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About Andrew Mittelman, MD

Assistant Professor of Emergency Medicine
Boston Medical Center

SAEM Clinical Images Series: Doubly Double Vision

palsy

A 52-year-old female with a past medical history of hypertension and prediabetes presented to the emergency department with double vision that started one day prior to arrival. She stated that her double vision improved when she closed one eye. She denied trauma, headache, neck pain, dizziness, dysphagia, numbness, tingling, weakness, or gait instability.

 

Vitals: BP 181/119; HR 76; RR 18; T 98.4°F; O2 saturation 96% on room air

General: No acute distress, well-appearing

Neurologic: AOx3; Following commands. Speech without dysarthria. PERRLA. EOM: incomplete abduction of the L and R eye. No facial asymmetry. Tongue protrudes midline. No pronator drift. 5/5 strength in all extremities. Sensation is intact throughout. Finger to nose is normal. Gait is narrow and steady.

None

Cranial nerve 6 (CN VI), also known as the abducens nerve, is responsible for ipsilateral eye movement. CN VI palsy presents clinically with the inability to abduct the eye resulting in horizontal diplopia. Patients often present complaining of double vision that is worse with lateral gaze. Other symptoms on presentation may include headache, nausea, vomiting, hearing loss, and recent viral symptoms. CN VI is typically diagnosed clinically by an inability to abduct the eye. It is the most common oculomotor palsy in adults and can be caused by damage anywhere along the course of the abducens nerve. Etiologies in adults include ischemia, trauma, neoplasm, demyelinating lesions, increased intracranial pressure, and infection. Risk factors include microvascular disease such as hypertension and inflammatory conditions. Bilateral CN VI nerve palsy without associated intracranial abnormalities is rare. Importantly, abducens nerve palsy is the second most common oculomotor palsy in children and a frequent presenting sign of an intracranial tumor. Children with CN VI palsy should be evaluated for ataxia and other gait disturbances which may indicate a brainstem glioma.

Depending on the presenting symptoms and medical history, the workup should include an MRI/MRA brain to evaluate for microvascular ischemia and cerebrovascular accident. Treatment of CN VI palsy should be targeted at the underlying cause. In cases of CN VI palsy due to microvascular ischemia, symptoms often self-resolve. In children, treatment includes alternating patching of the eyes, but this has not been shown to be effective in adults.

Take-Home Points

  • CN VI palsy is the most common oculomotor palsy in adults and presents with an inability to abduct the eye.
  • Treatment of CN VI palsy should target the underlying pathology which may include infection, trauma, neoplasm, or increased intracranial pressure.
  • CN VI palsy in children may indicate an intracranial tumor and workup should include a full neurologic examination and intracranial imaging when appropriate.

  • Graham C, Gurnani B, Mohseni M. Abducens Nerve Palsy. 2023 Aug 24. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan–. PMID: 29489275.

    Merino P, Gómez de Liaño P, Villalobo JM, Franco G, Gómez de Liaño R. Etiology and treatment of pediatric sixth nerve palsy. J AAPOS. 2010 Dec;14(6):502-5. doi: 10.1016/j.jaapos.2010.09.009. PMID: 21168073.

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Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2024-09-28T21:34:14-07:00Oct 7, 2024|Neurology, SAEM Clinical Images|
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SAEM Clinical Images Series: Didn’t See That Coming

hyphema

A 23-year-old healthy male presented to the emergency department with left eye pain, soreness, and blurry vision after being hit in the left eye with a Nerf gun bullet two days prior. He had no prior ophthalmologic history and does not wear corrective lenses.

Left eye: Visual acuity 20/30. Intraocular Pressure 17. Pupil 3mm, irregular, minimally reactive. Slit lamp exam revealing 3+ RBCs, vertical layering of blood along the nasal aspect.

None

Vertical hyphema

Blunt trauma induces shearing forces upon the vasculature of the ciliary body and iris, resulting in the accumulation of red blood cells (RBCs) in the anterior chamber. This space normally contains only clear, aqueous humor. RBCs slowly settle to the bottom of the anterior chamber in a gravity-dependent manner. Classically this develops in a horizontal pattern, but patients who subsequently sleep on their side may experience vertical hyphema formation. Although trauma is the most common etiology, hyphema can occur due to any hematologic abnormality. It is a frequent complication of sickle cell disease. As in all cases of ocular trauma, globe rupture must be immediately ruled out before proceeding with a comprehensive ophthalmologic examination.

The patient had a Grade I hyphema.

Grade 0: No visible layering, but red blood cells within the anterior chamber (microhyphema)

Grade I: Layered blood occupying less than one-third of the anterior chamber

Grade II: Blood filling one-third to one-half of the anterior chamber

Grade III: Layered blood filling one-half to less than total of the anterior chamber

Grade IV: Total filling of the anterior chamber with blood (also known as 8-ball hyphema)

Take-Home Points

  • A hyphema is a collection of blood in the anterior chamber of the eye.
  • Before measuring intraocular pressure, remember to inspect the anterior ocular anatomy with consideration for globe rupture. If this is not excluded, avoid tonometry as it can cause extrusion of aqueous humor and further damage to the globe.
  • Blunt trauma is the most common cause of hyphema. However, non-traumatic hyphema should prompt investigation for hematologic disorders such as Sickle cell disease.

  • Brandt MT, Haug RH. Traumatic hyphema: a comprehensive review. J Oral Maxillofac Surg. 2001 Dec;59(12):1462-70. doi: 10.1053/joms.2001.28284. PMID: 11732035.
  • Gragg J, Blair K, Baker MB. Hyphema. 2022 Dec 26. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan–. PMID: 29939579.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2024-09-28T21:19:11-07:00Sep 30, 2024|Ophthalmology, SAEM Clinical Images|
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SAEM Clinical Images Series: Below the Chin, Badness Lies Within

neck swelling

A 50-year-old male with insulin-dependent Type 2 Diabetes presented to the emergency department with three days of pain and swelling on the right side of his neck. He endorsed progression of his symptoms, reporting that he was now having fevers, myalgias, and intermittent difficulty swallowing solid foods.

 

Vitals: BP 153/96; HR 110; T 100.0°F; RR 16; O2 sat 97%

General: Appears uncomfortable

HEENT: Mild right-sided facial swelling. No trismus. No gingival inflammation or swelling or induration to suggest abscess. There is focal swelling and tenderness to palpation, without overlying erythema, throughout the right submandibular triangle, and along the sternocleidomastoid.

MSK: Limited active right shoulder range of motion secondary to pain

WBC: 10.4

Hgb: 14.4

Plts: 213

Na: 131

K: 3.7

A1C: 13

Lemierre syndrome (LS) is a rare complication of bacterial pharyngitis/tonsillitis and involves an extension of the infection into the lateral pharyngeal spaces of the neck with subsequent septic thrombophlebitis of the internal jugular vein (as seen on CT). Patients may present with trismus, dysphagia, and fever. Due to the possibility of widespread septic emboli, patients may experience sequelae of systemic infection with dyspnea, focal neurologic deficits, and abdominal pain. Treatment consists of prompt antibiosis and rapid source control.

Most cases of bacteremia in Lemierre syndrome are caused by Fusobacterium necrophorum, an anaerobic gram-negative rod that colonizes the oropharynx. This bacterium causes platelet aggregation and thrombus formation through hemagglutinin production and direct activation of the coagulation cascade. However, up to one-third of patients are found to have a polymicrobial infection with streptococcus and staphylococcus species frequently present.

Take-Home Points

  • Lemierre syndrome (LS) is a rare infection. However, the incidence of LS has been increasing in recent decades due to more judicious use of antibiotics for pharyngitis.
  • A high index of suspicion must be maintained to diagnose Lemierre syndrome, with special attention to alternative diagnoses such as Ludwig angina, retropharyngeal abscess, or meningitis.
  • A thorough investigation of associated symptoms is imperative as these may represent sequelae of septic emboli.

  • Foo EC, Tanti M, Cliffe H, Randall M. Lemierre’s syndrome. Pract Neurol. 2021 Oct;21(5):442-444. doi: 10.1136/practneurol-2021-002928. Epub 2021 May 7. PMID: 33963085.
  • Forrester LJ, Campbell BJ, Berg JN, Barrett JT. Aggregation of platelets by Fusobacterium necrophorum. J Clin Microbiol. 1985 Aug;22(2):245-9. doi: 10.1128/jcm.22.2.245-249.1985. PMID: 4031037; PMCID: PMC268368.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2024-09-06T22:10:20-07:00Sep 20, 2024|ENT, Infectious Disease, SAEM Clinical Images|
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SAEM Clinical Images Series: Bulge in the Belly

bulge

A 45-year-old male status-post right nephrectomy secondary to a renal mass presented to the emergency department with right-sided flank pain. He endorsed low-grade intermittent right-sided flank pain since the nephrectomy one year prior, associated with an increasingly enlarging mass extending laterally from his right abdomen. Over the course of the past several days, the mass had become larger and more painful. He denied any fevers, chills, or signs of systemic illness, and reported no urinary symptoms.

Vitals: T 98°F; HR 88; RR 17; BP 121/67; SpO2 97% on RA

Respiratory: Clear to auscultation in all lung fields. No diminished breath sounds in the right lower lobe.

Abdomen: Soft, non-tender to palpation. 10 cm mobile, non-erythematous mass protruding from the right flank.

White Blood Cell (WBC) Count: 5.5 K/uL

BUN: 10 mg/dL

Creatinine: 0.88 mg/dL

Lactate: 1.1 mmol/L

Urinalysis (UA): WBC 0-5, Neg Bacteria, Neg Nitrites, Neg Leukocyte Esterase, Neg Ketones

The major risk factor that predisposes patients to the development of abdominal wall hernias is a decrease in the strength of the abdominal wall musculature. Additionally, cardiovascular co-morbidities, such as obesity, hypertension, and diabetes, can increase the risk. Urologic procedures predispose patients to flank hernias in particular due to the postoperative weakening of the muscular wall. The patient in question had a right-sided nephrectomy, which likely predisposed him to the development of this hernia (Figure 1).

The critical complications that can develop secondary to a hernia are incarceration and strangulation (which can result in subsequent necrosis). Initial management focuses on a rapid assessment to evaluate for these complications, while also providing pain control. Incarcerated hernias are erythematous, edematous, tender to palpation, and unable to be reduced. If strangulated, patients will additionally have signs of peritonitis. Ancillary laboratory tests, such as an elevated lactate, may also suggest ischemia secondary to strangulation. CT imaging should be acquired in cases of suspected incarceration or strangulation (Figure 2: CT showing right-sided abdominal wall hernia containing fat and non-obstructed bowel loops without evidence of strangulation). Patients without evidence of emergent hernia complications can be managed with outpatient surgical follow-up.

Take-Home Points

  • Abdominal wall hernias are classified by their location: ventral, groin, pelvic, and flank.
  • Major risk factors for their development include prior abdominal surgeries that weaken the musculature as well as cardiovascular co-morbidities.
  • Evaluation should include a physical exam, laboratory work (particularly a complete blood count, comprehensive metabolic panel, and lactate), and CT Abdomen/Pelvis.
  • If an incarcerated or strangulated hernia is suspected, surgery should be consulted emergently.
  • Hernias that can be reduced at the bedside can be managed with outpatient surgical follow-up.

  • Pastorino A, Alshuqayfi AA. Strangulated Hernia. 2022 Dec 19. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 32310432.
  • Zhou DJ, Carlson MA. Incidence, etiology, management, and outcomes of flank hernia: review of published data. Hernia. 2018 Apr;22(2):353-361. doi: 10.1007/s10029-018-1740-1. Epub 2018 Jan 27. PMID: 29380158.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2023-12-05T20:31:20-08:00Dec 8, 2023|Gastrointestinal, SAEM Clinical Images|
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SAEM Clinical Images Series: Man with a Recurrent Rash

rash

A 33-year-old male presented to the emergency department with a diffuse pruritic rash that appeared several days after starting Trimethoprim/Sulfamethoxazole (TMP-SMX) for a dental infection. Initially beginning on the torso and low back, the rash spread to the palms, soles, and genitalia. Progression stopped after discontinuing TMP-SMX. He conveyed a remote history of a similar rash following use of an unknown medication, and noted that several of the current lesions arose at the same location as previous.

 

Skin: Widely distributed violaceous, non-blanching patches with a dusky center. Lesions ranged from 3 cm to 10 cm, and included palms and soles. There was no mucosal involvement.

Non-contributory

Fixed drug eruption (FDE). FDE is an uncommon, potentially life-threatening CD8+ T-helper cell-mediated hypersensitivity reaction to certain drugs, commonly NSAIDs, antibiotics, and antiepileptic [1].

Skin findings typically arise within two days of exposure and then more rapidly with subsequent exposures [2]. Characteristically, recurrent lesions appear at the same sites as prior lesions (hence “fixed”) but may arise in additional locations. The rash is classically divided into two phases: an acute phase of pruritic violaceous patches and plaques with central duskiness, followed by a residual phase of hyperpigmentation that can last several months. The sulfonamide moiety of TMP-SMX is a common cause of FDE [3]. Management of FDE anchors on identification and discontinuation of the causative agent. The majority of cases involve five or fewer lesions, however generalized or bullous cases (> 10% total body surface area, or involvement of 3 or more anatomic sites) [1], may require aggressive wound care and carry a mortality rate up to 22% [4]. Topical or systemic steroids are common adjuncts and there is limited evidence suggesting the utility of systemic cyclosporine for severe cases [1]. Patients need to be carefully advised on the risks of specific medication use and can expect a gradual resolution of lesions over the coming months.

Take-Home Points

  • FDE is a potentially life-threatening hypersensitivity reaction to certain drugs.
  • Recurrent lesions in similar distribution is a hallmark of FDE. Avoidance of the causative agent is the mainstay of management.

  1. Anderson HJ, Lee JB. A Review of Fixed Drug Eruption with a Special Focus on Generalized Bullous Fixed Drug Eruption. Medicina (Kaunas). 2021 Sep 1;57(9):925. doi: 10.3390/medicina57090925. PMID: 34577848; PMCID: PMC8468217.
  2. Flowers H, Brodell R, Brents M, Wyatt JP. Fixed drug eruptions: presentation, diagnosis, and management. South Med J. 2014 Nov;107(11):724-7. doi: 10.14423/SMJ.0000000000000195. PMID: 25365443.
  3. Chow TG, Khan DA. Sulfonamide Hypersensitivity. Clin Rev Allergy Immunol. 2022 Jun;62(3):400-412. doi: 10.1007/s12016-021-08872-3. Epub 2021 Jul 1. PMID: 34212341
  4. Lipowicz S, Sekula P, Ingen-Housz-Oro S, Liss Y, Sassolas B, Dunant A, Roujeau JC, Mockenhaupt M. Prognosis of generalized bullous fixed drug eruption: comparison with Stevens-Johnson syndrome and toxic epidermal necrolysis. Br J Dermatol. 2013 Apr;168(4):726-32. doi: 10.1111/bjd.12133. Epub 2013 Feb 16. PMID: 23413807.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2023-11-01T14:08:31-07:00Nov 10, 2023|Allergy-Immunology, Dermatology, SAEM Clinical Images|
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SAEM Clinical Images Series: Wolf in Sheep’s Clothing

wolf

A 55-year-old female with a history of hyperlipidemia presents after a syncopal episode. She had mild nausea and diarrhea on the morning of presentation but otherwise had no prodromal symptoms before suddenly losing consciousness in a grocery store. Of note, she recalls a similar syncopal episode in the remote past, also preceded by gastrointestinal symptoms at that time. At present, she is symptom-free.

Vitals: BP 135/71; HR 52; Temp 98°F; RR 18; SpO2 100% on room air

General: Tired appearing

CV: 2+ peripheral pulses. Regular rate and rhythm, no murmurs, rubs, or gallops.

Pulmonary: No increased work of breathing. Lungs clear to auscultation bilaterally.

GI: Soft, non-distended, non-tender to palpation.

Non-contributory

Wolff-Parkinson-White Syndrome (WPW)

Short PR interval (< 0.12 seconds) and slowed upstroke of the QRS complex, referred to as a delta wave, which are both seen in our patient. These particular EKG findings define a “Wolff-Parkinson-White Pattern.”

WPW is a pre-excitation syndrome characterized by an accessory pathway caused by a congenital failure of cells to resorb near the AV valves. This accessory pathway conducts impulses faster than the AV node, causing a short PR interval. WPW Syndrome consists of characteristic EKG findings as well as symptomatic arrhythmias. Patients with WPW may classically present after a syncopal episode due to an arrhythmia involving the accessory pathway. Most commonly, WPW is associated with atrioventricular nodal reentrant tachycardia (AVNRT) and atrial fibrillation.

First-line treatment for WPW-mediated tachyarrhythmia consists of procainamide, which blocks conduction through the accessory pathway. An exception to this would be the hemodynamically unstable patient, who should be cardioverted. AV nodal blocking agents should be avoided in patients with tachyarrhythmias as they can cause increased conduction to the ventricles through the accessory pathway, leading to potential ventricular arrhythmias and hemodynamic instability. Ablation of the accessory pathway is indicated in those with symptomatic tachyarrhythmias and leads to successful remission in about 90 percent of cases.

Take-Home Points

  • The WPW pattern on EKG consists of a short PR interval and a delta wave.
  • Patients with WPW Syndrome classically present with symptomatic arrhythmias (including syncope) and EKG findings consistent with WPW pattern.
  • The most common arrhythmias seen in WPW include AVNRT and atrial fibrillation, which should be managed with procainamide. Avoid the use of AV nodal blocking agents.

  • Conover MB. Diagnosis and management of arrhythmias associated with Wolff-Parkinson-White syndrome. Crit Care Nurse. 1994 Jun;14(3):30-9; quiz 40-1. PMID: 8194348.
  • Dagres N, Clague JR, Kottkamp H, Hindricks G, Breithardt G, Borggrefe M. Radiofrequency catheter ablation of accessory pathways. Outcome and use of antiarrhythmic drugs during follow-up. European heart journal. 1999 Dec 1;20(24):1826-32.
  • Wolff L, Parkinson J, White PD. Bundle-branch block with short P-R interval in healthy young people prone to paroxysmal tachycardia. 1930. Ann Noninvasive Electrocardiol. 2006 Oct;11(4):340-53. doi: 10.1111/j.1542-474X.2006.00127.x. PMID: 17040283; PMCID: PMC6932258.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2023-11-12T13:55:35-08:00Nov 6, 2023|Cardiovascular, ECG, SAEM Clinical Images|
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SAEM Clinical Images Series: A Serious Pain in the Neck

lemierre

An otherwise healthy 34-year-old male presented to the Emergency Department with two weeks of anterior neck pain. Symptoms began with several days of pain in his mandibular molars, progressing to pain and swelling in the neck. In the last several days, the patient developed warmth and redness in the chest wall associated with subjective fever and chills. Additionally, the patient reports difficulty swallowing solid foods secondary to odynophagia associated with intermittent globus sensation. He has no history of immunocompromise and denies any drug or alcohol use. Of note, he has not seen a dentist in many years.

 

lemierre

Vitals: BP 115/80; HR 120; T 101°F; RR 16; O2 sat 97%

General: Well appearing in no acute distress

HEENT: Poor dentition, mild trismus. No gingival inflammation or swelling or induration to suggest abscess. The floor of the mouth is unremarkable.

Skin: The neck and upper chest demonstrate erythema and tenderness with an enlarged area of fluctuance on the superior aspect of the left breast (Figure 1).

White blood cell (WBC) count: 6.3 k/uL

Lactate: 1.6 mmol/L

Glucose: 95 mg/dL

Creatinine: 0.72 mg/dL

Lemierre Syndrome, also known as septic thrombophlebitis of the internal jugular vein, is a rare condition with an incidence of 3-15 cases per million people. This condition occurs when an oropharyngeal or odontogenic infection spreads locally from pharyngeal tissue to the internal jugular vein. The pathogens classically arise from normal oral flora, most commonly Fusobacterium necrophorum. The presentation may be associated with trismus and/or dysphagia. Subsequent complications, including localized abscess formation and bacteremia, stem from a combination of surrounding tissue invasion and systemic septic embolization.

Given the potential for regional lymphatic spread and septic embolization, patients may present with both local and systemic findings. Skin exam may reveal regionalized cellulitic or infectious changes overlying the neck or chest (Figure 1).

Respiratory signs and symptoms may suggest the presence of pulmonary septic emboli or mediastinitis.

Constitutional symptoms including fever, chills, and fatigue are common though nonspecific. The differential is broad and includes a number of infectious, lymphatic, endocrine, and neoplastic conditions.

It is essential for the clinician to consider the alternative diagnosis of Ludwig’s Angina through careful evaluation of the oral floor.

Given the potential for oropharyngeal and respiratory compromise, emergency clinicians must maintain a high index of suspicion for this condition. Diagnostics should include laboratory studies with blood cultures, as well as CT imaging of the neck and chest to evaluate for filling defects of the internal jugular vein.

When entertaining the diagnosis, early antibiosis is prudent. Treatment should include both an extended course of antibiotic therapy as well as surgical source control of abscesses. Given the propensity for thrombus development (Figure 2), anticoagulation may be considered, but its indication here remains controversial. Patients with Lemierre Syndrome will require surgical consultation and hospital admission.

Take-Home Points

  • Lemierre Syndrome is a septic thrombophlebitis of the internal jugular vein most commonly occurring via direct spread from the oral cavity. Distinction from Ludwig’s Angina is imperative.
  • Given the proximity to critical structures and the potential for systemic organ dysfunction from septic emboli, emergency physicians need to maintain a high clinical suspicion for this rare diagnosis.
  • Treatment includes parenteral antibiotics and prompt consultation of medical and surgical subspecialists to identify the infectious source as well as mitigate against systemic spread and/or thrombus propagation.

  • Kuppalli K, Livorsi D, Talati NJ, Osborn M. Lemierre’s syndrome due to Fusobacterium necrophorum. Lancet Infect Dis. 2012 Oct;12(10):808-15. doi: 10.1016/S1473-3099(12)70089-0. Epub 2012 May 25. PMID: 22633566.

Copyright

Images and cases from the Society of Academic Emergency Medicine (SAEM) Clinical Images Exhibit at the 2023 SAEM Annual Meeting | Copyrighted by SAEM 2023 – all rights reserved. View other cases from this Clinical Image Series on ALiEM.

By |2023-10-15T21:15:48-07:00Oct 16, 2023|HEENT, Infectious Disease, SAEM Clinical Images|
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