ACMT Toxicology Visual Pearl: Needle to Necrosis
Which of the following agents, when injected along with heroin, is associated with the skin changes pictured?
- Cocaine
- Fentanyl
- Methamphetamine
- Xylazine
Photo by Dr. Matthew Salzman
SAEM Clinical Images Series: Utility of Bedside Ultrasonography
A 24-year-old G1P0010 female with a PMHx of ovarian cyst (unknown laterality) and emergency contraceptive use 3 months prior presented with sudden onset abdominal pain (upper > lower) that awoke her from sleep four hours prior to presentation with associated nausea and mild lower back pain. The pain is 10/10, sharp, stabbing, and diffuse. Additionally, she reported trace white vaginal discharge at baseline. No acute increase. She had intermittent vaginal bleeding since contraception use over the past two months, which has now resolved. She denied fever, chills, vomiting, chest pain, shortness of breath, diarrhea, or constipation. No pertinent surgical history.
Constitutional: Uncomfortable. Appearing to be in acute pain.
Cardiovascular: Tachycardia. Regular rhythm and normal heart sounds.
Pulmonary: No respiratory distress. Breath sounds normal.
Abdominal: Diffusely tender abdomen with voluntary guarding, otherwise soft. Normoactive bowel sounds. Negative Murphy’s sign.
Pelvic: Scant white vaginal discharge and CMT. No vaginal bleeding, lacerations, or external lesions.
Neurologic: A&O x 3
WBC: 18.9 k/uL
Hgb: 10.5 g/dL
BMP, lipase, Alk phos/Bili/ALT/AST, PT/PTT, and lactate: Unremarkable
Serum HCG: Negative
Urinalysis (UA): Unremarkable
COVID: Negative
An ideal RUQ ultrasound visualizes the liver, Morrison’s pouch, superior and inferior poles of the right kidney, and diaphragm in the coronal plane. Here, we see a thickened hepatic capsule, septations, and trace ascites.
Fitz-Hugh-Curtis syndrome (FHCS) is characterized by perihepatitis in the setting of pelvic inflammatory disease (PID). It traditionally presents with right upper abdominal pain with associated nausea, vomiting, and fever in women of childbearing age. While overall considered a rare manifestation of PID, the true incidence of FHCS is poorly defined in the literature [1]. The pathophysiology of spread is also poorly understood. It is speculated that bacteria (N. gonorrhoeae, C. trachomatis) travel to the liver via blood, lymphatics or peritoneal fluid, causing perihepatitis [1]. Diagnosing FHCS poses a diagnostic challenge to clinicians. Traditionally, the diagnosis is made via laparoscopic exploration of the abdomen with visualization of the characteristic “violin-string” adhesions, with growing evidence also supporting the use of contrast-enhanced CT [1]. Limited evidence exists to support the use of ultrasonography in diagnosing FHCS. One case report published in 1993 used RUQ abdominal ultrasound to identify septations (violin-string adhesions) and ascites to ultimately diagnose FHCS, later confirmed by serologic and operative evidence [2]. Another case report from 2018 used ultrasonography to identify a thickened hepatic capsule in an 18-year-old female with RUQ pain, later confirming FHCS by CT without the need for laparotomy [3]. While more research is needed, identification of FHCS via bedside ultrasonography in the emergency setting followed by appropriate antibiotic therapy can be an effective approach to FHCS, ideally reserving laparoscopy only for lysis of adhesions in refractory cases.
Take-Home Points
- RUQ abdominal ultrasound findings of a thickened hepatic capsule, ascites, and septations should raise suspicion for Fitz-Hugh-Curtis syndrome in the emergency setting.
- Moon, Y.H., Kim, J.H., Jeong W.J., Park, S.Y. Ultrasonographic findings in Fitz-Hugh-Curtis syndrome: a thickened or three-layer hepatic capsule. Yeungnam Univ J Med 35(1), 127-129 (2018).
- Theofanakis, C.P., Kyriakidis, A.V. Fitz-Hugh–Curtis syndrome. Gynecol Surg 8, 129–134 (2011). https://doi.org/10.1007/s10397-010-0642-8
- van Dongen PW. Diagnosis of Fitz-Hugh-Curtis syndrome by ultrasound. Eur J Obstet Gynecol Reprod Biol. 1993 Jul;50(2):159-62. doi: 10.1016/0028-2243(93)90181-b. PMID: 8405645.
ACMT Toxicology Visual Pearl: Poison Dart Frog
The toxin from the golden poison dart frog most resembles which of the following in its mechanism of action?
- Botulinum toxin
- Bufotoxin
- Grayanotoxin
- Palytoxin
- Tetrodotoxin
Photo adapted from Wilfried Berns (Wikimedia Commons)
SAEM Clinical Images Series: Pediatric Genitourinary Bleeding
A 4-year-old female with no significant past medical history is brought to the Emergency Department by her grandmother for concern for two days of progressive vaginal bleeding. The grandmother first noted blood in the patient’s underwear the previous morning when she was helping the patient wipe and she noticed it again prior to arrival, this time saturating the patient’s underwear. There is no history of any recent falls or trauma, abdominal pain, pain to the vagina, dysuria, prior incidents of vaginal bleeding, or any noticeable behavioral changes per the grandmother. The patient lives at home with her mother but has been at her grandmother’s house for the past four days (the household consists of female cousins, grandmother, and grandfather). Of note, the patient’s father took her to a trampoline park with her younger sister two days ago.
ACMT Toxicology Visual Pearl – Apricot Kernels: Eat or pass?
What toxin is found in bitter apricot kernels?
- Cardiac glycoside
- Cyanogenic glycoside
- Dinitrophenol
- Lysergic Acid
SAEM Clinical Images Series: More Than Skin Deep
A 57-year-old female college counselor living in the northeastern United States with no PMH presented for evaluation of rash, joint pain, and dyspnea for the past three weeks. The patient first noticed the rash on her upper back, describing it as being itchy. The rash then spread to her face, scalp, and thighs. Two weeks ago, she noticed swelling in her hands and had a gradual onset of dyspnea on exertion. The patient has pain in her hands and when moving her fingers. She denied fever, cough, chills, chest pain, headache, vision changes, focal weakness, abdominal pain, nausea, vomiting, and diarrhea. She denied recent travel, sick contacts, significant time spent outdoors, known tick bites, new medications, and changes in her diet. She has never had a rash like this before.
Vitals: BP 110/70; HR 86 BPM; RR 18 breaths/min; T 37°C; SpO2 96% on RA
Skin: Warm and dry. There is a macular, violaceous rash to the upper back and upper thighs. The patient’s hands are slightly edematous with nontender papules on the palmar aspect of the hands.
CV: Heart sounds are normal. No jugular venous distention or lower extremity edema.
Lungs: There are faint bibasilar rales heard on auscultation of the chest.
Extremities: Full ROM of the joints and there are no bony deformities. The patient does not have muscular tenderness.
Neuro: Within normal limits; muscle strength 5/5 in all four extremities.
CBC w/ differential: Normal
BMP: Na 142, K 3.8, Cl 106, HCO3 24, BUN 16, Cr 0.44, Glu 112, Ca 8.5, Mg 2.2, Phos 3.4
LFT’s: AST 105, ALT 76, ALP 68, Tbili 0.2 Alb 3.7
PT/PTT/INR: 12.0s/32.2/1.04
D-dimer: 347
ESR: 62
CRP: 0.75
Ferritin: 625
CK: 195
LDH: 276
Procalcitonin: undetectable
Amyopathic dermatomyositis – specifically anti-melanoma differentiation-associated gene 5 (anti-MDA5) positive dermatomyositis as determined by subsequent inpatient auto-immunological workup. Compared to other dermatomyositides, anti-MDA5 positive dermatomyositis is characterized by an absence of traditional muscular involvement. Additionally, patients can present with respiratory symptoms related to interstitial lung disease (ILD). One phenotype of this condition is associated with a rapidly progressive ILD, but respiratory involvement may be delayed years after the initial symptoms are noticed. The patient’s clinical images demonstrate a macular, violaceous rash in the “shawl sign” and “holster sign” distribution patterns typical of dermatomyositides. Palmar papules (not to be confused with Gottron’s papules which are found on the dorsal surface of the metacarpophalangeal and interphalangeal joints) are fairly specific for anti-MDA5 positive dermatomyositis
There are no specific guidelines for treating anti-MDA5 positive dermatomyositis. Patients are typically started on a high-dose steroid regimen. A rheumatology consult should be obtained to determine if the patient would benefit from treatment with immunosuppressants. Given her complaints of dyspnea, the patient should undergo a non-contrast CT of the chest to evaluate for evidence of scarring or pulmonary fibrosis.
Take-Home Points
- Anti-MDA5 positive dermatomyositis is associated with rapidly progressive ILD has a poor prognosis.
- This rare form of dermatomyositis should be suspected if the patient has respiratory complaints in addition to the hallmark cutaneous findings commonly observed in all types of dermatomyositides. Palmar papules are fairly specific for anti-MDA5 positive dermatomyositis. It often lacks typical historical and physical features of muscular weakness.
- Treatment involves high-dose corticosteroids and consideration of immunomodulator therapy.
- Allenbach Y, Uzunhan Y, Toquet S, Leroux G, Gallay L, Marquet A, Meyer A, Guillaud C, Limal N, Gagnadoux F, Hervier B, Borie R, Deligny C, Terrier B, Berezne A, Audia S, Champtiaux N, Devilliers H, Voermans N, Diot E, Servettaz A, Marhadour T, Castelain V, Humbert S, Blanchard-Delaunay C, Tieulie N, Charles P, Gerin M, Mekinian A, Priou P, Meurice JC, Tazi A, Cottin V, Miyara M, Grange B, Israël-Biet D, Phin-Huynh S, Bron C, De Saint Martin L, Fabien N, Mariampillai K, Nunes H, Benveniste O; French Myositis Network. Different phenotypes in dermatomyositis associated with anti-MDA5 antibody: Study of 121 cases. Neurology. 2020 Jul 7;95(1):e70-e78. doi: 10.1212/WNL.0000000000009727. Epub 2020 Jun 2. PMID: 32487712; PMCID: PMC7371381.
- Nombel A, Fabien N, Coutant F. Dermatomyositis With Anti-MDA5 Antibodies: Bioclinical Features, Pathogenesis and Emerging Therapies. Front Immunol. 2021 Oct 20;12:773352. doi: 10.3389/fimmu.2021.773352. PMID: 34745149; PMCID: PMC8564476.
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.
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.
- 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.
- 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.
- 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
- 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.