, loss of the paratracheal stripe or a 4- to 5-mm or greater
separation between the calcified intima and the lateral edge of the aortic knob. A PE usually
will show nonspecific signs such as atelectasis or an elevated hemidiaphragm. Rare PE
signs include Hampton’s hump, a wedge-shaped, pleural-based infiltrate representing an
area of infarction, and Westermark’s sign, which is an absence of pulmonary shadows distal
to a central embolism. Pneumonia typically produces one or more areas of pulmonary
consolidation, a pleural effusion, or cavitation. Esophageal rupture is classically associated
Chapter 12 CHEST PAIN84
with subcutaneous emphysema, pneumomediastinum, a left-sided pleural effusion, or a left-
sided pneumothorax.
16. Are cardiac enzymes useful in the evaluation of chest pain in the ED?
Yes. See Chapter 29.
17. Are there any bedside tests or medications that may help to identify the origin
of acute chest pain?
Several bedside tests may be helpful, but they are rarely diagnostic in themselves. Relief with
nitroglycerin occurs in both angina and esophageal spasm, whereas acute myocardial
infarction and unstable angina (ACSs) may remain unrelieved. The use of nitroglycerin as a
diagnostic test should be avoided. Antacids or gastrointestinal cocktails, consisting of viscous
lidocaine and an antacid, frequently resolve esophageal pain but also relieve pain in 7% of
patients with angina. The use of antacids as a diagnostic test should be avoided. Pain from
pericarditis is frequently worse in the supine position and relieved when leaning forward. Pain
from esophageal disease is worsened with changes in position such as leaning forward or
lying down. Musculoskeletal pain is worsened with movement.
18. Are there any other useful diagnostic imaging studies to help determine the
cause of chest pain?
Select low-to-moderate risk patients may be risk stratified for ACS with coronary computed
tomography (CT) angiography. Aortic dissection may be diagnosed by a thoracic
arteriogram, a rapid-sequence CT with intravenous contrast scan, magnetic resonance
imaging (MRI), or by a transesophageal echocardiogram. A suspected PE may be
confirmed by a ventilation-perfusion scan, spiral CT scan of the thorax, or pulmonary
angiography. Esophageal rupture may be diagnosed by an esophagogram with a water-
soluble contrast material.
19. What special considerations must be taken into account when evaluating
chest pain in geriatric, diabetic, or female patients?
Although the sources of chest pain in the elderly do not differ significantly from the general
population, their presenting symptoms are often atypical. Instead of chest pain, ischemic
heart disease may manifest as sudden progressive dyspnea, abdominal or epigastric
fullness, extreme fatigue, confusion, or syncope. Patients with diabetes mellitus may have
altered pain perception, resulting in an atypical presentation similar to that of the elderly.
The risk of coronary heart disease in women increases with menopause. Women with
ischemic heart disease present in atypical patterns more frequently than men. This is
because of the higher prevalence of less common causes of ischemia such as vasospastic
and microvascular angina.
KEY POINTS: CHEST PAIN
1. The primary goal of the evaluation of acute chest pain is the inclusion or exclusion of a
life-threatening disease process.
2. A normal ECG on initial presentation does not exclude an ACS.
3. Of patients with ACS, 25% do not have a primary complaint of chest pain.
4. Chest pain relieved by nitroglycerin or antacids is not diagnostic for cardiac or noncardiac
disease.
5. Chest pain in elderly and diabetic patients is caused by common diseases but often presents
in atypical fashion.
Chapter 12 CHEST PAIN 85
WEBSITES
American Heart Association: www.americanheart.org
BIBLIOGRAPHY
1. Anderson JL, Adams CD, Antman EM, et al: ACC/AHA 2007 guidelines for the management of patients with
unstable angina/non-ST-elevation myocardial infarction: executive summary. Circulation 116:803–877, 2007.
2. Antman EM, Hand M, Armstrong PW, et al: 2007 focused update of the ACC/AHA 2004 guidelines for the
management of patients with ST-elevation myocardial infarction: a report of the American College of
Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 51:210–247,
2008.
3. Brown JE, Hamilton GC: Chest pain. In Marx JA, Hockberger RS, Walls RM, et al, editors: Rosen’s Emergency
medicine: concepts and clinical practice, ed 6, St. Louis, 2002, Mosby, pp 183–192.
4. Gibler WB, Cannon CP, Blomkalns AL, et al.: Practical implementation of the guidelines for unstable angina/
non-ST-segment elevation myocardial infarction in the ED. Circulation 111:2699–2710, 2005.
5. Goodacre S, Angelini K, Arnold J, et al: Clinical predictors of acute coronary syndromes in patients with
undifferentiated chest pain. QJM 96(12):893–898, 2003.
6. Goodacre S, Locker T, Morris F, et al: How useful are clinical features in the diagnosis of acute,
undifferentiated chest pain? Acad Emerg Med 9:203–208, 2002.
7. Hamilton GC, Malone S, Janz TG: Chest pain. In Hamilton GC, Sanders AB, Strange GR, et al, editors: Emergency
medicine an approach to clinical problem-solving, ed 2, Philadelphia, 2003, Saunders, pp 131–153.
8. Ioaunides JP, Salem D, Chew PW, et al: Accuracy of imaging technologies in the diagnosis of acute cardiac
ischemia in the emergency department. Ann Emerg Med 37:471–477, 2001.
9. Jones ID, Slovis CM: Emergency department evaluation for the chest pain patient. Emerg Med Clin North Am
19:269–282, 2001.
10. Lee PY, Alexander KP, Hammill BG, et al: Representation of elderly persons and women in published
randomized trials of acute coronary syndromes. JAMA 286:708–713, 2001.
11. Lee TH, Goldman L: Evaluation of the patient with acute chest pain. N Engl J Med 342:1187–1195, 2000.
12. Panju AA, Hemmelgarn BR, Guyatt GH, et al: The rational clinical examination. Is this patient having a
myocardial infarction? JAMA 280(14):1256–1263, 1998.
13. Pope JH, Aufderheide TP, Ruthazer R, et al: Missed diagnosis of acute cardiac ischemia in the emergency
department. N Engl J Med 342:1163–1170, 2000.
14. Ringstrom E, Freedman J: Approach to undifferentiated chest pain in the emergency department: a review of
recent medical literature and published practice guidelines. Mt Sinai J Med 73(2):499–505, 2006.
15. Rusnak RA, Stair TO, Hansen K, et al: Litigation against the emergency physician: Common features in cases
of missed myocardial infarction. Ann Emerg Med 18:1029–1034.
16. Savonitto S, Ardissino D, Grauger CB, et al: Prognostic value of the admission electrocardiogram in acute
coronary syndromes. JAMA 281:707–713, 1999.
17. Smith SW, Whitman W: Acute coronary syndromes: Acute myocardial infarction and ischemia. In Chan TC,
Brady WJ, Harrigan RA, et al, editors: ECG in emergency medicine and acute care, Philadelphia, 2005,
Elsevier, pp 151-172.
20. Because approximately 2% to 4% of patients with chest pain caused by acute
myocardial infarction are discharged to home, what factors have been
associated with failure to make the diagnosis?
n
Young age group
n
Failure to obtain an accurate history
n
Incorrect interpretation of the ECG
n
Failure to recognize atypical presentations
n
Hesitance to admit patients with vague symptoms
n
Reliance on laboratory assays, such as cardiac enzymes
n
Insufficient experience or training
Chapter 12 CHEST PAIN86
18. Steele R, McNaughton T, McConahy M, et al: Chest pain in emergency department patients: if the pain is
relieved by nitroglycerin, is it more likely to be cardiac chest pain? CJEM 8(3):164–169, 2006.
19. Swap CJ, Nagurney JT: Value and limitations of chest pain history in evaluation of patients with suspected
acute coronary syndromes. JAMA 2005; 294: 2623–2629.
20. Takakuwa KM, Halpern EJ: Evaluation of a triple rule-out coronary CT angiography protocol: use of 64-Section
CT in low-to-moderate risk emergency department patients suspected of having acute coronary syndrome.
Radiology 248(2):438–446, 2008.
21. Turnipseed ST, Trythall WS, Diercks DB, et al: Frequency of acute coronary syndrome in patients with normal
electrocardiogram performed during presence or absence of chest pain. Acad Emerg Med 16(6):495–499,
2009.
87
CHAPTER 13
ABDOMINAL PAIN
Rick A. McPheeters, DO, FAAEM
1. What is the difference between visceral and somatic pain? How is this of
practical importance?
Evolving patterns of pain frequently reveal the source and give an idea of the extent to which
the process has advanced. Early, the patient may describe a deep-seated, dull pain (visceral
pain) emanating from hollow viscera or the capsule of solid organs. This pain is poorly
localized but generally falls somewhere along the midline of the abdomen. Later, as
inflammation progresses to the parietal peritoneum, the pain becomes better localized,
lateralized over the involved organ, sharper in intensity (somatic or parietal pain), and
constant. Visceral pain that is superseded by somatic pain frequently signals the need for
surgical intervention. A clear understanding of the process enables the clinician to identify
more precisely the cause and rate of progression of pathology.
2. What is the difference between localized and generalized peritonitis?
As the peritoneum adjacent to a diseased organ becomes inflamed, palpation or any
abdominal movement causes stretching of the sensitized peritoneum and, consequently, pain
localized at that site (localized peritonitis). If irritating material (e.g., pus, blood, or gastric
contents) spills into the peritoneal cavity, the entire peritoneal surface may become sensitive
to stretch or motion, and any movement or palpation may provoke pain at any or all points
within the abdominal cavity (generalized peritonitis).
KEY POINTS: MESENTERIC ISCHEMIA
1. Abdominal pain out of proportion to physical findings.
2. Diffuse abdominal tenderness, rebound, and rigidity are ominous signs.
3. Definitive diagnosis by mesenteric arteriography or surgical exploration.
3. Which tests for peritoneal irritation are best?
Rebound tenderness is the traditional physical examination finding for peritonitis. In a patient with
likely generalized peritonitis (e.g., obvious distress, excruciating pain every time the ambulance
hits a bump), the standard tests for rebound tenderness are unnecessarily harsh. Asking the
patient to cough generally supplies adequate peritoneal motion to give a positive test. When in
every respect the examination is normal, one highly sensitive test for peritoneal irritation is the
heel-drop jarring (Markle) test. The patient is asked to stand, rise up on tiptoe with knees straight,
and forcibly drop down on both heels with an audible thump. Among patients with appendicitis,
this test was found to be 74% sensitive, compared with 64% for the standard rebound test.
4. Why is it important to establish the temporal relationship of pain to vomiting?
Generally, pain preceding vomiting is suggestive of a surgical process, whereas vomiting
before onset of pain is more typical of a nonsurgical condition. Epigastric pain that is relieved
by vomiting suggests intragastric pathology or gastric outlet obstruction.