SAEM Clinical Image Series: Eye Pain

necrotizing

A 59-year-old gentleman experiencing homelessness with a history of hepatocellular carcinoma, hepatitis C, alcohol use disorder, and tobacco dependence presented to the emergency department (ED) with severe, worsening right eye pain, blurry vision, swelling, redness, and purulent discharge after scraping his upper face on concrete during a mechanical fall two weeks prior. Of note, his partner presented to the ED at the same time with a necrotic infection of the breast as well as multiple skin lesions reportedly due to insect bites.

Vitals: T 102.4°F; HR 108; BP 121/94

Head: Lice nits visible in his hair

Eye: Unable to open right eye without assistance; eyelids crusted and necrotic with underlying orbicularis oculi muscle visible; EOM full but painful in all fields of gaze; visual acuity 20/60 in each eye; pupils 2 mm, equal and minimally reactive.

White blood cell (WBC) count: 27,600/μl

Comprehensive metabolic panel (CMP): Na 121; K 2.8; Cl 83; AST 113; ALT 45

Wound culture: Positive for MRSA, Streptococcus pyogenes, Enterobacter cloacae, and Staphyloccocus epidermis

This patient’s presentation is consistent with periorbital necrotizing fasciitis complicated by severe sepsis.

This patient had type 1 necrotizing fasciitis given the polymicrobial source of infection with both aerobic and anaerobic organisms growing from his wound culture. Type 2 necrotizing fasciitis is attributable to streptococcal and/or staphylococcal infection alone. Group A strep is the most common organism responsible for necrotizing fasciitis, found in about 50% of cases.

Independent risk factors for necrotizing fasciitis include advanced age, diabetes mellitus, heart disease, liver cirrhosis, alcohol use disorder, and trauma. Furthermore, persons who experience homelessness are at risk of skin lesions due to insect bites, burns, and physical trauma which predispose them to secondary bacterial infections because of inadequate hygiene resources.

A systematic review of periorbital necrotizing fasciitis showed that 35% of cases were triggered by trauma, while 14% were caused by other infections such as acute dacryocystitis, sinus infections, and infections of the parotid glands.  Thus, it is likely that the patient’s contact with his partner who had a necrotic soft tissue infection secondary to insect bites, as well as his recent trauma to the eye, predisposed his development of this condition.

Initiation of broad-spectrum intravenous (IV) antibiotics with vancomycin, piperacillin/tazobactam, and clindamycin, as well as IV fluids.

In this case, the patient received the above antibiotics, underwent operative debridement, frequent wound care including dilute hypochlorous acid, local vancomycin administered via intra-orbital catheter, as well as lid reconstruction with glabellar flap. He was ultimately discharged on a two-week course of oral moxifloxacin and linezolid, healing well at his one-month follow-up appointment.

 

Take-Home Points

  • Skin problems are a common reason that persons experiencing homelessness seek medical care, given their risk factors for both primary insults and subsequent superinfection.
  • Common sources of infection for periorbital necrotizing fasciitis include trauma, surgery, and other infections of the upper face.
  • The standard of care for periorbital necrotizing fasciitis consists of IV and local antibiotics, and operative debridement.

  • Amrith S, Hosdurga Pai V, Ling WW. Periorbital necrotizing fasciitis — a review. Acta Ophthalmol. 2013 Nov;91(7):596-603. doi: 10.1111/j.1755-3768.2012.02420.x. Epub 2012 Apr 20. PMID: 22520175.

 

SAEM Clinical Image Series: Pediatric Rash

pediatric rash

A 17-month-old girl with a history of eczema presents to the pediatric emergency department for evaluation of a rash. The rash is different from her usual eczema, developed three days prior to presentation, and is described as red with yellow crusting. Her mother also noticed blistering in her groin and under her axilla. She has associated fussiness and decreased feeding, but no fever.

Vitals: T 37.7°C; HR 161; BP 115/75; RR 24; O2 sat 100% on room air

General: Fussy but consolable

Eyes: No conjunctival erythema or discharge

Mouth: Yellow crusting and fissuring surrounding mouth; no intra-oral lesions

Neck: No nuchal rigidity

Cardiovascular: Tachycardic with regular rhythm; no murmurs

Respiratory: Normal rate; normal breath sounds

Abdomen: Non-tender to palpation; non-distended; normal bowel sounds

Neurologic: Alert

Skin: Diffusely erythematous; scaling rash over the face with areas of yellow crusting; erythematous areas with blistering/desquamation to the anterior trunk, axilla, and inguinal regions

Complete blood count (CBC) and comprehensive metabolic panel (CMP) unremarkable.

Staphylococcal scalded skin syndrome caused by impetigo.

This case describes a patient with a rash, blistering/desquamation of axilla and groin, and systemic symptoms consistent with staphylococcal scalded skin syndrome (SSSS). Clinical features of SSSS include erythema to intertriginous areas, rapid progression of erythema, and systemic symptoms such as fever, irritability, and poor oral intake. Mucous membranes are not typically involved. Physical exam findings include perioral crusting and fissuring (seen in photo), blanching erythema, desquamation, shallow skin erosions, and a positive Nikolsky sign. SSSS is caused by exfoliative toxin A (ETA) and exfoliative toxin B (ETB), two exotoxins produced by certain strains of S. aureus. ETA and ETB cause the breakdown of keratinocyte adhesions within the epidermis, leading to desquamation. Infection with S. aureus at any site can cause SSSS, including bacterial conjunctivitis, wound/skin infection, staphylococcal pneumonia, pyomyositis, septic arthritis, and endocarditis. SSSS is more common in children, a phenomenon thought to be due to a lack of protective antibodies against staphylococcal antigens. The diagnosis of SSSS is clinical but can be confirmed with histopathology. In this case, the extensive yellow, crusting lesions of the face suggest impetigo, a superficial skin infection predominantly caused by S. aureus, as the etiology of SSSS. Children with eczema are at increased risk of impetigo due to disruption of the normal skin barrier. Complications of SSSS include fluid losses due to extensive skin breakdown, electrolyte abnormalities, sepsis, and death.

Penicillinase-resistant penicillins (oxacillin, nafcillin) or first- or second-generation cephalosporins. Clindamycin monotherapy should be avoided due to high rates of resistance. Management of SSSS in most cases also includes hospitalization for IV antibiotics and supportive care. In patients with significant skin involvement, admission to either an ICU or burn unit is warranted for close monitoring and wound care.

Take-Home Points

  • Staphylococcal scalded skin syndrome (SSSS) is caused by the release of S. aureus exfoliative toxins A and B into the bloodstream, thus SSSS can be caused by any infection caused by S. aureus.
  • Penicillinase-resistant penicillins are the first-line therapy in patients with SSSS. First- and second-generation cephalosporins, as well as vancomycin, can also be considered.
  • Treatment with clindamycin monotherapy should be avoided in patients with SSSS due to high levels of resistance among strains of S. aureus which cause SSSS.

  • Mishra AK, Yadav P, Mishra A. A Systemic Review on Staphylococcal Scalded Skin Syndrome (SSSS): A Rare and Critical Disease of Neonates. Open Microbiol J. 2016 Aug 31;10:150-9. doi: 10.2174/1874285801610010150. PMID: 27651848; PMCID: PMC5012080.
  • Paller A, Mancini, A. Hurwitz Clinical Pediatric Dermatology: A Textbook of Skin Disorders of Childhood and Adolescence. Edinburgh, Scotland: Elsevier; 2015.
  • Handler MZ, Schwartz RA. Staphylococcal scalded skin syndrome: diagnosis and management in children and adults. J Eur Acad Dermatol Venereol. 2014 Nov;28(11):1418-23. doi: 10.1111/jdv.12541. Epub 2014 May 20. PMID: 24841497.
  • Braunstein I, Wanat KA, Abuabara K, McGowan KL, Yan AC, Treat JR. Antibiotic sensitivity and resistance patterns in pediatric staphylococcal scalded skin syndrome. Pediatr Dermatol. 2014 May-Jun;31(3):305-8. doi: 10.1111/pde.12195. Epub 2013 Aug 23. PMID: 24033633; PMCID: PMC4349361.
  • Neubauer HC, Hall M, Wallace SS, Cruz AT, Queen MA, Foradori DM, Aronson PL, Markham JL, Nead JA, Hester GZ, McCulloh RJ, Lopez MA. Variation in Diagnostic Test Use and Associated Outcomes in Staphylococcal Scalded Skin Syndrome at Children’s Hospitals. Hosp Pediatr. 2018 Sep;8(9):530-537. doi: 10.1542/hpeds.2018-0032. PMID: 30139766; PMCID: PMC6317540.

 

SAEM Clinical Image Series: Painful Weeping Rash

rash

A 67-year-old nontoxic appearing male patient with a history of coronary artery disease, hyperlipidemia, transient ischemic attack, gout, renal colic, and squamous cell carcinoma presents with concern for multiple new painful lesions on his body. The rash first appeared five months ago but disappeared for some time before reappearing. It has worsened over the past few weeks. He has pain, erythema, pruritus, and urticarial, blistering, crusted lesions. He has had clear drainage from ruptured blisters. His only recent change in medication is an increase in his allopurinol (initiated four months ago; increased three weeks ago). He has tried Benadryl and steroids with minimal relief and is quite frustrated as this is his fourth emergency department visit for this complaint.

Skin: Multiple areas of 1-3 cm bullae (both tense and flaccid as well as open/ulcerated) on the trunk, groin, axilla, inguinal folds, palms, and dorsum of feet, not on soles; papules coalesce into annular plaques; no mucosal involvement

None. Complete blood count (CBC) from seven days prior showed normal counts and 9.4% eosinophils.

This patient has bullous pemphigoid. Also included on the differential is bullous lupus erythematosus, urticaria, DRESS (Drug Reaction with Eosinophilia and Systemic Symptoms), epidermolysis bullosa, and erythema multiforme.

Diagnosis may be made through clinical recognition of the typical features. The workup for a definitive diagnosis begins with histopathologic direct immunofluorescence from a skin biopsy of the edge of a blister and the surrounding normal-appearing skin, which is then confirmed with indirect immunofluorescence of the patient’s serum.

Take-Home Points

  • Bullous pemphigoid is a chronic, inflammatory, subepidermal, blistering disease. It is the result of an attack on the basement membrane of the epidermis by IgG +/-IgE immunoglobulins and activated T lymphocytes.
  • It primarily affects elderly individuals in their 50s-70s, with an average age at onset of 65 years, and is often associated with stroke or dementia.
  • The most common treatments for bullous pemphigoid are anti-inflammatories (topical and oral steroids), immunosuppressants, and doxycycline. Treatment regimens are aimed to minimize the systemic side effects of the treatment itself, while also decreasing inflammation, blister formation, and autoantibody production.
  • Oakley, A. Bullous pemphigoid. Jan 2016. [Online] Available at:
    https://dermnetnz.org/topics/blistering-skin-conditions/
  • Chan, L. Bullous Pemphigoid. Oct 2020. [Online] Available at: https://emedicine.medscape.com/article/1062391-overview

 

By |2021-12-02T13:13:48-08:00Dec 6, 2021|Dermatology, SAEM Clinical Images|

SAEM Clinical Image Series: Pediatric Rash

pediatric rash

A previously healthy 8-year-old female presents to the pediatric emergency department due to a rash. Her symptoms started three days prior to presentation with a painful rash on her lower extremities. The rash subsequently spread to the buttocks and upper extremities, and she developed intermittent diffuse abdominal pain, a nonproductive cough, and pharyngitis. The patient denies subjective fever. Known sick contacts include the patient’s mother, who tested positive for COVID-19 two and a half weeks prior.

 

Vitals: T 98.5°F; HR 93; BP 115/68; RR 16; O2 sat 100% on room air

Constitutional: Well-developed and in no acute distress

HEENT: Normocephalic, atraumatic; moist mucus membranes; no conjunctival injection; posterior pharyngeal erythema without exudates; tonsils are three bilaterally; lips are not cracked; no “strawberry tongue”;

Neck: Normal range of motion; no lymphadenopathy

Cardiovascular: Regular rate and rhythm; normal heart sounds and pulses

Pulmonary: Effort is normal; normal breath sounds; no wheezing

Abdominal: Abdomen is flat; minimal tenderness to palpation without guarding; no organomegaly

Skin: Diffuse petechial rash and painful, palpable, nonblanching purpura in the dependent regions (most notable on the buttocks and lower extremities)

COVID-19: Detected

Complete blood count (CBC): WBC 10K, hemoglobin 13, platelets 469

Comprehensive metabolic panel (CMP): Na 138, K 4.1, Cl 103, CO2 26, BUN 7, Cr 0.38, Glucose 94, ALT 23, AST 26, Albumin 4.5

Lipase: 10

Urinalysis (UA): Normal

C-reactive protein (CRP): 3.4

Erythrocyte sedimentation rate (ESR): 24

Procalcitonin: 0.03

Fibrinogen: 363

BNP: <10

Troponin: 0.00

Ferritin: 83

Triglycerides: 37

 

  • COVID-19-Associated Multisystem Inflammatory Syndrome in Children (MIS-C): According to CDC criteria, patients must be under 21 years of age, with a fever higher than 38°C/subjective fever for longer than 24 hours, laboratory evidence of inflammation, severe illness requiring hospitalization, and two or more organ systems involved (cardiac, renal, respiratory, hematologic, gastrointestinal, dermatologic, or neurologic), with no alternative plausible diagnoses and recent COVID-19 infection.
  • Immunoglobulin A Vasculitis (Henoch-Schönlein Purpura): According to the EULAR/PRINTO/PRES criteria, symptoms must include cutaneous findings (palpable purpura or petechiae without the presence of thrombocytopenia), plus at least one of the following: diffuse abdominal pain with acute onset, arthritis/arthralgia, renal involvement in the form of proteinuria or hematuria, or deposition of Immunoglobulin A seen on renal histology.
  • Kawasaki Disease: The diagnostic criteria include fever for five days or longer and four of the following: bilateral conjunctival injection, cervical lymphadenopathy, polymorphous rash, oral mucous membrane changes (including fissured lips, pharyngeal erythema or strawberry tongue), peripheral extremity changes (edema of the hands/feet or desquamation).

Immunoglobulin A (IgA) Vasculitis.

This patient presented with palpable purpura and petechiae without the presence of thrombocytopenia, as well as diffuse abdominal pain. The majority of cases of IgA Vasculitis are preceded by a respiratory pathogen, with the most common being streptococcus, staphylococcus, and parainfluenza virus. Although not well-documented due to its recent conception, COVID-19 is likely to be the cause of this patient’s vasculitis. Usual management of IgA Vasculitis is supportive care, with admission and specialty referral for complications including intussusception and glomerular involvement. Given the severity of the differential diagnoses, this patient was admitted to the hospital for observation and discharged the following day with close follow-up

Take-Home Points

  • COVID-19 can cause a variety of rashes in the pediatric population, and appropriate workup including inflammatory markers, complete blood count, and comprehensive metabolic panel must be initiated to rule out severe disease. Consider obtaining a troponin, EKG, chest x-ray, echocardiogram, ferritin, prothrombin time, partial thromboplastin time, international normalized ratio, fibrinogen, urinalysis and cultures to assess for end-organ damage. If positive, and the patient appears ill, consider Multisystem Inflammatory Syndrome in Children (MIS-C).
  • IgA Vasculitis is usually caused by a respiratory pathogen. Keep it on your differential when assessing children who test positive for Covid-19.
  • Complications of IgA vasculitis include intussusception, heme-positive stool, microscopic hematuria, and periarticular disease.

  • Centers for Disease Control and Prevention, Health Alert Network. (2020). Case Definition for Multisystem Inflammatory Syndrome in Children (MIS-C). [online] Available at: https://emergency.cdc.gov/han/2020/han00432.asp.
  • Trnka P. Henoch-Schönlein purpura in children. J Paediatr Child Health. 2013 Dec;49(12):995-1003. doi: 10.1111/jpc.12403. Epub 2013 Oct 18. PMID: 24134307.
  • Ozen S, Pistorio A, Iusan SM, Bakkaloglu A, Herlin T, Brik R, Buoncompagni A, Lazar C, Bilge I, Uziel Y, Rigante D, Cantarini L, Hilario MO, Silva CA, Alegria M, Norambuena X, Belot A, Berkun Y, Estrella AI, Olivieri AN, Alpigiani MG, Rumba I, Sztajnbok F, Tambic-Bukovac L, Breda L, Al-Mayouf S, Mihaylova D, Chasnyk V, Sengler C, Klein-Gitelman M, Djeddi D, Nuno L, Pruunsild C, Brunner J, Kondi A, Pagava K, Pederzoli S, Martini A, Ruperto N; Paediatric Rheumatology International Trials Organisation (PRINTO). EULAR/PRINTO/PRES criteria for Henoch-Schönlein purpura, childhood polyarteritis nodosa, childhood Wegener granulomatosis and childhood Takayasu arteritis: Ankara 2008. Part II: Final classification criteria. Ann Rheum Dis. 2010 May;69(5):798-806. doi: 10.1136/ard.2009.116657. PMID: 20413568.
  • Royle J, Burgner D, Curtis N. The diagnosis and management of Kawasaki disease. J Paediatr Child Health. 2005 Mar;41(3):87-93. doi: 10.1111/j.1440-1754.2005.00555.x. PMID: 15790316.

 

SAEM Clinical Image Series: A Rapidly Spreading Rash

spreading rash

A 40-year-old male with a past medical history of HIV presented for evaluation of a non-pruritic rash. Six days ago, he suddenly felt a stinging sensation at the back of his head and neck similar to a bug bite. He then noticed bumps were starting to form and developed a shock-like pain in the area. Three days ago, the rash spread from the back of his head towards his chest. Yesterday, the rash spread further and now extends medially and upwards covering most of his left neck and ear. The pain continued to worsen, at which point the patient shaved the left side of his head in an attempt to help the rash. Today, the pain became unbearable, which prompted his visit to the emergency department for further evaluation and management.

Head: Normocephalic, atraumatic; left side of patient’s head is shaved.

Eye: Pupils equal, round, reactive to light; extraocular movements intact; no corneal ulcers or dendritic lesions with fluorescein staining.

Visual acuities: Right 20/25, left 20/25, baseline 20/25

Ear, nose, throat: Mucous membranes are dry; oral thrush and tonsillar erythema appreciated; localized erythema, crusting and blistering rash of varying sizes and ages along with the outer ear including the tragus, antihelix, and antitragus; helix mildly swollen. On otoscopy, the tympanic membranes appear pearly grey, shiny, translucent with no bulging, and without cerumen impaction.

Neck: Full range of motion appreciated but both horizontal and vertical movement is slow secondary to pain; no lymphadenopathy.

Neurological: Awake, alert, and oriented to date, place, and person; moves all extremities; cranial nerves II through XII grossly intact; strength 5/5 in all extremities; gait steady; no ataxia, dysmetria, or dysarthria.

Skin: Erythematous, localized, crusted, blistering vesicular rash of various sizes and ages appreciated along the left V3 distribution, C3 to T3 dermatomes anteriorly, and C2 to C6 dermatomes posteriorly.

HIV-1 antibody: positive

CD4 helper t-cells: 48 (L)

HIV-1 RNA PCR: 36,490

The lesions can be characterized as vesicles in various stages of healing. Some lesions are crusted, others are bullous, and a few are pustular. The C2-C6 dermatomes are affected posteriorly, and the C2-T3 dermatomes are involved anteriorly.

The diagnosis is Disseminated Herpes Zoster. The rash in reactivation varicella zoster virus (VZV) is preceded by tingling, itching, or pain, and begins as maculopapular then progresses to vesicles, pustules, and bullae. The rash typically involves a single dermatome and does not cross the midline. Rash present in multiple dermatomes (>3) or a rash that crosses the midline signifies disseminated disease. Hutchinson’s sign is a lesion on the lateral dorsum and tip of the nose indicating the involvement of the nasociliary branch of the ophthalmic division of the trigeminal nerve. The nasociliary branch innervates the eye, thus these lesions are highly suspicious for herpes zoster ophthalmicus. Herpes zoster ophthalmicus on fluorescein examination appears as pseuododendritic lesions with no terminal bulbs (not to be confused with herpes simplex virus (HSV) keratitis, which has dendritic lesions with terminal bulbs). Vesicles in the auditory canal (herpes zoster oticus) may be a part of Ramsay Hunt syndrome with ear pain and paralysis of the facial nerve.

The patient is immunocompromised and requires hospitalization for intravenous (IV) antiviral therapy and pain management. VZV primary infection results in viremia, diffuse rash, and seeding of sensory ganglia where the virus establishes latency. Herpes zoster is the result of viral reactivation with spread along the sensory nerve in that dermatome. Antiviral therapy aids in the resolution of lesions, reduces the formation of new lesions, reduces viral shedding, and decreases the severity of acute pain, but does not affect the development of post-herpetic neuralgia.

Immunocompetent patients may receive Valacyclovir 1 g PO q8hrs (preferred) or Acyclovir 800 mg PO 5x/day x 7d if the onset of rash is <3 days or >3 days with the appearance of new lesions.

Immunocompromised, transplant, and cancer patients are all at high risk for dissemination, chronic skin lesions, acyclovir-resistant VZV, and multi-organ involvement. Immunocompromised patients and patients with disseminated zoster require aggressive multimodal treatment, admission to the hospital, and IV antiviral therapy regardless of the time of onset of rash. Recommended therapy is Acyclovir 10 mg/kg IV q8h or Foscarnet 40 mg/kg IV q8h for acyclovir-resistant VZV. All patients require adequate analgesia, typically with non-steroidal anti-inflammatory drugs, opioids, Gabapentin, Nortriptyline, and Lidocaine patches on intact skin.

Take-Home Points

  • Disseminated herpes zoster is defined as reactivation of VZV in three or more dermatomes. It requires admission, IV antiviral therapy, and pain control.
  • If VZV reactivation involves the face, one must evaluate for herpes zoster ophthalmicus and oticus.
  • Perform a thorough neuro exam including evaluation of cranial nerves V, VII, and VIII.
  • VZV requires airborne precautions.
  1. Cohen JI. Clinical practice: Herpes zoster. N Engl J Med. 2013 Jul 18;369(3):255-63. doi: 10.1056/NEJMcp1302674. PMID: 23863052; PMCID: PMC4789101.

 

 

 

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.

Non-contributory

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.

 

 

 

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