Block 9: Critical Care-Emergency Medicine Board Review: Q&A
1. You are supervising pediatric residents in an urgent care clinic. One of the residents presents a patient who has a
history of systemic lupus erythematosus and is well known to the clinic. She presents today with a decreased
appetite and emesis. The resident is concerned about the patient’s appearance. When you join her in the patient’s
room, you find a pale, diaphoretic 15-year-old girl who has a heart rate of 130 beats/min and cool, mottled
extremities. Her cardiovascular examination reveals distant heart sounds, no murmurs, and jugular venous
distention.
Of the following, the BEST explanation for this patient’s current findings is
A. arrhythmia
B. dehydration
C. pericardial tamponade
D. pleural effusion
E. sepsis
Preferred Response: C
The patient described in the vignette is in shock with decreased perfusion. Jugular venous distention results from
increased filling pressure in the right atrium, a direct result of fluid and, thus, pressure in the pericardial space
(pericardial tamponade). The pressure is transmitted to the thin-walled right atrium and subsequently the venous
return of the superior and inferior vena cavae. As these veins drain by passive (nonpulsatile) flow, any increase in
the filling pressure requires that they overcome a greater pressure. As the filling of the right atrium decreases, so too
does its stroke volume.
With progression, tachycardia develops in an effort to maintain cardiac output: cardiac output = heart rate x
stroke volume. The diminished cardiac output leads to cardiogenic shock and the resulting signs and symptoms of
pallor; diaphoresis; and poorly perfused, cool, mottled extremities noted in this patient. The distant heart sounds
are the result of excessive fluid in the pericardium creating even further space between the stethoscope and the heart.
Although the blood pressure was not reported for this patient, it is not uncommon for those who have large
pericardial effusion and tamponade to demonstrate pulsus paradoxus. Pulsus paradoxus is defined as a decrease in
the blood pressure of more than 10 mm Hg during inspiration. Normally, a mild (4— to 6-mm Hg) decrease in blood
pressure occurs as the negative intrathoracic pressure in combination with increased pulmonary capacitance leads to
a decrease in pulmonary venous return to the left atrium and a resulting decrease in left ventricular output. When
this normal physiologic phenomenon is exaggerated, such as in cases of significant pericardial effusion, severe
asthma, and other respiratory diseases, it is referred to as pulsus paradoxus.
Arrhythmia, dehydration, pleural effusion, or sepsis may lead to critical illness, but the alarming constellation of
poor peripheral perfusion, jugular venous distention, distant heart sounds, diaphoresis, and an underlying condition
that is associated with pericardial disease described for the patient in the vignette point specifically to pericardial
tamponade.
2. You are evaluating an 18-month-old girl for vomiting. She has a history of febrile seizures and recurrent ear
infections. She is receiving no medications. Over the past several weeks, her parents have noticed that she has been
"increasingly clumsy." She has vomited each of the last three mornings but has had no diarrhea or fever. Physical
examination findings are normal except for an ataxic gait and hyperreflexia.
Of the following, the MOST appropriate next step is
A. administration of an antiemetic
B. computed tomography scan of the head
C. electroencephalography
D. lumbar puncture
E. reassurance and re-evaluation in 3 to 5 days
Preferred Response: B
Initial symptoms of increased intracranial pressure often consist of headaches and confusion that may be
accompanied by lethargy. The child described in the vignette exhibits signs of a progressive increase in pressure,
such as vomiting (especially in the morning) and changes in motor tone. Physical examination findings include a full
or bulging fontanelle and widened sutures. These signs, as well as pupillary changes and papilledema, should
prompt rapid evaluation to prevent permanent neurologic injury and progression of the increased pressure with
potential neurologic catastrophe.
Intracranial pressure is maintained by the balance of the contents of the cranial vault, which includes brain, blood,
and cerebrospinal fluid. Increases in intracranial pressure can occur with a wide variety of disease processes, such as
brain tumors, hydrocephalus, infections, head trauma, and hypoxic-ischemic injury. Intracranial pressure increases
when the compensatory mechanisms of the cranial vault are exceeded and produce numerous symptoms, depending
on the age of the patient and the underlying pathology.
Computed tomography scan or magnetic resonance imaging of the head is the first priority in evaluating
suspected increased intracranial pressure. Meningitis is unlikely in this patient due to the chronicity of symptoms
and absence of fever. Accordingly, lumbar puncture is not indicated at this time. Electroencephalography might be
indicated if atypical migraines or seizures were suspected, but the initial priority is to evaluate the patient for
potential life-threatening disease processes. The child has no evidence of viral infection, and reassurance or
administration of antiemetics is not appropriate.
3. A 3-month-old infant is brought to the office for fussiness, increased sleeping, and poor feeding. According to
his mother, he was doing well until 4 days ago, when his formula intake decreased from 6 oz every 3 to 4 hours to 1
to 2 oz every 4 hours and she had to awaken him to feed. He has had no vomiting, diarrhea, or fever. He was born at
term, and the mother had no antenatal infections. On physical examination, the infant is difficult to console and has
a high-pitched cry. His temperature is 98.2°F (36.8°C), heart rate is 160 beats/min, and respiratory rate is 30
breaths/min. His anterior fontanelle is flat, pupils are 4 mm and equally reactive, and there is no evidence of corneal
abrasions. His lungs are clear, heart sounds are normal, and abdominal evaluation findings are benign. His
extremities are warm, well-perfused, and have normal tone. Results of the initial laboratory evaluation, including a
complete blood count with differential count, electrolytes, and urinalysis, are normal. The fecal occult blood test
result is negative.
Of the following, the MOST appropriate next study is
A. abdominal ultrasonography
B. chest radiography
C. computed tomography scan of the brain
D. serum ammonia determination
E. urine organic acid screen
Preferred Response: C
The differential diagnosis of the irritable infant is extensive and includes conditions that affect all organ systems.
The evaluation should be based on a complete history and physical examination as well as a high index of suspicion
for serious occult causes. For the patient described in the vignette, the concern should be high for nonaccidental
head injury, despite the lack of trauma history or external or cutaneous findings on physical examination, and
should prompt the physician to obtain neuroimaging (eg, computed tomography scan or magnetic resonance
imaging).
Of note, recent studies have reconfirmed the incidence of occult head injuries and the importance of neuroimaging
in the evaluation of suspected child abuse. Almost 30% of children undergoing child abuse evaluation in one study
had occult brain injury despite the absence of neurologic symptoms, and as many as 10% of brain injuries may be
missed if only skeletal surveys and ophthalmologic examinations are performed.
The presenting signs and symptoms of nonaccidental head trauma due to inflicted traumatic brain injury (also
known as "shaken baby syndrome") often are nonspecific. It is estimated that as many of 30% of cases are not
diagnosed initially, in part because the findings may be attributed to other conditions, such as viral syndrome, colic,
or formula intolerance. The history also may be misleading, with most caretakers reporting no trauma. In some
instances, the sole finding may be a disproportionately large head circumference. The absence of external findings
is related largely to the biomechanics of the injurious event. Vigorous shaking, with or without impact, leads to
traction on the dural bridging veins. Shearing of these veins causes bleeding into the subdural space. Especially in
those cases where there was no impact of the infant's head during the shaking episode, bruising or swelling is likely
to be absent.
Abdominal ultrasonography to evaluate for intussusception or hydronephrosis, serum ammonia and urine organic
acid determinations to evaluate for metabolic errors, or chest radiography to look for cardiomegaly or pulmonary
infiltrates may be indicated in the evaluation of the irritable infant. However, in contrast to abusive head trauma, it
is likely that signs, symptoms, or abnormalities on screening laboratory evaluations would provide clues to these
other diagnoses.
4. A 14-year-old boy who has epilepsy presents to the emergency department after a generalized tonic-clonic
seizure that began on the playground at school. He continued to convulse en route in the ambulance, where he
received 15 mg diazepam rectally and intravenous access was achieved. In the emergency department, he continues
to be unresponsive, exhibiting tachycardia and non-suppressable bilateral synchronous rhythmic clonic jerks.
Of the following, the MOST appropriate medication to administer next is
A. fosphenytoin 20 mg/kg intravenously
B. pentobarbital 5 mg/kg intravenously
C. phenobarbital 20 mg/kg intravenously
D. phenytoin 7 mg/kg orally
E. valproic acid 15 mg/kg intravenously
Preferred Response: A
Standard recommendations for pharmacologic treatment of status epilepticus and refractory status epilepticus in
adults were established in the 1990s. They also represent the standard of care for children and remain valid at the
time of this writing.
Because the boy described in the vignette continues to have seizures after administration of a reasonable dose of
diazepam (step 2), he now should receive either phenytoin 20 mg/kg intravenously or fosphenytoin 20 mg
phenytoin equivalents/kg intravenously. Use of phenobarbital before phenytoin is not standard. Pentobarbital is
reserved for use when other treatments have failed to induce a medical coma, a state of complete unresponsiveness
manifested by a characteristic electroencephalographic pattern of "burst suppression" (bursts interspersed with flat
or nearly flat tracing). Intravenous valproic acid and levetiracetam are new options for use in selected cases, but they
are not standard at this time.
5. A mother brings her 6-month-old boy to the emergency department because of decreased activity and poor
feeding for the past 2 days. She says that he has not had a fever. In the emergency department, his temperature is
37.0°C, heart rate is 150 beats/min, respiratory rate is 45 breaths/min, and blood pressure is 65/40 mm Hg. His
capillary refill time is greater than 4 seconds, and peripheral pulses are difficult to palpate. An initial chest
radiograph is obtained. The emergency department staff obtain laboratory studies, order blood cultures, and
administer a total of 60 mL/kg of isotonic fluid as well as antibiotics. The infant becomes less responsive, with a
heart rate of 170 beats/min, respiratory rate of 60 breaths/min, blood pressure of 50/28 mm Hg, and capillary refill
time of greater than 6 seconds. A repeat chest radiograph is obtained.
Of the following, the MOST appropriate next step is administration of
A. amphotericin B
B. dopamine infusion
C. isotonic fluid (20 mL/kg)
D. sodium bicarbonate
E. vasopressin infusion
Preferred Response: B
The child described in the vignette is in shock, as evidenced by tachycardia and poor perfusion. Following
aggressive resuscitation with fluid, he deteriorates clinically, and radiography documents cardiomegaly and
pulmonary edema, which is highly suggestive of cardiac disease. The appropriate treatment is respiratory
stabilization, diuretic administration, and initiation of inotropic medications to improve cardiac function. The choice
of inotropic agent depends on the type of shock seen. Dopamine is a good choice in this scenario due to its positive
effect on contractility and systemic vascular resistance.
Shock, the inadequate delivery of oxygen to meet the metabolic demand of tissues, is an important cause of
morbidity and mortality in pediatrics. It is critical to recognize and treat shock promptly because mortality rates of
20% to 50% have been reported. Shock is the culmination of disturbances in cardiac output and systemic vascular
resistance and generally is divided into several types.
Vasopressin is a powerful vasoconstrictor that has a role in severe shock, but because it often causes tachycardia and
can reduce splanchnic blood flow, it usually is reserved for shock resistant to standard inotropes. The chest
radiograph for the child in the vignette demonstrates significant pulmonary edema, which likely only would be
worsened by additional fluid boluses. Because there is no evidence of systemic fungal infection, amphotericin B
therapy is unnecessary. Administration of sodium bicarbonate is not indicated because the patient’s metabolic status
is not known and there is little documented evidence of its benefit in acute resuscitation, especially in infants.
6. A father brings his 2-year-old son to the emergency department in status epilepticus. He reports that the boy
spent several hours in the garage with him while he was repairing the car. On questioning, the father states that over
the course of the afternoon the child seemed sleepier than usual, then became lethargic, vomited, and seemed like he
was "drunk." On the way to the hospital he began having seizures. In the emergency department, the boy is given a
dose of lorazepam to stop the seizure and is endotracheally intubated because of respiratory depression. His initial
laboratory results are:
• Sodium, 138 mEq/L (138 mmol/L)
• Potassium, 4.9 mEq/L (4.9 mmol/L)
• Chloride, 100 mEq/L (100 mmol/L)
• Bicarbonate, 6 mEq/L (6 mmol/L)
• Glucose, 120 mg/dL (6.7 mmol/L)
• Blood urea nitrogen, 10 mg/dL (3.6 mmol/L)
• Calcium, 5.5 mEq/L (5.5 mmol/L)
• Serum osmolality, 335 mOsm/kg (335 mmol/kg)
Of the following, the MOST likely cause of this child’s clinical condition is ingestion of
A. ethylene glycol
B. gasoline
C. motor oil
D. organophosphate insecticide
E. turpentine
Preferred Response: A
The progressive lethargy, ataxia, seizures, anion gap metabolic acidosis of 30 mEq/L, and osmolar gap of 53
mmol/L described for the boy in the vignette are highly suggestive of alcohol poisoning. This is a particular
diagnostic possibility because the boy may have had access in the garage to such potential toxic alcohols as ethylene
glycol (antifreeze) and methanol (windshield wiper fluid). The hypocalcemia suggests ethylene glycol exposure
because the metabolism of ethylene glycol uses the patient’s calcium stores to create calcium oxalate, which is
excreted in the urine as crystals.
Other findings in ethylene glycol poisoning may include flank pain, hematuria, and acute renal failure. Rapid
diagnosis is critical for a patient who has symptomatic ethylene glycol poisoning because delay in treatment can lead
to renal damage, cerebral herniation, multiple organ system failure, and death. Often, initial treatment is based on
clinical suspicion before alcohol values are available.
Indirect laboratory evidence of alcohol toxicity includes an anion gap acidosis and an osmolar gap greater than
10 mmol/L. Initial treatment involves stabilization of vital functions, administration of sodium bicarbonate to
correct acidosis, and administration of the antidote fomepizole (or ethanol, if fomepizole is unavailable). Fomepizole
inhibits alcohol dehydrogenase, which metabolizes the nontoxic parent alcohols into their toxic byproducts. Because
alcohols are absorbed so quickly from the gastric mucosa, there is little role for gastrointestinal decontamination.
Hemodialysis is indicated for severe poisonings.
Many household products are toxic and frequently accessible to young children. Gasoline and turpentine are volatile
hydrocarbons that cause pulmonary injury after aspiration. Motor oil also is a hydrocarbon, but because of its high
viscosity and low volatility, it poses little risk for aspiration or toxicity. Organophosphate insecticides inhibit
acetylcholinesterase and cause a cholinergic crisis manifested by bradycardia, hypersalivation, bronchorrhea,
diarrhea, and muscle weakness.
7. A mother brings her 2-year-old son to the office 30 minutes after spilling a cup of hot coffee onto his arm and
chest. Physical examination reveals a 2x3-cm ruptured blister on his chest that has an erythematous, tender base and
a 3x5-cm area of erythema on his right upper arm.
Of the following, a TRUE statement regarding the management of the burns is that
A. the burns should be cleaned with soap and water after debridement of the blistered area
B. the patient should be given a 5-day course of prophylactic cephalexin
C. the patient should be referred to a burn center because of the extent of his burns
D. the patient will require skin grafting for the burn on his chest
E. the burn on his upper arm should be dressed with bacitracin ointment and gauze
Preferred Response: A
Most burn injuries in children are minor and can be managed on an outpatient basis. Decisions regarding
appropriateness of outpatient treatment are based on several criteria, including the depth (or degree) of the burn, the
extent of the body surface area (BSA) involved, the causative mechanism, and the location of the injury.
According to guidelines developed by the American Burn Association, pediatric patients should be referred to a burn
center for specialized care for partial-thickness burns covering greater than 10% of the total BSA; burns that involve
the face, hands, feet, genitalia, perineum, and major joints; full-thickness burns; and burns caused by chemicals or
electricity.
Superficial (first-degree) burns involve injury to the epidermis only and are characterized by intact, erythematous,
and painful skin. Partial-thickness (second-degree) burns injure both the epidermis and the dermis and often are
characterized further as superficial partial thickness if they involve only superficial layers of the dermis or deep
partial thickness when deeper dermal layers are damaged. Superficial partial-thickness burns are erythematous and
painful, with blister formation. When the blisters rupture, the base of the burn is moist and bright red. Deep partialthickness burns also are painful and erythematous, but the blister base may be pale and relatively less painful (but
not anesthetic) than in a superficial partial-thickness burn. Full-thickness (third-degree) burns injure the
epidermis and dermis and are dry, leathery, and insensate in the central portions of the burn where sensory nerves
have been destroyed.
The percentage of BSA involvement can be estimated using the “rule of nines” modified for infants and children.
This system assigns BSA percentages for various body parts and accounts for the relative BSA changes that occur
during growth from infancy to adulthood. Measuring the burn area with the patient’s palm (including the fingers),
which is approximately 1% of the BSA, also can be used to estimate the burn extent.
Treatment of superficial burns, such as that on the arm of the boy described in the vignette, involves analgesia and
local cleansing. Topical antibacterial therapy is not indicated for these injuries because the intact epidermis still
provides an adequate barrier. Partial-thickness burns, as described on the chest of the boy in the vignette, should be
cleaned with mild soap and water after broken blisters are debrided, then covered with an antibacterial ointment
such as bacitracin or silver sulfadiazine and a nonadherent dressing. A physician who has expertise in burn care
should evaluate full-thickness burns, which often require excision and grafting of the wound in addition to topical
therapy, as for partial-thickness burns. All burns should be evaluated daily for the first 48 hours because the ultimate
depth and extent may not be evident until this time. The use of prophylactic systemic antibiotics is not indicated.
The patient’s tetanus immunization status should be assessed and updated if indicated.
8. A 7-year-old boy is brought to the emergency department because of altered mental status. His parents report that
he was well when he came home from school today, but when he came in the house for dinner after playing outside
with his friends, he complained of abdominal pain and had an episode of nonbilious and nonbloody emesis. Over the
next 30 minutes, he became increasingly lethargic until his parents could not arouse him. They called emergency
medical services, and he was transported to the emergency department by ambulance. On physical examination, he
is unresponsive and drooling, his temperature is 98.8°F (37.1°C), heart rate is 50 beats/min, respiratory rate is 36
breaths/min, blood pressure is 100/60 mm Hg, and oxygen saturation is 82% on room air. His pupils are mid-size
and sluggishly reactive, and his breath sounds are coarse bilaterally, with increased work of breathing. You suspect a
toxin exposure.
Of the following, the MOST appropriate treatment of this patient is
A. atropine
B. N-acetylcysteine
C. naloxone
D. octreotide
E. physostigmine
Preferred Response: A
The patient described in the vignette is exhibiting the classic symptoms of cholinergic poisoning. These symptoms
can be remembered using the mnemonic "SLUDGE" (salivation, lacrimation, urination, diarrhea, gastric
emesis) and are due to irreversible inhibition of acetylcholinesterase and excess acetylcholine at the neuromuscular
junction. The resulting overstimulation of cholinergic receptors causes the muscarinic symptoms noted previously.
Nicotinic symptoms, which include muscle twitching, weakness, and paralysis, also may result. Organophosphate
exposure can occur though ingestion as well as dermal absorption and inhalation. These compounds are found
commonly in the home environment as components of lawn and garden care products, scabicides, and insecticides.
The treatment of cholinergic poisoning involves patient stabilization, decontamination, and administration of
antidotes. Significantly symptomatic patients may require intubation for airway protection and pulmonary toilet as
well as assisted ventilation with 100% oxygen for respiratory muscle weakness and hypoxia. Systemic
decontamination with activated charcoal as well as dermal decontamination should be performed. Dermal
decontamination may be facilitated by cleansing the skin with a dilute bleach solution. Contaminated clothes should
be discarded because laundering may not remove the toxin.
The mainstay of stabilization and treatment for cholinergic poisonings is the administration of atropine. Atropine
competes with acetylcholine at the cholinergic receptors and decreases the muscarinic cholinergic effects. The doses
of atropine used in this setting are higher than those used for symptomatic bradycardia from other causes. An initial
atropine dose of 0.05 mg/kg should be administered and doubled every 3 to 5 minutes until the pulmonary
muscarinic symptoms (bronchorrhea, bronchospasm) are controlled. Nicotinic neuromuscular symptoms are treated
by adding pralidoxime, a cholinesterase reactivating agent, to atropine therapy.
N-acetylcysteine is used to treat acetaminophen poisoning, which causes few, if any, acute symptoms. Naloxone is
an opiate antagonist used to treat symptomatic opiate overdoses, which are characterized by miosis, bradycardia, and
respiratory depression without bronchorrhea. Octreotide is a somatostatin analog that inhibits insulin release and is
indicated in the treatment of sulfonylurea overdoses, which cause profound hypoglycemia unresponsive to dextrose
administration. Physostigmine is a cholinergic agent that may be used in significantly symptomatic anticholinergic
poisonings. Because the patient's symptoms are not consistent with overdoses of any of these drugs, treatment with
these agents is not indicated.
9. You are evaluating a 6-month-old girl in the pediatric intensive care unit who is being treated for congestive heart
failure due to a presumed viral myocarditis. On physical examination, her heart rate is 170 beats/min, respiratory
rate is 50 breaths/min, and blood pressure is 75/40 mm Hg. She is currently receiving 3 L/min of oxygen via nasal
cannula and has an oxygen saturation of 92%. The infant appears alert, exhibits diaphoresis, has decreased aeration
bilaterally at the lung bases, and has a fourth heart sound. Her liver is palpable 5 cm below her right costal margin,
and her peripheral pulses are diminished. She is receiving milrinone and furosemide infusions. Results of laboratory
studies from 2 hours ago include:
• Serum sodium, 140 mEg/L (140 mmol/L)
• Serum potassium, 4 mEq/L (4 mmol/L)
• Serum chloride, 105 mEq/L (105 mmol/L)
• Serum albumin, 4.0 g/dL (40 g/L)
• Hematocrit, 45.0% (0.45)
• Blood urea nitrogen, 20.0 mg/dL (7.1 mmol/L)
• Serum creatinine, 0.6 mg/dL (53.0 mcmol/L)
Of the following, the MOST appropriate treatment to improve this child’s congestive heart failure is
A. administration of 15 mL/kg of 5% albumin
B. discontinuation of the furosemide infusion
C. increase in oxygen administration to 4 L/min
D. initiation of continuous positive airway pressure
E. transfusion with 15 mL/kg packed red blood cells
Preferred Response: D
Pulmonary edema results from a variety of pulmonary and cardiac disease processes that increase pulmonary
capillary pressure, decrease pulmonary capillary integrity, or decrease plasma oncotic pressure. Each of these
processes results in fluid outflow from the pulmonary capillaries into the pulmonary interstitium. Increased
pulmonary capillary pressure usually results from cardiac failure (as is the case for the infant in the vignette) or
obstruction to flow by stenotic pulmonary veins or tumor compression. Increased capillary permeability typically is
seen in sepsis, pneumonia, acute respiratory distress syndrome, near-drowning, or toxin exposure. Decreased
oncotic pressure generally results from hypoalbuminemic states, as may occur in renal or liver disease.
Treatment of pulmonary edema should be directed at addressing the underlying disease process, but general
measures to stabilize the patient’s respiratory status and reduce pulmonary fluid also are crucial. The administration
of positive end-expiratory pressure (PEEP) has been demonstrated to be very effective in the management of
pulmonary edema due to both pulmonary and cardiac diseases. PEEP decreases the work of breathing and improves
pulmonary function by reopening and maintaining the patency of alveolar units. This reduces pulmonary resistance
rather than forcing fluid from the interstitium. Severe cases of pulmonary edema likely require positive inspiratory
pressures as well.
Supplemental oxygen should be administered, both to increase alveolar oxygen tension and to decrease pulmonary
vasoconstriction. However, small increases in supplemental oxygen (eg, from 3 to 4 L/min) increase alveolar
oxygen tension only slightly. Diuretics are helpful for management of pulmonary edema and, therefore, should not
be discontinued. For patients who have hypoalbuminemia, administration of albumin may restore normal oncotic
pressure. Transfusion of packed red blood cells would only be of benefit if the patient was anemic.
10. A 10-year-old boy is brought to the emergency department after he struck a boulder while riding his all-terrain
vehicle, causing the vehicle to roll over on him. He was not wearing a helmet. Bystanders reported that he had a
brief loss of consciousness, but he is now alert and answers questions appropriately. He reports that he is nauseous,
has a severe headache, and is unable to hear with his left ear. On physical examination, his heart rate is 120
beats/min, respiratory rate is 20 breaths/min, and blood pressure is 130/80 mm Hg. He has multiple facial abrasions,
a 6-cm laceration on his forehead, and bloody drainage from his left ear. His midface is stable to palpation, his
extraocular movements are normal, and there is no deformity of his nasal bone.
Of the following, his clinical presentation is MOST consistent with a(n)
A. diffuse axonal injury
B. occipital skull fracture
C. orbital floor fracture
D. subdural hematoma
E. temporal bone fracture
Preferred Response: E
Nausea, headache, bleeding from the external auditory canal, and hearing loss in the setting of blunt head
trauma, as described for the boy in the vignette, are consistent with a temporal bone fracture. Other findings
may include facial paralysis, cerebrospinal oto- or rhinorrhea, and vertigo. Because temporal bone fractures result
from significant force, many patients have multiple other intracranial and orthopedic injuries.
Although temporal bone fractures can be associated with other skull fractures, an occipital fracture usually is
characterized by occipital scalp swelling, and an orbital floor fracture is characterized by maxillary tenderness,
periorbital swelling, and abnormal extraocular movements. A subdural hematoma or diffuse axonal injury causes
altered mental status.
11. Your first patient of the day is a 2-year-old girl who is brought in by her mother after a brown spider was found
in the child’s bed. The mother has brought the spider for you to inspect. On physical examination, there is a 2-cm
bulla with 4 cm of surrounding erythema on the medial aspect of the girl’s calf. The child otherwise appears well
and occasionally scratches at the lesion.
Of the following, the MOST appropriate course of action for this patient is to
A. begin dapsone therapy
B. begin local wound care
C. prescribe a 5-day course of prednisone
D. refer the child to a surgeon for excision of the bite area
E. transfer the patient to the emergency department for antivenom
Preferred Response: B
In the United States, two spider species are responsible for most spider bite-related illness and injury: Lactrodectus
sp (black widow spiders) and Loxosceles sp. Black widow spider bites cause a systemic syndrome characterized by
autonomic dysfunction, muscle cramping, and rigidity due to neurotoxins in the venom. Spiders of the genus
Loxosceles, of which the brown recluse spider (Loxosceles recluse) is best known, are recognized primarily as a
cause of necrotic skin lesions, although systemic symptoms, including a flulike illness, hemolytic anemia, and renal
failure, may occur.
The spider responsible for the skin lesion described for the child in the vignette is a brown recluse, which can be
recognized by its brown color, violin-shaped marking on the thorax, and three sets of eyes. Found throughout the
central and southern United States, they live in dark, protected environments such as wood piles or storage sheds but
can be found indoors in bedsheets and clothing hampers. They are nocturnal, and human bites typically occur at
night. Brown recluse spider venom contains a variety of proteolytic enzymes that can cause extensive tissue damage.
The bite itself usually is painless and may go unnoticed until pain, erythema, and pruritus develop at the site. The
initial erythematous maculopapular lesion becomes bullous and increases in size over the subsequent 48 hours. After
that time period, an eschar develops and subsequently separates, leaving a deep ulcer at the site. Systemic symptoms
include fever, chills, vomiting, and arthralgias. Because children are smaller and receive a larger per kilogram
venom dose, they are affected more commonly by the systemic syndrome, known as loxoscelism.
Black widow spider bites also are painless and leave little more than two small red, pinpoint marks on the skin. The
venom causes severe muscular cramping, tremors, and autonomic symptoms such as drooling and sweating. The
symptoms seen after black widow spider bites frequently are mistaken for a variety of other conditions, including
cholinergic crisis and acute abdominal processes.
Treatment of brown recluse spider bites, black widow spider bites, and bites of all other spiders indigenous to North
America is largely supportive and includes conscientious wound care and tetanus immunization, if indicated. The
muscular cramping caused by a black widow spider bite is controlled readily with benzodiazepines, narcotics, and
calcium gluconate. An antivenom is available, although its use is indicated only when autonomic symptoms or pain
cannot be managed with usual measures. Skin grafting may be necessary if tissue necrosis occurs following a brown
recluse spider bite. Many therapeutic modalities have been advocated to limit the extent of the brown recluse bite
wound, including dapsone, early wound excision, hyperbaric oxygen, and steroids, but none have proven effective.
Loxosceles antivenom is not available in the United States.
Skin findings caused by a wide variety of other pathologic conditions often are attributed to brown recluse spider
bites. The differential diagnosis is extensive and includes conditions such as staphylococcal and streptococcal skin
lesions, cutaneous anthrax, atypical mycobacterial infection, sporotrichosis, ecthyma gangrenosum, herpes simplex
and zoster, vasculitic lesions, erythema chronicum migrans, and erythema nodosum. Because necrotic skin lesions
can be caused by a number of serious conditions, and documented spider bites are rare, clinicians should consider
alternative diagnoses when faced with a necrotic skin lesion, if the spider is not available for inspection.
12. You are evaluating a 17-year-old boy whom you have known since early childhood. He is complaining of
headaches over the past 2 weeks. He has a history of asthma, which has been well controlled, and he is an otherwise
healthy member of the varsity football team at school. He has had a significant weight gain of 30 lb (13.5 kg) since
his visit to you 1 year ago. He denies using illicit or prescription drugs. On physical examination, he appears very
muscular and has a blood pressure of 180/120 mm Hg. You repeat the measurement using a leg cuff to ensure
adequate cuff size and obtain the same result.
Of the following, the BEST management plan is
A. angiotensin-converting enzyme inhibition as an outpatient
B. beta blocker therapy as an outpatient
C. diuretic therapy as an inpatient
D. repeat blood pressure measurement in 1 to 2 weeks
E. vasodilator therapy as an inpatient
Preferred Response: E
Hypertension is a major cause of morbidity and mortality in adults, and growing data suggest that it is becoming a
greater clinical problem in the pediatric population, particularly adolescents. Although yet to be defined clearly, the
lifelong risks for the child who has hypertension or a prehypertensive state are likely to be substantial. Blood
pressure is affected by height, weight, sex, and race. A complete medical history, particularly family history and
medications (including over-the-counter supplements), and a thorough physical examination are essential to early
and accurate diagnosis of hypertension and assessment of its secondary causes, comorbidities, and potential
complications.
Measurement of the blood pressure is a salient component of the yearly health supervision visit for children
beginning at 3 years of age. When the patient is calm and relaxed, blood pressure should be measured in the right
arm with the patient seated and the arm resting at the level of the heart. The stethoscope should be placed about 2 cm
superior to the cubital fossa, just over the brachial artery.
It is extremely important to use the proper size cuff for each patient. The bladder of the cuff (not the cuff material)
is the most important determinant of cuff size. The bladder width should cover 60% to 70% of the upper arm length.
The cuff bladder length should cover 80% to 100% of the circumference of the arm to ensure complete compression
of the brachial artery during cuff inflation. A cuff that is too small will result in a falsely elevated reading. A cuff
that appears too large will not affect the measurement adversely. Most errors in blood pressure measurement occur
in obese or highly muscularized patients when a cuff is used that is too small.
Severe hypertension and hypertensive crisis should be managed aggressively. The latter typically results from the
ingestion of drugs that cause hypertension, injury, or disease of the kidney or previously unrecognized, progressive
hypertension. Symptoms of severe hypertension may include headache, changes in vision, epistaxis, seizure,
pulmonary edema with congestive heart failure, and those that may arise from renal failure.
The patient described in the vignette has a significantly elevated blood pressure that involves marked and
reproducible systolic and diastolic hypertension. The best management plan is to monitor his blood pressure while
the cause is ascertained and treatment begun, which involves admission to the hospital and initial treatment with an
intravenous antihypertensive agent. The goal of such therapy is to reduce the blood pressure by 25% or less over the
first 8 hours and gradually normalize it over the next 48 hours to avoid complications (eg, cerebrovascular accident).
The choice of chronic antihypertensive therapy depends, in part, on the cause of the hypertension, but for immediate
short-term management, vasodilators (eg, calcium channel blockers, hydralazine, nitroprusside) are useful.
These agents reduce the afterload against which the left ventricle pumps, thereby reducing its work and oxygen
consumption. Alternatively, short-acting beta blockers could be used in the acute setting. When using beta blockers,
however, the clinician must bear in mind their potential complications, including exacerbation of underlying asthma.
Of importance, pharmacologic management of severe hypertension and hypertensive crisis should use medications
that can be titrated to effect readily and have a fast onset of action. Diuretics, particularly the thiazide class, often are
used as first-line antihypertensive agents for those who have mild or moderate hypertension that can be controlled
on an outpatient basis. These may be used in combination with other agents, including but not limited to
angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, if adequate control is not obtained with a
single agent. The significant hypertension reported for the boy in the vignette requires immediate action; repeating
the blood pressure measurement in 1 to 2 weeks is not appropriate.