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Emergency Medicine Cases

EMERGENCY MEDICINE CASES

CASE 1
Chief complaint
"Leave me alone!"

History and physical examination


A 64-year-old man with a history of chronic alcoholism is brought to the emergency
department by the police, who found him agitated, combative, and shouting at
imaginary monsters. Vital signs are: temperature 39 C (102.2 F), blood pressure
130/85 mm Hg, pulse 110/min, and respirations 24/min.

ccs Note
Any patient with a high fever
on the CCS should undergo
blood cultures, a chest x-ray,
and urinalysis. This is a generic
fever evaluation.

The patient appears disheveled, agitated, and he is sweating profusely. He is


staring around. Examination of the head, eyes, ears, nose, and throat shows poor
dentition, a supple neck, and intact cranial nerves. Cardiovascular examination
shows tachycardia, with no rubs or gallops. His lungs are clear, and his abdomen is
benign. There is no clubbing, cyanosis, or edema of the extremities, although there
is a resting tremor of the hands. Neurologic examination is nonfocal, and there is
no evidence of external injury.

Differential diagnosis
Delirium tremens
Alcoholic hallucinosis
Acute schizophrenia
Bacterial meningitis
Subdural hematoma
Acute intoxication

CCS Note
The CCS will value an
appropriate process more so
than jumping straight to the
diagnosis. Hence, a CT scan
of the head with fever and
change in mental status is
acceptable, even if the results
are normal.

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USMLE Step 3: Internal Medicine

CCS Note
There is no specific test to
diagnose alcohol withdrawal.
It is a diagnosis of exclusion,
along with a history of highvolume alcohol consumption.

Initial diagnostic plan

Results

1. Electrolytes

1. Sodium 146 mEq/L; chloride 108 mEq/L; BUN


30 mg/dL; creatinine 1.3 U/L

2. Blood alcohol level

2. 0.00 mg/dL

3. Serum magnesium level

3. 0.8 mg/dL (1.8-3.0 normal)

4. Arterial blood gases

4. pH 7.46; pC0 2 32 mm Hg; p0 2 84 mm Hg; HC0 3


24 mm Hg; 0 2 saturation 96%

5. CT scan of head

5. No bleeding

6. Lumbar puncture

6. Normal

7. Toxicology screen

7. Negative

8. Blood cultures

8. No growth

9. Urinalysis

9. No white cells

Assessment
The presentation of a patient with a history of alcohol abuse who is disoriented, agitated, hallucinating, and perspiring is classic of delirium tremens. Acute confusion and fever are suggestive of
meningitis and this can be excluded with a lumbar puncture if the diagnosis is not certain. The
acute change in mental status may also be due to a central nervous system bleed precipitated by
falling. The more mild alcohol withdrawal syndrome is often referred to as "impending DTs:' The
symptoms can generally be managed with oral benzodiazepines. Alcoholic hallucinosis presents
with visual hallucinations (as opposed to auditory hallucinations) and is generally distinguished
from acute schizophrenia by the history of prolonged alcohol use followed by a period of cessation. The treatment is the same as for delirium tremens.

CCS Note
In patients with a clear
presentation of alcohol
withdrawal, medical therapy,
such as lorazepam or
chlordiazepoxide, should be
ordered before the results of
the tests are known.

Further diagnostic plan

Results

1. Chest x-ray

1. No infiltrates

2. Vitamin B12 level

2. Normal

3. Liver function tests

3. Normal

Treatment plan
1. Chlordiazepoxide 50-100 mg intravenously every 4 to 6 hours and as needed (could also
choose other agents, e.g., diazepam, lorazepam, or phenobarbital)

2. Intravenous thiamine and folic acid


3. Intravenous fluids DSNS; adjust depending on patient's hemodynamic status
4. Magnesium sulfate replacement
5. Clonidine can also be helpful to suppress some of the cardiovascular hyperexcitability
6. Atenolol can be used as an adjunct to the benzodiazepines for the tachycardia
7. Admission to general floor if the withdrawal is mild or to the intensive care unit if the patient
IS se1zmg

Discussion
Abstinence or withdrawal syndrome refers to a constellation of symptoms that develop only after a
period of relative or absolute abstinence from alcohol. The syndrome may develop in the periodic
drinker, as well as the chronic drinker. Delirium tremens is the most serious form of the syndrome
and should not be confused with the more mild signs and symptoms of alcohol withdrawal, such

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Emergency Medicine Cases

as tremulousness. Seizures may develop, which may be fatal. Delirium tremens is an acute medical
emergency with a mortality rate of about 15% if left untreated.
Delirium tremens is characterized by:
Delusions
Generalized seizures
Profound confusion
Visual hallucinations
Tremor
Agitation
Increased activity of the autonomic nervous system, e.g., dilated pupils, fever, tachycardia, and perspiration
The symptoms generally develop starting 9 to 12 hours after the last drink, peaking at 48 to 72
hours. Laboratory hallmarks include hypomagnesemia, decreased arterial pH, and a decreased
p0 2 There are also derangements in the serum electrolytes--most often related to dehydration.
The initial evaluation should be thorough, paying special attention to the fact that there may be
associated injuries to the patient due to the state of agitation and altered mental status. These
patients have often fallen before they arrive for medical attention. They have been in poor
states of health and are often suffering from malnutrition. Special attention should be given
to the issue regarding glucose administration in the intravenous fluids. The alcoholic patient
generally lives on a diet high in carbohydrates (alcohol) and low in thiamine, and tends to have
no vitamin-B reserves. The administration of glucose will consume the patient's last stores of
thiamine and may precipitate Wernicke syndrome. There is no definitive proof, however, that
giving the thiamine just before or after the dextrose really makes any difference because they
are given so closely together.
The goal of therapy is to provide medication that is crosstolerant for alcohol and that will blunt
the patient's state of agitation and thereby prevent exhaustion. This is best achieved with benzodiazepines or chlordiazepoxide; however, the specific agent used is not as important as using
a sufficiently high amount of the medication. Phenytoin is not useful for withdrawal-related
seizures.

Final diagnosis
Alcohol withdrawal

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USMLE Step 3: Internal Medicine

Case Review
Delirium Tremens
Symptoms start at least 8 to 12 hours after the last drink
Symptoms peak at 36 to 72 hours, resolves in 3 to 5 days
Autonomic hyperexcitability, such as tachycardia, hypertension, tremor, and agitation
May have hallucinations and seizures
Treat with benzodiazepines
Alcoholic Hallucinosis
Similar in onset to delirium tremens and alcohol withdrawal
Predominantly characterized by visual hallucinations, autonomic lability absent
Treat with benzodiazepines as in alcohol withdrawal
Use haloperidol as well to suppress hallucinations
Patient recovers in 1 to 3 weeks
Acute Schizophrenia
No relationship in time to alcohol use
Tremors may occur with tardive dyskinesia
No temporal relationship between the development of the tremors and alcohol
Tremors and autonomic instability do not dramatically increase with a few hours
No fever
Generally auditory hallucinations, not visual
Bacterial Meningitis
Fever, headache, stiff neck, and photophobia
Definitively needs a lumbar puncture to exclude meningitis
Ceftriaxone, vancomycin
Subdural Hematoma
History of head trauma
May have focal neurologic findings
Signs of increased intracranial pressure if large and acute, such as headache and vomiting
Diagnose by noncontrast head CT scan
Surgical drainage

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Emergency Medicine Cases

CASE 2
Chief complaint
"I can't walk right."

History and physical examination


A 19-year-old white man who was playing rugby six hours ago comes to the
emergency department complaining of a severe headache for the last two
hours. While playing, he sustained head trauma and had a brief period of loss of
consciousness from which he awoke and was his normal self. He also started to
complain of nausea, vomiting, and weakness of the right side, as well as an inability
to walk. He has no other medical problems.
Vital signs are: temperature 37.8 C (100 F), blood pressure 120/80 mm Hg, pulse
88/min, and respirations 18/min. Neurologic examination shows a small laceration
of the left temporal region. His right eye is normal, and his left eye is dilated. There
is a right hemiplegia. The remainder of the physical examination is unremarkable.

Differential diagnosis

CCS Note
All patients with head trauma
and a loss of consciousness
should undergo a head CT
scan without contrast, no
matter how brief the loss of
consCiousness.

Subdural hematoma
Concussion
Epidural hematoma
Contusion
Subarachnoid hemorrhage

Initial diagnostic plan

Results

1. CT scan of head, without contrast

1. Convex hyperdensity between the brain and


the skull, consistent with an acute epidural
hematoma. A midline shift to the right is seen.

Assessment

CCS Note

Rapidly evolving and often lethal, acute epidural hematomas are formed by laceration of a dural
vessel, which produces a clot between the skull and the dura. Hemorrhage originates most often
from a branch of the middle meningeal artery that has been lacerated by a fracture. In 90% of
adult patients with an epidural hematoma, skull fracture is demonstrated by x-ray or at surgery
or autopsy. The classic history is a brief loss of consciousness from which the patient awakens
and is completely well; then the clot forms, compressing the brain surface and increasing the
overall intracranial pressure. The increased pressure results in headache, vomiting, and weakness of contralateral limbs. The temporal lobe is displaced, compressing the brainstem and the
adjacent ipsilateral occulomotor nerve.

Although not repeatedly


mentioned in every one of
these cases, every patient
scheduled to have surgery
should have a CBC to assess
the platelet count and a
prothrombin time to assess
the risk of bleeding during
the procedure.

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USMLE Step 3: Internal Medicine

Treatment plan
1. Intubation and hyperventilation to a pC0 2 of 25- 30 mm Hg

CCS Note
Stress ulcer prophylaxis is
given for any patient who has
had head trauma, burns, or
intubation.

2. Intravenous mannitol use


3. Neurosurgical evaluation for surgical evacuation of the hematoma
4. Maintain systolic blood pressure at > 100 mm Hg
5. Stress ulcer prophylaxis with proton pump inhibitors, H 2 blockers, or sucralfate
6. Admission to the intensive care unit

Discussion
In acute epidural hematoma, careful observation of the level of consciousness and the neurologic status is imperative if an epidural hematoma is considered. Early removal of the hematoma before transtentorial herniation is essential for a favorable outcome. Approximately 73o/o of
patients who were decerebrate before surgery died, but only 1o/o of patients who were conscious
before surgery died. The two essential components of a successful procedure are removing the
clot to relieve brain compression and securing the source of bleeding to prevent recurrence.
As the clot is removed, hemostasis is achieved by electrocoagulation and ligation of the main
trunks of the middle meningeal vessels as they appear on the dura.
The acute management of increased intracranial pressure involves hyperventilation and mannitol
injection. Hyperventilation lowers the pC0 2 of the arterial blood, and the cerebral vessels will
therefore constrict. This will decrease intracranial pressure. Mannitol is an osmotic diuretic that
also acutely decreases intravascular volume. Steroids are of no benefit in intracranial bleeding.
Their best indication is to decrease swelling around brain tumors, such as neoplasms and infection, which lead to increased intracranial pressure from edema.

CCS Note
Don't forget to address
location for every CCS case.
Don't leave your patient in the
emergency department after
the initial management
is complete.

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Final diagnosis
Epidural hematoma, acute

Emergency Medicine Cases

Case Review
Concussion
History of head trauma
Loss of consciousness with amnesia
Length of amnesia is related to the severity of the head trauma
No focal neurologic deficits
Normal head CT scan
No specific therapy

Contusion
Head trauma with loss of consciousness
Usually no focal deficits, but they might be present
Head CT scan is the best test
Rarely requires surgical intervention and resolves spontaneously

Subdural and Epidural Hematoma


History of head trauma
More frequent neurologic deficits
Head CT will distinguish which one is present
Larger lesions need surgical removal
Herniation may occur and will need acute management with hyperventilation and mannitol

Subarachnoid Hemorrhage
Secondary to trauma or spontaneous rupture of congenital intracranial aneurysm
Fever, headache, photophobia, and neck stiffness are typical
Distinguish from meningitis by the more acute onset or loss of consciousness
Gives a loss of consciousness and focal deficits in 30 to 50%
CT scan without contrast
CSF with xa nthochromia
L.__

--

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USMLE Step 3: Internal Medicine

CASE 3
Chief complaint
Nausea and vomiting

History and physical examination


A 21-year-old college student is brought to the emergency department with nausea
and vomiting. Her roommate states that she has been depressed lately and is
sleeping more than usual. Things got worse after she failed two final exams last
week. Since the day before, she has not seemed herself. She started complaining of
nausea this morning and has been vomiting for the past six hours. She has no other
medical problems and denies daily use of medicines. Her roommate is worried that
she took some pills.
She is awake but appears somnolent and in mild respiratory distress. Vital signs
are: temperature 38.3 C (101 F), blood pressure 110/60 mm Hg, pulse 130/ min,
and respirations 26/min. Cardiovascular examination shows a regular rhythm and
hyperdynamic precordium. Her lungs are clear, and her abdomen has normal bowel
sounds and is slightly tender. There is no evidence of edema in her extremities.

Differential diagnosis
Drug overdose, unspecified
Acetaminophen overdose
Salicylate (aspirin ) overdose
Gastroenteritis
Alcohol intoxication

CCS Note

All patients with acute altered


mental status of unclear
etiology can receive naloxone,
thiamine, and dextrose as part
of their initial set of orders.

Initial diagnostic plan

Results

1. Complete blood count

1. WBC 12,000/mm 3; platelets and hemoglobin within

normal limits
2. Serum electrolytes

2. Sodium 146 mEq/L, potassium 5 mEq/L, chloride


108 mEq/L, bicarbonate 17 mEq/L, glucose
110 mg/dL

3. BUN, creatinine

3. BUN 28 mg/dL, creatine 2.1 U/L

4. Anion gap

4. 21 mEq/L

5. Arterial blood gasses

5. pH 7.46/pC0 2 23 mm Hg/p0 2 90 mm Hg/HC0 3


17 mmHg; metabolic acidosis with respiratory
alkalosis

6. Serum ethanol level

6. 0 mg/dL

Assessment
The presentation of an acute change in mental status in a depressed patient should lead you to
suspect a possible drug overdose. A respiratory alkalosis and metabolic acidosis should prompt
yo u to suspect salicylate intoxication. A blood alcohol level can help to rule out this ingestion . The

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management approach should take into account the patient's altered mental status. Other complications of aspirin overdose that are not present in this patient are tinnitus, pulmonary edema, and
coma (resulting from edema).
Aspirin is a very complex metabolic poison. It causes an acute respiratory alkalosis at first by
central brainstem stimulation. Later, there is predominant metabolic acidosis. The acidosis
is actually a lactic acidosis because aspirin poisons the mitochondria, leading to anaerobic
metabolism and the production of lactate. Aspirin is directly toxic to the kidney tubules and
lung parenchyma and may give acute tubular necrosis and acute respiratory distress syndrome.
The direct effect of aspirin on the brain leads to encephalopathy.

Further diagnostic plan

CCS Note
For patients with potential
overdoses, it is acceptable to
order activated charcoal before
obtaining the results of specific
diagnostic tests. Although
charcoal may not help every
overdose, it has no adverse
effects.

Results

1. Plasma salicylate level

1. Salicylate level100 mg/dL (elevated)

2. Urine or blood toxicology screen

2. Negative for all but salicylate

Treatment plan
1. Activated charcoal to block further absorption of the drug

2. Intravenous fluids to help restore volume status


3. Intravenous bicarbonate for urine alkalinization, which aids drug excretion
4. Psychiatric consultation

Discussion

CCS Note

Salicylates (aspirin) have great potential for both accidental ingestion by children and as a suicide
substance for adults. Acute ingestion of > 100 mg!kg leads to an initial respiratory alkalosis and later
may cause a mixed respiratory alkalosis and metabolic acidosis. Acute ingestion invariably presents
with vomiting, and this often aids in distinguishing aspirin from acetaminophen overdose.

Consultations should rarely,


if ever, be ordered for singlebest answer questions.
However, you are expected to
ask for them much more often
on the CCS.

The initial management calls for the prevention of absorption. This is best accomplished at home
by induced emesis (with an agent like ipecac syrup) and should be considered for all patients
without altered mental status. Gastric lavage, used more often in the emergency department, is
used on patients who present within one hour of ingestion as another method to empty the gastric contents. Activated charcoal is administered to absorb the ingested toxin, thereby blocking
further systemic absorption. Following these initial measures, alkalinization of the urine should
be performed to promote ionization of the salicylate and to thus reduce further reabsorption.
For this purpose, intravenous bicarbonate is given. Effectiveness is monitored by measuring the
pH of the urine, not serum.
Lastly, hemodialysis would be indicated for:
1. Persistent acidosis with pH <7.1

2. Initial salicylate levels > 160 mg/dL or > 130 mg/dL after six hours
3. Coma/seizures
4. Renal failure
5. Congestive heart failure

Final diagnosis
Salicylate intoxication

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USMLE Step 3: Internal Medicine

Case Review
Salicylate Intoxication
Hyperventilation from central stimulation; patients complain of dyspnea
Tinnitus, renal failure, and metabolic acidosis
Respiratory alkalosis occurs first; acidosis predominates later
Diagnose with serum level and treat with bicarbonate to eliminate aspirin by urinary excretion

Benzodiazepine Overdose
Rarely, if ever, cause death by themselves
Central nervous system depressant leading to lethargy and slow heart and respiratory rates
Never with a fever (as in this patient)

Barbiturates
Central nervous system depressant, even to the point of coma
Diagnose by drug level
Phenobarbital excretion may be enhanced with alkalinization of urine

Hallucinogens
Rarely make you sleepy
Do not cause mortality
No specific antidotes

Cocaine
May give the hyperventilation, tachycardia, and fever (as found here in this case)
Does not present with sleepiness, as in this case
Hyperexcitability is common
No specific antidote

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Emergency Medicine Cases

CASE4
Chief complaint
"I have blood in my stool."

History and physical examination


A 76-year-old white man comes to the emergency department after passing stool
that was surrounded by a large volume of blood. The patient states he had two
similar episodes seven months ago but did not seek medical attention. He denies
abdominal pain, fever, or diarrhea. He has a history of a myocardial infarction and
valvular disease. He is on no medications.
Vital signs are: temperature 37.0 C (98.6 F), blood pressure 90/70 mm Hg, pulse
100/min, and respirations 16/min. There are orthostatic changes. His abdomen is
soft and nontender. Rectal examination shows no hemorrhoids or stool, but there is
bright red blood in rectum. Cardiovascular examination shows 3/6 systolic ejection
murmur radiating to carotids.

Differential diagnosis

CCS Note

Hemorrhoids
Angiodysplasia
Colonic polyps
Ulcerative colitis
Crohn disease
Diverticulosis
Solitary rectal ulcer

Initial diagnostic plan

Results

1. Complete blood count

1. Hematocrit 29% (normal39-49o/o)

2. BUN

2. 32 mg/dL (normal8-18 mg/dL)

3. Creatinine

3. 0.9 mg/dL (0.6-1.3 mg/dL)

4. Prothrombin time/partial thromboplastin time

4. Normal

5. Electrocardiogram

5. Normal

The most important initial


consideration on the CCS
in gastrointestinal bleeding
is hemodynamic stability. If
the patient is hypotensive
or tachycardic, a bolus of
intravenous normal saline
or Ringer's lactate should be
ordered with the first set of
orders.

Assessment
Large volume bleeding from the colon in adults is usually caused by diverticular disease,
angiodysplasia, or ulcerative colitis. Benign or malignant neoplasms and ischemic colitis rarely
cause massive bleeding. The site of bleeding in the colon can be identified in 70-80% of patients.
Massive bleeding originates in the right as often as in the left colon. Diverticulosis is most often
left-sided. Bleeding diverticula and angiodysplasia are common in the right colon. When active
hemorrhage is occurring, radionuclide scintigraphy or angiography can be performed to identify
the site of hemorrhage.

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USMLE Step 3: Internal Medicine

Colonoscopy will show lesions in the colon also, but they are harder to see during large-volume
bleeding. Colonoscopy is the primary method of identifying angiodysplasia. Nasogastric tube
placement is occasionally useful because 10% of cases of hematochezia originate from the upper
gastrointestinal tract. BUN characteristically rises because of absorption of nitrogenous breakdown products of blood from the gastrointestinal tract.

CCS Note
Specific endoscopy is
not as important as fluid
resuscitation and correction
of coagulopathy. Order fluids,
CBC, type, and cross first, then
do scope later.

Further diagnostic plan

Results

1. Colonoscopy

1. Classic spider angioma-like lesions in the

right colon
2. Radionuclide scintigraphy, if bleeding
is too rapid to make colonoscopy
effective

2. Negative

3. Nasogastric tube placement if you are


uncertain as to whether it is an upper
or lower gastrointestinal source of
bleeding

3. Negative

Treatment plan
1. Normal saline infusion until blood is available for transfusion

CCS Note
Nasogastric tube placement is
one of the least useful tasks
in gastrointestinal bleeding.
Lavaging the stomach with
saline or ice has no efficacy
in stopping the bleeding. The
nasogastric tube is useful
in guiding the site of the
initial endoscopy.

2. Endoscopic electrocoagulation
3. Blood transfusion
4. Surgical consultation for the possibility of colonic resection if bleeding is persistent and
massive (>4-6 units of blood in < 24 hours)

Discussion
Angiodysplasia is characterized by painless bleeding, which may be mild to massive.
Angiodysplasia is sometimes associated with aortic stenosis. Signs of bleeding can range from
brisk hematochezia to occult blood loss, leading to iron-deficiency anemia. Many patients are
elderly with a history of cardiac disease, especially aortic stenosis. In older patients with cardiac
disease, it is especially important to maintain the hematocrit above 30%. Hematochezia refers
to the passage of gross blood per rectum.
Brisk colonic hemorrhage due to angiodysplasia responds to endoscopic electrocoagulation. In
high-risk patients unable to be controlled by endoscopy, selective arterial catheterization should
be performed either for local infusion of vasopressin or for deliberate embolization. Vasopressin
is rarely necessary and should be avoided in a patient with cardiac disease because it causes vasospasm. Most cases stop spontaneously. If massive bleeding continues, subtotal colectomy, laser
therapy, or electrocoagulation is indicated. Fresh frozen plasma is used with coagulopathy.

Final diagnosis
Lower gastrointestinal bleed

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Emergency Medicine Cases

Case Review
Angiodysplasia
Second most common cause of lower gastrointestinal bleed in older patients
Bright-red blood per rectum (but this is the same in hemorrhoids and diverticulosis)
Diagnosed by direct visualization on colonoscopy
Angiography is sometimes necessary for diagnosis
Usually stops spontaneously; some cases need local coagulation through the endoscope
Hemorrhoids
Most common cause of red blood in the stool
Blood found on toilet tissue
Diagnose by rectal examination or anoscopy
Diverticulosis
Most common cause of significant lower gastrointestinal bleeds
Found on endoscopy
Rarely needs a nuclear bleeding scan or angiogram
Inflammatory Bowel Disease (Crohn Disease and Ulcerative Colitis)
Usually presents at a younger age
Fever, mucus, and diarrhea are characteristic
Diagnosed at endoscopy
Treat with 5-ASA derivatives, such as mesalamine, steroids, and infliximab (if fistulizing)

MEDICAL

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USMLE Step 3: Internal Medicine

CASE 5
Chief complaint
Confusion and irritability

History and physical examination


A 73-year-o\d woman with insulin-requiring diabetes mellitus is brought to the
emergency department by her family for a flulike illness earlier in the week and
because she has not been eating well. Over the past 24 hours, she has "not been
herself," with marked irritability and confusion. This morning she had been difficult to
awaken. There is no history of fever, neck stiffness, or focal neurologic deficits. She is on
no other medications. She is currently lying on a stretcher and is difficult to arouse.
Vital signs are: temperature 37.8 C (100.0 F), blood pressure 105/72 mm Hg, pulse
110/min, and respirations 16/min. Her pupils are equal, round, and reactive to light
and accommodation. She has normal heart sounds and tachycardia. Her lungs are
clear and abdomen is benign. Changes consistent with venous stasis are evident
in the extremities. Neurologic examination is nonfoca\; there are no gross deficits;
however, she is unable to follow commands.

Differential diagnosis
Hypoglycemia
Acute delirium
Drug overdose
Cerebrovascular accident
Sepsis syndrome

Initial diagnostic plan

Results

1. Measurement of blood glucose by finger stick

1. 35 mg/dL

2. Serum electrolytes

2. Normal

3. CBC

3. Normal

Assessment
Hypoglycemia is a relatively common complication of therapy with insulin and oral hypoglycemic agents and should be thought of first when approaching a diabetic patient with a change
in mental status. Other common symptoms that may be seen in association with this condition
include irritability, tremulousness, diaphoresis, seizure, stupor, and coma. Meningitis is unlikely
in the absence of fever and neck stiffness. Strokes usually present with a focal deficit rather than
generalized delirium, as seen in this patient.

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Emergency Medicine Cases

Further diagnostic plan

Results

1. Blood cultures

1. No growth

2. Urine cultures

2. No growth

3. If the patient does not recover after


administration of glucose, consider
thyroid function tests, vitamin B12
level, lumbar puncture, toxicology
screen, and CT scan of the head

CCS Note
Treating unstable patients is
always more important on the
CCS than specific diagnostic
testing. Giving glucose to a
disoriented person is more
important than waiting for
specific diagnostics.

Treatment plan
1. Intravenous dextrose (50 mL of 50% dextrose should be given initially). Oral administration

should be avoided in patients who are not alert.


2. Further evaluation would be required if the patient's status does not markedly improve with
glucose administration.

Discussion
The most common causes of hypoglycemia in diabetic patients are a change in dietary habits
without an appropriate change in medication, an increase in metabolic demands (either from
activity or infection), and medication overdose. The diagnosis is easy to establish and the condition must be corrected promptly. In nondiabetic patients, possible causes of hypoglycemia include
insulinoma, severe liver disease, alcohol intoxication, adrenal insufficiency, myxedema, and severe
malnutrition. Reactive hypoglycemia occurs following a meal usually 2 to 4 hours after eating. It
is due to an excess of insulin released after glucose stimulation often after gastric resection. When
the diagnosis is in question, an insulin level can be obtained.

Final diagnosis
Hypoglycemia

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USMLE Step 3: Internal Medicine

Case Review
Sepsis
May or may not be febrile
Hypotension and tachycardia are present
Positive blood culture
Low serum bicarbonate
Cerebrovascular Accident
Accompanying focal neurologic findings
Abnormal CT scan or MRI
Drug Overdose
Look for the drug in the history
Response to empiric naloxone and dextrose
Urine toxicology screen
Hypoglycemia
Frequent in patients maintained on insulin and sulfonylureas
Characterized by tachycardia, sweating, nausea, feeling of warmth
Giving glucose can be both diagnostic as well as therapeutic

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Emergency Medicine Cases

CASE 6
Chief complaint
"''m spitting all the time and am tired."

History and physical examination


A 60-year-old farmer is brought to the emergency department because of excessive
salivation and somnolence. After spraying his crops, he developed diarrhea,
polyuria, and excessive salivation. He also is complaining of dyspnea and anxiety.
Vital signs are: temperature 37.0 C (98.6 F), blood pressure 90/60 mm Hg,
pulse 56/min, and respirations 24/min. He appears to be somnolent and in
mild respiratory distress. His skin is warm and dry. Physical examination shows
miosis, wheezing bilaterally, and a soft abdomen with hyperactive bowel sounds.
Neurologic examination is nonfocal but shows lethargy.

Differential diagnosis
Organophosphate poisoning
Cholinergic crisis

CCS Note

Assessment
Cholinesterase inhibitors are found in a wide variety of insecticides for home and commercial use. Some chemical warfare agents are cholinesterase inhibitors. These compounds
inhibit acetylcholinesterase and therefore allow accumulation of acetylcholine at nerve endings. Organophosphates bind irreversibly with the enzyme, whereas carbamates are considered
reversible inhibitors. All are rapidly absorbed from the skin and gastrointestinal and respiratory
tract. Miosis, salivation, bronchospasm, and lethargy occur shortly after exposure. Diarrhea,
miosis, bronchorrhea, bradycardia, and bronchospasm also occur. Fasciculations, anxiety,
seizures, and lacrimation will occur. Death could also occur from respiratory depression and
pulmonary edema.

Initial diagnostic plan

Results

1. Red blood cell cholinesterase level

1. Decreased

Oxygen is always appropriate


for a person who is
hyperventilating, such as this
patient, or for those who
are described as being in
respiratory distress. Although
this patient's cause of
respiratory distress will soon
be reversed, starting the
oxygen and stopping it later
are better than not having
started it at all.

Treatment plan
1. Atropine

2. Pralidoxime (2-PAM)
3. Management of airway
4. Remove the patient from the site of exposure
5. Remove clothing

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USMLE Step 3: Internal Medicine

Discussion
CCS Note
On the CCS, doses are less
important than are the routes
of administration.

Hospitalize all patients with suspected or documented acetylcholinesterase-inhibitor poisoning.


Careful management of the airway is important because bronchial secretions may accumulate,
and bronchospasm and hypoventilation may occur. Supplemental oxygen is helpful. At times
mechanical ventilation may be required. Remove the patient's clothing. The patient's skin must
be washed carefully. Atropine, the specific treatment, must be administered. Large doses may be
required. Start with 2 mg intravenously and follow with repeat doses of 2 to 4 mg every 5 to 10
minutes until signs of atropinization occur, such as flushing, mydriasis, tachycardia, and drying
of secretions. Pralidoxime may release organophosphates from acetylcholinesterase and should
be given to all patients with significant intoxication.

Final diagnosis
Organophosphate poisoning

208

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Emergency Medicine Cases

CASE 7
Chief complaint
Sudden shortness of breath

History and physical examination


A 35-year-old woman comes to the emergency department with progressive
shortness of breath that began last evening after dinner. She has had a
nonproductive cough and pain on her right side with inspiration. This morning,
she woke with a cough productive of a scant amount of blood-streaked sputum. Of
note, the patient recently returned from a vacation in Australia.
Vital signs are: temperature 37.4 C (99.3 F), blood pressure 100/70 mm Hg, pulse
140/min, and respirations 28/min with splinting. Physical examination shows no
oral ulcers or nasal flaring. The remainder of the examination is unremarkable.

Differential diagnosis
Pneumothorax
Pulmonary embolism
Pneumonia
Bronchitis
Pulmonary hypertension
Myocarditis
Cardiomyopathy

Initial diagnostic plan

Results

1. Chest x-ray

1. Normal

2. Complete blood count, biochemical profile

2. Normal

3. Arterial blood gasses

3. pH 7.47, pC0 2 29 mmHg; p0 2 70


mmHg; 94% 0 2 saturation; drawn on
room air

4. Electrocardiogram

4. Sinus tachycardia

Assessment
Pulmonary embolus must always be considered in the setting of acute onset of shortness of breath.
The patient's recent trip from Australia suggests a prolonged period of immobilization, putting
her at risk for a deep venous thrombosis. Tachycardia, fever, pleuritic chest pain, and hemoptysis
are all consistent with pulmonary embolus. Other possibilities include myocarditis with associated
congestive heart failure, pneumothorax, pneumonia, and increasing pleural effusion. Chest x-ray
should help to differentiate between these etiologies. A chest x-ray of a patient with pulmonary
embolism is most often normal but may show atelectasis. "Classic" findings, such as a wedgeshaped infarction, are rare. An electrocardiogram that shows sinus tachycardia or nonspecific
ST-T-wave changes are the most common findings. Signs of acute right heart strain such as right
axis deviation are rarely seen. Arterial blood gas evaluation most often shows a pure respiratory

CCS Note
Oxygen for dyspneic patients
is always appropriate. Do not
worry about making your
arterial blood gas inaccurate
by giving the oxygen at the
same time as doing the test.
On the CCS, the diagnostic
test is considered to be done
prior to administrating the
therapy.

209

USMLE Step 3: Internal Medicine

CCS Note
Do not wait for the results of
the spiral CT angiogram or
the V/Q scan in order to start
heparin. Order the heparin
once the results of the chest
x-ray, EKG, and blood gasses
are obtained.

alkalosis with hypoxia and an elevated alveolar-arterial (A-a) gradient. You can still have a pulmonary embolus with a normal blood gas. Spiral CT is generally the best test to confirm the presence
of a pulmonary embolism. A ventilation-perfusion CV!Q) scan can be a helpful initial evaluation
to rule out pulmonary embolus after chest x-ray, blood gas, and ECG are obtained. A low probability ventilation-perfusion scan makes the diagnosis of pulmonary embolus very unlikely when
the pretest probability is low. A high probability scan has an 85 to 90% specificity.
Underlying pulmonary disease can make interpretation difficult. Patients with significant lung
disease at baseline should always undergo a chest CT scan. The degree of clinical suspicion is
paramount in interpreting indeterminate scans. The index of suspicion should be raised for
patients who demonstrate an unusual number of risk factors: venous stasis, hypercoagulable
states, obesity, prior history of pulmonary embolus, or malignancy. CT angiography is increasingly accurate, and a normal spiral CT scan strongly excludes a clot.
Pulmonary angiogram remains the "gold standard" for the diagnosis of pulmonary embolism.
However, it is more invasive and involves the injection of contrast material and therefore has
more complications.
A CT scan of the chest can be used to diagnose pulmonary emboli if they are large and in the
proximal pulmonary artery. You should answer chest CT if the baseline chest x-ray is very
abnormal. The more abnormal the chest x-ray, the less accurate the ventilation perfusion scan
will be.
D-dimers are very sensitive in the diagnosis of pulmonary emboli; however, they are very nonspecific. D-dimers are the metabolic breakdown product of fibrin. They rise with the presence
of any form of clot. Lower extremity dopplers are very specific if positive. If positive, no further
testing is necessary since it will not change management.

Further diagnostic plan

Results

1. Spiral CT scan

1. Pulmonary embolus present

Treatment plan

CCS Note
The most important thing
about CCS is not just which
tests and treatments to order,
but in what sequence you
order them.

1. Start on heparin
2. Supplemental oxygen
3. Doppler studies of lower extremities
4. Venous interruption filter is indicated if anticoagulation is dangerous or ineffective
5. Consider thrombolytic therapy in patients with significant hemodynamic instability

Discussion
The immediate effect of a pulmonary embolus is obstruction of pulmonary blood flow to the
distal lung, resulting in 1) wasted ventilation, 2) atelectasis, 3) wide alveolar-arterial (A-a)
gradient, and 4) right heart strain.
Vasoconstriction of adjacent pulmonary vascular beds occurs due to hypoxemia and release
of serotonin by platelets. Severe pulmonary hypertension may result in hypotension because
of right-sided failure. More than 90% of all pulmonary emboli originate in the proximal deep
veins of the lower extremities. Virchow triad of stasis, hypercoagulability, and injury to the vessel wall identify factors that predispose to the development of venous thrombosis. Embolization
from upper extremity thrombi is rare.

210

MEDICAL

Emergency Medicine Cases

Patients with a suspected pulmonary embolus should be given supplemental oxygen and placed at
bed rest to reduce oxygen consumption. Heparin anticoagulation should be started and continued
for 7 to 10 days. If the patient is not a candidate for prolonged systemic anticoagulation or has
another pulmonary embolus during heparinization, placement of an inferior vena caval (IVC)
filter should be considered. Thrombolytic agents may be useful in cases of severe pulmonary
embolism with shock; however, the precise role of thrombolytic therapy in pulmonary embolus
is uncertain at present and is not a standard recommendation. The best use of thrombolytics is in
those with hemodynamic instability. Thrombolytics can also be used if there are recurrent emboli
while on heparin or if there is worsening after IVC filter replacement. Thrombolytic therapy
has been shown to reduce right heart pressure due to acute pulmonary embolism but has not
improved survival.
Embolectomy is a potential therapy in cases of severe pulmonary embolism; however, it is rarely
used because of the invasiveness of the procedure and the poor rate of survival. Embolectomy is
your treatment of last resort. When all else has been done (0 2 , heparin, IVC filter, thrombolytics)
and the patient is severely symptomatic, answer embolectomy. Heparin is usually started with
bolus followed by constant infusion to prolong partial thromboplastin time to 1.5 to 2.5 (normal).
The best target is partial thromboplastin time 2x control. The amount of the bolus is dependent
on weight.
Warfarin sodium should be started when the patient has stabilized, with the goal of increasing
the INR to 2 to 3 times normal. Anticoagulation for a pulmonary embolus is generally maintained for 3 to 6 months. If the patient has an underlying hypercoagulable (thrombophilia)
state, it may be continued indefinitely.

CCS Note
The specific diagnostic
etiology of the clot, such as
factor V Leiden abnormality,
protein C or S deficiency, or
antiphospholipid syndrome,
is less important on the
CCS. Remember, the CCS
is a test of management,
not pathophysiology. An
underlying thrombophilia does
not change the intensity of
anticoagulation with warfarin.
You should still maintain the
patient at an INR of 2 to 3.

Final diagnosis
Pulmonary embolus

MEDICAL

211

USMLE Step 3: Internal Medicine

Case Review
Pulmonary Embolism
Presence of risks such as malignancy, immobility, recent surgery, particularly orthopedic
Sudden dyspnea with a clear lung examination and a normal chest x-ray
Heparin and coumadin therapy
IVC filter placement if heparin can't be used
Thrombolytics in severe hemodynamic instability
Pneumonia
Cough, dyspnea, pleuritic chest pain, and fever
Abnormal chest x-ray, sputum Gram stain and culture
Pneumothorax
Sudden dyspnea
Only a tension pneumothorax will give tracheal deviation and jugular venous distension
Diagnosed by chest x-ray
Chest tube placement
Pulmonary Hypertension
Gradually, slowly progressive dyspnea
Abnormal echocardiogram or right heart catheterization
Trial of calcium channel blockers, prostacyclin, or sildenafil

212

Emergency Medicine cases

CASES
Chief complaint
''I've been nauseous and have been vomiting all day."

History and physical examination


A 44-year-old business executive comes to the emergency department with
complaints of severe nausea and vomiting over the past 12 hours. He had been
under a great deal of pressure recently and had taken numerous over-the-counter
cold preparations and acetaminophen around the clock for a severe upper
respiratory tract infection. He has had several emergency department visits for
alcohol intoxication, including one episode of alcohol withdrawal. He is a chain
smoker and has several glasses of wine with dinner each evening.
Vital signs are: temperature 37.9 C (100.2 F), blood pressure 110/75 mm Hg, pulse
100/min, and respirations 20/min. Physical examination is unremarkable, except for
mild right upper quadrant (RUQ) tenderness without rebound or guarding.

Differential diagnosis

CCS Note

Acetaminophen overdose
Appendicitis
Acute gastroenteritis
Acute cholecystitis
Acute pancreatitis
Hepatitis

Initial diagnostic plan

Results

1. Complete blood count

1. White blood cell count 12,800/mm 3, hemoglobin


13.0 g!dL, platelets 210,000/mm3

2. Electrolytes

2. Normal

3. Liver function tests

3. AST (SGOT) 74 U/L, ALT (SGPT) 92 U/L,


total bilirubin 1.6 mg/dL

4. Prothrombin time

4. 12.2 seconds

5. Amylase level
6. Abdominal ultrasound

5. Normal
6. Normal

Sometimes you cannot


identify the diagnosis on the
initial history in the CCS. Do
not worry. Order tests around
the history, and the specific
diagnosis will be revealed
later. Just don't count on
consultants to help you.

Assessment
The differential diagnosis in a 44-year-old patient presenting with nausea and vomiting is quite
broad. It is important to recognize that many over-the-counter cold preparations contain acetaminophen. In addition to this, the patient has been taking large doses of supplemental acetaminophen. Patients with significant alcohol ingestion are at increased risk for developing clinical acetaminophen toxicity, as they may have some level of baseline hepatic injury. The absence
of significant associated fever and a normal white blood cell count speak against appendicitis,
pancreatitis, and cholecystitis, although these are all considerations in this patient.

213

USMLE Step 3: Internal Medicine

CCS Note
Normal values are routinely
provided with the test
results on the CCS. Do not
worry about memorizing
uncommon test results, such
as acetaminophen levels.

Further diagnostic plan

Results

1. Serum acetaminophen levels

1. 150 tJ-g/mL

2. Aspirin level

2. 0 mg/dL

Treatment plan
1. Gastric lavage or induced emesis with ipecac if they are not already vomiting; most useful

within 1 hour of ingestion. There is a nonsignificant effect after two hours. Ipecac is rarely used
in the emergency department. Ipecac delays the administration of antidotes orally. It is most
useful for those with an accidental ingestion at home.
2. Acetylcysteine (Mucomyst); may be beneficial up to 24 hours after ingestion
3. Charcoal administration in between the doses of acetylcysteine (space their administration
apart by one hour)

Discussion
Early clinical manifestations of acetaminophen overdose include anorexia, nausea, vomiting,
diaphoresis, and malaise. Hepatotoxicity is the major concern in such patients, with peak injury
occurring 72 to 96 hours after ingestion.

CCS Note
Order acetaminophen
and aspirin levels with any
overdose case on the CCS.
Coingestion is frequent. You
won't lose points, even if the
aspirin level is normal (as seen
in this case). Missing an occult
aspirin or acetaminophen
overdose on the CCS is more
dangerous than finding an
additional normal level.

The serum acetaminophen level is plotted against time after ingestion to determine if the
patient is at risk for the sequelae of acetaminophen overdose. The level is more accurate after
four hours. Prior to this, absorption is still occurring and the level may still be rising.
The initial management of a patient with acetaminophen overdose focuses on minimizing
absorption of the drug with gastric lavage or induced emesis. Ipecac is rarely, if ever, used in the
emergency department; it is primarily for home management of overdoses in those who have not
arrived at the hospital. Charcoal may interfere with absorption of acetylcysteine (the antidote) if
given at the exact same time, so the doses should be interspersed. Acetylcysteine should be administered as quickly as possible for up to 24 hours after ingestion of acetaminophen.
Patients with hepatic injury due to acetaminophen toxicity may require liver transplant. A single
dose of 10 to 15 grams is sufficient to result in evidence of hepatic injury. Fatalities can occur with
> 15-gram ingestion. However, in chronic alcoholics, toxicity may begin with as little as 4 grams.
In the first 4 to 12 hours, the early symptoms are nausea, vomiting, diarrhea, and abdominal
pain, which often resolve. Twenty four to 48 hours later, evidence of hepatic injury begins. The
injury is not directly caused by the acetaminophen but rather by a toxic metabolite formed by
the hepatic cytochrome p450 system.

Final diagnosis
Acetaminophen overdose

214

Emergency Medicine cases

Case Review
Acetaminophen Overdose

Greater than 10 grams of ingestion results in toxicity if the liver is normal (>4 grams in alcoholics)
Vomiting in the first 24 hours followed by an asymptomatic period
Liver necrosis in 3 to 4 days
Severity is assessed with a drug level
Acetylcysteine within the first 24 hours, charcoal
Alcoholic Hepatitis

Large-volume drinking in the history


Right upper quadrant pain and tenderness with vomiting
Elevated transaminases, usually AST > ALT and elevated bilirubin on presentation
No specific therapy
Acute Cholecystitis

Right upper quadrant pain and tenderness, some fever, rarely jaundiced
Anorexia and nausea are common
Ultrasound shows gallstones, white blood cell count often mildly elevated
Treat with antibiotics and surgery if no immediate improvement
Acute Pancreatitis

Usually secondary to alcohol use or gallstones


Severe vomiting and midepigastric pain and tenderness
Elevated amylase and lipase levels
Abnormalities on ultrasound or CT scan
Conservative management with intravenous fluids, nasogastric tube suction, and analgesics

MEDICAL

215

USMLE Step 3: Internal Medicine

CASE 9
Chief complaint
''I'm wheezing, and my lips are swollen."

History and physical examination


A 27-year-old woman comes to the emergency department complaining of
wheezing and swelling of the lips. The symptoms began acutely just after eating
a chicken-and-nut dish at a nearby Chinese restaurant. She also complains of
tightness in her chest and mild difficulty breathing. She has no significant past
medical history and is taking no medicines. She had a similar episode a year ago
after she had eaten some cookies at a friend's house.
Vital signs are: temperature 36.8 C (98.2 F), blood pressure 110/50 mm Hg,
pulse 110/min, and respirations 24/min. The patient appears anxious and in mild
respiratory distress. She has diffuse facial erythema and swelling of the lips and
tongue. There is no stridor. Her heart has a regular rhythm and is tachycardic.
There is diffuse bilateral wheezing on auscultation. The remainder of the physical
examination is unremarkable.

Differential diagnosis
Acute anaphylaxis
Foreign body aspiration
Asthma
Pulmonary embolus

CCS Note
An oximeter alone is sufficient
when one is not investigating
C02 retention and when
a specific A-a gradient is
not important. An ABG is
important in COPD or in
Pneumocystis pneumonia.

216

Initial diagnostic plan

Results

1. Pulse oximetry

1. Oxygen saturation 92%

Assessment
The onset of wheezing, shortness of breath, facial erythema, and swelling of the tongue are
common manifestations of anaphylaxis. The diagnosis is made easier by the development of
these symptoms occurring shortly after exposure to the causative agent-in this case, nuts.
There are no tests that will determine the specific agent. The most important factor in a case
of acute allergic reaction is evidence of instability, such as dyspnea, hypotension, or signs of
airway obstruction, such as stridor. An allergic reaction characterized only by a rash is much
less dangerous. The presence of wheezing in this case is very worrisome.

Emergency Medicine Cases

Treatment plan
1. Supplemental oxygen

2. Establish intravenous access and start normal saline


3. Epinephrine 1:1000 subcutaneously every 15 minutes until improvement
4. Diphenhydramine intramuscularly or intravenously every 4 to 6 hours
5. Corticosteroids intravenously every 6 hours
6. Endotracheal intubation if there is severe airway obstruction secondary to laryngeal edema
that does not rapidly improve with epinephrine
7. Albuterol inhalers in patients who are wheezing

CCS Note
Oxygen should be
administered at the same
time as ordering the oximeter
in a patient with shortness
of breath. When a test and a
treatment are ordered at the
same time, the test reflects the
pretreatment state.

Discussion
Anaphylaxis is an acute systemic reaction resulting from the interaction of a foreign antigen
with surface immunoglobulin E located on mast cells and basophils in a previously sensitized
person. This results in the release of histamine, leukotrienes, and other factors that lead to
smooth-muscle contraction and vasodilation. Anaphylactic reactions can present with a spectrum of symptoms, and, in the majority of cases, will develop within one hour of exposure to
the offending agent.
Vasodilation results in the leakage of plasma into the extravascular space, which may result
in urticaria and angioedema, hypovolemia and shock, pulmonary edema, obstruction of the
upper airway, and cardiac arrhythmia. The most critical issue in anaphylaxis is whether or not
the person's airway is obstructed and if their blood pressure is low. Intravenous fluids must be
given with the epinephrine at the beginning if the blood pressure is low.
The systems most frequently affected are the skin, lungs, gastrointestinal tract, and cardiovascular system. The diagnosis is generally easily made if the symptoms occur shortly after exposure
to the causative agent. If not, the diagnosis may be more difficult and can be confused with such
diagnoses as a vasovagal episode, foreign body aspiration, and cold urticaria.
Countless substances can cause anaphylactic reactions, but the most common offenders are
drugs, insect stings, and food substances, such as peanuts and fish. Because anaphylaxis may
be rapidly fatal, the most important step in management involves a rapid assessment of the
patient's airway, breathing, and cardiovascular status.
Following an initial assessment, epinephrine should be administered as the first-line agent.
Then, antihistamines (such as diphenhydramine or hydroxyzine), H2 blockers, and steroids
may be added. All patients with an episode of severe anaphylaxis should be observed for at least
6 to 8 hours, due to the possibility of a late second reaction.

Note
Diphenhydramine is the
superior antihistamine in case
of anaphylaxis. It is more
hemodynamically effective
than the others.

Beta blockers are contraindicated in those at risk for anaphylaxis because they can make it
worse. Also, because epinephrine is used as one of the main treatments for anaphylaxis, beta
blockers will interfere with the ability of the epinephrine to be effective.

Final diagnosis
Anaphylaxis, acute secondary to nuts

217

USMLE Step 3: Internal Medicine

CASE 10
Chief complaint
"My son fell and hit his head."

History and physical examination


An 18-year-old man fell to the ground while playing soccer and hit his head. He
was unconscious for two minutes. He is complaining of a headache but cannot
recall the incident. His friends state that after the time of the injury he had difficulty
walking, which improved by the time he arrived in the emergency department.
Vital signs are: temperature 37.0 C (98.6 F), blood pressure 120/80 mm Hg, pulse
92/min, and respirations 16/min. The patient is alert and oriented to time, person, and
place. The mini mental examination is intact, and there are no neurologic deficits.

Differential diagnosis
Cerebral contusion
Cerebral concussion
Acute epidural hematoma
Subdural hematoma

CCS Note
Don't forget location at the
end of each case! Minor
head trauma without
focal neurologic deficits or
abnormalities on a head CT
scan can be managed at
home. The observation can be
done by a family member.

CCS Note
Contrast is used to detect
cancer and infections, such as
an abscess, not blood.

Initial diagnostic plan

Results

1. CT scan of head

1. Normal

Assessment
Clinically, cerebral concussion has two important signs: amnesia and unconsciousness.
Retrograde amnesia is defined as amnesia for events immediately preceding injury; antegrade
amnesia means amnesia for events happening after the injury has occurred. A period of unconsciousness lasting up to five minutes is common. Longer periods of unconsciousness are likely
to be related to at least minor degrees of brain contusion. The length of the amnesia is roughly
related to the severity of the trauma: The harder you are hit, the more you forget. Events fill in
later, starting with the most remote and moving toward the time of the injury. Young children
occasionally manifest generalized seizures or transient cortical blindness after concussion.
These are alarming phenomena but are not negative prognostic factors. Acute subdural hematoma is a potentially life-threatening problem that needs to be considered. It usually becomes
symptomatic minutes to hours after injury. One third of patients have lucid intervals.
A lucid interval is a period of normal alertness and mental status after the injury, followed
by worsening neurologic deficits and altered sensorium. Although lucid intervals may occur
with both subdural and epidural hematoma, they are somewhat more common with epidural
hematoma.

Treatment plan
1. Observation for 24 hours after the head CT scan

2. Neurologic checks every three hours

218

MEDICAL

Emergency Medicine cases

Discussion
X-ray films are often obtained but are not usually helpful. CT scans are not usually required in
the absence of focal neurologic deficit. If obtained, they are most often normal. Observation for
lethargy, vomiting, or focal neurologic signs should be instituted for 24 hours.
In cerebral concussion, neurologic deficits are maximal at the time of injury and are followed
by rapid and steady improvement. All brainstem reflexes will be normal. The CT scan will be
normal. Concussions affect 1.5 to 2 million persons in the United States each year and constitute over 50% of head injuries. Although CT scans are usually normal, pathologic studies
have revealed diffuse axonal damage. At discharge from the hospital, all patients have a normal
neurologic examination, but they may experience difficulty returning to former levels of activity for 3 to 6 months.
The main management of a concussion consists of observation for signs of more serious head
trauma, such as subdural and epidural hematoma. Subdural and epidural hematomas rarely
develop, even with an initially normal CT scan. This is why the period of neurologic checks
every few hours is necessary.

Final diagnosis
Cerebral concussion

Case Review
Concussion
Head trauma often with loss of consciousness
Never any focal neurologic findings
Never any abnormalities on head CT scan
No specific therapy; check for possible progression to bleeding

Contusion
Minor parenchymal petechiae; no collection of blood
Rarely with focal findings, blood mixed in with brain on CT scan
Never need surgery

Epidural and Subdural Hematomas


More severe head trauma
Epidural is arterial in nature; subdural is venous
Often with focal findings on neurologic examination
Both need surgical drainage if they are large
Readily visible on CT scan

MEDICAL

219

USMLE Step 3: Internal Medicine

CASE 11
Chief complaint
Extensive body burns

History and physical examination


A man was trapped in a house fire for 20 minutes. When he was finally rescued,
he was noted to be alert and breathing and had extensive burns on his right arm
and anterior chest.
He is currently awake and alert with a patent airway and moving air without
difficulty. There is some soot around his mouth, and he is not hoarse. Vital signs
are currently stable. There are extensive second- and third-degree burns along
the entire right arm and anterior torso. There are also some scattered first-degree
burns over both lower extremities and back. He weighs 220 lbs. Heart and lung
examinations are normal except for tachycardia; there is no wheezing. His abdomen
is soft and nontender.

Differential diagnosis
Skin burns
Airway burn
Carbon monoxide poisoning

Note
The most common cause
of death in burns is carbon
monoxide poisoning.
That makes 100% oxygen
administration the most
important initial therapy
for burns.

CCS Note
Order fluids with the initial set
of labs in serous burns; you
can only specify "bolus" or
"continuous," not the specific
amounts.

Initial diagnostic plan

Results

1. Carboxyhemoglobin

1. Elevated at 23%

2. Chest x-ray

2. Normal

3. Complete blood count

3. Hemoglobin 14 g/dL

4. Electrolytes (chemistry)

4. Normal

Assessment
Diagnosing skin burns in this case is not difficult. However, the critical issue is in determining the
exact extent of the burns. The depth of the burn is graded as first, second, or third degree. Firstdegree burns are erythematous, and only the superficial layer of skin is affected. Second-degree
burns are often associated with blistering and a white or fibrinous exudate. Third-degree burns
may appear blackened, charred, or leathery. Patients often lack sensation in these areas because
of loss of both epidermal and dermal elements, including hair follicles and pain receptors. The
most common causes of death in the initial period following second- and third-degree burns are
hypovolemic shock, infection, and airway injury. Airway injury is a variable problem, depending
on the nature of the burn. Even without a direct burn of the airway, inhalation injury can lead to
serious illness because of the elevation of carboxyhemoglobin levels. Carboxyhemoglobin does
not deliver oxygen to tissues, and functionally, it is the same as being anemic.
Evidence of respiratory tract injury includes tachypnea, soot in the mouth, erythema of the
palate, stridor, laryngospasm, and other evidence of respiratory distress. Laryngeal edema and
respiratory failure can develop in 6 to 24 hours after the injury. The airway and lung may appear
normal at first, but life-threatening abnormalities may appear later.

220

Emergency Medicine Cases

Further diagnostic plan

Results

1. Immediate bronchoscopy

1. Reveals no significant inhalation injury

Treatment plan
1. 100% oxygen

2. Fluid resuscitation 4 mL/kg/o/o body surface area burned (Ringer lactate)


3. Prevention of infection with topical antibiotics
4. Endotracheal intubation if there is evidence of significant respiratory injury

CCS Note
If you are given a burn case
with evidence of respiratory
burn, such as hoarseness,
wheezing stridor, or burns
in the mouth, you should
perform endotracheal
intubation with the first set
of orders.

Discussion
Care in the acute period should focus on maintaining adequate ventilation and oxygenation,
replacement of acute volume loss, correcting metabolic abnormalities, and prevention of infectious complications. The decision regarding intubation is based on the degree of airway inflammation and level of oxygenation.
The patient should be started on 100% supplemental oxygen. Oxygen therapy decreases the
half-life of the carboxyhemoglobin. The full extent of an inhalation injury may not be apparent
for 12 to 24 hours.
Hypovolemic shock often results from second- or third-degree burns encompassing >25% of
the body surface area (BSA). Fluid is infused at 2-4 ml per kg per o/o BSA is given in the first
24 hours. Normal saline or Ringer's lactate is acceptable. Patients may require replacement of
plasma and albumin as well. Emphasis should be placed on maintaining adequate urine output
to avoid renal failure. Hypovolemia can result in metabolic acidosis.

CCS Note
The CCS asks route of
administration, not dose.
Hence, in burns, topical
antibiotics, not systemic or
intravenous antibiotics, are
used prophylactically.

Calculations for body surface area (BSA) are as follows:


Head 9%
Arms 9% each
Legs 18% each
Chest 18%
Back 18%
Perineum 1o/o
Silver sulfadiazine is administered topically to all burned areas, and the wounds should be
debrided and dressings changed twice per day. Operative debridement of deep partial-thickness
burns and skin grafting should be done as soon as feasible. This helps to avoid subeschar infection and improves wound closure. Streptococcal and staphylococcal infection often complicates
the initial course.
Excision of burn eschar may be done to improve healing or if evidence of arterial compression
is present. Patients may require skin grafting.

Final diagnosis
Burns

221

USMLE Step 3: Internal Medicine

CASE 12
Chief complaint
"My eyelids are swollen."

History and physical examination


A 40-year-old laboratory technician comes to the emergency department after
he was splashed with an unknown chemical while working. He is complaining of
swollen eyelids and red eyes. His pain is worsening, and he has blurred vision.
His eyelids are edematous, and conjunctiva is hyperemic. The limbus show patchy
blanched areas with conjunctival sloughing, especially in the interpalpebral area.

Differential diagnosis

CCS Note
In ocular chemical injury,
irrigation is far more important
than doing diagnostic testing.
The nature of the chemical
is irrelevant in terms of the
choice of irrigating solution.
Normal saline is preferred
as the irrigating solution in
all cases.

Eye alkali burn


Thermal burn
Eye acid burn

Initial diagnostic plan

Results

1. Visual acuity

1. Patient unable to perform test

Assessment
Apart from the history, the diagnosis of chemical burns is usually based on the presence of
swollen eyelids with marked conjunctival hyperemia and chemosis. There is usually corneal
haze and diffuse edema, with wide areas of epithelial cell loss and corneal ulceration. After
instillation of fluorescein, corneal ulcerations can be better visualized with blue light. Other
burns can be caused by thermal exposure or by acid or alkali substances. Burns due to ultraviolet radiation (snow blindness, welder arc, or a flash burn) also can occur.

Further diagnostic plan

Results

1. Blue light examination with


fluorescein staining

1. Corneal ulcerations

Treatment plan
1. Irrigation of eyes with copious amount of isotonic saline after optical anesthesia

CCS Note

2. Eversion of eyelids to look for and remove foreign material

Eye patches have no proven


efficacy. They are only proven
harmful with contact lens
injuries because of bacterial
colonization of the cornea.

3. Antibiotic optic ointment


4. Keep eyes moist, consider eye patch
5. Analgesia orally
6. Hospitalize patient if burns are severe
7. Ophthalmology consultation

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MEDICAL

Emergency Medicine Cases

Discussion
Ocular burns secondary to alkali material are very serious because after apparent removal of the
offending agent, lodging of tiny particles within the cul-de-sac may continue to cause progressive
damage to the eye. As a rule, acid burns cause damage more rapidly but are generally less serious
than alkali burns because they do not cause progressive destruction of ocular tissues. Alkaline
(base) injury to the eye continues to penetrate the cornea and damage the eye. Superficial thermal corneal burns have a good prognosis, although corneal ulcers may occur as a result of loss of
corneal epithelium. Corneal haze due to corneal edema is frequently seen in thermal burns of the
cornea and may lead to decreased vision.

Final diagnosis
Ocular burn

MEDICAL

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