DRH-EM Education

Heat emergencies represent a continuum of disorders that range in severity from heat cramps to heat exhaustion to life-threatening heat stroke. In most circumstances, heat emergencies can be avoided through common sense, public education, and prevention. People most at risk for heat injuries include athletes, military personnel, and laborers who work outdoors in the heat. Classic heat injury, as is the case with this patient, usually occurs during periods of high environmental heat stress. Physical exertion is not required if environmental temperatures and humidity create a situation where heat gain overwhelms native heat losses. Exertional heat injury usually affects individuals who are participating in athletic events in conditions of high heat stress. Clinical features are what determine the severity of heat illness. This patient is presenting with symptoms characteristic of heat exhaustion. Other symptoms can include muscle cramps, headache, and vomiting. On physical examination of patients with heat exhaustion, the temperature may be normal or elevated. However, patients with heat exhaustion will not have mental status changes. Mental status changes are a sign of heat stroke which can be life-threatening.

Dry skin, or anhidrosis (A), can classically be found in patients with heat stroke but this is not a requirement for the diagnosis since patients with severe heat illness can also present with diaphoresis. Heat exhaustion is characterized by the inability to maintain adequate cardiac output due to strenuous exercise and environmental heat stress. Acute dehydration may be present. Athletes with heat exhaustion have difficulty continuing with exercise. Other signs of heat exhaustion include hypotension (B), syncope, and tachycardia (D). The presence of these factors does not necessarily portend severe complications from the illness. Severe heat illness, heat stroke, presents with neurological symptoms such as hallucinations, seizure, mental status changes, or coma.

The class Arachnida contains the largest number of venomous species known, but most are not harmful to humans. Humans fear spiders and scorpions, but of this class of species ticks probably cause the greatest morbidity. One of the more venomous spiders known is the black widow spider or Latrodectus species. They are found throughout the United States, except Alaska. Symptoms of a black widow spider bite include a pinprick sensation followed by local redness and swelling, but sometimes the bite is not felt. Over the next hour, patients develop dull cramping in the area of the bite that eventually spreads to the entire body. Pain is centered in the chest in patients who suffer an upper extremity bite, and pain is centered in the abdomen in patients who suffer a lower extremity bite. The abdomen may become boardlike and can mimic pancreatitis, appendicitis, or a perforated peptic ulcer. Signs and symptoms usually abate within a few hours and definitely resolve in two to three days. Management is supportive with benzodiazepine treatment for muscle spasms.

Symptoms of a brown recluse spider (B) bite include local burning pain at the site of the bite. After a few hours, a bleb forms in the center of the bite with a surrounding erythematous ring. The area can look like a target sign or a bull’s eye. Over the next few days, the bleb darkens and begins to necrose with eventual involvement of the underlying subcutaneous fat along with the skin. Systemic symptoms such as fever, malaise, vomiting, and rash can develop and lead to shock in severe cases, although fatalities are rare. This patient does not have a bite characteristic of a brown recluse spider. A scorpion (C) sting is characterized by immediate pain at the site of the sting. Over some time, patients can develop numbness and weakness locally and will have heightened sensitivity in the sting area. Systemic symptoms such as restlessness, vomiting, muscle spasms, nystagmus, and myoclonus can develop in severe cases but are more rare. Scorpion sting symptoms can mimic those found in patients with black widow spider bites but are much less common. Most tarantulas (D) are nontoxic. They are unusual in that their abdominal hairs can be thrown and embedded in human skin, leading to allergic reactions. There is not a toxic bite. The patient in this question is not presenting with allergic reaction symptoms.

Decompression sickness occurs due to the liberation of gas bubbles associated with a decrease in ambient pressure. This can occur in divers breathing compressed air as well as high altitude pilots or astronauts. The gas bubbles likely obstruct blood flow, leading to direct tissue ischemia. They also activate a variety of inflammatory processes, leading to thrombosis and capillary leaking. Symptoms of decompression sickness typically occur minutes to hours after surfacing. Decompression sickness can include pain syndromes involving the joints (“the bends”) as well as more serious manifestations including pulmonary (“the chokes”), cardiovascular, and neurologic symptoms (“the staggers”). Treatment of decompression sickness is similar to the treatment of an arterial air embolism and includes administration of oxygen, increasing tissue perfusion with intravenous fluids, and rapid decompression with hyperbaric oxygen.

Arterial air embolism (A) is an example of a barotrauma of ascent and results from entry of air into the arterial system with resultant embolization. The brain is the most commonly affected organ. Arterial air embolism should be suspected in any diver with loss of consciousness upon surfacing. Inner ear barotrauma (C) is an example of barotrauma of rapid descent or ascent and results from rupture of the round window or tearing of the vestibular membrane due to a forceful Valsalva maneuver done during descent to clear the ears. Symptoms include vertigo (as seen in the patient above) but this condition is easily differentiated from decompression sickness due to the onset of symptoms during descent rather than after surfacing. Nitrogen narcosis (D) occurs with deep dives and includes symptoms such as loss of fine motor skills and higher-order brain functions, resulting in bizarre and dangerous behavior. Presentation is similar to alcohol intoxication.

Atrial fibrillation in hypothermia tends to be relatively benign and resolves spontaneously with rewarming. Persistent atrial fibrillation after complete rewarming is unlikely to be due to hypothermia and may suggest an underlying medical pathology. Cardioversion increases the risk of ventricular fibrillation and is contraindicated unless the patient is unstable. Anticoagulation for temporary atrial fibrillation is not indicated and could worsen the coagulopathy already present in hypothermia.

This patient presents with rhabdomyolysis after an electrical injury and should be treated with aggressive intravenous hydration. Electrical injuries are common and are the cause of about 5% of burn unit admissions and 6% of occupational fatalities. The extent of the injury is related to the type of circuit (alternating current (AC) versus direct current (DC)), the resistance, amperage, duration of contact and voltage. The initial exposure to electricity can cause severe burns spreading from the point of impact. Additionally, the energy from the shock is transmitted into the body and can cause significant muscle breakdown. Breakdown is increased if the patient experiences tetany or prolonged exposure to the electrical source. The classic finding of rhabdomyolysis is a urine dip that is positive for blood with only scant or no RBCs on microscopy. The urine dipstick falsely reports myoglobin as hemoglobin in this case. A serum creatinine kinase level should be obtained. Initial treatment is with aggressive fluid resuscitation to maintain urinary output as myoglobin accumulation can lead to renal failure. Electrolyte abnormalities (specifically hyperkalemia from cellular breakdown) should be closely monitored and treated as well.

A CT scan of the abdomen (A) is not necessary to look for a bleeding source. Intravenous antibiotics (B) are not necessary as this urinalysis does not indicate the presence of infection. Packed red blood cells (D) are not needed at this time as the patient does not exhibit signs of bleeding.

The partial pressure of oxygen decreases as barometric pressure decreases at altitude. At 8,000 feet or greater above sea level, the environment becomes hypoxic and high-altitude syndromes can occur due to hypoxia. These include acute mountain sickness (AMS), high-altitude pulmonary edema, high-altitude cerebral edema, retinopathy, and certain neurologic syndromes. High-altitude cerebral edema (HACE) is the most severe form of acute mountain sickness. At altitude, cerebral vasodilation occurs and leads to increased blood flow and blood volume. This is due to a leaky blood-brain barrier either from lack of autonomic autoregulation or increased vascular permeability, or a combination of the two. HACE is characterized by progressive global cerebral dysfunction and causes confusion, altered mental status, and ataxia. Ataxia is a cardinal and early sign of HACE, and all patients with acute mountain sickness should be monitored for ataxia. Other features, such as headache, nausea, or vomiting, may be absent. Retinal hemorrhages are also common, and cranial nerve palsies of the third and sixth cranial nerves may occur due to increased intracranial pressure. Concomitant pulmonary edema is common. Death from HACE is due to brainstem herniation, so early identification and management are critical. The highest priority is descent. If this is not possible, temporizing measures (though often unavailable) include supplemental oxygen, corticosteroids, and use of a portable hyperbaric oxygen chamber. Computed tomography of the head may demonstrate white matter hyperattenuation more than gray matter with effacement of the sulci and flattening of the gyri.

This patient presents with signs and symptoms consistent with a left middle cerebral artery stroke as well as subcutaneous emphysema that developed during ascent from diving. Any focal neurologic deficit that results during ascent or immediately thereafter should be considered a cerebral arterial air embolism until proven otherwise. Rapid uncontrolled ascent against a closed glottis causes the volume of gas in the lungs to expand according to Boyle’s law (pressure and volume of a gas are inversely related at a constant temperature). As this gas expands, it can lead to pulmonary barotrauma, including pneumothorax, pneumomediastinum, (as indicated by this patient’s subcutaneous emphysema on exam), and alveolar rupture. Alveolar rupture leads to gas leakage into the pulmonary veins, which can then move into the systemic circulation and lodge in distal arterioles as arterial gas emboli. Cerebral gas embolism presents with typical stroke symptoms and is one of the most serious complications of pulmonary barotrauma. Air embolization can be prevented by exhaling during ascent, which prevents the rapid expansion of volume within the lungs as pressure decreases. Treatment includes fluid resuscitation and rapid recompression with 100% hyperbaric oxygen. Hyperbaric oxygen works by decreasing the size of the air embolism as well as easing washout of other gases by increasing the diffusion gradient for nitrogen from the air embolism to plasma.

Barotitis (B), or ear barotrauma, is the most common diving disorder and results from unequalized increasing pressure on the tympanic membrane on descent. Symptoms include unilateral ear pain and fullness, as well as vertigo and disorientation from rupture of the tympanic membrane and uneven caloric stimulation of the middle ear. Treatment is conservative. Decompression syndrome (C), or “the bends,” usually occurs within six hours after ascent. It results from the expansion of inert gas that dissolved in tissues during descent. As the pressure of these inert gases exceeds atmospheric pressure, it can exit tissue in the form of bubbles, which often lodge in veins, leading to localized venous obstruction and inflammatory cascades. Patients either present with significant pain (type I) or ascending paresthesias or paralysis (type II). Treatment is the same as for arterial gas embolization. Nitrogen narcosis (D) results from the increased partial pressure of nitrogen in CNS tissue and therefore occurs at significant depth. Symptoms are similar to alcohol intoxication and include altered coordination and impaired judgment.

The ECG demonstrates the presence of J waves or Osborn waves which are seen in hypothermia. One of the first cardiac effects of hypothermia is bradycardia secondary to decreased firing of the cardiac pacemaker cells in cold temperatures. Osborn waves may appear at any temperature below 32°C. The waves are an upward deflection at the terminal portion of the QRS complex. They may represent abnormal ion flux in cold temperatures along with delayed depolarization and early repolarization of the left ventricular wall. As temperatures continue to drop, the ECG will demonstrate prolonged intervals: PR, followed by QRS and then QTc.

Both diabetic ketoacidosis (A) and digoxin toxicity (B) may lead to hyperkalemia. In diabetic ketoacidosis, hyperkalemia develops as a result of the acidic pH in the blood and the transport of hydrogen ions intracellularly in exchange for a potassium ion. Digoxin toxicity poisons the cellular Na+/K+ ATPase resulting in elevated extracellular levels of potassium. The ECG manifestations of hyperkalemia begin with peaked T waves. Multiple other findings eventually develop including a shortened QT interval, ST depression, bundle branch blocks, widened QRS, prolonged PR interval, flattened T wave and ultimately a sine wave. Hyperparathyroidism (C) may lead to hypercalcemia. In hypercalcemia, the ECG shows a shortened QT interval, flattened T waves and QRS widening at very high levels.

Hepatic injury, as denoted by aspartate aminotransferase 2100 U/L, alanine aminotransferase 1900 U/L, is so extremely common in heat stroke that its absence should push one to reconsider the diagnosis. The hallmarks of heat stroke include severe hyperthermia (> 40.5oC) and neurologic dysfunction. Neurologic dysfunction occurs due to a progressive increase in heat stores because of the body’s decreasing ability to perfuse the distal extremities. As the heat stores increase, intracranial pressure increases with a subsequent decrease in cerebral blood flow. There are two types of heat stroke, each with their own patient population and clinical presentation. Classic heatstroke is due to exogenous heat production, while exertional heatstroke is due to endogenous heat production. Patients with classic heat stroke are commonly elderly with chronic diseases or those with limited access to shelter against the heat or oral hydration that present with symptoms usually in the setting of a prolonged, severe heat wave. Patients with exertional heat stroke are commonly young, athletes, or military personnel that present with symptoms after strenuous exercise in the heat. Classic heat stroke patients are usually anhidrotic, while those with exertional heat stroke tend to present diaphoretic. Diagnosis is primarily clinical, though laboratory testing should always be performed, as end-organ damage is common and can help further differentiate the types of heat stroke. Classic heat stroke tends to cause respiratory alkalosis, mild coagulopathies, mild creatinine kinase elevations, and elevated troponin. It is more common to see lactic acidosis, disseminated intravascular coagulation, rhabdomyolysis, and hypoglycemia in those with exertional heat stroke. With a mortality rate of 21–63%, treatment must be immediate and aggressive. Cooling is the mainstay of treatment with the primary goal to maximize evaporative cooling and prevent heat-generating shivering. Antipyretics are not useful in cooling, as they counteract hypothalamic-mediated hyperthermia and not environmental hyperthermia. Alongside cooling, immediate supportive treatment with intravenous fluids, supplemental oxygen, and reversal of coagulopathies should be started.

Acute kidney injury, as denoted by blood urea nitrogen 30 mg/dL, creatinine 1.5 mg/dL (B), and elevated troponin 0.8 ng/mL (D) can occur in classic heat stroke but are rare in exertional heat stroke. Rhabdomyolysis, as denoted by creatinine kinase 2500 U/L (C), is common in exertional heat stroke and less so in classic heat stroke. While each of these laboratory findings is possible in heat stroke, hepatic damage is still the most common finding.

In ANY case of chemical exposure to the eye the first step is irrigation of the eye, and while pH should ideally be measured immediately it should NOT delay irrigation. Note that tetracaine is an acidic substance and if administered prior to pH measurement it may give a false reading.  The pH of this patient’s eye is 8, and the goal pH of the eye should be 7.0-7.4  and irrigation should continue until that is achieved to prevent further liquefactive necrosis in this case (remember that acidic injury causes coagulative necrosis and basic injury causes liquefactive necrosis).  Emergent Ophtho consult is indicated. Once the goal pH is met, the eye should subsequently be stained with fluorescein and examined for any abrasion or ulceration.

This image depicts Seidel’s sign (fluorescein moves away as contents (which appear yellow-green) leak out at site of globe rupture). When a globe rupture is suspected you should avoid any manipulation of the eye (tonometry is contraindicated!). While awaiting emergent ophthalmology consultation for operative repair, a CT orbit should be performed to rule out posterior ocular injury as well as identification of the foreign body. A tetanus vaccine should be documented as up-to-date, as well as prophylactic systemic antibiotics, any pain should be adequately controlled, and anti-emetics provided (to prevent further extrusion of ocular contents due to increased intraocular pressure when vomiting).

Patient is presenting with a Grade I hyphema. Treatment recommendations for a mild hyphema are bed rest, head of bed elevation to encourage layering out of red blood cells and clot formation. Ophtho follow up and discussion of risk of rebleeding from clot contraction are also indicated.  Only severe cases of Grade IV aka “eight-ball” hyphema require surgical drainage/admission.  An exception to this management plan is sickle cell patients, in which a hyphemia is emergent and requires ophtho consultation immediately.  Additionally, anti-coagulation medications may cause or increase risk of developing a hyphema.

Diffuse superficial punctate keratitis (SPK) is usually an acute process arising from contact lens complications, UV exposure from welding or snow blindness, chemical exposure, topical eye medication toxicity, or in extreme dry eye cases. Symptoms include red eye, pain, photophobia, foreign body sensation, +/- mildly decreased visual acuity. Defining features of SPK on fluorescein stain include: pinpoint corneal epithelial defects that enhance. Classically, pain is relieved by the instillation of anesthetic drops, suggesting corneal epithelial involvement.

Non-contact lens wearers with a small amount of SPK should receive artificial tears +/- lubricating ointment. Severe amounts of SPK should also receive topical antibiotics such as erythromycin ointment for 3-5 days. Ophthalmology followup is usually on a non-emergent basis.

Contact lens wearers with a small amount of SPK should discontinue contact lens use until the condition resolves, with artificial tears +/- lubricating ointment. Severe amounts of SPK should also receive topical antibiotics such as fluoroquinolone or tobramycin. Urgent ophthalmology followup should be given.

A hordeolum or stye is an abscess of the eyelid. It presents with pain, erythema, and swelling. Most resolve without intervention. Warm compresses for 15 minutes four times a day may help facilitate drainage. If the hordeolum does not improve in one to two weeks, the patient should be referred to an ophthalmologist for potential incision and drainage or antibiotics.

mnemonic: the Hordeolum is HOT and the Chalazion is COLD, but regardless of what it is warm compress you’ll hold

The hordeolum is an infectious process so will be inflammed and painful, while the chalazion is a painless “cold” cyst, regardless first line treatment is conservative

Retinal detachment’s should be suspected in patient’s with monocular vision loss symptoms. They can be seen in older diabetic patients, however should be suspected in younger patients with trauma such as motor vehicle crashes, skydiving, bungee jumping, and other activities with sudden deceleration forces are risk factors. Patients with myopia (such as this patient) are at higher risk of traumatic retinal detachment. Diagnosis can be made with indirect ophthalmoscopy or ultrasound. Ultrasound will show a discrete hyperechoic retinal line projecting out from the posterior globe.  Patients usually present with painless vision changes, including flashes of light, floaters, or the classic “curtain-like” loss of vision. Retinal detachment is an ophthalmologic emergency and early intervention can prevent worsening of the detachment.

Involvement of the macula is important to determine. If the retinal detachment involves the macula (“mac on”) it is LESS emergent than if the macula is not involved (“mac off”), this is because emergent surgical correction can salvage the macula in a “mac off” situation.

Retinal detachment is usually a thicker line which will not cross over the optic nerve as the retina is an extension of the nerve. This is in comparison to posterior vitreal hemorrhage which appears as a whispy thin line which can cross over the optic nerve. See the video link below.

http://5minsono.com/rdvd/

This patient presents with dacryocystitis and should be treated with oral anti-staphylococcal antibiotics. Dacryocystitis is an acute infection of the lacrimal sac secondary to lacrimal duct obstruction. Given the obstruction of the lacrimal duct, topical abx treatment of the eye alone will not provide penetration into the infected area. It is typically caused by Staphylococcus aureus. Symptoms include swelling, redness, pain and tenderness to palpation over the lacrimal sac. Diagnosis can be aided with a fluorescein stain, aka fluorescein disappearance test, which sill either show lack of clearance of fluorescein dye to the eye over 5 minutes or fluorescein spilling out as tears (normal eye will clear fluorescein in <5 minutes). In addition to oral antibiotics, patients should be treated with warm compresses and gentle massage of the area. Complications of improperly treated dacryocystitis include peri-orbital and orbital cellulitis.

This patient’s fluorescein exam is consistent with a corneal abrasion. It is caused by direct mechanical damage, leading to a partial-thickness corneal injury. Athletes, contact lens wearers, welders, and glass workers may present more often with these injuries. Diagnosis is confirmed when fluorescein dye highlights the usually linear or punctate abrasions. Multiple vertical corneal abrasions may indicate a retained foreign body beneath the eyelid. Corneal abrasion fluorescein exam findings are not to be confused with open globe injuries (streaking of the dye from the site of injury), corneal ulcers (circular patches of dye uptake with ragged, “heaped up” edges), and herpes simplex keratitis (dendritic pattern uptake). Patients commonly present with eye pain and tearing with a usually known mechanism of injury. The mainstay of treatment includes pain control, infection prophylaxis, updating tetanus as needed and preventative care to avoid abrasions in the future. For non-contact wearers prescribe erythromycin ointment, as this does not cover pseudomonal infections, contact lens wearers should be prescribed  ciprofloxacin or tobramycin ophthalmic drops

A lateral canthotomy should be performed in this woman who presents with classic symptoms for a traumatic injury causing retrobulbar hematoma and resultant orbital compartment syndrome. She displays the triad of symptoms including loss of vision, ophthalmoplegia, and proptosis. A retrobulbar hemorrhage from a ruptured infraorbital or ethmoidal artery with intact orbital walls may lead to orbital compartment syndrome. Loss of vision is irreversible 60–100 minutes after the onset of ischemia and so lateral canthotomy and inferior cantholysis should be performed in order to decompress the orbit and preserve vision. Intraocular pressure-lowering agents such as intravenous carbonic anhydrase inhibitors, topical beta-blockers, alpha agonists, and intravenous mannitol are temporizing measures.

This patient has traumatic endopthalmitis. Suspicion should be high in any patient with recent trauma or intraocular surgery and signs/symptoms of infection or with hypopyon (purulent/white layering of fluid in anterior chamber). Manipulation of the eye should be avoided due to concern for globe rupture in this patient (e.g. ocular US/tonometry). A stat CT orbit is indicated to examine for foreign body. Systemic antibiotics are indicated in traumatic endopthalmitis, treatment should be broad-spectrum and common courses include vanc/ceftazidime. While at DRH vanc/cefepime is commonly used to treat various infections, BE AWARE that cefepime has relatively poor penetration into the vitrea and is not recommended. Common pathogens include staph/strep and oddly enough bacillus cereus.  Topical antibiotics alone are insufficient. It is essential to consult ophthalmology as definitive management is generally surgical: vitrectomy and intra-vitreal abx injection.

The patient presents with brisk hemorrhage from the nose with a failed anterior pack suggestive of a posterior nasal bleeding source. The initial management of any patient presenting with epistaxis should focus on the airway and assessment of hemodynamic status. This should be followed by application of direct pressure and localization of the bleeding cause. Anterior epistaxis results from bleeding from Kiesselbach’s area, which can be directly visualized during evaluation. Posterior bleeding usually originates from the nasopalatine branch of the sphenopalatine artery, which cannot be visualized directly. In a patient where a properly placed anterior pack does not control bleeding, placement of a posterior pack should be performed. In the Emergency Department, this is typically performed by placing a Foley catheter into the nares and advancing it into the posterior pharynx followed by inflation of the balloon and application of anterior traction to tamponade bleeding while waiting for ENT to arrive. After placement of a posterior pack, patients should be given prophylactic antibiotics to avoid the development of sinusitis and toxic shock (via colonization of packing material). Patients with posterior packs must be admitted to the hospital and likely require intensive care management. Posterior packing has been shown to decrease partial pressures of oxygen and increase the partial pressure of carbon dioxide. Dysrhythmias, bradycardia and aspiration have been described after posterior packing.

After a properly placed anterior pack fails to control bleeding, placement of a contralateral pack (B) is unlikely to contribute to hemostasis. Similarly, replacing the anterior pack (D) is unnecessary and will delay definitive management. Although the patient will require admission (A) this does not obviate the need to control bleeding emergently in the Emergency Department.

This patient is exhibiting signs and symptoms consistent with cavernous sinus thrombosis. These signs and symptoms are the result of structures affected by cavernous sinus thrombosis. The internal carotid artery passes through the cavernous sinus. The third, fourth, sixth, and portions of the fifth cranial nerves also course through the sinus. This close proximity of veins, arteries, nerves, and paranasal sinuses accounts for the classic presentation of cavernous sinus thrombosis. The clinical presentation is usually due to the venous obstruction as well as impairment of the cranial nerves that are near the cavernous sinus. Headache is the most common presenting symptom and is usually followed by fevers, periorbital edema, and cranial nerve signs. Lateral gaze palsy secondary to an abducens nerve (CN VI) palsy is most common as it lies freely within the sinus while the others course within the lateral walls of the sinus. CST is usually a late complication of an infection of the paranasal sinuses. Cavernous sinus thrombosis is a clinical diagnosis although imaging is often used in cases of diagnostic uncertainty or to confirm the diagnosis. MRI with MR venography (MRV) is the preferred imaging choice as the MRV will show the absence of venous flow in the affected cavernous sinus. Staphylococcus aureus accounts for approximately 70% of all infections.

While the oculomotor nerve (B) and trochlear nerve (D) course through the cavernous sinus and may also be affected in cavernous sinus thrombosis, the abducens nerve lies freely in the cavity and is most commonly affected. The optic nerve (C) is rarely affected due to its location outside of the cavernous sinus.

The patient is complaining of symptoms consistent with iatrogenic tympanic membrane perforation that occurred during disimpaction. Tympanic membrane perforations (TMPs) can result from a complication of infection (acute otitis media, myringitis); blast injury (explosion, slap, lightening); barometric pressure changes (flying in airplane, scuba diving); and improper attempts at wax removal or ear cleaning. The pars tensa is the most common area of the TM to perforate because it is the most anterior and thinnest portion. Patients typically experience decreased or complete hearing loss, pain, and bleeding. In the setting of tympanic membrane perforation, the goal is to keep the ear dry, provide analgesics, and arrange for follow-up with an ENT. Most heal within a few months.

The patient does not require admission (A) to the hospital. ENT care can be arranged for as an outpatient. Traumatic tympanic membrane perforations do not require otic antibiotics (B) unless the ear was contaminated such as from diving in seawater or the rupture is secondary to infection. The patient should receive more than a cotton ball (D) in her ear. Her management should include analgesia and ENT follow-up because complications of tympanic membrane rupture include facial nerve palsy, vertigo, and hearing loss.

This patient has Ménière’s disease. This disorder is associated with increased endolymph within the cochlea and labyrinth. The common triad is tinnitus, vertigo, and unilateral hearing loss (sensorineural). A key finding in Ménière’s disease is fluctuating hearing loss. Episodes are abrupt in onset and associated with nausea and vomiting. There are often long, symptom-free intervals between attacks.

Benign paroxysmal positional vertigo (A) is sudden in onset, short-lived, and positional in nature. It is not associated with tinnitus or hearing loss. Salicylate (aspirin) toxicity (C) is associated with tinnitus and reversible hearing loss. The patient has a history of osteoarthritis and may be using aspirin for her pain; however, salicylate toxicity is usually associated with bilateral hearing loss. Symptoms of vertigo are also uncommon in such patients. Vestibular neuronitis (D) manifests with severe vertigo positional in nature but not associated with hearing loss. It is usually preceded by a viral upper respiratory infection.

Cholesteatoma is a mass of keratinized squamous epithelium that occurs in the middle ear or mastoid process occurring most frequently in teenagers. This ear-related metaplasia is not associated with cholesterol or gallbladder problems, as the name suggests. There are two types of cholesteatoma. The congenital type is less common and occurs medial to the tympanic membrane. The acquired type is more common and grows from the tympanic membrane. Conductive hearing impairment prevails, with imbalance and facial weakness being the most common associated symptoms. Examination may reveal inflammation, retrotympanic waxy appearing polyps or white-pasty discharge from the tympanic membrane. As such, this can easily be confused with chronic, suppurative otitis media. Microscopic excision surgery is required to prevent complications and to maintain or improve hearing.

Acoustic neuromas (A) present with sensorineural, not conductive, hearing impairment. Furthermore, these masses occur in the inner ear and temporal bone on the vestibular nerve and would not likely be viewable during an otoscopic examination. Otitis media (C) presents with otalgia, hearing loss, fever and tympanic membrane abnormalities like erythema, bulging, or cloudiness. Although retrotympanic masses can result from chronic suppurative middle ear infections, current infection is unlikely in the above patient. Squamous cell carcinoma (D) is an epithelial cell malignancy that typically occurs on the external, not middle, ear due to prolonged sun exposure. It has an ulcerated, erythematous appearance with or without bleeding.

This patient is exhibiting signs and symptoms of posterior epistaxis. Posterior epistaxis is less common than anterior epistaxis and is most commonly due to bleeding from the sphenopalatine artery, located at the posterior aspect of the middle nasal turbinate. Patients with posterior epistaxis typically complain of bleeding from both nostrils. Inspection of the posterior pharynx may reveal profuse bleeding. In treating epistaxis, start by having the patient gently blow his nose or suction out the blood. If the bleeding is profuse, apply cotton balls soaked in a topical anesthetic and vasoconstrictor for at least five minutes. A good option is 1% tetracaine plus 0.05% oxymetazoline solution. In posterior epistaxis, this may not achieve hemostasis or allow visualization of the location of bleeding. Management of posterior epistaxis should be with either a Foley catheter or dual balloon pack. A 10 to 14 French Foley catheter with a 30 cc inflatable balloon may be inserted past the site of the bleeding and inflated with 5 to 7 cc of air or saline. It should then be pulled back onto the site of the posterior bleed and inflated until it is snug. An anterior nasal pack should then be placed in both nares. A dual balloon pack is placed by anesthetizing the nare and advancing the pack past the site of the bleeding. The posterior balloon is inflated with 5 to 7 cc of saline or air and pulled back onto the site of bleeding. It is the further inflated until it is snug. The anterior balloon is then inflated. The opposite nare should be packed as well. Complications of posterior epistaxis packing include aspiration, hypoxia, hypercarbia, and symptomatic bradycardia. Antibiotics should be administered after all packing; however, there is significant controversy regarding whether prescribing antibiotics actually prevents toxic shock syndrome as there is no evidence to support this. All patients with posterior packing should be admitted to a telemetry bed for further monitoring while the packing is in place.

The facial artery (A) may be injured during oncologic surgery of the parotid gland or in severe facial trauma. Kiesselbach plexus (B) is the most common source of anterior bleeding. Given that this patient has profuse bleeding that appears bilateral, the source is most likely to be posterior. The labial artery (C) is most commonly injured in children who suffer electrical burns of the commissure of the lip while chewing on electrical cords.

This patient is showing signs and symptoms consistent with necrotizing or malignant otitis externa. Necrotizing otitis externa is defined as the progression of otitis externa through the periauricular tissue and into the temporal bone. It most commonly occurs in immunocompromised or diabetic patients. The causative agent is typically Pseudomonas aeruginosa. Signs and symptoms of necrotizing otitis externa include persistent, excruciating pain that interferes with sleep and continues despite topical treatment. Additional signs and symptoms include fever, erythema of the periauricular tissues, and facial or vagal nerve palsy. Diagnosis of necrotizing otitis externa is by CT of the temporal bone. The key to management is with systemic antibiotics. Antipseudomonal double-coverage is preferred with a penicillin-based antipseudomonal and an aminoglycoside. Ciprofloxacin is a reasonable alternative in patients who cannot take one of these antibiotics. Surgical debridement may be necessary. Mortality is as high as 50% if untreated. Patients should be evaluated by ENT for further management.

Moraxella catarrhalis (A) and Streptococcus pneumoniae (D) are two of the most common causes of otitis media; however, this patient has signs and symptoms of malignant otitis externa given his exam findings with severe persistent pain. Staphylococcus aureus (C) is a common cause of cellulitis; however, cellulitis of the external ear is rare and the edema of the external ear and severe pain are more consistent with necrotizing otitis externa.

In this case, the patient has symptoms concerning for mastoiditis. Mastoiditis is most common in children between 1 and 3 years old. It is a complication of acute otitis media with extension of the infection into the mastoid bone. Patients typically present with ear proptosis, fever, an injected tympanic membrane on the infected side, and postauricular erythema. Organisms involved in this infection are similar to those in otitis media, including Streptococcus pyogenes, Staphylococcus aureus, and Pseudomonas aeruginosa. Diagnosis is confirmed by CT, and consultation with ENT is indicated. If the patient has not taken antibiotics before, the initial treatment is with oral antibiotics if the disease is mild and close follow-up can be ensured. If a patient develops mastoiditis after an appropriate course of oral antibiotics, then admission, ENT consultation, and intravenous antibiotic therapy are warranted. Antibiotics with good gram-positive coverage like ampicillin-sulbactam or third-generation cephalosporins are the first-line choice.

B. This patient has already completed one course of antibiotic therapy, so starting her on a different oral antibiotic is not appropriate. Admission is warranted for more aggressive management.

C. Discharging the patient with instructions for supportive care is not the right course of action, again, because initial antimicrobial treatment failed. Admission and additional antibiotics are needed to treat the acute infection process.

D. At this point in the patient’s care, intravenous antibiotic therapy is the next step. Mastoidectomy should be considered only if intravenous antibiotic therapy fails and the infection spreads beyond the mastoid.

Acute mastoiditis is usually a complication of untreated or inadequately treated acute otitis media. It has also been described as a complication of leukemia, mononucleosis, sarcoma of the temporal bone, and Kawasaki disease. Acute mastoiditis is a natural extension of otitis media because the mastoid air cells are generally inflamed during acute otitis media. The aditus ad antrum is a narrow connection between the middle ear and mastoid air cells. When this is obstructed, there is increased risk for abscess development and bone destruction. Progression results in destruction of the mastoid bone trabeculae resulting in acute mastoid osteitis. Clinically, patients present with otalgia, fever, headache, and erythema. Pain is universally present. Physical exam findings mimic acute otitis media in addition to postauricular or supra-auricular tenderness and edema. Most cases resolve after administration of antibiotics. For persistent cases, surgical intervention is required for drainage.

Orbital cellulitis (A) is a complication of ethmoid sinusitis, not mastoiditis. Otorrhea (C) can occur in mastoiditis (secondary to marked otitis media with ruptured tympanic membrane). However, it is uncommon. Otorrhea is more commonly observed with otitis externa. Trismus (D) is a complication of suppurative parotitis.

The patient has symptoms consistent with acute otitis media. He is a candidate for a “wait-and-see” prescription for an antibiotic if his symptoms do not improve in 48 to 72 hours. He meets the criteria for “wait and see” including age ≥ to 2 years old, unilateral infection, symptoms for fewer than 48 hours, and temperature is less than 39⁰C. Assuming there are no contraindications, amoxicillin (90 mg/kg/day PO for 5-10 days) is the first-line treatment. Amoxicillin-clavulanate is appropriate if the patient has failed a course of amoxicillin. Cephalosporins like cefdinir or cefuroxime or clindamycin are appropriate in penicillin-allergic patients. Streptococcus pneumoniae is the most common bacterial organism, although most cases are viral.

A. Given the tympanic membrane visualized, antipyretics alone are not sufficient if there is no improvement within 48 to 72 hours. Complications from untreated bacterial otitis media include mastoiditis and hearing complications.

B. If the wait-and-see approach fails, the patient should complete a course of antibiotics. Referral to an ENT for possible tympanostomy should only occur after repeated episodes of otitis media.

C. Immediate use of antibiotics has been shown not to improve outcomes when using these criteria. In addition, there is an increased risk of diarrhea and antibiotic resistance for those who take antibiotics.

The patient has thrombotic thrombocytopenic purpura (TTP). The classic pentad of TTP includes CNS abnormalities, renal pathology, fever, microangiopathic hemolytic anemia, and thrombocytopenia. However, diagnostic criteria have recently been simplified to include all adults with microangiopathic or microvascular hemolytic anemia and thrombocytopenia with no other explanation for these findings. TTP shares many clinical and laboratory features of HELLP syndrome. HELLP syndrome is less common before 24 weeks gestation. The derangements in hemoglobin and platelet levels are more severe in TTP. The mainstay of treatment for TTP is plasmapheresis (plasma exchange), which can achieve remission of disease in 80% of patients. If plasmapheresis cannot be immediately performed, fresh frozen plasma (FFP) should be administered until apheresis can be performed.

DDAVP stimulates the release of VWF, Factor VIII, and tissue factor. It may be used in bleeding episodes with mild Hemophilia A and von Willebrand disease. It does not affect Factor IX and so would not help in Hemophilia B. DDAVP does have beneficial effects on platelet function but would not help in the setting of thrombocytopenia.

D-dimer has an NPV of 99% in the diagnosis of DIC. If this test is negative, the clinician can be nearly certain the patient does not have DIC.

This patient most likely has tumor lysis syndrome, characterized by hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia. The tetany (chvostek’s sign of tapping on facial nerve causing muscle twitching) and hyper-reflexia are likely secondary to the hypocalcemia. A uric acid level is the most important test to aid in this diagnosis. Treatment is generally supportive with fluids and correction of electrolyte abnormalities. While hypoparathyroidism can cause low calcium, it will not cause the renal insufficiency seen in tumor lysis syndrome. Neither a CBC nor a peripheral smear are likely to aid in this diagnosis.

The patient in this question has hemolytic uremic syndrome, of which the acute renal failure is the leading cause of morbidity and mortality. If anuric, these patients require plasma exchange therapy, dialysis, and/or monoclonal antibody treatment.

This patient is most likely suffering from leukostasis secondary to blast crisis. The most important treatment in this case is immediate induction chemotherapy. If induction chemotherapy is unavailable, leukaphoresis and hydroxyurea may be used as temporizing measures but the definitive treatment is induction chemotherapy. IV rasburicase is the treatment for severe tumor lysis syndrome.

This patient most likely has AML, which can present with the above gingival findings due to infiltration by tumor cells. Of note, the CBC can vary in patients with AML. Normocytic anemia and thrombocytopenia are common, however the white blood cell count may be low, normal, or elevated. Lymphadenopathy is rare in AML, in contrast to ALL in which it is a common presenting symptom. Definitive diagnosis of AML is by bone marrow biopsy.

Hypercalcemia is generally a product of another underlying disorder and not a primary process in itself. Causes are grouped into four categories: malignancy (primary hematologic, metastases to the bone, or parathyroid producing tumor), hyperparathyroidism, increased intake (milk-alkali syndrome, vitamin D or A toxicity), and increased bone breakdown (immobilization, Paget disease). Clinically, patients experience lethargy, weakness, myalgias, constipation, and anorexia. The clinical presentation is often remembered by the mnemonic “bones, stones, groans and psychiatric overtones.” The first step in treatment is aggressive hydration. The addition of intravenous bisphosphonates (e.g. zoledronic acid) inhibits calcium release from bone. It is usually reserved for hypercalcemia associated with malignancy.

Plasma exchange is the treatment for patients presenting with thrombotic thrombocytopenic purpura (TTP). Patients with this diagnosis have high mortality and should be treated as soon as possible. In a patient with altered mental status, severe thrombocytopenia, and neurologic symptoms, thrombotic thrombocytopenic purpura should be suspected. Patients commonly present with weakness, gastrointestinal symptoms, or neurologic symptoms. Neurologic manifestations may include transient neurologic deficits, confusion, coma, and headache. The classic presentation of fever, renal failure, anemia, thrombocytopenia, and severe neurologic symptoms only occurs in a small percentage of patients. The pathophysiology of TTP involves abnormal platelet aggregation secondary to an abnormality in ADAMTS13, which leads to microangiopathic hemolytic anemia, characterized by schistocytes on blood smear, thrombocytopenia, and end-organ damage.

IV immunoglobulin (A) is the treatment for patients presenting with immune thrombocytopenia (ITP). Patients with ITP will have thrombocytopenia without any clear etiology and therefore should be a diagnosis of exclusion. Patients with ITP will not have evidence of microangiopathic hemolytic anemia or signs of end-organ damage. A lumbar puncture (B) is indicated in a patient suspected to have a CNS infection. In a patient with a normal white blood cell count and no fever, a CNS infection is less likely. Also, the chances of an epidural hematoma would be higher in a patient who has a platelet count of 15 x 109/L. The risks of a lumbar puncture outweigh the benefits in a patient with severe thrombocytopenia and low clinical suspicion for infection. A platelet transfusion (D) is unnecessary in a patient with significant thrombocytopenia unless there is evidence of active bleeding or a procedure is indicated and there is a risk of significant bleeding during the intervention. There is also a potential risk with platelet administration in patients with TTP, since platelet aggregation may worsen as the result of transfusion.

Severe neutropenia is defined as having an absolute neutrophil count less than 500 cells/microL which increases the risk of spontaneous serious bacterial infection. Neutropenia can be inherited or more usually acquired while on chemotherapy. Viral infections can cause transient neutropenia and if discovered incidentally further workup may be indicated. Patients with known severe neutropenia such as a patient with a neutrophil count less than 500 cells/microL in the last week who presents to the emergency department with a fever should be immediately evaluated and started on broad–spectrum antibiotics, even if well appearing. A delay of more than 60 minutes in antibiotic administration to patients with severe neutropenia is associated with an increase in morbidity, mortality, and length of stay.

This patient with sickle cell disease (SCD) presents with acute chest syndrome requiring broad-spectrum antibioticsand intensive care unit (ICU) admission. SCD is a genetically determined disease due to an abnormal allele for hemoglobin beta chains. The end result of this abnormality is a sickled cell that is less deformable and can cause increased viscosity and sludging of the blood. Additionally, cells are sequestered in the spleen and the liver leading to destruction. Patients experience chronic hemolysis, vaso-occlusive events, thrombosis and ultimately, end organ injury. Splenic autoinfarction occurs early in life and makes patients more susceptible to encapsulated organisms such asStreptococcus pneumoniae, Haemophilus influenzae and Neisseria meningitides. Acute chest syndrome is the leading cause of death in SCD and is defined as fever, chest pain, and the presence of new pulmonary infiltrates. Management consists of supportive care, supplemental oxygen if needed, broad spectrum antibiotics, andadmission to the ICU.

The patient in the question stem is suffering from vasoocculsive crisis, or pain crisis of the bones. In adults, this is the most common in the chest, long bones, and back. The mainstay of treatment is narcotics and IV fluids.

Acute cerebrovascular accident is a complication in sickle cell patients due to intravascular sickling and vasoocclusion. It typically manifests as ischemic changes of large intracranial arteries. However, in older patients, hemorrhagic changes can be seen as arterial walls have been weakened from prior infarcts. The ideal treatment is exchange transfusion; it is the most effective method to reduce the percentage of sickled hemoglobin and to reduce intravascular sickling and vasoocclusion. Exchange transfusion also helps minimize the risk of transfusion-associated circulatory overload and associated pulmonary edema, in addition to reduced risk of stroke recurrence. Unfortunately, there are no published evidence regarding the safety and efficacy of thrombolytics in sickle cell patients with acute ischemic strokes. If exchange transfusion is available, this option should be pursued first.

This patient is likely suffering a vasoocclusive pain episode, triggered by a likely viral upper respiratory infection. The provided information does not suggest any life-threatening complications (acute stroke, acute chest syndrome, acute bacterial infection, aplastic crisis, symptomatic anemia) that would require further blood tests or imaging at this time.

For patients who are hypovolemic, IV normal saline resuscitation would be indicated. However, there is no indication in this patient that he is dehydrated. If pain is not adequately controlled with initial PO/IM, then IV pain medication may be attempted.

Acute chest syndrome is the leading cause of death in adult sickle cell patients. It is a syndrome that includes pneumonia, pulmonary infarction, pulmonary embolism, bone marrow infarction, and fat emboli. To make the diagnosis, patient must have consolidation or infiltrate on CXR, and at least 1 of the following symptoms: fever >38.5°C, chest pain, tachypnea, cough, wheezing, or PaO2 <60mmHg. Treatment includes pain control, fluid hydration, antibiotics to cover for both typical and atypical organisms, and oxygen. Bronchodilators may be used, especially if patients already have underlying reactive airway diseases. Glucocorticoids should be avoided as studies have shown rebound vasoocclusion and pain crises following the cessation of steroids.

Although there is limited evidence regarding transfusion therapy in acute chest syndrome, transfusion is considered a mainstay therapy for acute chest syndrome. Some guidelines suggest simple blood transfusion in mild-moderate acute chest syndrome cases, while recommending exchange transfusion in moderate-severe cases.

Mild acute chest syndrome criteria include: O2Sat >90% on room air; segmental/lobar infiltrates involving no more than 1 lobe on CXR; and response to simple transfusion of no more than 2units RBC.

Moderate acute chest syndrome criteria include: O2Sat at least 85% on room air; segmental/lobar infiltrates involving no more than 2 lobes on CXR; and response to transfusion of 3 or more units RBC.

Severe acute chest syndrome criteria include: respiratory failure requiring mechanical ventilation; O2Sat <85% on room air; segmental/lobar infiltrates involving at least 3 lobes on CXR.

Very severe acute chest syndrome criteria include: presence of ARDS or life-threatening lung failure.

Given the initial transcutaneous oxygen saturation 88% on room air, this patient is classified as moderate acute chest syndrome. Hematology should be consulted for transfusion therapy.

Acute dactylitis is the most common presenting symptom for patients with sickle cell disease. It most common occurs in patients 6-18 months of age, and represents bone infarction. It is not an infection.

The genotype HbSC is associated with a higher level of total hemoglobin and a less-severe course; however, these patients are at greater risk for avascular joint necrosis. In patients with HbS beta thalassemia, the severity of disease is determined by the severity of the thalassemia mutation. Patients with mild HbS beta+ thalassemia will have near-normal lives, whereas the natural history of HbS beta0 thalassemia is similar to HbSS.

This patient is most likely suffering from transfusion-related acute lung injury (TRALI), one of the leading causes of transfusion-related mortality. It is most closely associated with platelet and fresh frozen plasma transfusions, though cases have been reported with packed red blood cells since there is some residual plasma in the packed cells. Symptoms begin abruptly during transfusion or within six hours and resemble adult respiratory distress syndrome with noncardiogenic pulmonary edema, dyspnea, hypoxemia, and bilateral infiltrates on chest radiograph. It is thought to be caused by granulocyte recruitment and degranulation. As with all transfusion-associated complications, the transfusion should be stopped immediately and supportive care instituted. Most cases resolve spontaneously.

ABO incompatibility (A) causes intravascular hemolysis of transfused red blood cells, producing hemoglobinemia and hemoglobinuria. The onset is immediate. Symptoms include fever, chills, headache, nausea, vomiting, a sensation of chest restriction, and severe joint pain. ABO incompatibility is most often due to human error. An allergic transfusion reaction (B) can vary in severity from simple pruritus with urticaria to anaphylaxis with wheezing and bronchospasm. This patient’s respiratory symptoms are not bronchospastic in nature. Although TRALI can be confused with acute transfusion-associated circulatory overload (TACO) (C), TRALI is associated with hypotension, whereas TACO is associated with a rapid rise in blood pressure.

Pancytopenia (a reduction in all blood cell lines: erythrocytes, leukocytes, and platelets) with a low reticulocyte count is suggestive of aplastic anemia. The use of medications known to cause bone marrow suppression further suggests drug-induced aplastic anemia. Bone marrow generates pluripotent stem cells that differentiate into red blood cells (erythrocytes), white blood cells (leukocytes), and platelets (thrombocytes). Immature red blood cells are called reticulocytes. When red blood cell production is increased, the erythrocyte count becomes elevated. If this level is reduced, concern is raised about the integrity of bone marrow stem cell production. When red blood cell counts are low (anemia), the hormone erythropoietin is released to accelerate red cell production. Aplastic anemia is a rare type of anemia that is caused by drugs or chemicals in 50% of cases. Drugs that suppress bone marrow production include chloramphenicol, anticonvulsants (e.g., carbamazepine), insecticides, sulfonamides, and gold. Medical conditions associated with aplastic anemia include viral hepatitis, radiation, pregnancy, and autoimmune diseases. Aplasia may affect a single cell line (e.g., pure red cell aplasia) or all cell lines. Symptoms of aplastic anemia may include fatigue, malaise, infection (from neutropenia), or mucosal bleeding (from thrombocytopenia). Bone marrow analysis is needed for definitive diagnosis.

Disseminated bacteremia (A) with certain organisms (e.g., Streptococcus pneumoniae, Neisseria gonorrhoeae) may present with purpura or petechiae. However, these patients are septic with fever, hypotension, lactic acidosis, and usually normal or elevated white blood cell counts and normal red blood cell counts. Disseminated intravascular coagulation (B) is a consumptive coagulopathy with multiple etiologies (e.g., sepsis, trauma, pregnancy, cancer) that can also present with excessive bleeding and petechiae. Thrombocytopenia and schistocytes are characteristic, as well as abnormal coagulation tests. Red blood cell and white blood cell lines are typically unaffected. A type I hypersensitivity reaction (D) is an immunoglobulin E (IgE)-mediated process that results in a massive, abrupt immune response affecting multiple organ systems (e.g., skin, respiratory, circulatory). Anaphylaxis is an example.

Sacroiliitis is an inflammatory disorder of the sacroiliac joint in the posterior pelvis. It is a feature of spondyloarthropathies such as ankylosing spondylitis. Patients may present with low back pain or pain in the buttock or leg. There is tenderness to palpation of the sacroiliac joint but no pelvic instability. Patients with ankylosing spondylitis are usually men less than 40 years of age and often report back pain and stiffness that is worse upon waking up and improves with activity throughout the day. Plain films of the spine may demonstrate “squaring” of the vertebral bodies (bamboo spine). Referral to a rheumatologist and treatment with nonsteroidal anti-inflammatory drugs (NSAIDs) are recommended. Emergent causes of low back pain (e.g., spinal cord compression, spine infection, trauma) should be considered and screened with directed history and physical examination. Concerning features of back pain include history of trauma, recent surgery, intravenous drug use, old age, history of cancer, fever, focal neurologic deficits (e.g., weakness, numbness), urinary or bowel dysfunction, and unexplained weight loss. Patients with these features should be worked up for emergent causes of back pain such as malignancy, cord compression, or infection with advanced imaging, blood cultures, and potentially consultation to a spine surgeon.

Central cord syndrome (A) is the most common spinal cord syndrome and presents with upper extremity weakness greater than lower extremity weakness. It is caused by extreme neck extension. Pott’s disease (B) is vertebral osteomyelitis. Patients usually present with fever and other signs of infection such as tachycardia, leukocytosis, and erythema overlying the area of infection. A psoas abscess (C) is an infected fluid collection of the iliopsoas muscle compartment. Patients are usually ill-appearing and septic with fever and back pain, flank pain, or lower abdominal pain that does not improve throughout the day.

Fluoroquinolone drugs, including levofloxacin, have been associated with spontaneous tendon ruptures. Fluroquinolones are a commonly prescribed antibiotic class. The class includes ciprofloxacin, moxifloxacin and levofloxacin. The fluoroquinolone class of drugs has a number of side effects, the most serious of which are prolongation of the QTc and spontaneous tendon rupture. Tendon rupture appears to be more common in older patients. The overall risk is between 0.1 – 0.4%. These drugs are discouraged for use in pregnant women and children secondary to their effect on cartilage.

Sciatica is a lumbosacral radiculopathy that is caused by compression of the spinal nerve root(s). 90% of all cases are due to disc herniation, although spinal stenosis, spondylolisthesis, and piriformis syndrome are other notable causes. Symptoms typically develop suddenly during physical activity and consist of back pain radiating down the leg, though the pain may radiate bilaterally. Weakness and numbness in the affected limb may also be present. The straight leg raise (SLR) is a good screening test for sciatica with 92% sensitivity and 28% specificity. The patient’s affected leg is extended and passively elevated. Pain elicited in a sciatic nerve distribution past the knee indicates a positive test. Pain elicited in the back alone is not considered positive. The crossed straight leg raise compliments the straight leg raise well in that it has a sensitivity of 28% and specificity of 90%. The crossed straight leg raise is performed by passively elevating the extended unaffected leg. A positive test is signified by pain evoked in a sciatic nerve distribution in the affected leg. Atraumatic sciatica does not necessitate imaging. Imaging should be sought when there is concern for infection or malignancy or when significant neurologic deficits are present (e.g., marked weakness, numbness, or bowel/bladder dysfunction). MRI is the preferred imaging modality in these cases. Treatment of sciatica is largely symptomatic with the use of non-narcotic analgesics, preferably nonsteroidal anti-inflammatory drugs, and activity as tolerated. Steroids and neuropathic pain medications have not shown significant efficacy in sciatica. With conservative management, most patients’ symptoms resolve after six weeks. Surgical treatment via discectomy is reserved for patients who have failed conservative management. However, while studies have shown short-term improvement in pain control after surgery, no difference in long-term pain control has been found between conservatively and surgically managed patients.

Crossed leg raise alone (A) has good specificity, but poor sensitivity. Crossed straight leg raise and straight leg raise (B) should be used together, however the straight leg test has the highest sensitivity and the crossed straight leg raise has the highest specificity. Straight leg raise alone (C) has good sensitivity, but poor specificity.

This young patient with low back pain and morning stiffness that improves with exercise most likely has ankylosing spondylitis. Ankylosing spondylitis is an inflammatory arthritis that primarily affects the spine and is associated with human leukocyte antigen (HLA-B27). Diagnosis is made using a combination of clinical symptoms, lab testing, and radiographic findings suggestive of sacroiliac joint pathology. Classically, X-ray imaging shows fusion of vertebrae (“bamboo spine”) as the peripheral fibers of the intervertebral annulus fibrosus discs ossify. However, symptoms can be present up to 10 years before radiographic evidence of the disease is apparent. Patients generally present with arthritic symptoms most apparent in the lower back, but can also have enthesopathy (as in this patient’s Achilles tendon pain), uveitis, and fibrosis of the upper lobes of the lung. The sacroiliac joint can be tested by flexing, abducting, and externally rotating one leg (FABER test). If pain is elicited on the posterior, contralateral side, it is suggestive of sacroiliac joint pathology. If pain is elicited on the anterior, ipsilateral side, it is suggestive of pathology within the hip. The mainstay of treatment is nonsteroidal anti-inflammatory drugs (NSAIDs) along with tumor necrosis factor antagonist medications.

Osteoarthritis (B) can also cause back pain, but generally affects older patients and usually improves with rest rather than worsening. The sacroiliac joints are rarely affected. Rheumatoid arthritis (D) can cause arthritic pain in younger individuals with morning stiffness, but usually affects small joints (hands, feet, and cervical spine). Osteofibrous dysplasia (C) is a fibrovascular defect of the long bones that leads to replacement of cortical bone with fibrous tissue. The disease is usually painless and spinal involvement is extremely rare.

Rhabdomyolysis is the result of the breakdown of skeletal muscle releasing the intracellular contents into the bloodstream. In minor cases, patients are asymptomatic but with severe cases the condition is life threatening with severe electrolyte disturbance and renal failure. The ultimate final pathway in rhabdomyolysis is the accumulation of intracellular cytoplasmic calcium which leads to myocyte destruction. This occurs as a result of direct cell membrane damage and ATP depletion. The hallmark of diagnosis is the presence of elevated serum creatine kinase and myoglobinuria. Management of rhabdomyolysis involves treating or removing the underlying cause, correcting electrolyte abnormalities and prevention of renal failure. Intravenous fluid administration is the mainstay of therapy titrating to a goal urine output of 3 mL/kg/hr.

Standard therapy used to include alkalinization of both serum and urine with the administration of sodium bicarbonate. An alkaline pH of the urine (A) above pH of 6.5 is the goal in alkalinization. This is not achieved with intravenous normal saline as described in the vignette. Intravenous fluid should be continued until clearance of the plasma creatine kinase. Precise guidelines do not exist, but the goal CK should be a level less than 1000 U/L, not 15,000 U/L (B). A creatinine less than 1.0 mg/dL (C) is not a standard goal of hydration for rhabdomyolysis. If renal failure is present, hydration will continue until improvement although no specific value is identified as the target.

The subacromial space is an area between the coracoacromial arch and the greater tuberosity of the humerus. It contains the long head of the biceps tendon, the supraspinatus tendon, and the subacromial bursa. Subacromial bursitis is most often an overuse injury due to chronic impingement. Patients who participate in frequent overhead activity are most at risk. The most common complaints are pain with overhead movement and difficulty finding a comfortable position at night due to pain. On physical examination, they likely will have a positive Neer impingement sign (pain with arm in 180 degrees forward flexion, followed by internal rotation) and Hawkins impingement sign (pain with arm in 90 degrees abduction, elbow flexed at 90 degrees, followed by internal rotation). Initial treatment is conservative with rest, nonsteroidal anti-inflammatory drugs and activity modification. Some patients may need additional physical therapy or a subacromial bursa steroid injection. Those with continued pain may proceed to further imaging with ultrasound or MRI and consideration of decompression surgery with orthopedics.

Acromioclavicular separation (A) involves partial or complete tearing of the acromioclavicular and coracoclavicular ligaments. It follows an injury to the shoulder, most often a direct or blunt hit to the shoulder. On examination, there is often a notable deformity at the AC joint along with associated tenderness to palpation. Adhesive capsulitis (B) or “frozen shoulder” is an inflammatory reaction within the capsule and synovium of the glenohumeral joint. It results in significant global loss of active and passive range of motion of the shoulder (forward flexion, abduction, external rotation and internal rotation). It can occur following an injury or spontaneously in those with autoimmune disorders such as diabetes or hypothyroidism. Full-thickness supraspinatus tear (C) most often occurs following an acute injury and presents with an inability to abduct the arm and a positive empty can test (unable to hold arm in 90 degrees of abduction with internal rotation).

Rhabdomyolysis is the breakdown of striated muscle resulting in release of intracellular contents into the extracellular fluid and circulation. This can result in a spectrum of disease severity ranging from asymptomatic elevation of muscle enzymes to life-threatening electrolyte imbalances, acute renal failure, multiorgan failure, and death. There are several causes of rhabdomyolysis such as exertion, drugs and toxins, trauma, infections, electrical current, hypoxia, hyperthermia, or metabolic disorders. However, in the United States, it occurs most often due to prolonged muscle compression in the intoxicated patient who lays motionless or in the elderly with dementia following a fall. Patients classically present with complaints of muscle weakness, myalgias, and tea-colored urine. Physical examination may reveal muscle weakness, tenderness and swelling, or skin color changes, such as blistering or discoloration. Compartment syndrome should be considered if the exam reveals a firm compartment, pain on passive extension, and neurovascular compromise. The diagnosis of rhabdomyolysis can be made with a creatine kinase level greater than five times normal. Other laboratory abnormalities may include an elevated serum myoglobin, myoglobinuria, large blood on urinalysis with the absence of red blood cells, hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, and hypoalbuminemia. The mainstay of treatment is with high volumes of normal saline to maintain a urine output of 200 to 300 mL/hr. Urine alkalinization theoretically enhances renal myoglobin clearance and can be achieved by adding bicarbonate to the intravenous fluids to maintain a urine pH greater than 6.5. This can be used as an adjunct, however, there are potential adverse effects such as hypernatremia, fluid overload, and exacerbation of hypocalcemia.

Elevated creatinine (B) may be seen in rhabdomyolysis that is complicated by acute renal failure, however, it is not diagnostic. Hypokalemia (C) is not diagnostic of rhabdomyolysis. Potassium levels are typically elevated in rhabdomyolysis. Large blood on urinalysis with red blood cells present (D) is not diagnostic of rhabdomyolysis, however, large blood on urinalysis with the absence of red blood cells is diagnostic of rhabdomyolysis and is due to myoglobinuria.

Pain with passive stretch of the effected compartment is the most common symptom early in compartment syndrome. Compartment syndrome develops when pressure builds within a confined anatomical space. Increasing pressure leads to decreased perfusion compromising tissue. Tissue ischemia eventually leads to death of muscle, nerve and bone tissue. Although it is typically associated with major trauma and crush injuries, it can develop after a relatively minor injury. Any compartment that is prescribed by fascial planes can develop compartment syndrome. However, the lower extremities are the most common location due to their higher risk for injury and their relatively low-volume compartments. Long-bone fractures account for 75% of all traumatic compartment syndromes. Patients will present with pain that is often out of proportion to examination.

Although pallor (B), parasthesias (C), pulse deficit (D) and paralysis are four of the classic symptoms, pain with passive stretch of the muscles involved is the most common early finding. Early recognition is key as prompt decompression can be limb saving.

Grade IA recommendation is for early activity and to avoid bed rest (by RCT).

The first choice for patients with mild to moderate back pain should be acetaminophen or a nonsteroidal anti-inflammatory drug (NSAID) like ibuprofen or naprosyn. In patients with severe pain, opiate medications may be necessary. However, it is important to note that no studies have demonstrated the superiority of one pain medication (or class of medication) over another in the treatment of back pain. Patients with milder symptoms should initially be treated with acetaminophen or an NSAID. These medications are well tolerated in short courses with minor side effects. NSAIDs have not been shown to be superior to acetaminophen.

Pseudogout generally affects middle-aged and elderly patients. Pseudogout is a type of crystal-induced synovitis that is caused by calcium pyrophosphate crystals. These crystals are positively birefringent and are rhomboid shaped. Patients will present complaining of joint pain, swelling, and redness. Joints most commonly affected are the knee, wrist, ankle, and elbow. Pseudogout is a type of inflammatory arthritis that is diagnosed and confirmed by synovial fluid analysis. Synovial fluid for an inflammatory arthritis will have a white blood cell count between 200 and 50 000 with a predominance of neutrophils (generally greater than 50%). The appearance of the synovial fluid will be cloudy and yellow with positive birefringent, rhomboid shaped crystals. Treatment includes the use of nonsteroidal anti–inflammatory drugs and opioid analgesics. Corticosteroids are an option in patients with a history chronic kidney disease or patients the provider thinks may be of benefit. Avoid corticosteroids in uncontrolled diabetics given the risk of worsening hyperglycemia. Colchicine is not routinely used due to its side effect profile, however, it may be used in refractory cases or in cases where NSAIDs and corticosteroids cannot be used.

Gout (A) is also a type of inflammatory crystal-induced synovitis, however, it is caused by uric acid crystal deposition. Gout generally affects middle-aged and elderly patients. Uric acid crystals are needle shaped and are negatively birefringent. Patients will present complaining of arthritis, edema, and erythema. The joints most commonly affected are the great toe, tarsal joints, and knee. Synovial fluid analysis will be similar to pseudogout, as both are an inflammatory arthritis. Differentiating the two is based on the characteristic crystal formation. Thus, crystal analysis is imperative to the correct diagnosis. However, treatment remains the same as with pseudogout and so synovial fluid analysis is performed more to rule out septic arthritis. Osteoarthritis (B) is a symmetric and chronic polyarticular joint disease distinguished by the lack of constitutional symptoms. Patients may present with acute exacerbations of monoarticular pain that consists on joint pain and inflammation. Synovial fluid analysis will demonstrate a white blood cell count of less than 200 cells with fewer than 25% neutrophils. The synovial fluid will be have a clear and transparent appearance without crystals. Treatment consists of rest and analgesics. Septic arthritis (D) is a condition that can rapidly lead to irreversible joint destruction if not recognized and treated. Patients will typically present with a monoarticular arthritis and may have associated fever, chills, and malaise. Septic arthritis should be differentiated from periarticular processes such as cellulitis, bursitis, and tendinitis. A true arthritis will produce pain that is exacerbated through active and passive range of motion. Synovial fluid analysis for septic arthritis will demonstrate a significantly elevated white blood cell count typically greater than 50 000 cells with a predominance of neutrophils (greater than 50%). The synovial fluid will be cloudy and yellow in appearance. Admission for parenteral antibiotics and repeated needle aspiration, arthroscopy, or open surgical drainage is required.

Septic arthritis is a bacterial or fungal infection of a joint typically spread hematogenously unless there is direct bacterial contamination. The synovium is highly vascular and lacks a basement membrane making it susceptible to bacterial seeding. Certain conditions predispose individuals to septic arthritis including diabetes, sickle cell disease, immunocompromise, alcoholism or pre-existing joint disease like rheumatoid arthritis or gout. Fever is present in less than half of cases of septic arthritis so with clinical suspicion an arthrocentesis is indicated. The knee is the most common joint affected and patients have pain (especially on passive range of motion) and decreased range of motion often accompanied by warmth, erythema and fever. This patient may have an acute gouty flare, but the clinician must exclude an infection. On joint fluid analysis, the white blood cell count of a septic joint is typically > 50,000.

Indomethacin (B) is a non-steroidal anti-inflammatory agent commonly used in the treatment of acute gout. Gout is arthritis caused by deposition of monosodium urate monohydrate crystals in the joint space. Acute flares involve a monoarticular arthritis with a red, hot, swollen and tender joint. Acute episodes of gout result from overproduction or decreased secretion of uric acid. However, measurement of serum uric acid (C) does not correlate with the presence or absence of an acute flare. A radiograph of the knee (D) may show chronic degenerative changes associated with gout but will not help to differentiate gouty arthritis versus septic arthritis.

Septic Arthritis

• Patient will be complaining of fever, monoarticular pain with decreased ROM
• Labs will show WBC > 50,000 with > 75% PMNs
• Diagnosis is made by arthrocentesis
• Most commonly caused by:
  • Age < 35: N. gonorrhea, S. aureus overall
• Treatment is IV ABX, surgical washout

Allopurinol therapy should never be initiated until an acute attack has subsided. Allopurinol is a xanthine oxidase inhibitor that decreases uric acid production but also produces a more soluble metabolite. Allopurinol is therefore effective regardless of the cause of the hyperuricemia. Gout is caused by deposition of uric acid crystals in the synovium, bursae, tendon sheaths, skin, heart valves, and kidneys, which can lead to arthritis, tophi, renal stones, and gouty nephropathy. Typically, patients present with acute, exquisitely tender, monoarticular arthritis. The joint is usually warm and erythematous. The first metatarsophalangeal joint (MTP) joint is most commonly affected. Detecting negatively birefringent, needle-like crystals in the synovial fluid from an arthrocentesis confirms the diagnosis. First line treatment are NSAIDs. Indomethacin has traditionally been the NSAID of choice, but any NSAID can be used with similar efficacy.

Ethanol metabolism blocks renal excretion of uric acid which increases the risk for developing gouty arthritis. However, allopurinol is not contraindicated in individuals who consume ethanol (B). Hyperuricemia (C) is present (usually >8 mg/dL) in the gout patient, and when symptomatic, these patients should be treated. Colchicine (D) can be used in combination with allopurinol to help decrease the likelihood of a gouty flare while the uric acid level is decreasing after an acute attack has subsided. Colchicine decreases inflammation associated with lactic acid production and phagocytosis of urate; it terminates most gouty attacks within 6 to 12 hours but is limited by GI side effects.

Gout

• Patient will be a middle-aged man
• Complaining of acute onset of pain in the first MTP (Podagra)
• Labs will show needle-shaped crystal with negative birefringence
• Most commonly caused by uric acid crystals
• Treatment is:
  • Acute: NSAIDs, steroids, colchicine 
  • Chronic: allopurinol or colchicine
• Comments: Can be triggered by loop and thiazide diuretics

The correct answer is disseminated gonorrhea. The skin lesions above are hemorrhagic pustules which are essentially pathognomonic for gonorrhea.

The correct answer is admission and ortho consult. While this patient’s arthrocentesis is consistent with pseudogout due to the presence of rhomboid crystals, this can certainly occur in conjunction with a septic arthritis. In fact, gout and pseudogout patients are at higher risk for bacterial infection of their joints.

The correct answer is anserine bursitis. The anserine bursa is located on the medial aspect of the knee 2-3 inches below the joint, and can become inflamed due to trauma, gout, or repeated stress. Treatment is generally conservative with rest, ice, elevation, and NSAIDS.

The correct answer is slipped capital femoral epiphysis. A Klein line is a line drawn on an AP film along the superior aspect of the femoral neck.  It should pass through a portion of the femoral head.  If it does not, this is consistent with SCFE.

The correct answer is positively birefringent crystals. This x-ray demonstrates chondrocalcinosis, or calcium deposition in the joint space, diagnostic of pseudogout (calcium pyrophosphate crystals). Negatively birefringent crystals are caused by uric acid crystals in gout. Fat globules can be seen in fractures, and an elevated WBC count would be expected in a septic joint. This is certainly possible in this patient as any gouty arthritis increases the risk for septic joint, however the more likely finding is calcium pyrophosphate crystals.

This patient’s mechanism of injury as well as the significant ligamentous laxity is concerning for a knee dislocation.  CT angiography should be performed to rule out a popliteal artery injury.