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A 61-year-old woman presents with vertigo that starts every time she moves her head. She has no hearing changes, tinnitus, or significant medical history. Her blood pressure is 178/85; there are no neurologic deficits. Bedside positional testing demonstrates nystagmus with a long latency and transient duration; it is suppressible with repeated testing. What is the most likely diagnosis?
- Benign paroxysmal positional vertigo
- Ménière disease
- Transient ischemic attack
- Vertebral basilar artery insufficiency
The correct answer is A, Benign paroxysmal positional vertigo.
Why is this the correct answer?
Benign paroxysmal positional vertigo (BPPV) is suggested by the onset of vertigo with changes in head position and by the age of the patient. More importantly, the physical examination confirms that this patient has peripheral vertigo; the nystagmus has a long latency, has a transient duration, and is fatigable with provocative testing (the Dix-Hallpike maneuver). Furthermore, it is not associated with any other neurologic deficits. This is distinct from central vertigo, such as that caused by strokes and tumors. Central vertigo tends to have nystagmus with a short latency and a sustained duration, is not fatigable, and tends to be accompanied by other cranial and peripheral nerve deficits.
BPPV is the most common cause of vertigo overall, accounting for approximately 40% of vertigo diagnoses and affecting roughly 10% of all adults by age 80. The incidence of BPPV increases with age, with peak onset between age 50 and 60. Women are more commonly affected than men, with almost a 3-to-1 female-to-male ratio. Osteoporosis, vitamin D deficiency, and a history of prior head trauma have all been associated with the development of BPPV. BPPV is believed to be caused by loose calcium carbonate otoliths moving aberrantly within the semicircular canals of the inner ear, ultimately resulting in the false sensation of rotation. The posterior semicircular canal is most commonly affected and accounts for approximately 60% to 90% of all cases of BPPV.
Patients usually present with brief episodes of vertigo, typically lasting less than 1 minute, that are provoked by head position changes (eg, rolling over in bed, getting out of bed, tilting the head upward to reach objects on high shelves, or tilting the head downward to tie shoes). BPPV can be diagnosed with a series of bedside maneuvers known as the Dix-Hallpike maneuver, which provokes directional and torsional nystagmus depending on the involved semicircular canal. If a Dix-Hallpike test result is negative, a supine roll test may be performed to evaluate for lateral semicircular canal BPPV. The first-line treatment for BPPV is an attempt at repositioning the misplaced otolith with a procedure known as the Epley maneuver. This is effective in approximately 90% of cases. Pharmacologic treatments such as meclizine, ondansetron, and diazepam may be used to temper nausea and emesis in patients with BPPV but are not as effective as the Epley maneuver.
Why are the other choices wrong?
Ménière disease is unlikely because this patient lacks the typical aural symptoms. The classic triad for Ménière disease is intermittent episodes of ear fullness, tinnitus, and vertigo. In BPPV, the nystagmus has a long latency, has a transient duration, and is fatigable with provocative testing.
A transient ischemic attack is an important consideration but is unlikely because of the lack of central signs on physical examination, including ataxia. In BPPV, the nystagmus has a long latency, has a transient duration, and is fatigable with provocative testing.
Vertebral basilar artery insufficiency is an important consideration in the differential diagnosis, but this condition is unlikely because of the lack of central signs on physical examination. Vertebral basilar artery insufficiency should always be considered in patients with vertigo that occurs when they look up (when raising the head compresses the vertebral artery). In BPPV, the nystagmus has a long latency, has a transient duration, and is fatigable with provocative testing.
REFERENCES
Goldman B, Johns P. Vertigo. In: Tintinalli JE, Ma OJ, Yealy DM, et al, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill Education; 2020:1145-1153.
Chang AK. Dizziness and vertigo. In: Walls RM, Hockberger RS, Gausche-Hill M, et al, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Vol 1. 10th ed. Elsevier; 2023:142-151.
Kim JS, Zee DS. Benign paroxysmal positional vertigo. N Engl J Med. 2014 Mar;370(12):1138-1147.
UpToDate article on benign paroxysmal positional vertigo, available in full with a subscription: https://www.uptodate.com/contents/benign-paroxysmal-positional-vertigo
A 58-year-old man with known severe coronary artery disease presents via ambulance after a witnessed cardiac arrest. He has been intubated by EMS, and CPR is in progress. His end-tidal carbon dioxide (EtCO2) drops from 20 mm Hg to 9 mm Hg during the course of 10 minutes; the waveform maintains a normal morphology. Bedside echocardiogram shows ventricular fibrillation. What is the most likely cause of the drop in EtCO2?
- Cardiac tamponade
- Displacement of endotracheal tube
- Inadequate chest compressions
- Internal hemorrhage
The correct answer is C, Inadequate chest compressions.
Why is this the correct answer?
Monitoring of end-tidal carbon dioxide (EtCO2) during cardiopulmonary arrest has become the standard of care in most emergency departments. EtCO2 may be used as a marker of perfusion during resuscitation of a patient in cardiac arrest. Near-normal EtCO2 levels (20 mm Hg) suggest that good chest compressions are being provided and that perfusion is adequate. EtCO2 should ideally be maintained above 10 mm Hg. A gradual decrease in EtCO2 may indicate that the person giving chest compressions is becoming fatigued and CPR should be provided by a different team member or an automated device.
EtCO2 monitoring provides a real-time assessment of ventilation and perfusion in the setting of cardiac arrest, and it may also provide important prognostic information. Changes in EtCO2 during resuscitation may indicate issues with ventilation, such as incorrect initial placement of the endotracheal tube or subsequent displacement of the endotracheal tube. Although colorimetric CO2 detectors may change colors early in esophageal intubation, an adequate waveform will not be noted. A sudden decrease in CO2 with a poor waveform during resuscitation likely indicates displacement of the endotracheal tube. A sudden increase in EtCO2 may indicate a return of spontaneous circulation. An EtCO2 <10 mm Hg at the 20-minute mark of resuscitation has been associated with a poor prognosis.
Why are the other choices wrong?
Since no cardiac tamponade was noted on bedside echocardiogram, cardiac tamponade is not a likely cause of the gradual decrease of EtCO2 in this case. Cardiac tamponade can decrease EtCO2 by decreasing blood flow to the lungs.
Displacement of the endotracheal tube would cause a sudden decrease in EtCO2 with concomitant loss of waveform. A gradual decrease in EtCO2 may be seen with expanding pneumothorax, which can be a complication of CPR.
Significant internal hemorrhage is unlikely to be the cause in this patient with a witnessed cardiac arrest. In trauma, however, ongoing hemorrhage should be considered as a potential cause of decreasing EtCO2.
REFERENCES
Long B, Koyfman A, Anantharaman V, et al. Cardiac resuscitation. In: Tintinalli JE, Ma OJ, Yealy DM, et al, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill Education; 2020:153-164.
UpToDate article on capnography, available in full with a subscription: https://www.uptodate.com/contents/carbon-dioxide-monitoring-capnography
Life in the Fast Lane article on capnography in cardiac arrest: https://litfl.com/capnography-in-cardiac-arrest/
ALiEM article on end-tidal CO2 in cardiopulmonary resuscitation: https://www.aliem.com/end-tidal-co2-in-cardiopulmonary-resuscitation/
What is the most significant risk factor for hospital-acquired pneumonia?
- Chronic lung disease
- Dialysis
- Immunocompromise
- Mechanical ventilation
The correct answer is D, Mechanical ventilation.
Why is this the correct answer?
Hospital-acquired pneumonia (HAP) is pneumonia that develops more than 48 hours after hospital admission. Mechanical ventilation is the most significant risk factor for HAP. Pneumonia that develops 48 hours or more after endotracheal intubation is known as ventilator-associated pneumonia (VAP). Given the significant morbidity and mortality of VAP, many ICUs have instituted "VAP prevention bundles." Preventive measures include avoiding intubation when possible, minimizing sedation during intubation as much as possible, preventing aspiration by elevating the head of the bed and draining subglottic secretions, and assessing readiness to extubate daily. Other risk factors for HAP include older age, chronic lung disease, aspiration, multiple trauma, opioid exposure, and paralysis.
Why are the other choices wrong?
Patients with chronic lung disease may have an increased risk of HAP, but it is a less significant risk factor than mechanical ventilation. However, underlying lung disease may increase mortality in patients who develop HAP.
Patients requiring dialysis do not have an increased risk of HAP. However, comorbidities (including renal failure requiring dialysis) may increase mortality in patients who develop HAP.
Immunocompromised patients are more likely to develop HAP than healthy individuals, but mechanical ventilation is a more significant risk factor than immunocompromise for the development of HAP. However, an immunocompromised state may increase the risk of morbidity and mortality from HAP.
REFERENCES
UpToDate article on preventing hospital-acquired and ventilator-associated pneumonia in adults, available in full with a subscription https://www.uptodate.com/contents/risk-factors-and-prevention-of-hospital-acquired-and-ventilator-associated-pneumonia-in-adults
Anderson E, French S, Maloney GE. Community-acquired pneumonia, aspiration pneumonia, and noninfectious pneumonia infiltrates. In: Tintinalli JE, Ma OJ, Yealy DM, et al, eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 9th ed. McGraw-Hill Education; 2020:439-449.
Which aspect of the physical examination can best distinguish toxicity from an anticholinergic agent from that of a sympathomimetic agent?
- Heart rate
- Pupils
- Skin
- Temperature
The correct answer is C, Skin.
Why is this the correct answer?
The skin is a helpful indicator to distinguish between these two conditions. Dry skin is expected with anticholinergic toxicity, and damp or sweaty skin is expected with sympathomimetic toxicity. An anticholinergic (more accurately, antimuscarinic) toxidrome can result from exposure to a variety of agents, including drugs (eg, atropine, benztropine, diphenhydramine, various antipsychotics, and tricyclic antidepressants) and plants (eg, angel's trumpet and jimsonweed). The antimuscarinic state results from antagonism at central and peripheral nervous system muscarinic receptors.
Manifestations include coma; delirium; diminished bowel sounds; dry and, at times, flushed skin; hyperthermia; mydriasis; tachycardia; urinary retention; and picking behavior. The sympathomimetic toxidrome also includes hyperthermia, mydriasis, and tachycardia, but the presence of diaphoresis can help distinguish it from the anticholinergic toxidrome. Hypertension is expected with ingestion of sympathomimetic agents, but it can also occur with antimuscarinics. Agitation and psychosis rather than delirium are also more typical with sympathomimetic agents than with antimuscarinic agents. Exposure to cocaine and phencyclidine can result in a sympathomimetic toxidrome, as can various amphetamines, including ecstasy (MDMA), methamphetamine, and cathinones (recently sold in the United States as bath salts).
Why are the other choices wrong?
Tachycardia is expected with both anticholinergic and sympathomimetic agents. The skin is a better indicator to differentiate between the two.
Mydriasis is expected with both anticholinergic and sympathomimetic agents. Typically, the skin is used to differentiate between the two conditions. Dry skin is more common in the anticholinergic state.
Hyperthermia can occur with both anticholinergic and sympathomimetic agents. Differentiation between the two toxidromes can be difficult, so knowing that the skin findings can be different is important. Dry skin is typically found with the anticholinergic state, and damp or sweaty skin is found with the sympathomimetic state.
REFERENCES
Nelson LS, Howland MA, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS. Initial evaluation of the patient: vital signs and toxic syndromes. In: Nelson LS, Howland MA, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS, eds. Goldfrank’s Toxicologic Emergencies. 11th ed. McGraw-Hill Education; 2019:28-31.
Homer FMG. Anticholinergic agents. In: Wolfson AB, Cloutier RL, Hendey GW, Ling LJ, Rosen CL, Schaider JJ, eds. Harwood-Nuss’ Clinical Practice of Emergency Medicine. 7th ed. Wolters Kluwer; 2021:1530-1533.
UpToDate article on anticholinergic poisoning, available in full with a subscription: https://www.uptodate.com/contents/anticholinergic-poisoning
What factor is associated with a diagnosis of SCIWORA (spinal cord injury without a radiographic abnormality)?
- Axial loading mechanism
- CT findings
- Lumbar spine tenderness
- Presentation in younger children versus adults
The correct answer is D, Presentation in younger children versus adults.
Why is this the correct answer?
Spinal cord injury without radiographic abnormality (SCIWORA) is thought to occur more commonly in children than in adults because of the relative laxity of the ligaments of the spine in children. Additionally, the large size of the head and the increased mobility of the cervical spine in younger children are thought to contribute to this phenomenon. For the same reasons, SCIWORA is more common in younger children than in older children and adults. SCIWORA is also thought to occur from mechanisms such as spinal traction or even spinal ischemia due to stretching, attributed to this relative mobility. That being said, older patients are also at risk due to spinal stenosis or kyphosis. Central cord syndrome is a manifestation of SCIWORA.
The term SCIWORA was coined and recognized before the use of MRI became more commonplace in emergency departments. With the use of MRI, more of these injuries are being identified as spinal cord contusion or ischemia. At one time, high-dose steroids were thought to have benefit in patients with spinal cord injuries. However, this therapy has fallen out of favor. It is now generally accepted that the benefits are somewhat controversial and are outweighed by the risks.
Why are the other choices wrong?
The most common mechanism of injury in SCIWORA is flexion and extension. This can happen in motor vehicle collisions. Axial loading injuries usually occur from falls and are a less common cause of SCIWORA.
SCIWORA is a neurologic deficit that does not demonstrate any bony radiographic abnormality which would be diagnosed on plain x-rays or CT scans. SCIWORA is a spinal cord injury that would need diagnosis via MRI. With increased use of MRI, these injuries are being identified more often as spinal contusions or ischemia or ligament-related injuries.
Because of its relative mobility and laxity, the cervical spine is the most common location of SCIWORA. It is least commonly seen in the lumbar spine.
REFERENCES
Preston-Suni K, Kaji AH. Spinal trauma. In: Walls RM, Hockberger RS, Gausche-Hill M, et al, eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Vol 1. 10th ed. Elsevier; 2023:340-367.
Frisch AN. Spinal cord injuries. In: Wolfson AB, Cloutier RL, Hendey GW, Ling LJ, Rosen CL, Schaider JJ, eds. Harwood-Nuss’ Clinical Practice of Emergency Medicine. 7th ed. Wolters Kluwer; 2021:204-209.
UpToDate article on SCIWORA, available in full with a subscription: https://www.uptodate.com/contents/spinal-cord-injury-without-radiographic-abnormality-sciwora-in-children