SAEM Clinical Images Series: Penile Lesion with a Poor Prognosis

A 49-year-old male presented to the emergency department of an academic hospital with the chief concern of penile pain. Prior medical history is notable for end-stage renal disease on hemodialysis three times per week, but the patient has not been dialyzed in the past four days, hypertension, insulin-dependent diabetes mellitus, heart failure with reduced ejection fraction (59% two months prior), seizure disorder, prior pulmonary embolism (eight months prior), a left nephrectomy seven months ago due to a gunshot wound, bradycardia status post permanent pacemaker, duodenal ulcer, and dry gangrene of the left foot. The patient was recently admitted to the hospital eight days prior to presentation for purulent urethral discharge where he received a course of topical antibiotics and was discharged. The patient stated he had 10/10 sharp penile pain since discharge from the hospital. He followed up with all “appropriate” appointments. He noticed that his penis started becoming discolored. He then noticed the pain start and grow in intensity without radiating anywhere else except the glans. He denies any discharge or pain with urination with 2-3 small volume voids daily but denies urine trapping.

GU: There is erythema, tenderness, and discoloration of the penile gland. There is no crepitus or swelling.

The rest of the physical exam is benign.

K: 6.5

Magnesium: 2.6

BUN: 70

Creatinine: 8.7

Alkaline phosphatase: 1562 (baseline 1069-1409)

Hemoglobin: 8.9 (at baseline)

WBC: 18.7 (monocyte predominance)

Calcinosis is characterized by the presence of precipitated calcium crystals in soft tissue. The condition is divided into 5 subtypes based on etiology and severity: dystrophic, metastatic, idiopathic, iatrogenic, and calciphylaxis (1). Dystrophic calcinosis cutis is caused by local trauma to the tissue, such as by repeated intravenous access, heel sticks, or other procedures, and is present in patients with normal calcium and phosphorus levels (1). Metastatic calcinosis cutis occurs in patients with underlying disorders of calcium or phosphorus metabolism (and therefore abnormal calcium and phosphorus levels) and can also be associated with calcium deposition in blood vessels, lungs, kidneys, and intestines (1). Iatrogenic calcinosis cutis is caused by the extravasation of intravenous calcium gluconate, calcium chloride, or fluids containing phosphorus (1). Idiopathic calcinosis cutis occurs in the absence of underlying causes like metabolic disorders or tissue damage. Calciphylaxis is the most serious subtype, defined as a vasculopathy of small and medium vessels that leads to ischemic necrosis.

Calciphylaxis is also known as uremic gangrene syndrome or calcific uremic arteriolopathy and is most often seen in patients with chronic renal failure, specifically those on hemodialysis. It is associated with extreme pain, infection, and a 60% to 80% mortality rate in the setting of few and frequently ineffective therapeutic options (2,3). Because of the rich vascular network of the penis, penile calciphylaxis is rare and is often associated with a poor prognosis having an overall mortality rate of 64% and an average of 2.5 months to death (4).

Take-Home Points

  • Calciphylaxis is the presence of calcium crystals in soft tissues and is often seen in hemodialysis patients.
  • Penile calciphylaxis is a rare finding that often portends a poor prognosis with a high mortality rate.

  • Nunley JR. Calcinosis cutis.
  • Vedvyas, C., Winterfield, L. S., & Vleugels, R. A. (2012). Calciphylaxis: a systematic review of existing and emerging therapies. Journal of the American Academy of Dermatology, 67(6), e253–e260.
  • Nigwekar SU, Kroshinsky D, Nazarian RM, Goverman J, Malhotra R, Jackson VA, Kamdar MM, Steele DJ, Thadhani RI. Calciphylaxis: risk factors, diagnosis, and treatment. Am J Kidney Dis. 2015 Jul;66(1):133-46. doi: 10.1053/j.ajkd.2015.01.034. Epub 2015 May 7. PMID: 25960299; PMCID: PMC4696752.
  • Yang TY, Wang TY, Chen M, Sun FJ, Chiu AW, Chen YH. Penile Calciphylaxis in a Patient with End-stage Renal Disease: A Case Report and Review of the Literature. Open Med (Wars). 2018 May 9;13:158-163. doi: 10.1515/med-2018-0025. PMID: 29756051; PMCID: PMC5941707.

SAEM Clinical Images Series: Face and Chest Rash

chicken pox

A 23-year-old female with a past medical history of asthma presented with a rash that began five days ago on her face and spread to her chest. The lesions are painful and pruritic, spreading slightly to her extremities. She noted a slight sore throat and nasal congestion. She denied any known fever and had no known vaginal or oral lesions. She has a 5-year-old daughter at home with no known symptoms. She is sexually active with one male partner who has no rash or illness. She is vaccinated for COVID-19. She is unsure of childhood illnesses and believes she was never properly immunized as a child in Central America.

Vitals: BP 110/55; Temperature 37°C; pulse ox 97%

Skin: Face, thorax, and extremity papules are noted with an erythematous base, some vesicular, others with occasional crust or scabs. No dermatomal distribution. There is relative sparing of extremities with more lesions noted on the trunk and face. Negative Nikolsky sign. Otherwise, no other findings on physical examination.


Herpes varicella-zoster, or chickenpox, is a viral infection transmitted by airborne droplets and direct contact. Before immunization, 90% of cases occurred in children. While primary infection in children is generally benign, adult and infant infections can have severe complications including encephalitis and pneumonia. Erythematous vesicular lesions appear in successive crops typically starting on the face and spreading to the trunk. Extremities usually have more minor involvement with sparing of palms and soles. Vesicles progress quickly to crusted erosions in 8-to-12-hour periods. Treatment should focus on symptomatic care.

Antivirals can slow the severity of the course if given within 24 hours of the onset. Severely immunocompromised patients should receive acyclovir 10 mg/kg IV every 8 hours for 7 to 10 days.

Take-Home Points

  • Chickenpox presents with several “crops” of lesions: papules, vesicles, and scabs.
  • Adult primary disease is not common and is more severe than pediatric illness.
  • Antivirals are not indicated after the first day of illness in immunocompetent adults with mild to moderate disease.

  • Gomez-Gutierrez AK, Flores-Camargo AA, Casillas Fikentscher A, et al. Primary varicella or herpes zoster? An educational case report from the primary care clinic. Cureus Apr 2022;14(4):e23732.
  • Hughes CM, Liu L, Davidson WB, et al. A Tale of Two Viruses: Coinfections of Monkeypox and Varicella Zoster Virus in the Democratic Republic of Congo. Am J Trop Med Hyg. 2020 Dec 7;104(2):604-611. doi: 10.4269/ajtmh.20-0589. PMID: 33289470
  • Kennedy PGE, Gershon AA. Clinical Features of Varicella-Zoster Virus Infection. Viruses. 2018 Nov 2;10(11):609. doi: 10.3390/v10110609. PMID: 30400213
  • Wolff K, Johnson RA Saavedra AP. Fitzpatrick’s Color Atlas of Clinical Dermatology. 7th ed. McGraw Hill. 2013:673-675.

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).
  • 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.

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.

Vitals: BP 95/68; HR 96; RR 24; 98% on room air; Temp 36.2°C; Wt 18.2 kg

General: Well-appearing 4-year-old female acting appropriately with grandmother and mother at the bedside.

Abdomen: Soft, nontender, nondistended.

Genitourinary: Normal appearing external genitalia without any skin tears/lacerations. Vaginal exam: Slow oozing bleed noted with round “doughnut” shaped tissue protruding at the vaginal opening.

Hemoglobin: 12.2 g/dL

Urinalysis (clean catch): Blood: Large; >200 RBCs, Ketones: 20, Nitrite: Negative, Leukocytes: Moderate, 19 WBCs

FSH/LH/Testosterone: Within normal limits

Urethral prolapse is a rare condition occurring in prepubertal female pediatric patients. It often presents to the emergency department with complaints of vaginal bleeding, difficulty urinating, or dysuria. The most common predisposing factors to this condition include obesity, cough, trauma, constipation, or a history of any activity that causes a sudden recurrent increase in pelvic pressure, such as a trip to the trampoline park as was the case in this patient [1]. On physical examination, urethral prolapse appears as an annular-like mucosal mass with a central dimple located between the labia majora on examination [1]. Initial treatment is medical management with topical estrogen cream in conjunction with Sitz baths and outpatient follow-up with pediatric urology or gynecology. However, persistence of the prolapse or necrosis of the distal urethra often warrants emergent pediatric urology consultation [2,3]. Recurrent cases or cases refractory to medical management will often require surgery. The patient in this case was treated with a 4-week estrogen cream taper. The patient followed up with pediatric gynecology without further complication or need for further intervention.

Child Abuse, Vaginal Trauma, Malignancies (ie: sarcoma botryoides), Infection, Vaginal foreign body, Urethral Prolapse, Precocious puberty, Hypothyroidism, and Exogenous hormone

Take-Home Points

  • Consider urethral prolapse in any prepubertal female who presents to the Emergency Department with a triage complaint of vaginal bleeding.
  • Treatment for urethral prolapse is typically conservative with topical estrogen cream and prompt follow up with pediatric urology or gynecology.
  • Always keep a broad differential for prepubertal pediatric patients with genitourinary and vaginal bleeding complaints
  • HHillyer S, Mooppan U, Kim H, Gulmi F. Diagnosis and treatment of urethral prolapse in children: experience with 34 cases. Urology. 2009 May;73(5):1008-11. doi: 10.1016/j.urology.2008.10.063. Epub 2009 Mar 13. PMID: 19285715.
  • Laufer M, Emans S. Overview of vulvovaginal conditions in the prepubertal child. Published 2021. Accessed January 5, 2022.
  • Teach S. Evaluation of vulvovaginal bleeding in children and adolescents. Published 2021. Accessed January 5, 2022.

By |2023-11-12T14:19:13-08:00Nov 17, 2023|Ob/Gyn, Pediatrics, SAEM Clinical Images|
Go to Top