Emergency Medicine Cases: Case 1
Emergency Medicine Cases: Case 1
Emergency Medicine Cases: Case 1
CASE 1
Chief complaint
"Leave me alone!"
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.
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.
MEDICAL
191
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.
Results
1. Electrolytes
2. 0.00 mg/dL
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.
Results
1. Chest x-ray
1. No infiltrates
2. Normal
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)
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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MED ICAL
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
193
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
194
CASE 2
Chief complaint
"I can't walk right."
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
Results
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.
MEDICAL
195
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.
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.
196
Final diagnosis
Epidural hematoma, acute
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
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.__
--
197
CASE 3
Chief complaint
Nausea and vomiting
Differential diagnosis
Drug overdose, unspecified
Acetaminophen overdose
Salicylate (aspirin ) overdose
Gastroenteritis
Alcohol intoxication
CCS Note
Results
normal limits
2. Serum electrolytes
3. BUN, creatinine
4. Anion gap
4. 21 mEq/L
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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MEDICAL
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.
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
Treatment plan
1. Activated charcoal to block further absorption of the drug
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.
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
199
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
200
CASE4
Chief complaint
"I have blood in my stool."
Differential diagnosis
CCS Note
Hemorrhoids
Angiodysplasia
Colonic polyps
Ulcerative colitis
Crohn disease
Diverticulosis
Solitary rectal ulcer
Results
2. BUN
3. Creatinine
4. Normal
5. Electrocardiogram
5. Normal
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.
201
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.
Results
1. Colonoscopy
right colon
2. Radionuclide scintigraphy, if bleeding
is too rapid to make colonoscopy
effective
2. Negative
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
202
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
203
CASE 5
Chief complaint
Confusion and irritability
Differential diagnosis
Hypoglycemia
Acute delirium
Drug overdose
Cerebrovascular accident
Sepsis syndrome
Results
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.
204
Results
1. Blood cultures
1. No growth
2. Urine cultures
2. No growth
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
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
205
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
206
CASE 6
Chief complaint
"''m spitting all the time and am tired."
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.
Results
1. Decreased
Treatment plan
1. Atropine
2. Pralidoxime (2-PAM)
3. Management of airway
4. Remove the patient from the site of exposure
5. Remove clothing
207
Discussion
CCS Note
On the CCS, doses are less
important than are the routes
of administration.
Final diagnosis
Organophosphate poisoning
208
MEDICAL
CASE 7
Chief complaint
Sudden shortness of breath
Differential diagnosis
Pneumothorax
Pulmonary embolism
Pneumonia
Bronchitis
Pulmonary hypertension
Myocarditis
Cardiomyopathy
Results
1. Chest x-ray
1. Normal
2. Normal
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
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.
Results
1. Spiral CT scan
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.
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MEDICAL
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
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
CASES
Chief complaint
''I've been nauseous and have been vomiting all day."
Differential diagnosis
CCS Note
Acetaminophen overdose
Appendicitis
Acute gastroenteritis
Acute cholecystitis
Acute pancreatitis
Hepatitis
Results
2. Electrolytes
2. Normal
4. Prothrombin time
4. 12.2 seconds
5. Amylase level
6. Abdominal ultrasound
5. Normal
6. Normal
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
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.
Results
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
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
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
MEDICAL
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CASE 9
Chief complaint
''I'm wheezing, and my lips are swollen."
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
Results
1. Pulse oximetry
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.
Treatment plan
1. Supplemental oxygen
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
CASE 10
Chief complaint
"My son fell and hit his head."
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.
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
218
MEDICAL
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
MEDICAL
219
CASE 11
Chief complaint
Extensive body burns
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.
Results
1. Carboxyhemoglobin
1. Elevated at 23%
2. Chest x-ray
2. Normal
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
Results
1. Immediate bronchoscopy
Treatment plan
1. 100% oxygen
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.
Final diagnosis
Burns
221
CASE 12
Chief complaint
"My eyelids are swollen."
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.
Results
1. Visual acuity
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.
Results
1. Corneal ulcerations
Treatment plan
1. Irrigation of eyes with copious amount of isotonic saline after optical anesthesia
CCS Note
222
MEDICAL
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
223