Practice

A60-year-old female returns to the ED3 days after anterior nasal packing for epistaxis. She now complains of *fevers, chills, myalgias*, and diffuse abdominal pain. Her temperature is *39.2◦C*, blood pressure is *82/44*, and heart rate is *132*. She has a diffuse, raised, blanching, erythematous rash that resembles severe sunburn. What is the MOST beneficial course of treatment? (A) Intravenous access, blood transfusion, leave the nasal packing in place due to likely disseminated intravascular coagulation, and admission. (B) Intravenous access, fluid resuscitation, administer intravenous antibiotics, remove the nasal packing, and admission. (C) Intravenous access, fluid resuscitation, epinephrine for anaphylaxis, and admission. (D) Order aCTscan of the abdomen to evaluate for abscess. (E) Reassure the patient she has sinusitis and a viral exanthemaand discharge home.

10-4The answer is B (Chapter 145). The presentation is strongly suggestive for toxic shock syndrome (TSS). Menstrual causes of TSS have decreased since the withdrawal of highly absorbent tampons. Nonmenstrual causes of TSS include wound infections, mastitis, respiratory infections following viral pneumonia, and enterocolitis. Additionally, nasal packing has been associated with S. aureus invasion. The diffuse rash is known as erythroderma. Patients may experience massive vasodilation and cardiac dysfunction, requiring profound fluid resuscitation. The history and the erythroderma are not consistent with anaphylaxis. Vague, diffuse abdominal pain is characteristic of the disease, andwhile investigationmaybe indicated, the nasal packing is a likely source andaCT is not initially indicated. Erythroderma is not consistent with a viral exanthem. Vancomycin plus clindamycin is an appropriate antibiotic regimen for staphylococcal TSS. Although patientsmaydevelopbleedingcomplications due to thrombocytopenia, the nasal packing must be removed, as it is the source of the disease.

A 45-year-old male with end-stage renal disease presents to the ED with *2 days, of fever* up to *39.0◦C*. His initial blood pressure is *74/40* and his heart rate is *130.* There is a dialysis catheter in his right internal jugular vein. There is mild erythema around the site but no frank pus. His last *dialysis* was 3 days ago. What intervention is necessary for definitive treatment of this infection? (A) Catheter removal (B) Emergent dialysis (C) Intravenous fluids (D) Levofloxacin 750mg intravenously (E) Vancomycin 1 g intravenously

10-6The answer is A (Chapter 146). This patient has characteristics suggestive of severe sepsis. *Source control is a key component of successful therapy in sepsis*. Definitive treatment of sepsis would be removal of the nidus of infection if feasible. Patients receiving dialysis through temporary external catheters are at higher risk for bacteremia than those with AVfistulas. Coagulase-negative staphylococcus and S. aureus comprise the majority of infections. Enterococcus and enteric gramnegative organisms must also be considered. While this patient should receive fluid resuscitation and antimicrobial therapy, this patient is unlikely to recover without removal of the source of infection. It wouldbe prudent to assess this patient's chemistry panel, but it is more likely that he is suffering from sepsis than dialyzable conditions such as uremia or hyperkalemia.

Which of the following causes of syncope decreases in incidence with age? (A) Cardiac syncope due to dysrhythmia (B) Cardiac syncope due to structural abnormalities (C) Neurologic syncope (D) Orthostatic hypotension (E) Vasovagal syncope

2-19The answer is E (Chapter 56). The incidence of vasovagal syncope actually decreases with age due to decreased responsiveness of the autonomic nervous system. Orthostatic hypotension is common in the elderly due to a less-sensitive thirst mechanism and a decreased endocrine response to volume depletion. Orthostatic hypotension is also related to increased medication use in older patients. Advancing age increases the risk of syncope but cardiovascular risk is thought to be a better predictor. Cardiac syncope due to dysrhythmias or structural conditions is very commonandmore likely with increasing age. Neurologic syncope is a rare cause of syncope at any age, since it must be transient and allow a return to baseline neurologic function. Vertebrobasilar insufficiency can transiently affect the reticular activating system and cause a brief loss of consciousness, but other posterior circulation signs and symptoms also occur, such as vertigo or diplopia.

A 34-year-old male with no past medical history presents to the ED complaining of 1 day of *nausea, vomiting, and epigastric pain* after drinking "a lot" over the weekend. He denies hematemesis, bright red blood per rectum or melena. He states that he has never been much of a drinker but drank excessively this weekend when some college friends were in town. He has *vomited more than 15 times* and has not been eating much because of the nausea and vomiting. His finger *stick glucose is 97* and his vital signs are stable. His exam is significant for *dry mucous membranes*. He is anicteric. His abdomen is soft with mild *discomfort* in the *epigastric region* with no abdominal distention, masses, rebound, or guarding.Which of the following is MOST important in determining the patient's diagnosis? (A) Electrolytes (B) Improvement with GI cocktail. (C) Lipase (D) Ultrasound of gallbladder (E) Urine ketones

The answer is *A* (Chapter 221). Although alcoholic ketoacidosis (AKA) is most common in chronic alcoholics, it also occurs in first time binge drinkers. Patients usually present with nonspecific complaints of abdominal pain, nausea, and vomiting. The anion gap in AKA is positive and ranges between 16 and 33 and is caused by ketonemia, primarily from ␤-hydroxybutyrate. The blood glucose ranges fromlow to mildly elevated. Urine ketones may be often low or negative initially as the nitroprusside reagent used to measure urine and serum ketones only measure acetoacetate. Acetone and ␤-hydroxybutyrate are not reactive and are more common early in the process of AKA. Gastritis can accompany AKA; however, improvement of symptoms with a "GI cocktail" does not rule out AKA, and without a high suspicion, AKA might be missed. Pancreatitis may also accompanyAKA,but this patient does not have a history and physical consistent with pancreatitis. The patient's exam and history are also not consistent with gallbladder disease, so an ultrasound would not aid in making the diagnosis of AKA.

A 12-year-old boy arrives by EMS due to lethargy and *dehydration*. Parents report that he has been tired the past few days with increase *thirst and going to the bathroom a lot*. You appreciate a *fruity odor* to his breath along with *tachypnea and dehydration*. Diabetic ketoacidosis (DKA) is suspected. Bedside *glucose* reads as *high*. Venous blood gas has pH of 7.12 and HCO3 of 8. You instruct the nurse that the priority is: (A) Administer insulin subcutaneously (B) Administer sodium bicarbonate (C) IVF therapy (D) Obtain serum ketone level (E) Portable chest radiograph

The answer is *C *(Chapter 139). If presenting in shock, 20 mL/kg IVF bolus with normal saline is indicated, but once patient and vital signs stabilize, correction of dehydration over 24-48 hours provides best outcomes. Sodium bicarbonate infusion is not recommended and can increase chances of cerebral edema in children with DKA. Insulin therapy is key to halting ketone production and acidosis after IVFs begun. Controlled correction is best achieved by regular insulin infusion at 0.1 units/kg per hour. Subcutaneous regular insulin can complicate management in children due to risk of decreasing glucose levels too quickly and hypokalemia. Serum ketone levels are not helpful for initial management of DKA. Severity of acidosis and hyperosmolar state would be more useful in assessing risk factors for cerebral edema. Portable chest radiograph is not indicated, since patient's tachypnea (Kussmaul breathing) is a response to his metabolic derangement.

You are treating an obtunded 72-year-old female for severe sepsis due to pneumonia. You have administered 3 L normal saline and broad-spectrum antibiotics. After performing endotracheal intubation, you place a central venous oxygen saturation catheter and arterial line in preparation for early goal directed therapy. The patient's blood pressure is now 88/34, *central venous pressure* is *11 mm Hg,* and venous oxygen saturation is 66%. Lab values are not yet available. What is the MOST appropriate next step? (A) Administer 1 Lnormal saline intravenously. (B) Begin infusion of dobutamine 0.5-1.0 mcg/kg/minIV. (C) Begin infusion of norepinephrine 5mcg/minIV. (D) Nofurther actions, the endpoints of early goal directed therapy have been met. (E) Transfuse 2 units packed redblood cells.

The answer is *C* (Chapter 146). Early goal directed therapy in severe sepsis is guided by an algorithmic approach (Figure 10-9). After initial supplemental *oxygen or intubation, fluid resuscitation, and broad-spectrum antibiotics,* patients must be repeatedly reassessed for response to therapy. Target values include a mean arterial pressure >65mm Hg, central venous pressure of 8 mm Hg, venous oxygen saturation of 70%, and urine output >0.5 mL/kg/hr. This patient demonstrates persistent hypoperfusion after initial fluid resuscitation with a mean arterial pressure of 52 mm Hg (mean arterial pressure is approximated by diastolic plus one-third of the pulse pressure). Although many patients have large fluid deficits, a central venous pressure of 11 mm Hg suggests adequate resuscitation. The next step in management is inotropic support, and norepinephrine or dopamine is the typical agent ofchoice for initial management. Dobutamine may be used in select settings with invasive monitoring, but typically not until after dopamine administration. The patient should be transfused until the hematocrit is greater than30%, but would not be indiscriminately transfused unless anemia and severe blood loss were obvious.

A 26-year-old woman complains of a gradual-onset diffuse headache that started a few weeks ago. It is worse when she awakens in the morning and is better after prolonged sitting or standing. She has had transient episodes of blurry vision for a few days, and today she has double vision. On examination the patient is moderately obese .Visual acuity is normal. She is unable to abduct either eye. The fundoscopic exam is papilledema, Head CT is normal. What do you expect to find on LP? (A) High opening pressure (B) High protein level (C) HighRBC (D) HighWBC (E) Lowglucose

The answer is A (Chapter 159). The patient likely has idiopathic intracranial hypertension (IIH) also known as pseudotumor cerebri. This condition usually occurs in young women, especially those who are obese. It causes typical symptoms of elevated ICP: a headache that is worse in the morning or in the supine position or with activities that raise ICP such as coughing or straining. The headache is often chronic by the time the patient presents for care. Figure 123 shows papilledema, a classic fundoscopic finding in IIH that is not a cause of vision loss (the worst outcome from IIH) or the transient visual obscurations that are common in this disease. Elevated ICP of any etiology may cause dysfunction of cranial nerves, particularly nerve VI (abducens nerve), which courses through tight canals and can be easily compressed by a downwardly displaced brainstem. Head imaging is normal in IIH, which makes LP safe despite the presence of papilledema. Lumbar puncture shows elevated opening pressure (>20-25 cm H2O) and otherwise normal CSF.

Noncontrast CT of the head is most sensitive for SAH howlong after the onset of bleeding? (A) Less than 12 hours (B) 12-23 hours (C) 24-71 hours (D) 3-7 days (E) 7-14 days

The answer is A (Chapter 160). Modern multidetector CT scanners are very sensitive for SAH and other ICH soon after the onset of bleeding—the earlier, the better. Recent studies find such scanners to be almost 100% sensitive for SAH within 12 hours of the onset of symptoms and more than 90% sensitive between 12 and 24 hours after onset. CT is only about50% sensitive at 1 week. It is possible that in the near future patients presenting early after the onset of a high-risk headache will not need more than a CT scan to rule out SAH. But at this time, the standard of care is to follow a negative head CT with an LP.

A 72-year-old woman awoke at 6 am with great *difficulty speaking or moving the right side *of her body. She arrives in the ED by ambulance at 6:45am. her husb and corroborates the history and says she was *normal last night* when she went to sleep. Physical exam shows moderate *right-sided weakness and sensory loss* and *aphasia*. Blood pressure is 140/90. Head CT shows signs of an early left *middle cerebral artery stroke*, no bleeding. Glucose, platelets, and coagulation studies are normal. She has no risk factors for bleeding. It is now 7:30 am. What is the most appropriate treatment at this time? (A) Aspirin (B) Heparin (C) Nimodipine (D) Norepinephrine (E) Thrombolysis

The answer is A (Chapter 161). On first glance, this patient may appear to be a good candidate for thrombolysis; however,wedo not know whether the stroke occurred within the time window *(maximum 4.5 hrs) for thrombolysis*—therefore, it should be withheld. In patients with stroke, it is critical to ascertain when they were last normal. This patient was last known to be normal the previous night. She awoke with her deficits, so the stroke could have occurred at any point between the onset of sleep and awakening. Aspirin is the appropriate ED treatment for acute nonhemorrhagic stroke, though if thrombolytics are administered aspirin shouldbewithheld for the first 24 hours. Heparin and other anticoagulants have been shown to be either nonbeneficial or harmful in acute stroke, even in the presence of atrial fibrillation. Nimodipine helps prevent vasospasm inSAH,but antihypertensives are contraindicated in acute ischemic stroke unless the blood pressure is above 220/120 mm Hg, and even then treatment should be very gentle, parenteral,andwith close monitoring. Vasopressor therapy to induce hypertension is being studied in acute stroke, but is not standard care at this time.

Both Wernicke encephalopathy and normal pressure hydrocephalus present with what abnormality? (A) Ataxia (B) Headache (C) Mydriasis (D) Ophthalmoplegia (E) Urinary incontinence

The answer is A (Chapter 163). Ataxia is a common manifestation of many neurologic diseases. Wernicke encephalopathy is due to thiamine deficiency and usually occurs in alcoholics. It is characterized by the triad of altered mental status, ataxia, and ophthalmoplegia. Mortality is up to 20% and the diagnosis is often missed. Thiamine repletion reverses the abnormalities sometimes within hours. Magnesium is a necessary cofactor for thiamine, so it must also be repleted. Normal pressure hydrocephalus occurs in the elderly and presents with the triad of dementia, ataxia, and urinary incontinence. Head imaging shows hydrocephalus with other characteristic findings. Surgical shunting benefits the subgroup of patients who respond well to large-volume CSF drainage. Headache and mydriasis are not typical of either disorder

A45-year-old woman complains of dizziness that started suddenly a few hours ago while getting out of bed. If she moves her head toward the right, particularly when lying down, she develops a strong feeling that the roomis spinningandbecomesnauseated; she has vomited several times. When her head is kept still, the symptoms resolve completely. She denies hearing loss or tinnitus. She has no medical problems and does not smoke or use illicit drugs. Neurologic examination, including coordination, is normal. When the Dix-Hallpikemaneuver is performedandthe head is tilted to the right, her symptoms as well as rotatory nystagmus ensue after a 3second delay and resolve after 30 seconds. What is the diagnosis? (A) Benign paroxysmal positional vertigo (BPPV) (B) Cerebellar stroke (C) M´eni´ere disease (D) Vertebral artery dissection (E) Vertebrobasilar insufficiency

The answer is A (Chapter 164). BPPV is the most common type of peripheral vertigo. Peripheral vertigo is usually described as a strong spinning sensation that is triggered or substantially worsened by head movement. Symptoms often resolve with avoidance of head movement and fatigue after repeated provocation. The finding of vertigo and nystagmus occurring after a few seconds delay during the Dix-Hallpike maneuver and resolving within a minute is almost pathognomonic for BPPV. Cerebellar strokes may cause vertigo but invariably present with ataxia as well. M´eni´ere disease presents with repeated bouts of peripheral vertigo often associated with tinnitus andhearing loss.Vertebral artery dissection may cause central (not peripheral) vertigo, usually occurs after rapid rotation or extreme positioning of the neck, and often the initial symptom is occipital or nuchal pain. Vertebrobasilar insufficiency may cause numerous symptoms referable to the brainstem or cerebellum (including central vertigo) and is a disease of the elderly or those with major atherosclerosis risk factors.

A 25-year-old man was brought to the ED by paramedics for a *seizure*. He had been seizing with generalized tonic-clonic jerking for* 30 minutes continuously*; this stopped after multiple doses of* lorazepam* and a *20 mg/kg* loading dose of *fosphenytoin.* It has been 40 minutes since the seizure stopped and he was* intubated*. He remains unresponsive to verbal stimuli. He is afebrile, pupils are equal and reactive, and the neck is supple. Glucose level is 150mg/dL.Besides CT of the head, LP, and a broad laboratory workup, what needs to be ordered for the patient immediately? (A) Continuous electroencephalography (B) Hyperventilation (C) Hypertonic saline (D) Mannitol (E) Thiamine

The answer is A (Chapter 165). This patient has suffered *status epilepticus, *which is 30 minutes of continuous seizing or multiple seizures without recovery of mental status between seizures. Patients with such long seizures may stop having perceptible muscle activity butmay still have ongoing damaging electrical seizures in the brain, so-called nonconvulsive status epilepticus. This should be suspected when a patient is not waking up within 30 minutes of cessation of motor activity. Continuous *electroencephalography* is essential in these cases. Hyperventilation, hypertonic saline, and mannitol are important short-term treatments in life-threatening elevations of ICP, but there is no evidence of this here. Thiamine deficiency does not cause status epilepticus.

A 40-year-old previously healthy man is brought to the ED by his wife because he has been confused for the past 2 days. She says he has been forgetful and has difficulty speaking. The patient only complains that his *"head hurts" * and generally answers questions with one or two words. On exam, his temperature is 38.3◦C, he is disoriented, *hasmildphotophobia *and* meningismus* and moderate *aphasia* with an otherwise nonfocal neurologic exam. Ceftriaxone is given. A head CT is normal. Lumbar puncture reveals 150 WBCs/hpf (55% lymphocytes and 45% neutrophils) and 100 RBCs/hpf in tube no. 4. What is the most appropriate step at this time? (A) Acyclovir (B) Ampicillin (C) Dexamethasone (D) Neurosurgery consultation (E) Therapeutic hypothermia

The answer is A (Chapter 168). The patient very likely has herpes simplex virus *(HSV) meningoencephalitis. *The virus usually infects both the *meninges (causing headache, fever, and nuchal rigidity)* and the brain* parenchyma (encephalitis), *in particular the temporal lobe and/or the anterior frontal lobe resulting in cortical signs such as memory deficits and aphasia; seizures are common as well. MRI and sometimes CT show characteristic changes. CSF usually contains a *viral pleocytosis (WBC 10-300 with lymphocyte predominance)* as well as elevated RBCs due to HSV's destructive nature in this infection. Early initiation of acyclovir is important as it markedly reduces mortality. Ampicillin is indicated when the CSF cell count suggests meningitis and the patient is at risk for Listeria infection (age >50, neonate, or immunocompromised). In bacterial meningitis, dexamethasone should be given just before or concomitant with the first dose of antibiotics, not after the antibiotic has already been given. There is no role for cooling or a neurosurgeon in this case.

Which of the following would suggest that a patient's cognitive impairment is due to dementia rather than delirium? (A) Absence of underlying medical condition (B) Clouding of consciousness (C) Rapid onset (D) Visual hallucinations (E) Waxing and waning course

The answer is A (Chapter 284). Dementia tends to be a slow and progressive disorder with a consistent pattern and the notable absence of any clouding of consciousness. In contrast, the hallmark feature of delirium is decreased alertness and/or awareness of the external environment. The impairment may range from simple inattention to drowsiness, even stupor. Dementia and delirium may coexist in the same patient with the latter typically a response to some underlying medical condition: infection, metabolic derangement, intoxication, trauma, medication intolerance, etc. Visual hallucinations are common as is a rapid onset of symptoms and variable pattern often matching the underlying medical condition.

A 58-year-old man is brought in by paramedics after a witnessed syncopal episode while walking with friends. He denies headache, chest pain, or shortness of breath prior to the event, or now. He has hypertension and takes lisinopril.Vital signs are BP150/100,HR78,RR18, T 98.6, room air saturation 97%. Physical examination is notable for a harsh, systolic murmur at the right base, which radiates into the neck. His lungs are clear to auscultation.Atransthoracic echocardiogram is pending. The ECG shows normal sinus rhythm with left atrial enlargement but is otherwise normal. What is the MOST appropriate next step in management? (A) Admit patient (B) Arrange computedtomography (CT) of chest (C) Arrange EEG (D) Arrange outpatient electrophysiologic testing (E) Arrange outpatient tilt-table testing

The answer is A (Chapter 56). This patient has strong evidence of a structural cardiac abnormality, most likely aortic stenosis, and should be admitted for further evaluation of cardiac function. A transthoracic echocardiography is essential. Critical aortic stenosis is associated with a classic triad of chest pain, dyspnea on exertion, and syncope. Older patients with aortic stenosis and syncopewhoareasymptomaticuponEDpresentation should still be admitted due to the increases risk of death. Patients with documented cardiac syncopehave a 6-monthmortality exceeding 10%. Electrophysiologic testing is done for patients with dysrhythmias, preexcitation, or conduction delays. Tilt-table testing is performed on patients with recurrent unexplained syncope, suspected to have a reflex-mediated etiology. EEGswouldbe reserved for patients with suspected seizures.

Which of the following decreases the chance that a headache is due to SAH? (A) Associated cough and myalgia (B) Meningismus (C) Occipital-nuchal location (D) Older age patient (E) Onset during exertion

The answer is A (Chapters 159 and 160). Diagnosing SAH can be life saving, and taking a good history is the key to suspecting the diagnosis and initiating the workup. Characteristics that increase the risk of SAH include sudden onset; onset during exertion (evencoughingorValsalva); occipital-nuchal location; new, unusual, or particularly severe headache; and family history of SAH or intracranial aneurysm. The risk of SAH increases with age, with a steep rise in the middle ages (45-55 years old). Cough and myalgia suggest a secondary cause of headache, suchas influenza, rather than a primary cause such as SAH or migraine.

The previous patient's right-sided paralysis resolves after intervention. She is sitting comfortably with her family, eating lunch, and asking when she can go home. Her CBC, chemistry panel, chest x-ray, and urinalysis are all normal. Which of the following is the most appropriate next step in the management of this patient? (A) Admission for observation (B) Broad-spectrumantibiotics and admission (C) Dischargehomewith oral antibiotics (D) Dischargehomewith precautions to return to ED. (E) Observe for another 2 hours and if normal finger stick, discharge home.

The answer is A (Chapters 161 and 219). Hypoglycemia is a known complication in the treatment of diabetes. In patients who are taking sulfonylureas, a search for underlying causes should be sought. This patient has no evidence of an infection, so treatment with antibiotics is not indicated. Patients on sulfonylureas, medium- to long-acting insulins, or meglitinides should be admitted for serial glucose monitoring and treatment.

An 80-year-old woman with a history of atrial fibrillation presents with sudden-onset headache, vomiting, and somnolence. She takes *warfarin*. Her blood pressure is 160/90. She is sleepy but easily arousable and answers questions appropriately. She has moderate left-sided weakness and numbness and ignores the nurse standing to her left. Head CT shows a right intracerebral hemorrhage. The INR is 1.9. Which of the following actions is most likely to reduce this patient's mortality? (A) Administering aspirin (B) Administering fresh frozen plasma and vitaminK (C) Intubation for airway protection (D) Lowering the blood pressure (E) Therapeutic hypothermia

The answer is B (Chapter 160). Patients with intracranial hemorrhage (ICH) and coagulopathy are critically ill with a high mortality rate, even if the bleed is small and they look well. The coagulopathy, which is usually due to warfarin therapy, must be reversed immediately by the fastest available means—vitamin K and fresh frozen plasma (FFP) are the traditional means and are effective. More expensive but fast and reliable alternatives include prothrombin complex concentrates and recombinant-activated factor VII. Rapid reversal by any means markedly reduces mortality. Aspirin is absolutely contraindicated in ICH. Intubation is not yet indicated in this awake and talking patient. Lowering systolic blood pressure below 180 mm Hg is recommended in ICH—beyond that, there is mixed evidence on the value of further lowering; regardless, reversal of coagulopathy is a higher priority. Therapeutic hypothermia is probably beneficial postcardiac arrest, but has not yet been shown to be helpful in ICH or brain

A 25-year-old man is brought to the ED by a friend after a *seizure* that occurred an *hour ago*. The friend says that the patient has not been himself lately—he has been* sleepy* with a poor attention span and either does not talk much or *spews expletives inappropriately*. The patient is awake and complains of severe *tooth pain and a headache.* On exam, his temperature is 38.1◦C. He refuses to answer most questions. He has swelling, redness, and purulent discharge from the left second maxillary molar tooth (no. 15). There is no meningismus. He has a mild right *pronator drift*. *Noncontrast head CT is normal*. What diagnostic study should be ordered next? (A) Complete blood count (B) Contrast head CT (C) Erythrocyte sedimentation rate (D) Lumbarpuncture (E) Panorex film of the teeth

The answer is B (Chapter 168). The patient probably has a brain abscess. His infected tooth is the likely source, via direct spread to the brain (in this case, to the left frontal lobe based on the exam findings). CT scan without contrast may be normal, but with contrast one or multiple ring-enhancing lesions are seen and are diagnostic. Brain abscesses are uncommon now in the developed world, but are critical to diagnose because they are life threatening and the cure usually requires surgery. Direct spread of pathogens in otitis media, sinusitis, and odontogenic infection is responsible for at least a third of cases. The classic clinical triad of headache, fever, and focal neurologic deficits is surprisingly uncommon—therefore, the physician must pick up on subtle risk factors (e.g., signs of sinusitis or a new murmur in a patient with an abnormal heart valve). Complete blood count and erythrocyte sedimentation rate might be abnormal but would not aid in diagnosis. Lumbar puncture is relatively contraindicated if brain abscess is suspected and there are focal findings, but if it were performed, it might show abnormalities similar to bacterial meningitis. Panorex x-rays of the teeth would not be a high priority here.

A 30-year-old office manager complains of a gradual-onset headache that started yesterday and is now severe. He is covering his eyes with a blanket to avoid the room lights. He has no medical history and no drug allergies. His temperature is 38.5◦C and he has *nuchal* rigidity. His mental status and neurologic examination are normal, as is the fundoscopic exam. The charge nurse asks you to attend to two trauma patients. What is the most appropriate sequence of orders for this patient? (A) Ceftriaxone 2 g IV→headCT→set up for lumbar puncture (LP) (B) Ceftriaxone 2 g IV→set up for LP (C) HeadCT→set up for LP→Ceftriaxone 2 g IV after CSF obtained (D) Set up for LP→Ceftriaxone 2 g IVafter CSF obtained (E) Set up for LP (no order for antibiotics until CSF studies confirm bacterial meningitis)

The answer is B (Chapter 168). This patient has bacterial meningitis until proven otherwise. He needs antibiotics without delay. If an LP could be performed immediately, an-tibiotics could be ordered to be ready to administer as soon as CSF is obtained. If there is any delay before LP, antibiotics should be given immediately. Ceftriaxone (2 g intravenously) covers the most common meningeal pathogens; other antibiotics can wait until initial CSF studies confirm the diagnosis (unless clinical features strongly suggest a particular uncommon pathogen). If the suspicion for meningitis is high or if CSF is grossly purulent, then dexamethasone should be administered just before or along with ceftriaxone. In one randomized study, this intervention improved outcomes when the pathogen was pneumococcus. Head CT before LP is required if the patient has any of the following risk factors for elevated ICP or brain lesions: age >60, history of central nervous system disease, malignancy, immunocompromised state, altered mental status, an abnormal neurologic exam or papilledema, or a recent seizure. This patient does not have any of the risk factors, and there is nothing about his history that is concerning for a new mass lesion of the brain, so he does not require a head CT. The other choices would delay antibiotics and are therefore incorrect.

Which of the following causes an anion gap acidosis solely by the production of lactate? (A) Ethylene glycol (B) Iron (C) Ketoacidosis (D) Methanol (E) Uremia

The answer is B (Chapter 19). Elevated anion gaps are usually associated with metabolic acidosis. While the differential for elevated anion gap acidosis is broad, it is important to separate out processes that cause the elevation directly and those that cause it indirectly by producing lactate. Without this separation, important components in the differential for lactic acidosis will be missed. Biguanides, cyanide, iron, and theophylline are not unmeasured ions causing an elevated anion gap.Thesesubstances actually raise the anion gap by producing a lactic acidosis.

A 39-year-old alcoholic presents with ataxia, confusion, and confabulations. What vitamin deficiency is causing these symptoms? (A) VitaminA (B) Vitamin B1 (C) Vitamin B6 (D) Vitamin B12 (E) VitaminC

The answer is B (Chapter 199). Wernicke- Korsakoff syndrome is a complication seen most often in malnourished chronic alcoholics who are suffering from a vitamin B1 deficiency. Wernicke encephalopathy is believed to be the result of an acute deficiency thiamine. Korsakoff syndrome is believed to be a chronic long-term sequela of Wernicke encephalopathy. The administration of thiamine prior to administering D50 to avoid precipitation of Wernicke encephalopathy is unfounded.Thiamineisexcretedintheurine and therefore toxic levels are relatively unheard of.

A 64-year-old woman arrives by ambulance with crushing substernal chest pain for the past 40 minutes. She received aspirin and a large bore IV en route. Several tubes of blood are available. Her past medical history includes adult onset diabetes mellitus and hypertension, controlled by metformin and lisinopril, respectively. Vital signs include blood pressure (BP) 90/74, heart rate (HR) 115, respiratory rate (RR) 28, temperature (T) 37◦C, room air SaO2 96%. The patient appears ashen and diaphoretic, with cool, mottled extremities. She is awake but answers questions slowly. Jugular venous distention (JVD) is present. Heart sounds are regular with an S4 gallop but without murmurs or rubs. Lungs sounds are equal bilaterally and clear to auscultation. Her abdomen is soft, nontender, without palpable masses. Femoral pulses are equal. Extremities are cool, but without edema. Peripheral pulses are faint butequal. Despiteherslow responses, the patient follows commands and moves all four extremities. The initial ECG showed sinus tachycardia, with ST-segment elevation in leads II, III, and aVF. The secondECGis shownhere (Figure 2-1). While arrangements for echocardiography and early revascularization aremadewith the cardiologist, which of the following is the next MOST appropriate action? (A) Administer propranolol (B) Infuse 250-500mLof normal saline (C) Initiate thrombolytic therapy (D) Start a dobutamine drip (E) Start a phenylephrine drip

The answer is B (Chapter 54). This patient is in cardiogenic shock due to an RV infarction complicating her acute inferior STEMI. This acutely ill patient needs an emergency bedside transthoracic echocardiogram to assess cardiac contractility and to rule out any mechanical cause of shock such as acute pulmonary embolus or pericardial effusion. If she can be stabilized, transesophageal echocardiography would be appropriate. Since the patient does not have signs of pulmonary congestion, a judicious trial of crystalloid is indicated. Patients with RV infarcts may require several boluses of IV fluid. Early revascularization, either by PCI or coronary artery bypass graft (CABG), has been shown to increase survival of cardiogenic shock compared with the use of an intra-aortic balloon pump (IABP) along with thrombolytics or with thrombolytics alone. Mortality remains high (∼50%) despite appropriate treatment. Beta-blockers should be avoided in cardiac shock because of their negative inotropy and chronotropy. Pure ␣1adrenergic receptor agonists such as phenylephrine should be avoided since they increase cardiac afterload. If crystalloid therapy does not improve perfusion, vasopressors or inotropes should be considered. Dobutamine is indicated if the patient is not profoundly hypotensive. However, dobutamine should be avoided if the systolic BP remains below 90 mm Hg, due to its vasodilator potential. Dopamine is the preferred single agent if the systolic BP is below 70 mm Hg. Dopamine in combination with dobutamine can be more effective than either agent alone but pharmacologic therapy is only a temporizing measure until early revascularization is arranged.

A 68-year-old man presents to the ED after an episode of syncope at home witnessed by his grandson. The patient had allowed his grandson, who was practicing for a firstaid certificate, attempt to locate the "pulse in his neck." The grandson states the patient slumped over after about 5 seconds of neck pressure and was unresponsive. The patient woke up spontaneously after his grandson placed him supine on the floor and 911 was called. The patient has a history of hypertension and takes enalapril. He reports having a similar fainting episode 6 months ago while trimming his sideburns. He denies headache, chest pain, shortness of breath, abdominal pain, or weakness. Vital signs are BP 138/90, HR70, RR 18, T 98.6, room air saturation 96%. The physical examination, ECG, and bedside transthoracic echocardiogram are unremarkable. Which of the following is the MOST likely etiology of this presentation? (A) Aortic stenosis (B) Carotid sinus hypersensitivity (C) Orthostatic hypotension (D) Postprandial hypotension (E) Micturition syncope

The answer is B (Chapter 56). The patient's prior history of syncope during head turning and the current scenario suggest carotid sinus hypersensitivity syndrome. Direct pressure on baroreceptors in the carotid body may trigger an abnormal vagal response of bradycardia and asystole or a drop in BP without a decrease in heart rate. Both reactions may also occur simultaneously. This patient's sitting position at the time of syncope precludes a diagnosis of orthostatic hypotension. Neither micturition nor postprandial syncope are suggested by this scenario. Aortic stenosis should always be considered in the differential diagnosis of syncope in an elderly patient, but physical exam findings such as delayed carotid pulse and a harsh systolic murmur would be evident.

Which of the following is associated with a higher risk of stroke after a transient ischemic attack (TIA)? (A) Age<60 (B) Anemia (C) Duration of TIA symptoms >10 minutes (D) Family history of coronary artery disease (E) Visual symptoms during TIA

The answer is C (Chapter 161). TIA is transient neurologic dysfunction like a stroke but usually lasting less than an hour and lacking evidence of cerebral infarction. After a TIA, the 3-month risk of stroke is about 10%. Half of these strokes occur in the first 2 days after the TIA. A validated clinical risk score called ABCD2 stratifies patients' risk of stroke after a TIA. The following features increase the risk of stroke: age >60, hypertension at the time of the TIA, diabetes, duration of symptoms *greater than 10 minutes, *and weakness or speech disturbance. Adding diffusion-weighted MRI to this score probably improves risk prediction. However, expert guidelines do not yet incorporate this score in decision making about hospital admission; thus in most centers, patients with TIA should be admitted to the hospital for expedited workup and risk modification.

An 83-year-old woman presents with 30 minutes of left-sided weakness that started suddenly while she was on the phone. On exam, her blood pressure is 200/110, she has moderate weakness on her left face and left upper extremity, and she only pays attention to you if you are standing to her right.CT of the head is normal. Glucose, platelets, and coagulation studies are normal. By history she has no risk factors for bleeding. What is the most appropriate management? (A) Aspirin, no lowering of blood pressure (B) Careful lowering of blood pressure, aspirin (C) Careful lowering of blood pressure followed by thrombolysis (D) Careful lowering of blood pressure, no thrombolysis (E) Thrombolysis, no lowering of blood pressure

The answer is C (Chapter 161). This patient meets all criteria for thrombolysis with rtPA (based on the National Institute for Neurological Disorders [NINDS] trial) except for a blood pressure that is mildly higher than the upper limit (185/110) that is acceptable for thrombolysis. In such a case, the blood pressure should be gently lowered to facilitate thrombolysis. Importantly, we know with certainty that the patient's stroke began within the last 3 hours, a crucial factor in determining eligibility for thrombolysis; of note, though, a recent study European Cooperative Acute Stroke Study (ECASS III) showed a benefit for rtPA in the 3-4.5 hours window, so the acceptable time from symptom onset may be changing soon. Giving aspirinandnotloweringbloodpressure is a reasonable choice given the mixed evidence and controversies surrounding thrombolysis, but expert guidelines and standardof care would dictate thrombolysis in this case. If thrombolysis is not performed for any reason, then blood pressure should not be lowered unless it is greater than 220 mm Hg systolic or 120 mm Hg diastolic.

A 19-year-old man is brought to the ED by paramedics for a generalized *tonic-clonic seizure*. He was given rectal diazepam gel en route with no effect. His glucose level in the ambulance was 105mg/dL. He has now been *seizing* for *10 minutes* and an *IV* has been *placed*. What is the treatment of choice? (A) Intravenous dextrose (B) Intravenous fosphenytoin (C) Intravenous lorazepam (D) Intravenous phenobarbital (E) Rectal diazepam

The answer is C (Chapter 165). *Intravenous lorazepam * is the first-line treatment of choice in status epilepticus or impending status epilepticus, the latter being defined as seizure(s) for *more than 5 minutes *without recovery of consciousness. Lorazepam is effective, can be rapidly administered, and has a short onset of action. Doses of 2-4mg can be given and repeated. The fact that the patient failed diazepam in the field does not change lorazepam's first-line status. *Glucose* is not indicated in *normoglycemia.* *Fosphenytoin*, a water-soluble prodrug of phenytoin that can be rapidly administered, is a second-line agent and would be useful to *abort* a *seizure* that breaks through benzodiazepines or to *prevent* further *seizures* after control is established with benzodiazepines. Phenobarbital is a third-line agent in status epilepticus. Rectal diazepam and buccal midazolam are useful when there is no IV access.

A 40-year-old woman with a *known seizure disorder *presents with an *uncomplicated* generalized tonic-clonic seizure that lasted about 1 minute. She denies any recent illness or other symptoms. She takes *phenytoin*. Her physical exam is normal except for a mild tongue laceration. What is the most appropriate diagnostic workup? (A) Electrolytes, renal function, glucose level, liver function tests, coagulation studies, urine toxicology screen, and phenytoin level (B) Electrolytes, renal function, glucose level, liver function tests, coagulation studies, urine toxicology screen, phenytoin level, and CTscan of the head (C) Glucose and phenytoin levels (D) Glucose and phenytoin levels andCT scan of the head (E) Glucose and phenytoin levels, urine toxicology screen, and CT scan of the head

The answer is C (Chapter 165). Patients who have a known seizure disorder and have a single typical seizure do not need an extensive diagnostic workup unless there is reason to suspect that the seizure was provoked by a medically important or treatable factor (e.g., a dehydrated patient may have hyponatremia, which could provoke a seizure and can be treated). A *glucose level* and an *anticonvulsant* level suffice in this case. The tests listed in the other answers could all be appropriate in the right clinical circumstance, but not in this straightforward case. In particular, while *imaging* of the head is certainly* indicated in a first-time seizure*, it is rarely needed to work up a typical seizure in a patient with a known seizure disorder.

An 82-year-old man is brought in by ambulance during a summer heat wave unresponsive with a rectal temperature of 41◦C and dry skin. He lives alone in a trailer without air conditioning. No medications were found by emergency medical services (EMS) on the scene. Which of the following is the most appropriate initial management? (A) Cooling to body temperature of 37◦Cby immersion bath (B) CTscan of brain, serumand urine toxicological screens, and cooling blanket (C) Evaporative cooling and fluid resuscitation (D) Rectal acetaminophen, blood cultures, and broad-spectrumantibiotics (E) Thyroid function tests and administration of dantrolene sodium

The answer is C (Chapter 204). The likely diagnosis is heat stroke. CT scan of the brain, toxicological screens, endocrine evaluation, and search for infection may be important in this patient to rule out other causes of hyperthermia. However, the initial goal is rapid cooling and fluid resuscitation with normal saline. The goal temperature should be 39◦C to avoid overshoot hypothermia, and is best accomplished by evaporative cooling. Immersion cooling makes patient airway managementand cardiac monitoring difficult and is not advised. Cooling blankets work too slowly for a patientwithheat stroke. Ice packs to groin, neck, and axilla may be useful adjunctive cooling measures. Acetaminophen and dantrolene have no role in treatment of heat stroke.

A 64-year-old female is brought in by her family for right-sided paralysis. The family states the patient was watching TV and had *sudden onset of slurred speech* 35 minutes ago. When she tried to get up and walk, she was unable to move her *right side.* The family states that she thinks she has had the *flu* for a few days but *no fever*, cough, or abdominal pain. She has a past medical history of *diabetes and hypertension.* She takes metformin, glyburide, and metoprolol. She has not had any changes in her medications. Her vital signs show a BP of 169/93, heart rate of *56*, RR of 12, and her pulse oximetry of 99% on 2 L. She is speaking to you but has a* right-sided facial droop* and a *right-sided motor deficit*. Which of the following is the first step in this patient's management? (A) CTangiogram of head (B) ECG (C) Glucose level (D) Lactate level (E) MRI of head

The answer is C (Chapter 218). Although neurological causes such as cerebrovascular eventsandtransient ischemic attacks are high on the differential diagnosis, it is important to recognize that hypoglycemia may manifest in a stroke-like syndrome. In any patient where stroke is suspected, a bedside glucose level should be attained prior to the patient receiving further evaluation.

A 68-year-old woman complains of paresthesias of the legs and progressive difficulty walking over the last couple of weeks. She is a vegan with no medical problems. On exam the patient is thin. Her cranial nerves, strength, and light touch sensation are normal. Muscle tone is normal and there is no tremor. She performs the finger-to-nose and rapid alternating movement tests normally. When she walks she looks down at her feet, has a wide-based gait, and slaps her feet down with each step. When the patient stands with eyes closed she is very unsteady; with eyes open she is steady. What is most likely location of the lesion? (A) Basal ganglia (B) Cerebellum (C) Cerebral cortex (D) Posterior column of the spinal cord (E) Thalamus

The answer is D (Chapter 163). This patient probably has a severe deficit of proprioception (position sense), as evidenced by her incoordination in the absence of visual input. The next step on physical exam would be to formally test proprioception by asking her if she knows which way you move her toes or distal fingers while her eyes are closed. Proprioception is transmitted up the posterior column of the spinal cord, along with vibratory sensation. There are many etiologies of posterior column dysfunction. A classic one is vitamin B12 deficiency, which this patient probably has due to inadequate B12 intake. It is important for the emergency physician to be familiar with this diagnosis because if it is not treated promptly, it can lead to permanent disability. Basal ganglia dysfunction causes parkinsonism. Cerebellar lesions cause ataxia of the limbs and/or trunk that is present even when there is visual input. Cortical lesions cause abnormalities such as unilateral weakness and numbness, aphasia, and neglect. Thalamic lesions cause unilateral sensory deficits.

A 28-year-old woman complains of gradualonset double vision and a lazy left hand. The latter has made it difficult for her to type or even button her clothes unless she looks at the hand. She has no medical history other than a 1-month episode of near-blindness of her right eye as a teenager in Canada. Exam reveals that the patient is unable to adduct either eye beyond midline during horizontal gaze. Strength and reflexes are normal, including in the left hand. Light touch and proprioception are diminished in the left hand. Whenher neck is flexed, she developsan electrical shooting pain down her spine. What is the most likely diagnosis? (A) Amyotrophic lateral sclerosis (B) Central cordsyndrome (C) Conversion disorder (D) Multiple sclerosis (E) Myasthenia gravis

The answer is D (Chapter 167). MS is a chronic central demyelinating disease. It is suspected when a patient presents with multiple neurologic abnormalities separated by "space" (occurring in different parts of the brain or spinal cord) and "time" (time of onset of the abnormalities is different). The diagnosis is aided by MRI. Certain neurologic deficits are highly suggestive. This patient has two such deficits: bilateral internuclear ophthalmoplegia and "sensory useless hand." The shooting pain down the spine with neck flexion is called Lhermitte sign and is also characteristic of MS. Optic neuritis causing temporary vision loss is a common initial manifestation. Growing up far from the equator is a risk factor for MS. Amyotrophic lateral sclerosis causes upper and lower motor neuron weakness, not sensory abnormalities. Central cord syndrome presents with upper>lower extremity weakness and numbness usually after traumatic neck extension; it cannot affect the eyes. Conversion disorder is a diagnosis of exclusion and is unlikely in the setting of multiple neurologic deficits. Myasthenia gravis causes ophthalmoplegia, but not of the internuclear variety, and does not cause sensory abnormalities.

Which of the following increases the risk of post-LP headache? (A) Patient moving her legs while spinal needle is in subarachnoid space (B) Patient sitting up within 1 hour of completion of the procedure (C) Replacing the stylet before removing the spinal needle (D) Using a cutting (Quincke) spinal needle (E) Using a small (22-gauge) spinal needle

The answer is D (Chapter 169). Noncutting pencil-tipped spinal needles (Whitacre or Sprotte) substantially decrease the risk of post-LP headache compared with cutting (Quincke) needles. Smaller spinal needles (i.e., 22 gauge) also decrease the risk. Unfortunately, what comes in the standard LP kit is a 20-gauge Quincke needle; thus, the diligent emergency physician should separately obtain a 22-gauge noncutting needle in most cases. Replacing the stylet before withdrawing the spinal needle prevents arachnoid tissue from being sucked through the hole in the dura and causing a spinal fluid leak, the cause of post-LP headaches. Movement of the legs while the needle is in the subarachnoid space is considered safe. It has traditionally been taught that patients should not sit up for several hours after an LP, but a recent study showed a lower risk of post-LP headache with early mobilization.

Which of the following is most useful in distinguishing a grand-mal seizure from syncope? (A) Orofacial trauma (B) Prodromalsymptoms (C) Tonic-clonic movements (D) Transitory wide anion gap (E) Urinary incontinence

The answer is D (Chapter 56). Distinguishing grand-mal seizures from true syncope is essential yet very challenging. Historical features such a classic aura, prolonged postictal confusion, witnessed head turning, unusual posture or automatisms, and muscle pain suggest seizure. Patients with syncope may have premonitory symptoms of nausea or light headedness if the event is reflex mediated (vasovagal), but a dysrhythmia may occur without prodrome. Brief tonic-clonic movements can occur with syncope yet be mistaken for seizure. Trauma with or without defensive injuries to the hands or knees suggests a sudden event without warning, which could occur with dysrhythmia, noncardiac syncope, or seizure, so trauma is not a distinguishing feature. Urinary incontinence could occur with seizure or syncope. *A transitory wide anion gap occurs after a grandmal seizure* but not after an uncomplicated syncopal event.

According to the San Francisco Syncope Rules, which of the following are predictors for an adverse event in a patient with syncope? (A) Age>65 years (B) Elevated TSH level (C) Guaiac positive stool (D) History of congestive heart failure (CHF) (E) Positive pregnancy test

The answer is D (Chapter 56). The acronym CHESS summarizes the San Francisco Syncope Rules' five predictors of adverse events, including arrhythmia and mortality: history of *CHF,* hematocrit less than 30, abnormal ECG, shortness of breath, and systolic BP less than 90. An abnormal ECG would include any non-sinus rhythm, conduction delays, new changes to the QRS, or ST segment not previously seen on prior tracings. A new prolonged QT interval would meet the criteria and would warrant admission, due to risk of torsades des pointes. Patients with a clear cause of syncope, such as vasovagal, hypovolemia, situational (cough or micturition), medication-related events, which improved with treatment, and are stable during an observation period, may be discharged. Unfortunately, the etiology of syncope remains unclear in over half of the patients who presented to the ED.

A 50-year-old woman complains of a *severe headache* that started *suddenly 18* hours ago while she was *running* on a treadmill. Initially it affected only the *back of her head and neck* but is now diffuse. She is *nauseated.* She had a similar headache, though milder, a couple of weeks ago, and while she gets headaches on occasion, this one feels* different and is more severe.* She has h*ypertension *and is a*.smoker*.Vital signsandphysicalexam are normal. Head CT is normal. What is the most appropriate next step? (A) Admission for overnight observation (B) Carotid ultrasound (C) Confront the patient about secondary gain (D) Lumbarpuncture (E) Pain control and discharge

The answer is D (Chapters 159 and 160). This presentation is concerning for *SAH*. Suddenonset headache (i.e., reaching maximal intensity within minutes) is always concerning for SAH, especially if it starts during *exertion*. *Occipital-nuchal* location of pain is *common in SAH*, and the patient says this headache is unusual for her. Her *hypertension and smoking* are risk factors for SAH. Finally, 2 weeks ago, she had what sounds like a sentinel headache, which is usually a small leak from an aneurysm that is ready to rupture. The negative head CT decreases the likelihood of SAH, but not enough to obviate LP. *Admission without further workup* could dangerously *delay the diagnosis.* Carotid ultrasound might be helpful if carotid dissection were suspected, but not here. Occasionally, patients with frequentEDvisits for painwithout organic explanations do need to be confronted about secondary gain, but not this patient. Pain control and discharge would be appropriate if the patient did not have highrisk features or if this were a typical headache for her.

A 16-year-old girl presents to the ED with near syncope without antecedent headache, chest pain, shortness of breath, abdominal pain, or weakness. The patient was arguing with a boyfriend and reports feeling her extremities and lips tingling before she "practically passed out." She admits to social stressors but denies suicidal or homicidal ideation. Vital signs are BP 120/80, HR 72, RR 18, T 98.6, room air saturation 100%. Initial physical examination is normal. She had a prior ED visit for anxiety last month. Her urine pregnancy test is negative, her hemoglobin and hematocrit are normal, and an ECG shows normal sinus rhythm. What is the next MOST appropriate step in management? (A) Admitand arrange inpatient psychiatric consult (B) Arrange outpatient electrophysiologic (EP) testing (C) Arrange outpatient tilt-table testing (D) Ask patient to take slow deep breaths with her mouthopen (E) Discharge immediately

The answer is D(Chapter 56). Given her age, normal physical examination, and negative workup, this patient is most likely hyperventilated and had a near syncopal episode. Asking her to take slow deep breaths with her mouth open might reproduce her symptoms and provide her with insight into her breathing pattern in response to stress. This patient *does not require admission*, although she might benefit from a *referral for psychologica*l counseling. In general, patients with recurrent syncope associated with falls should undergo tilt-table testing. EP testing is indicated for patients with documented dysrhythmia, preexcitation, or underlying heart disease.

A 58-year-old male presents complaining of pain, swelling, and redness to his right lower extremity that has progressed over 4 days.He wasseenby his primary care physician 2days ago and was prescribed cephalexin. His temperature is 38.3◦C, blood pressure is 140/82, heart rate is 118, and respiratory rate is 16. A fingerstick glucose is 140. The white blood cell count is 18,000 cells/mm3. His right lower extremity has a strong dorsalis pedis pulse and is depicted below (Figure 10-2). Which of the following is the MOST appropriate antimicrobial treatment? (A) Cefazolin intravenously (B) Ciprofloxacin bymouth (C) Clindamycin intravenously (D) Trimethoprim/sulfamethoxazole by mouth (E) Vancomycin intravenously

The answer is E (Chapter 147). The patient is presenting with cellulitis and has failed outpatient therapy with an oral beta-lactam. He is also showing signs of systemic toxicity and should likely be hospitalized for parenteral therapy. A patient that warrants hospitalization should receive therapy for methicillinresistant S. aureus (MRSA) and Streptococcus pyogenes. Vancomycin would be an ideal agent. Alternative choicesmaybe linezolid or daptomycin. MRSA with resistance to clindamycin is high in some communities and should not be relied on for severe soft-tissue infections. Trimethoprim/sulfamethoxazole would provide adequate coverage for MRSA in a patient stable for outpatient treatment. However, it has minimal activity against S. pyogenes and should not be sole therapy. Cefazolin and other beta-lactam antibiotics are appropriate treatment for streptococcus and methicillin-sensitive S. aureus cellulitis, but treatment of severe disease should cover MRSA. MRSA in many communities develops rapid resistance to ciprofloxacin, and it should not be first-line treatment.

What cerebrospinal fluid (CSF) finding is most diagnostic of subarachnoidhemorrhage (SAH)? (A) Elevated opening pressure (B) Greater than 50 redblood cells (RBCs)/ microliter in tube no. 1 (C) High white blood cell count (WBC) (D) Lowglucose (E) Xanthochromia

The answer is E (Chapter 160).* Xanthochromia *is yellow discoloration of the CSF due to bilirubin accumulation from the enzymatic breakdown of hemoglobin in RBCs. It is* diagnostic of SAH. *Xanthochromia develops within 12 hours of SAH and lasts for up to 3 weeks. Unfortunately, most hospital laboratories determine the presence of xanthochromia simply by holding up the specimen against a white background; spectrophotometry is the more sensitive gold standard method. The RBC count in the CSF is important, especially in the first 12 hours after headache onset. The presence of RBCs in a CSF specimen is common due to trauma during the LP, so the presence of RBCs in tube no. 1 is not by itself specific for SAH. However, the RBC count in tube no. 4 should be normal (or in a traumatic tap, it should be substantially decreased from tube no. 1 and nearly normal) to exclude SAH. An elevated opening pressure or a slight elevation in the white blood count in the CSF may be seen in SAH, but is not diagnostic. The glucose level in the CSF should not be altered.

A 72-year-old man complains of the sudden onset of vertigo and a hoarse voice 2 hours ago. He has history of hypertension, diabetes mellitus, and gout. On neurologic examination, he has ptosis of the left eye, numbness on his left face, poor palatal rise on the left, a hoarse voice, numbness on his right upper and lower extremities, and dysmetria on left-sided finger-nose testing. What is the diagnosis? (A) Cerebellar stroke (B) Left middle cerebral artery stroke (C) Multiple sclerosis (D) Perilymph fistula (E) Wallenberg's (lateral medullary) syndrome

The answer is E (Chapter 164). The patient has Wallenberg syndrome, which is infarction of the lateral medulla, usually due to occlusion of the posterior inferior cerebellar artery. Due to the presence of multiple nerve tracts and nuclei in this small section of the brainstem, the syndrome is characterized by seemingly disparate neurologic deficits, including crossed sensory loss (ipsilateral face and contralateral trunk/extremity),* vertigo,* dysphagia/dysphonia, Horner syndrome, and ataxia (if the cerebellum is affected). Cerebellar stroke causes predominant ataxia and vague, often nonspinning vertigo. Middle cerebral artery stroke causes motor/ sensory loss in the contralateral face and upper extremity (less so in the lower extremity) as well as cortical signs such as aphasia or neglect. MS may cause disparate neurologic deficits, but it does so slowly over time. Perilymph fistula is caused by a sudden rise in middle ear pressure resulting in a tear in one of thewindowsseparating the middle ear and vestibular organs; symptoms include peripheral vertigo and hearing loss.

A 32-year-old woman presents after a *firsttime seizure* in which her *left arm *became *stiff* and then *shook *for 2 minutes while she *stared blankly*. She feels normal now and denies any recent illnesses or unusual symptoms.She *emigrated* from *Mexico* 2 years ago, has no medical history and no family history of seizures, and she denies drug use. Her vital signs and physical exam are normal. *MRI is shows bugs*- *slarvae (cysticerci)* of the tapeworm *Taenia solium.* What is the most likely cause of her seizure? (A) Brain tumor (B) Cocaine abuse (C) Hyponatremia (D) Primary epilepsy (E) Worms in her brain

The answer is E (Chapter 165). The most likely cause of this patient's seizure is* neurocysticercosis*, an infection of the brain by the larvae (cysticerci) of the tapeworm Taenia solium. It is the most common parasitic infection of the central nervous system in the world and the* most common *acquired cause of epilepsy in the developing world, particularly Latin America. The worm is usually acquired via ingestion of undercooked pork or fecally contaminated water. *CT or MRI imaging *may reveal parenchymal* calcifications (scarring) or hypodense *or *ring-enhancing lesions (active cysts),* the latter being seen in the MRI in Figure 12-4. Antiepileptic monotherapy is usually effective in preventing recurrent seizures. Antiparasitics along with or preceded by steroids can be considered in consultation with an infectious diseases specialist if there is evidence of active cysts. A brain tumor could explain this seizure but is less likely than cysticercosis in this patient from Mexico with no previous symptoms and a normal neurological exam. There is no evidence of cocaine abuse by history or exam. Hyponatremia is unlikely in the absence of a recent illness or medication use. Primary epilepsy is possible, but at the age of 32, this would be late onset, making cysticercosis more likely in a patient from Latin America.

A 3-year-old boy with a ventriculoperitoneal shunt placed 2 years ago for hydrocephalus presents with headache, vomiting, and listlessness. On exam, he is afebrile, lethargic, and ataxic. There is no meningismus or abdominal tenderness. Plain film shunt series is negative. What is the most likely cause of his symptoms? (A) Abdominal pseudocyst (B) Shunt fracture (C) Shunt infection (D) Shunt misplacement (E) Shunt obstruction

The answer is E (Chapter 169). The patient has typical symptoms of elevated ICP, implying shunt malfunction. Shunt obstruction is the most common mechanism of malfunction. The plain film shunt series (x-rays of skull, chest, and abdomen) helps to identify kinks, malpositioning, and perhaps fracture of the shunt, but does not detect obstruction. CT of the head could be performed, but it exposes the child to ionizing radiation and would likely just confirm the clinical findings of elevated ICP without determining the cause. The valve chamber could be palpated to help diagnose an obstruction—difficulty compressing the chamber indicates a distal obstruction, whereas slow refill of the chamber (more than 3 seconds) indicates a proximal obstruction. Regardless, a neurosurgeon should be consulted. Abdominal pseudocyst is an uncommon cause of shunt malfunction. Shunt fracture is also uncommon and is often evident either on physical exam (e.g., collection of fluid around the clavicle) or the shunt series. There are no signs of shunt infection. Shunt misplacement is a postoperative diagnosis and would usually be identified by the shunt series.

A 37-year-old male presents to the ED with *altered mental status*. He was found *unconscious* in the bathroom at work. On exam, he is arousable to painful stimulus, muttering incoherently. His airway is intact and he has bilateral breath sounds. His initial vital signs are blood pressure (BP) 95/47, P 110, respiratory rate (RR) 14, O2% 97% on room air, T 99.4. He has *dry mucus membranes*. Fingerstick *glucose is 396*. Lab work reveals a normal CBC, 3+ acetone, Na 121, Cl− 97, HCO3 9, *K 3.0,* Mg 2.9, Phos 1.5, AG 29. Which of the following is the first priority in caring for this patient? (A) IV bicarbonate (B) IV lactated ringers (C) IV phosphate (D) IV potassium (E) IV saline

The answer is E (Chapter 220). In patients with diabetes mellitus, it is very important to prioritize therapeutic interventions. The order of therapeutic priorities is *volume resuscitation first and foremos*t. Patients often have a fluid deficit of* 5-10 L*. Potassium deficits should be addressed next. Diabetic ketoacidosis (DKA) patients often have profound total-body potassium deficits. For an initial potassium level between *3.3 and 5.3* mEq/L, with established *urine output*, *potassium* should be replaced at a rate of 10 mEq KCL per hour for 4 hours. Insulin may be given, but only after volume resuscitation and potassium deficits have been addressed. It may be administered at a bolus of 0.1 units/kg and followed by a drip of 0.1 units/kg per hour. In general, IV phosphate therapy should only be initiated if the serum level is <1.0 mg/dL. Routine use of IV bicarbonate is not recommended in the treatment of DKA.

In the Framingham Heart Study, which of the following was theMOSTcommonetiology of syncope? (A) Cardiac (B) Orthostatic (C) Seizure (D) Vasovagal (E) Unknown or indeterminate

The answer is E (Chapter 56). The longitudinal Framingham study described 822 reports of syncope in the 7814 patients followed for 17 years. The causes of syncope were vasovagal (21%), cardiac (10%), orthostatic (9%), seizure (5%), neurologic (4.1%), and unknown (37%). Other studies also report anunknowncause in about40% of cases, despite extensive workups. Limited ED evaluations may not determine a specific cause of syncope in 50-60% of cases. The ED focus is to identify patients at increased risk of immediate decompensation or future serious morbidity or sudden death.

While observing the arrival of a trauma patient with an open tibia fracture, an otherwise healthy 22-year-old male hospital volunteer states he feels *lightheaded*. He appears *pale and diaphoretic* and *slowly* sinks to the floor. Fortunately, anobservant nurse prevents him from striking his head. He is unresponsive for 10 seconds, has a brief tonic-clonic movement but *spontaneously awakens*, and states "That was weird." A brief neurologic exam is nonfocal. Which of the following is theMOST likely cause of his condition? (A) Dysrhythmia (B) Grand-mal seizure (C) Hypoglycemia (D) Orthostatic hypotension (E) Vasovagal syncope

The answer is E (Chapter 56). This patient's report of *lightheadedness and the prodrome of pallor and sweating *after viewing an intense visual stimulus suggest vasovagal syncope, rather than orthostatic hypotension. Brief, tonic-clonic, or asynchronous movements may occur with any form of syncope. The duration and intensity of movements during grand-mal seizures often causes muscle pain. The patient's rapid recovery also makes the diagnoses of hypoglycemia or seizure unlikely. Although an acute dysrhythmia might not be entirely excluded in this scenario, it was not the most likely cause in a previously healthy young person.

A 25-year-old man is brought to the ED by his partner, who complains that the patient is* "out of it." *The partner describes episodes in which the patient* claims to smell and hear things *that aren't there, complains that people are out to get him, then *smacks his lips* for about a minute and doesn't interact. Finally he begins responding again but remains *confused* for several minutes before becoming normal. What is the diagnosis? (A) Complex partial seizure (B) Lysergic acid diethylamide (LSD) abuse C) Schizophrenia (D) Simple partial seizure (E) Tourette syndrome

Theanswer is A (Chapter 165). *Complex partial seizures* are *focal seizures that affect consciousness or mentation.* They usually originate in the *temporal lobe* and can cause odd symptoms or behaviors, such as *olfactory orauditory hallucinations*, automatisms, and affective symptoms such as fear or paranoia. LSD causes hallucinations and affective changes but not automatisms with unresponsiveness. Schizophrenia often causes auditory hallucinations and paranoia but is not paroxysmal nor does it affect consciousness. Simple partial seizures could explain all of the findings except the change in consciousness. Tourette syndrome is characterized by recurrent brief motor and verbal tics but not hallucinations or changes in mood or consciousness.

A 22-year-old motorcyclist is involved in a moderate speed crash. He complains of severe neck pain and inability to move his arms or legs. On exam, he has mid-cervical spine tenderness as well as paralysis and loss of sensation of his upper and lower extremities. Testing of which of the following would be most useful in distinguishing between complete or partial spinal cord injury? (A) Maximuminspiratory force (B) Pain and temperature sensation in the upper extremities (C) Reflexes (D) Sensation at the angle of the mandible (E) Sensation in the perineum

Theanswer is E(Chapter 255). In acute spinal cord injury, preserved perianal/perineal sensation, which is dependent on the sacral nerve roots, is an important finding that indicates a partial rather than complete cord injury. The other answer choices are useful functions to test, but they do not distinguish partial from complete cord injury. Maximum inspiratory force is important in upper cervical cord injury to determine the need for ventilatory support. Pain and temperature sensation in the upper extremities is affected by most partial and all complete cervical cord injuries. Reflexes may not be abnormal in acute cord injury—hyperreflexia may take hours to manifest. Interestingly, sensation at the angle of the mandible is carried by the C3 nerve root (rather than the trigeminal nerve).

A 36-year-old man presents with right neck pain that started while he was wrestling with his dog 2 days ago. Today he also has a *right-sided **frontotemporal* headache and complains that he can hear his heartbeat ringing in his right ear. Vital signs are normal. There is no evidence of head or neck trauma. Neurologic exam shows the abnormalities of the *right eye* seen in Figure 12-2. What is the most likely diagnosis? (A) Carotid artery dissection (B) Right third cranial nerve palsy (C) Severe neck strain (D) Temporal arteritis (E) Vertebral artery dissection

Theanswer isA(Chapter 161).Carotid artery dissection is uncommon but is a significant cause of stroke in the young. It usually occurs after major or minor neck trauma. The most *common symptom* is headache, which is usually *frontotempora*l, followed by neck pain; pulsatile tinnitus (hearing the heartbeat) occurs occasionally. Neurologic abnormalities, *classically a partial ipsilateral Horner syndrome* (no anhydrosis), often occur days after the onset of pain and can be quite subtle. In Figure 12-2, the patient's right eye miosis is obvious, but the ptosis is very mild. Neck strain wouldbe a diagnosis of exclusion and is less likely here given the classic presentation of carotid dissection. Third cranial nerve palsy produces severe ptosis, pupillary dilation, and ophthalmoplegia. Temporal arteritis occurs almost exclusively in those older than 50 years and is not associated with trauma. Vertebral artery dissection also occurs after neck trauma but usually causes occipital andnuchal painandbrainstem deficits such as vertigo and ataxia.

A77-year-old man is brought in by his family for unusual behavior. He has been *confused and paranoid* for a couple of days, repeatedly claiming that the neighbors are poisoning him. He is worse at night and is *sleeping irregularly.*He has a history of schizophrenia, diabetes, and benign prostatic hyperplasia. At triage the patient was *disoriented* to time and place and answered questions nonsensically. Vital signs are as follows: temperature 37.9◦C, blood pressure 110/85, heart rate 105, respiratory rate 18, oxygen saturation 98% on room air. On exam, he is oriented to self, place, and year and answers some questions appropriately but has difficulty paying attention and occasionally nods off to sleep. He complains, "my penis is on fire." What is the most likely explanation for the change in his mental status? (A) Delirium (B) Dementia (C) Mania (D) Paranoid personality disorder (E) Psychosis

Theanswer isA(Chapter 162). This patient is *delirious*. He has *waxing and waning* disorientation and attention deficit—he was more disoriented at triage than during examination. He *cannot focus* his attention. He has been *worse at night* and his *sleep-wake cycle is abnormal. Finally, he has concerning vital sign abnormalities that indicate an underlying acute medical condition.With a history of benign prostatic hyperplasia, a complaint of penile burning, and a fever with tachycardia and narrow pulse pressure, perhaps he has* urosepsis*, a very *common cause* of delirium in the elderly. Because of his schizophrenia, he is manifesting delirium with more paranoia than is typical, but psychosis alone does not cause disorientation, attention deficit, or vital sign abnormalities, nor does mania or paranoid personality. Dementia makes one more vulnerable to delirium but does not cause acute changes in mental status.

A 46-year-old woman with a history of diabetes and palpitations presents with sudden vertigo, loss of balance, inability to walk, and vomiting. Neurologic exam reveals severe limb and truncal ataxia, with the patient falling to the left when she sits at the edge of the bed. Emergent MRI shows a large left cerebellar infarction and mild hydrocephalus. Besides arranging for admission to the intensive care unit, what is an important step in the management of this patient? (A) Carotid ultrasound (B) Heparin (C) Maintaining the patient in Trendelenburg position (D) Neurosurgery consultation (E) Thrombolysis

Theanswer isD(Chapter 161). Largecerebellar infarctions, usually due to occlusion of the posterior inferior cerebellar artery, can be life threatening because the cerebellum can become edematous and impinge on the brainstem and may even herniate into the brainstem. Thus, patients can rapidly deteriorate and must be monitored closely in consultation with a neurosurgeon. Obstructing hydrocephalus implies a poorer outcome and the possible need for acute surgical decompression. Carotid ultrasound is not useful in a posterior circulation stroke. Patients with possible elevated intracranial pressure (ICP) should be placed at 30 degrees of head elevation, not Trendelenburg. Heparin is rarely part of the initial treatment of any acute stroke. Thrombolysis is contraindicated in cerebellar stroke because any bleeding can lead to cerebellar herniation. This coupled with the fact that head CT may be normal in cerebellar stroke (due to artifact from bones of the posterior fossa) highlights the importance of the neurologic exam in distinguishing stroke territories.

A45-year-old woman complains of dizziness that started suddenly a few hours ago while getting out of bed. If she moves her head toward the right, particularly when lying down, she develops a strong feeling that the roomis spinningandbecomesnauseated; she has vomited several times. When her head is kept still, the symptoms resolve completely. She denies hearing loss or tinnitus. She has no medical problems and does not smoke or use illicit drugs. Neurologic examination, including coordination, is normal. When the Dix-Hallpike maneuver is performed and the head is tilted to the right, her symptoms as well as rotatory nystagmus ensue after a 3second delay and resolve after 30 seconds. What is the diagnosis? (A) Benign paroxysmal positional vertigo (BPPV) (B) Cerebellar stroke (C) M´eni´ere disease (D) Vertebral artery dissection (E) Vertebrobasilar insufficiency

he answer is A (Chapter 164). BPPV is the most common type of peripheral vertigo. Peripheral vertigo is usually described as a strong spinning sensation that is triggered or substantially worsened by head movement. Symptoms often resolve with avoidance of head movement and fatigue after repeated provocation. The finding of vertigo and nystagmus occurring after a few seconds delay during the Dix-Hallpike maneuver and resolving within a minute is almost pathognomonic for BPPV. Cerebellar strokes may cause vertigo but invariably present with ataxia as well. M´eni´ere disease presents with repeated bouts of peripheral vertigo often associated with tinnitus andhearing loss.Vertebral artery dissection may cause central (not peripheral) vertigo, usually occurs after rapid rotation or extreme positioning of the neck, and often the initial symptom is occipital or nuchal pain. Vertebrobasilar insufficiency may cause numerous symptoms referable to the brainstem or cerebellum (including central vertigo) and is a disease of the elderly or those with major atherosclerosis risk factors.