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B. Postoperative Fever. In the immediate postoperative period fever may often be caused
by atelectasis. Pneumonia, urinary tract infection, line infections, wound infections, and
abscesses may also cause fever following surgery.
C. Fever of Unknown Origin. Numerous definitions of FUO exist, but most include a fever
documented on several different days over 2 or 3 weeks, with no diagnosis found following
repeated physical examinations and routine diagnostic tests. Diseases that may cause FUO are
listed in Table 2.6.1. One approach to evaluating the patient with FUO is shown in Figure 2.6.1.
The underlying etiology is eventually found in over 90% of FUO cases. Historically, the most
common cause of FUO was infection, followed by malignancies, and then rheumatologic
diseases. In more recent studies, rheumatologic causes have surpassed malignancies as the
second most common cause of FUO. FUO is much more likely to be caused by an unusual
presentation of a common disease than a common presentation of an unusual disease.
Initial Evaluation
Fever Persists >3 wk
FUO
Discontinue All
Nonessential
Medications
Fever
Resolves
in <72 h
Drug Fever
Fever Chart
to Document Fever
Focus Identified
Persistence of Fever >72 h
Abdominal Computed Tomography
Tc-Based Nuclear Scan
Obtain Tissue
to Confirm
Diagnosis
Use Duke Criteria to
Rule In or Rule Out
Infective Endocarditis
Yes
Leg Doppler Imaging
>Age 50 y
No
No
Yes
Clinical Status
Deteriorating?
Yes
Liver Biopsy
Temporal Artery
Biopsy
Laparoscopy
No
Undiagnosed FUO
Follow Clinically
Fever Persists
Positive for
Deep Vein
Thrombosis
Low-Molecular-
Weight Heparin
Infective Endocarditis
Suspected?
Figure 2.6.1. Approach to the evaluation of fever. FUO, fever of unknown origin.
18
Taylor’s DifferenTial Diagnosis Manual
2.7
I. BACKGROUND. Headache, or technically cephalgia, is an extremely common phenomenon in
the United States and around the globe.
A. Epidemiology. In 2008, headaches were the first-listed diagnosis for over 3 million ED
visits (2.4% of all ED visits) and 81,000 inpatient stays (0.2% of all inpatient stays). In
developed countries, tension-type headache (TTH) alone affects two-thirds of adult males
and over 80% of females.
Migraine prevalence and attack incidence data suggests that 3,000 migraine attacks occur
every day for each million of the general population. Current studies have estimated that migraine
headache affects 37 million people in the United States, or 12% of the entire population.
The toll of chronic daily headache is not insignificant either as up to one adult in 20
has a headache every or nearly every day. Amazingly though, about 10% of men and 5% of
women have never had a headache! The cost is also phenomenal. Migraine headaches cost
American employers $13–17 billion a year because of a collective 157 million missed work
days, impaired work function, and physician office visits.
II. PATHOPHYSIOLOGY
A. Classifications.
Headaches are typically classified into the categories of primary and sec-
ondary with the International Classification of Headache Disorders, second edition (ICHD-II)
system providing what many consider the gold standard.
B. Diagnosis. Primary headaches include migraines with all the various subsets (with and without
aura, retinal, ophthalmoplegic, basilar, etc.), TTH (episodic and chronic), cluster headaches,
and other trigeminal autonomic headaches (which includes paroxysmal hemicranias) and finally
“other” primary headaches (which include stabbing, cough, exertional, associated with sexual
activity, thunderclap etc.). Secondary headaches are far less common (10% of all headaches)
but potentially more dangerous. They include headaches related to head and neck trauma and
headaches related to cranial or cervical vascular disorders (which include conditions such as
transient ischemic attack (TIA), cerebrovascular accident (CVA), arteritis, intracranial/subarach-
noid hemorrhage, vascular malformations, cerebral venous thrombosis etc.). Other secondary
headaches take in headache attributed to nonvascular intracranial disorder (which includes head-
aches tied to Chiari malformation Type 1, high or low cerebrospinal fluid (CSF) fluid pressures,
increased intracranial pressure or hydrocephalus caused by neoplasm etc.), headache attributed
to a substance (which includes medication overuse, medication adverse events, substance with-
drawal etc.), headaches attributed to various intracranial and systemic infections (which include
meningitis, encephalitis etc.), headaches attributed to disorders of homeostasis (which include
hypoxia, hypothyroidism, fasting etc.), headache or facial pain attributed to multiple disorders of
the cranium, neck, eyes, ears, nose, sinuses, teeth, mouth, or other facial or cranial structures, and
lastly headaches attributed to psychiatric disorders such as somatization and psychotic conditions.
III. EVALUATION. The primary task of the family physician whether they are practicing in a clinic,
on a hospital service, or in an emergency room is to determine whether a patient has an organic,
potentially life-threatening cause of headache. Fortunately, the majority of headaches do not
have a serious cause, but serious causes of headache, such as meningitis and subarachnoid hem-
orrhage, must be excluded. In the vast majority of cases, the physician can accurately diagnose
a patient’s headache and determine whether additional laboratory testing or neuroimaging is
indicated by considering the various headache types in each category as listed above and obtain-
ing a thorough headache history followed by a focused clinical examination.
A. History. The history is the most important aspect of the evaluation of a patient with head-
ache, especially because primary and secondary headaches can share similar clinical features
Headaches
Mark D. Goodwin
Chapter 2 • Undifferentiated Problems
19
and associated symptoms. Historical items important to document should include previous
similar episodes, the date/time of onset, precipitating and ameliorating factors, character of
the pain as well as the level of intensity, the symptom course over time, duration, frequency,
location of pain, and associated symptoms such as nausea/vomiting, any autonomic features,
fever, chills, and focal neurologic signs/symptoms. A review of the patient’s other past medical
conditions and current medications is also critical, as this may point to an etiology (such as
caffeine or nonsteroidal anti-inflammatory drug [NSAID] withdrawal headaches). The history
of the headache can often provide a diagnosis with no further investigation or testing needed.
Certain signs and/or symptoms are often labeled as “red flags” when it comes to headaches.
While studies to support the use of these are lacking, the following conditions should prompt
additional evaluation—headache beginning after 50 years of age, a sudden onset of the head-
ache, headaches with increasing frequency and severity (especially if they report that this is “this
is the worst headache ever”), a new-onset headache in a patient with risk factors for cancer or
human immunodeficiency virus (HIV), a headache with signs of systemic infection, headaches
with focal neurologic signs or seizure, and a headache subsequent to intracranial hemorrhage.
B. Physical. The physical examination of the headache patient should identify causes of
secondary headaches and as such it should target areas identified as abnormal during the
headache history. The general physical examination should include vital signs, funduscopic
and cardiovascular assessment, and palpation of the head and face. The physician should
check for evidence of localized infections such as acute otitis media (AOM) and acute
bacterial sinusitis (ABS). A complete neurologic examination is essential. The examination
should include mental status, level of consciousness, cranial nerve testing, motor strength
testing, deep tendon reflexes, sensation, pathologic reflexes (e.g., Babinski’s sign), cerebellar
function and gait testing, and signs of meningeal irritation (Kernig’s and Brudzinski’s signs).
It is important to remember that signs like nuchal rigidity and maneuvers such as Kernig’s
and Brudzinski’s all have exceedingly low sensitivities (30%, 5%, and 5%, respectively).
C. Testing. Laboratory and neuroimaging are often not required in the headache patient
work-up, especially for patients who present with a primary form of headache. However,
if the history and/or physical examination suggest secondary causes, then labs and imaging
may be required. Blood counts and cultures would be indicated for those presenting with
signs/symptoms of systemic infection. In addition to the complete blood count (CBC)
and cultures, a lumbar puncture would be indicated in any patient in whom meningitis
is suspected. Urgent scanning is indicated if patients present with new sudden onset of
severe headache, headache associated with new abnormal neurologic signs, or a new type
of headache in patients infected with HIV and is best achieved using CT. Magnetic reso-
nance imaging (MRI), though more expensive, is better at defining pathologic intracranial
changes especially in the posterior fossa. An ESR would be indicated in patients presenting
with giant cell arteritis. Lastly, CT scanning without contrast medium, followed by lumbar
puncture if the scan is negative, is preferred to rule out subarachnoid hemorrhage.
Consider neurologic consultation if the headache diagnosis is uncertain, if the patient’s
conscious level is affected or if there is a period of amnesia, if the neurologic examination
is abnormal, or if the neuroimaging is abnormal. Neurosurgical consultation is warranted
if the patient presents with a subarachnoid hemorrhage or mass lesion (such as tumors or
abscess), or if a pituitary lesion is suspected.
IV. SUMMARY. Most primary headaches can be diagnosed by taking a comprehensive history to
exclude worrisome symptoms and documenting a normal general and neurologic examination.
Diagnostic testing is not necessary in these cases. Secondary headaches usually require addi-
tional diagnostic testing.
REFERENCES
1. Jonathan AE. Clinical policy: critical issues in the evaluation and management of adult patients pre-
senting to the emergency department with acute headache. From the American College of Emergency
Physicians Clinical Policies Subcommittee; American College of Emergency Physicians; 2008.07.001.
2. ICSI Health Care Guideline-Diagnosis and Treatment of Headache; Jan 2011, 10th edition.
20
Taylor’s DifferenTial Diagnosis Manual
3. Kevin H, Sara W, Marcia R. Direct cost burden among insured US employees with migraine. Headache
2008;48(4):553–563.
4.
Randall CC. Evaluation of acute headaches in adults. Am Fam Physician 2001;63(4):685–692.
5. John RM. Headache in primary care. Prim Care Clin Office Pract 2007;34:83–97.
6.
Jennifer L. Headaches in U.S. hospitals and emergency departments, 2008. Agency for Healthcare
Research and Quality, May 2011.
7. The International Classification of Headache Disorders, 2nd ed. May 2005.
2.8
I. BACKGROUND. Hypersomnia, or excessive daytime somnolence (EDS) is defined by the
International Classification of Sleep Disorders, Second Edition (ICSD-2) as “the inability to stay
awake and alert during the major waking episodes of the day, resulting in unintended lapses into
drowsiness and sleep (1).” EDS should be differentiated from generalized fatigue and nonspecific
tiredness, as patients often use the terms interchangeably. Generalized fatigue is more subjective
and typically related to problems of decreased physical energy, poor concentration and memory,
muscle exhaustion, or mood. Due to the prevalence and comorbidities associated with untreated
obstructive sleep apnea (OSA), patients with EDS should be considered for an OSA evaluation.
II. PATHOPHYSIOLOGY
A. Etiology.
Hypersomnia can be due to a primary sleep disorder, but is more commonly
secondary to disorders that disrupt normal sleep patterns such as sleep deprivation, medi-
cation side effects, poor sleep hygiene, sleep-disordered breathing, and other medical and
psychiatric conditions (2).
B. Epidemiology. EDS is a common problem affecting approximately 10% to 20% of adults
and children (1, 3) with an even higher prevalence in older adults (4) and patients with
psychiatric conditions. EDS is reported as a significant factor in motor vehicle incidents
and personal injuries in the United States and has been linked to poor health and reduced
cognitive function (2). Narcolepsy (the common tetrad includes sleep paralysis, cataplexy,
excessive daytime somnolence, and hypnagogic hallucinations) is an uncommon diagnosis
and affects approximately 50/100,000 people (1).
III. EVALUATION
A. History and Review of Systems.
A detailed and complete sleep history is important for
determining the appropriate evaluation in patients with EDS. Determining the patient’s
work schedule, diet, sleep routine, social stressors, home environment and living situation,
prescription and nonprescription drug use, as well as the comorbidities and behaviors of
bed partners will help in developing a differential diagnosis. A history of sleep attacks or
episodes of cataplexy (sudden and transient loss of muscle strength) can be very dangerous
and highly suggestive of narcolepsy (1). A full review of systems often highlights other medi-
cal and psychiatric disorders that may be causing daytime sleepiness. Abrupt symptom onset
should heighten concern for central nervous system tumors, ischemic stroke, or significant
metabolic disorders.
B. Sleep Patterns. Sleep deprivation is probably the most common cause of EDS (2). Sleep
deprivation can result from job-related factors (shift work), environmental situations (bed-
partner snores loudly, disruptive neighbors, gunshots outside, caring for ill family members),
or other medical diagnoses (periodic limb movement disorder, asthma, OSA).
C. Medication History. Many medications can induce somnolence or interrupt the normal
sleep cycle. These are listed in Table 2.8.1 (2, 5).
Hypersomnia
Jennifer J. Buescher
Chapter 2 • Undifferentiated Problems
21
TABLE 2.8.1 Medications That Can Be Involved in Hypersomnia
Prescription medications causing somnolence
Benzodiazepines
Nonbenzodiazepine sleep aids
Tricyclic antidepressants
Atypical antidepressants
Selective serotonin reuptake inhibitors
Antipsychotics
Lithium
Anticonvulsants
Antiparkinsonian agents
Opiates
Antihistamines
α1-Adrenergic antagonists (prazosin, terazosin)
α2-Adrenergic agonists
Skeletal muscle relaxants
Antimuscarinics and antispasmodics
Barbiturates
Prescription medication causing alertness or insomnia
Amphetamines
Modafinil and Armodafinil
Theophylline
β-Adrenergic agonists
β-Blockers
Corticosteroids
Decongestants
Selective serotonin reuptake inhibitors
Nonprescription and herbal agents affecting sleep
Amphetamines
Alcohol
Nicotine
Illicit drugs
Chamomile
Rosemary
Melatonin
Adapted from Pagel JF. Excessive daytime sleepiness. Am Fam Physician
2009;79(5):391–396; Roux FJ, Kryger MH. Medication effects on sleep. Clin Chest Med
2010;31:397–405.
22
Taylor’s DifferenTial Diagnosis Manual
D. Physical Examination. A general physical examination may give insight into medical
or psychological disorders that require further evaluation, such as OSA, asthma, nocturia/
urinary urgency, or anxiety.
E. Testing. The Eppworth Sleepiness Scale can help to quantify sleepiness (1). Intrinsic
sleep disorders are best evaluated using a Multiple Sleep Latency Test (MSLT) and the
Maintenance of Wakefulness Test (MWT) (2). OSA and limb movement disorders are best
evaluated by overnight polysomnography (2).
IV. DIAGNOSIS
A. Differential Diagnosis.
The differential diagnosis for hypersomnia is listed in Table 2.8.2.
B. Clinical Manifestations. Hypersomnia may present with significant fatigue, trouble with
work or school performance, marital or relationship problems, accidents or personal injury,
and can be the first sign of dementia or other neurologic disorders.
REFERENCES
1. Morrison I, Riha RL. Excessive daytime sleepiness and narcolepsy—an approach to investigation and
management. Eur J Int Med 2012;23:110–117.
2. Pagel JF. Excessive daytime sleepiness. Am Fam Physician 2009;79(5):391–396.
3. Calhoun SL, Vgontzas AN, Fernandez-Mendoza J, et al. Prevalence and risk factors of excessive daytime
sleepiness in a community sample of young children: the role of obesity, asthma, anxiety/depression,
and sleep. Sleep 2011;34(4):503–507.
4. Bloom HG, Ahmed I, Alessi CA, et al. Evidence-based recommendations for the assessment and man-
agement of sleep disorders in older persons. J Am Geriatr Soc 2009;57(5):761–789.
5. Roux FJ, Kryger MH. Medication effects on sleep. Clin Chest Med 2010;31:397–405.
TABLE 2.8.2 Differential Diagnosis of Excessive Daytime
Somnolence
Primary hypersomnias:
Narcolepsy with or without cataplexy
Idiopathic hypersomnia
Secondary hypersomnias:
Obstructive sleep apnea
Restless leg syndrome
Periodic limb movement disorder
Parkinson’s disease
Insufficient sleep syndrome (behavioral sleep deprivation)
Head trauma
Depression
Anxiety
Medication effects
Illicit drug use
Poor sleep hygiene
Data adapted from Morrison I, Riha RL. Excessive daytime sleepiness and
narcolepsy—an approach to investigation and management. Eur J Int Med
2012;23:110–117; Pagel JF. Excessive daytime sleepiness. Am Fam Physician
2009;79(5):391–396.
Chapter 2 • Undifferentiated Problems
23
2.9
I. BACKGROUND. Chronic insomnia is the difficulty of initiating or maintaining sleep that
causes significant daytime impairment and has been present for at least 1 month (1). Secondary
insomnia is a sleep disturbance caused by an underlying environmental, medical, or psychiatric
disorder (1).
II. PATHOPHYSIOLOGY
A. Etiology.
Primary insomnia is uncommon and is due to an intrinsic disorder of the sleep–
wake cycle. Secondary insomnia is much more common. Chronic pain, substance use or
abuse, restless legs syndrome, depression, circadian rhythm disturbance (i.e., shift work),
and obstructive sleep apnea are common causes of secondary insomnia (1, 2). Poor sleep
hygiene, alcohol, caffeine, and nicotine use are also common causes of difficulty with sleep
initiation and nonrestorative sleep (2).
B. Epidemiology. Between 10% and 30% of the population is affected by insomnia, but
only 10% to 15% of these patients suffer from intrinsic disorders of sleep (1, 3).
III. EVALUATION
A. History.
A thorough history should focus on determining the cause and duration of
insomnia. Precipitating events such as emotional trauma, illness, stress, and prescription or
other drug use should be explored with the patient and his or her bed partner.
B. Sleep Patterns. A thorough discussion of the patient’s sleep pattern and the sleep patterns
of other members of the household should include the timing and the content of evening
meals, bedroom environment (temperature, noise, comfort of bed), safety of the outside
neighborhood, work schedules, and sleep schedules (including daytime napping).
C. Review of Systems. The review of systems should be directed to the common medical and
psychological problems that are associated with insomnia.
D. Medications. Many medications affect sleep by causing or exacerbating restless legs syn-
drome or periodic limb movements, dreams or nightmares, or by interrupting normal sleep
architecture (2). Table 2.9.1 lists some of the more common medications that can interrupt
normal sleep patterns.
E. Physical Examination. The physical examination should focus on associated medical
conditions associated with insomnia. In primary insomnia, the physical examination is likely
to be normal.
F. Testing. Laboratory and diagnostic testing is infrequently useful in the diagnosis of pri-
mary insomnia. A detailed sleep diary kept by the patient or a home visit by the physician
can be helpful in determining extrinsic factors causing insomnia (1). Polysomnography can
assist in the diagnosis of comorbid conditions such as obstructive sleep apnea, restless legs
syndrome, and periodic limb movement disorder.
IV. DIAGNOSIS
A. Differential Diagnosis.
A differential diagnosis of insomnia is listed in Table 2.9.2.
B. Clinical Manifestations. Insomnia can cause significant functional impairment, dif-
ficulty in work or school, and marital or relationship problems. Chronic sleep loss from
untreated insomnia can cause fatigue-related accidents, poor concentration, decreased
memory, and job or school absenteeism and is associated with increased morbidity and
mortality from cardiovascular and psychiatric disorders (1, 3).
Insomnia
Jennifer J. Buescher
24
Taylor’s DifferenTial Diagnosis Manual
TABLE 2.9.1 Medications That Interrupt Sleep
Prescription drugs
Non-prescription medications
Carbamazepine Phenylephrine
Valproate sodium Pseudoephedrine
Phenytoin Caffeine
Gabapentin Stimulant diet pills
Pregabalin Nicotine
Selective serotonin reuptake inhibitors Alcohol
Lithium Illicit drugs
Venlafaxine
Risperidone
Clozapine
Methylphenidate
Dextroamphetamine
Albuterol
Theophylline
Prednisone
Beta blockers
Information from Foral P, Knezevich J, Dewan N, Malesker M. Medication-induced sleep
disturbances. Consult Pharm 2011;26(5):414–425.
TABLE 2.9.2 Differential Diagnosis of Insomnia
Primary insomnia Depression
Obstructive sleep apnea Nightmares or night terrors
Congestive heart failure Alzheimer’s or other dementia
Gastroesophageal reflux disease Urinary incontinence, nocturia
Chronic pain syndrome Chronic obstructive pulmonary disease
Fibromyalgia Illicit drug use
Asthma Alcohol use or abuse
Restless legs syndrome Circadian rhythm sleep disorders (shift work, jet lag)
Periodic limb movement disorder
Anxiety
Environmental disturbances (loud noises, bed partner
with sleep disorder, uncomfortable or unsafe
sleeping conditions)
Information modified from Foral P, Knezevich J, Dewan N, Malesker M. Medication-induced sleep
disturbances. Consult Pharm 2011;26(5):414–425; Harsora P, Kessmann J. Nonpharmacologic
management of chronic insomnia. Am Fam Physician 2009;79(2):125–130; Ramakrishnan K, Scheid
DC. Treatments options for insomnia. Am Fam Physician 2007;76(4):517–526.
Chapter 2 • Undifferentiated Problems
25
REFERENCES
1. Harsora P, Kessmann J. Nonpharmacologic management of chronic insomnia. Am Fam Physician
2009;79(2):125–130.
2. Foral P, Knezevich J, Dewan N, Malesker M. Medication-induced sleep disturbances. Consult Pharm
2011;26(5):414–425.
3. Ramakrishnan K, Scheid DC. Treatments options for insomnia. Am Fam Physician 2007;76(4):
517–526.
2.10
I. BACKGROUND. Nausea is the objectionable sensation of abdominal discomfort that produces
a sensation that one may vomit. Vomiting is an autonomic response leading to the active and
forceful expulsion of gastric contents (1). Nausea may or may not be followed by active vomiting.
II. PATHOPHYSIOLOGY
A. Etiology.
Nausea is a subjective symptom experienced in many of the disorders that also
cause vomiting. Vomiting is an autonomic response intended to protect humans from the
ingestion of harmful or toxic substances (1). Several neurologic abnormalities can trigger the
autonomic system and lead to vomiting.
B. Epidemiology. Acute nausea and vomiting are common symptoms and frequently seen in
outpatient, inpatient, and emergency settings. Chronic nausea and vomiting are less com-
mon but can lead to significant morbidity.
III. EVALUATION
A. History.
A thorough history should discuss the duration and frequency of vomiting, the
symptoms of other family members, exposure to toxic substances, and the relationship of
nausea and vomiting to meals or types of food.
B. Review of Systems. A complete review of systems should specifically address a history of fever,
character of abdominal pain, neurologic symptoms, and the signs and symptoms of dehydration.
C. Physical Examination. A complete abdominal exam should first attempt to rule out acute
life-threatening or severe problems such as intestinal obstruction, pancreatitis, and acute myo-
cardial infarction. Neurologic exam can help identify vomiting caused by a central nervous
system abnormality or vestibular problem (2). The physical exam should also evaluate for
complications caused by protracted vomiting, including dehydration and electrolyte disorders.
D. Testing. The evaluation of nausea and vomiting should be directed by the severity, onset,
and description of the symptoms and any abnormal findings on physical exam. A flat and
upright abdominal radiograph or abdominal CT is helpful in the evaluation of acute and
severe nausea or vomiting. Subsequent studies such as barium studies, upper GI series,
intracranial CT/MRI, and abdominal ultrasound may be warranted based on the differen-
tial diagnosis (1). Laboratory tests including a metabolic panel, pregnancy test, urinalysis,
liver function test, lipase, and toxicology screen should be ordered based on the clinical
assessment and should be used in the evaluation of the underlying cause and subsequent
complications from nausea and vomiting.
IV. DIAGNOSIS
A. Differential Diagnosis.
The diagnosis of nausea and vomiting can often be made on
clinical history and physical examination without further evaluation (2). Chronic or severe
symptoms may be more difficult to diagnose and may require more extensive laboratory
and diagnostic testing. Table 2.10.1 provides a list of common causes of acute and chronic
nausea and vomiting.
Nausea and Vomiting
Jennifer J. Buescher
26
Taylor’s DifferenTial Diagnosis Manual
B. Clinical Manifestations. Many patients with isolated or self-limited nausea and/or
vomiting will not seek medical attention; however, their symptoms can lead to temporary
functional limitations and missed work or school. Patients with persistent or severe nausea
and vomiting can experience significant weight loss, hypokalemia, electrolyte disturbances,
dehydration, metabolic alkalosis, dental caries, and esophageal abnormalities, and can expe-
rience significant social isolation and missed work or school.
REFERENCES
1. Scorza K, Williams A, Phillips D, Shaw J. Evaluation of nausea and vomiting. Am Fam Physician
2007;76(1):76–84.
2. American Gastroenterological Association. Medical position statement: nausea and vomiting.
Gastroenterology 2001;120(1):261–263.
TABLE 2.10.1 Differential Diagnosis of Nausea and/or Vomiting
Acute nausea and/or vomiting Chronic nausea and vomiting
Increased intracranial pressure Increased intracranial pressure
Meningitis/encephalitis/abscess Mass lesion
Closed head injury Hydrocephalus
Cerebrovascular injury Pseudotumor cerebri
Migraine Gastroparesis
Vestibular abnormalities Nonulcer dyspepsia
Labyrinthitis Irritable bowel syndrome
Motion sickness Psychiatric disorders
Bowel obstruction Bulimia nervosa
Intussusception Anorexia nervosa
Strangulated hernia Conversion disorder
Volvulus Anxiety
Cholecystitis/cholangitis Social phobia disorder
Pancreatitis Cyclic vomiting
Appendicitis Uremia
Infectious gastroenteritis Cirrhosis
Spontaneous bacterial peritonitis Medications/toxins
Pyelonephritis Alcohol intoxication
Acute myocardial infarction Chemotherapeutics
Nephrolithiasis Hormonal contraception
Acute pain Arsenic
Diabetic ketoacidosis Organophosphates/pesticides
Pregnancy Radiation therapy
Illicit drug use
Modified from Scorza K, Williams A, Phillips D, Shaw J. Evaluation of nausea and vomiting. Am Fam
Physician 2007;76(1):76–84.
Chapter 2 • Undifferentiated Problems
27