About Andrew Mittelman, MD

Assistant Professor of Emergency Medicine
Boston Medical Center

SAEM Clinical Images Series: Man with a Recurrent 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.


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.

SAEM Clinical Images Series: Wolf in Sheep’s Clothing


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.


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.

By |2023-11-12T13:55:35-08:00Nov 6, 2023|Cardiovascular, ECG, SAEM Clinical Images|

SAEM Clinical Images Series: A Serious Pain in the Neck


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.

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.

SAEM Clinical Images Series: Insidiously Contracted Hand


A 64-year-old Caucasian male with a history of alcohol use disorder and tobacco use disorder presents with painless bilateral hand contractures that have been worsening for the past several months. He denies any recent trauma, fever, chills, or decreased sensation. The patient works as a construction worker.

Vitals: BP 143/83 ; HR 94; RR 18; T 98.6°F; O2 saturation 98% on room air

Musculoskeletal: He has bilateral palmar contractures proximal to the fourth digits. No tenderness to palpation along digits. Passive extension of the digits is limited bilaterally but does not elicit pain. When asked to place his palm flat on the table, there is notable contracture of the bilateral fourth metacarpophalangeal (MCP) joint (a positive Hueston’s tabletop test). No erythema or cellulitic changes are appreciated.


Dupuytren’s Contracture is a clinical diagnosis that most commonly presents as painless loss of extension of the fourth and fifth phalanx. Collagen deposition and subsequent fibrosis within the palmar fascia cause nodule formation along the flexor tendons near the distal palmar crease. Clinically this appears as puckering, tethering, and/or dimpling of the skin of the palm (as shown in the photograph). Accompanying joint rigidity and loss of full extension of the digit typically can take years to fully develop. Pain or inflammatory findings are not commonly seen unless there is an underlying tenosynovitis. Without signs of infection, outpatient management with Hand Surgery is the appropriate initial management.

Risk factors for the development of Dupuytren’s contracture include northern European descent, age greater than 50 years, and diabetes. The condition has been associated with tobacco use disorder, alcohol use disorder, jobs that require repetitive handling tasks or vibration, and localized fibrotic pathologies including Peyronie’s disease.

Take-Home Points

  • Dupuytren’s contracture presents as a painless palmar contraction (typically proximal to the 4th or 5th digit) that impedes finger extension.
  • A progressive condition, Dupuytren’s is best managed through Hand Surgery referral provided there is no evidence of superinfection.
  • Repetitive motion occupations, tobacco use, alcohol use, and diabetes are key risk factors.

  • Shih B, Bayat A. Scientific understanding and clinical management of Dupuytren disease. Nat Rev Rheumatol 2010; 6:715.   Trojian TH, Chu SM. Dupuytren’s disease: diagnosis and treatment. Am Fam Physician 2007; 76:86.

By |2023-09-14T12:40:35-07:00Sep 15, 2023|Orthopedic, SAEM Clinical Images|

SAEM Clinical Images Series: A Painful Swollen Digit


A 50-year-old male with a history of polysubstance use disorder and poorly-controlled type 2 diabetes mellitus presents with left hand pain. One week ago, the patient sustained a macerating injury of the left distal middle digit. Since that time he has experienced worsening pain throughout the digit, now associated with diffuse swelling and discoloration. The patient also reports reduction in range of motion.

Vitals: Temp 97.6°F (36.4°C); BP 134/89; HR 87; Resp 16

General: Uncomfortable appearing male.

Musculoskeletal: Left hand third digit with fusiform edema, diffuse erythema, and warmth. Held in passive flexion at rest. Skin breakdown noted at distal fingertip with scant serous drainage. Tender to palpation, most markedly over the volar surface of the PIP joint. Patient reports severe pain with passive extension at the MCP, PIP, and DIP joints.

Glucose: 296

White Blood Cell (WBC) Count: 8,000/μl

ESR: 54 mm/hr

Infectious flexor tenosynovitis is an infection of the flexor tendon and synovial sheath with a significant risk of complications (e.g., tendon rupture, loss of function, amputation) if not promptly treated. Patients classically present 2-4 days after penetrating trauma to the hand (e.g., bite/scratch, puncture wound, laceration, injection).

This diagnosis is suggested clinically by four cardinal findings, the Kanavel signs:

1) diffuse “fusiform” swelling of the digit (most common)

2) digit held in passive flexion

3) tenderness to percussion over the flexor sheath

4) pain with passive extension

Although fundamentally a clinical diagnosis, the initial evaluation for infectious flexor tenosynovitis should include laboratory studies including complete blood count (CBC) and inflammatory markers (ESR/CRP). Radiographs may be performed to evaluate for occult traumatic injury or foreign body. Treatment includes emergent consultation of orthopedics or hand surgery, initiation of intravenous (IV) antibiotics, and hospital admission. Antibiotics should target gram-positive organisms (Staphylococcus, including MRSA, and Streptococcus). In immunocompromised patients, additional coverage against gram-negative organisms and anaerobes may be needed. Risk factors for poor outcomes include immunocompromise (HIV, diabetes, immunosuppression), intravenous drug use, peripheral vascular disease, and polymicrobial infection.

Take-Home Points

  • Infectious flexor tenosynovitis is a surgical emergency that is diagnosed clinically by the presence of one or more of the four Kanavel signs on physical exam.
  • History of trauma or penetrating injury and immunocompromised status should raise suspicion for infectious flexor tenosynovitis; common pathogens include Staphylococcus and Streptococcus species.
  • Treatment includes emergent consultation with orthopedics or hand surgery as well as early initiation of IV antibiotics.

  • Ritter K, Fitch R. Tenosynovitis. In: Knoop KJ, Stack LB, Storrow AB, Thurman R. eds. The Atlas of Emergency Medicine, 5e. McGraw Hill; 2021. Accessed November 30, 2022. https://accessmedicine-mhmedical-com.ezproxy.bu.edu/content.aspx?bookid=2969&sectionid=250459435.
  • Hyatt MT, Bagg MR. Flexor Tenosynovitis. OrthopClin N Am 2017;48:217-27.
  • Pang HN, Teoh LC, Yam AKT, Lee JYL, Puhaindran ME, Tan ABH. Factors affecting the prognosis of pyogenic flexor tenosynovitis. Journal of Bone and Joint Surgery. 2007;89(8):1742-1748.

SAEM Clinical Image Series: Silver Scales

A 6-year-old otherwise healthy female presented to the emergency department (ED) with a rash across all four extremities. She has had seven months of pruritic, expanding lesions starting on her shins, now beginning to expand on her forearms. No history of allergies or irritant exposure. Due to Covid-19, she has been unable to see a provider before today’s ED visit.

Vitals: T 98.3°F; BP 96/72; HR 92; RR 24; O2 sat 100%

Skin: Numerous patchy red lesions scattered across bilateral upper and lower extremities with silver plaque accumulation. No nailbed involvement. No mucous membrane involvement.


Psoriasis vulgaris, plaque subtype, is a common dermatologic condition often seen in the outpatient setting. Plaques are most commonly noted on the knees, elbows, and lower back. The silvery plaques in characteristic locations are a hallmark of this diagnosis but are rarely seen to this extent. Unfortunately for this patient, this was the initial presentation due to the inability to access care during the COVID-19 pandemic.

Initial management is with high-potency topical corticosteroids. Systemic steroids should be avoided to prevent exacerbation or eruption of pustular psoriatic lesions. In this case, given the patient’s age and disease severity, she was seen in the ED by Dermatology and initiated on corticosteroid topical therapy. She was encouraged to establish care with rheumatology to be routinely screened for associated life-altering pathologies including psoriatic arthritis and uveitis.

Take-Home Points

  • When making a visual diagnosis of plaque psoriasis, evaluate for erythema, edema, or signs of superinfection.
  • Avoid systemic steroids given the risk of rash exacerbation, especially upon withdrawal.
  • Younger patients and those with more than 10% body surface area involvement should be evaluated by a dermatologist for initiation of topical corticosteroids and possible escalation to phototherapy, methotrexate, retinoids, or biologic agents.
  1. Menter A, Cordoro KM, Davis DMR, Kroshinsky D, Paller AS, Armstrong AW, Connor C, Elewski BE, Gelfand JM, Gordon KB, Gottlieb AB, Kaplan DH, Kavanaugh A, Kiselica M, Kivelevitch D, Korman NJ, Lebwohl M, Leonardi CL, Lichten J, Lim HW, Mehta NN, Parra SL, Pathy AL, Farley Prater EA, Rupani RN, Siegel M, Stoff B, Strober BE, Wong EB, Wu JJ, Hariharan V, Elmets CA. Joint American Academy of Dermatology-National Psoriasis Foundation guidelines of care for the management and treatment of psoriasis in pediatric patients. J Am Acad Dermatol. 2020 Jan;82(1):161-201. doi: 10.1016/j.jaad.2019.08.049. Epub 2019 Nov 5. Erratum in: J Am Acad Dermatol. 2020 Mar;82(3):574. PMID: 31703821.




Go to Top