SAEM Clinical Images Series: An Ultrasonographic Rabbit Hole


An 86-year-old man with a past medical history of coronary artery disease, hypertension, hyperlipidemia, chronic kidney disease, COPD, choledocholithiasis requiring ERCP and sphincterotomy 2 years ago presented with five days of feeling unwell. History was limited due to cognitive impairment. His daughter had reported to staff he had been feeling unwell for five days, intermittently having nausea and generalized abdominal pain, subjective fevers, chest pain, and shortness of breath. His daughter also reported a history of intermittent lower abdominal cramping which was chronic for him. He denied changes to urination or bowel movements.

Vitals: BP 106/67, Temp 36.2°C, Pulse 115, Resp 20, SpO2 95%

General: Nontoxic appearing, no distress

Heart: Regular, no murmurs

Lungs: Clear bilaterally, normal work of breathing

Abdomen: Diffusely tender, greatest in left upper quadrant

CBC with differential: WBC 14.1, Neutrophil 12% (high)

Comprehensive metabolic panel (CMP): Total bilirubin 2.7 (high), AlkP 328 (high), AST/ALT normal

Lipase: Normal

Troponin x2: Negative

Chest x-ray: No acute abnormality

This patient has sonographic evidence of perforated gangrenous cholecystitis which was confirmed on subsequent CT scan. Gallbladder perforation is a complication of cholecystitis and has a reported incidence of 5-10%. It has been reported as early as two days after the onset of symptoms to as late as several weeks afterward. The most common site of perforation is the fundus due to relatively poor blood supply. In this case, the culprit perforation was in the proximal body adjacent to the stone which is suspected to have eroded through the wall.

Figure 1 depicts a minimally thickened gallbladder wall measured at 3.5 mm with a large shadowing stone-in-neck and associated perihepatic fluid collection (arrow) with a subtle intraluminal membrane and wall irregularity consistent with gangrenous cholecystitis. Figure 2 doppler images show no flow within the fluid collection and a suspiciously thin gallbladder wall (arrow). Figure 3 again highlights an irregular wall with small “hole sign” (arrow) signifying perforation of the gallbladder into the adjacent fluid collection. This patient was admitted to the hospital’s general surgical service and treated with IV broad-spectrum antibiotics and a percutaneous cholecystostomy tube placed by interventional radiology.

Take-Home Points

  • Look out for “hole signs” with adjacent fluid collection on your gallbladder ultrasounds which would suggest perforation.
  • Intraluminal membranes or wall irregularities suggest gangrenous cholecystitis.
  • Initial treatment includes broad-spectrum antibiotics and cholecystostomy tube decompression.

  • Indiran, V., Prabakaran, N. & Kannan, K. “Hole sign” of the gallbladder. Indian J Gastroenterol 36, 66–67 (2017).
  • Jeffrey RB, Laing FC, Wong W, Callen PW. Gangrenous cholecystitis: diagnosis by ultrasound. Radiology. 1983 Jul;148(1):219-21. doi: 10.1148/radiology.148.1.6856839. PMID: 6856839.
  • Sood, B.P., Kalra, N., Gupta, S., Sidhu, R., Gulati, M., Khandelwal, N. and Suri, S. (2002), Role of sonography in the diagnosis of gallbladder perforation. J. Clin. Ultrasound, 30: 270-274.

SAEM Clinical Images Series: One Month of Vaginal Bleeding

heterogenous uterus

A 28-year-old female G3P2002 presented to the emergency department for one month of vaginal bleeding. The patient was seen in the emergency department one month earlier for vaginal bleeding in the first trimester of pregnancy. Her estimated gestational age was six weeks by last menstrual period. At the time her beta-hCG was 7225 mlU/mL with no intrauterine pregnancy demonstrated on transvaginal ultrasound. Three days later, the patient had declining b-hCG and transvaginal ultrasound again with no intrauterine pregnancy. The patient was discharged home with a diagnosis of miscarriage. Since discharge, she endorsed an initial slowing of vaginal bleeding but over the last two weeks bleeding had become heavier and continuous; soaking up to eight pads a day. She endorsed worsening nausea and vomiting over the past two weeks. She has been sexually active since her last encounter. She denied abdominal pain, pelvic pain, cramping, dizziness, shortness of breath, or fevers.

Vitals: BP 136/70; Pulse 96; Temp 97.8°F; Resp 16; SpO2 100%

Constitutional: No distress

Cardiovascular: Normal rate, regular rhythm, normal heart sounds

Abdomen: Soft and non-tender; Gravid uterus approximately 10 weeks

Pelvic exam: Active vaginal bleeding of dark red blood originating from the cervical os. Cervical os is closed and otherwise normal in appearance. Multiple clots are seen in the vaginal canal and posterior fornix. Vaginal canal and external genitals are normal in appearance.

Beta-HCG: 91,401 mlU/mL

Hemoglobin: 12.8 g/dL

Our patient’s case is convoluted by reporting a miscarriage the month prior, with declining beta-HCG and transvaginal ultrasounds with no intrauterine pregnancy. While her symptoms never fully resolved she endorsed that her vaginal bleeding slowed and only started getting worse after resuming intercourse.

Her physical exam of a gravid uterus of approximately 10 weeks (despite reporting a miscarriage four weeks prior), persistent vaginal bleeding, and intractable nausea and vomiting are concerning for molar pregnancy [1]. Molar pregnancies typically present as abnormal uterine bleeding in the first or second trimester and are accompanied by symptoms of hyperemesis gravida secondary to the increase in beta-hCG [2]. The two main risk factors for gestational trophoblastic disease are the extremes of maternal age and prior molar pregnancy. However, there is an increased risk for molar pregnancy in patients with a history of prior spontaneous abortions and infertility [4]. Beta-hCG are typically greater than > 100,000 mlU/mL signifying excessive trophoblastic growth, however a value < 100,000 mlU/mL does not exclude the diagnosis of molar pregnancy as partial moles tend not to produce as much beta-HCG [3].

These images, taken by point of care ultrasound, show a heterogenic mass with mixed echogenicities within the uterine cavity consistent with gestational trophoblastic disease or molar pregnancy. Obstetrics and Gynecology was consulted for definitive management. The patient was taken to the operating room for dilation and curettage and was discharged the following day.

Take-Home Points

  • Physical exam findings of an enlarged uterus inconsistent with gestational age, vaginal bleeding, and intractable nausea and vomiting should clue you into a possible molar pregnancy.
  • Point-of-care ultrasound is an invaluable tool when assessing vaginal bleeding and will often help the clinician in the management or diagnostic pathway.
  • Beta-hCG < 100,000 mlU/mL does not rule out molar pregnancy. Obtain a good history, perform a thorough physical exam, and pick up your ultrasound probe.

  • Soper, John T. “Gestational Trophoblastic Disease.” Obstetrics & Gynecology, vol. 137, no. 2, 2021, pp. 355–370.,
  • Cline, David, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill Education, 2020.
  • Berkowitz, Ross S., and Donald P. Goldstein. “Molar Pregnancy.” New England Journal of Medicine, vol. 360, no. 16, 2009, pp. 1639–1645.,
  • Acaia, Barbara, et al. “Increased Frequency of Complete Hydatidiform Mole in Women with Repeated Abortion.” Gynecologic Oncology, vol. 31, no. 2, 1988, pp. 310–314.,

By |2024-02-11T20:06:03-08:00Feb 12, 2024|Ob/Gyn, SAEM Clinical Images|

SAEM Clinical Images Series: Back Lesion

skin lesion

An 18-year-old-female with no known past medical history presented with a lesion on her back that had been present and enlarging for five months. It was not painful unless she touched it, and then only mildly tender. She denied any known cause, wound, prior rash, or other lesions. Her review of systems and past medical history were negative.

Vitals: Normal

Skin: An erythematous lenticular, or biconvex, lesion with distinct borders is noted at the left posterior thorax below the scapula. It is soft with some slight nodularity on palpation, and only mild tenderness noted. There is no fluctuance. No other skin lesions are present. The rest of the examination is normal.

Ultrasound reveals a 1.7 x 0.8 x 1.1 cm superficial soft tissue mass inferior to the scapula on the left thorax.

CT scan of the chest confirms no intrathoracic extension or other lesions.

Biopsy is the next appropriate step. The lesion does not appear to be infectious, either viral, bacterial, or fungal. Furthermore, it has no appearance of an inflammatory reaction that would benefit from topical steroids. The differential includes a cystic structure, neurofibroma, or malignancy. Because of the concern for malignancy, a biopsy was performed in the emergency department after the ultrasound and CT scan confirmed there was no extension into the thorax. The biopsy revealed a pilomatrixoma, or pilomatricoma. Pilomatrixoma is a superficial benign skin tumor that arises from hair follicle matrix cells. They commonly occur in the first two decades of life with a mean age of 17 years. The most common presentation is an asymptomatic, firm, slowly growing mobile nodule. However, only 16% are accurately diagnosed on clinical examination. This case reveals the wide variation in visual presentation and confirms the inability to diagnose the lesion at the bedside. Complete surgical excision is curative.

Take-Home Points

  • Unknown skin lesions, with concern for malignancy, should be diagnosed by biopsy.
  • Pilomatrixoma is rarely diagnosed at the bedside.
  • Jones CD, Ho W, Robertson BF, Gunn E, Morley S. Pilomatrixoma: A Comprehensive Review of the Literature. Am J Dermatopathol. 2018 Sep;40(9):631-641. doi: 10.1097/DAD.0000000000001118. PMID: 30119102.

By |2024-01-28T21:32:23-08:00Feb 2, 2024|Dermatology, SAEM Clinical Images|

SAEM Clinical Images Series: Retrobulbar Spot Sign


A 59-year-old male with no known past medical history other than an incidental abdominal aortic aneurysm presented with sudden onset, painless vision loss in his left eye. The patient was watching TV two days prior when he saw a “brightness” in his left eye and then progressive blurriness until his vision faded away, all occurring within the span of a minute. At the time of presentation, he only sees a speck of light from that eye. He denied associated pain, flashes, floaters, jaw claudication, the sensation of a “curtain falling”, prior vision problems, or a history of blood clots.

Eyes: Eyelids and lashes normal. Visual acuity: 20/30 OD, Light Perception OS. EOMI. PERRL. OD visual fields intact. Afferent Pupillary Defect OD. Normal conjunctiva. IOP 16 OD, 14 OS. Otherwise CN 3-12 intact.

Complete blood count (CBC): Within normal limits

Basic metabolic panel: Creatine 1.3 (unknown baseline)

ESR: Unmarkable

Central Retinal Artery Occlusion (CRAO) is an ocular emergency that presents as acute painless monocular vision, caused by ischemia and infarction to the retina via thromboembolic disease to the central retinal artery. It requires immediate consultation with ophthalmology as well as neurology as it is considered a stroke equivalent.

The case described above and several previously published case studies highlight the utility of POCUS in identifying CRAO via the retrobulbar spot sign (RBSS) within the optic nerve in a rapid, non-invasive manner that can be done prior to waiting for dilation for a fundoscopy exam. This has the potential to expedite consultations with specialty teams and treatment.

Several studies also reveal the potential of POCUS to predict the etiology of CRAO (arterio-arterial embolization vs cardio-embolic vs vasculitis) and thus to predict the success of thrombolytic treatment in CRAO. In a prospective monocenter study of 46 patients with ophthalmologically confirmed CRAO, embolism from large artery atherosclerosis (LAA, i.e. carotids or aortic arch) was the etiology in 27 patients, cardioembolic in 10 patients, vasculitis in 5 patients, and unknown in 4 patients. Out of the LAA patients, 59% had RBSS compared with only 20% in cardioembolic and 0% in the vasculitis patients. Within the 11 patients that underwent thrombolysis, statistically significant visual improvement occurred in all 4 patients with RBSS negative CRAO, while the 7 patients with RBSS positive CRAO had persistent visual impairment with persistent occlusion of their arteries. This study concludes that their results support the hypothesis that RBSS is seen due to calcium deposits that will not be dissolved with thrombolysis. Another small single-center German study points out the utility of seeing RBSS as 100% specific for an embolic cause of CRA, excluding temporal arteritis from the differential.

Take-Home Points

  • POCUS can guide us in diagnosing a patient with painless vision loss prior to more time-consuming fundoscopy exam.
  • Stroke workup for CRAO is necessary, and don’t forget about secondary prevention/risk stratification which must be part of the management.
  • RBSS may predict poor response to systemic thrombolysis.

  • Ertl M, Altmann M, Torka E, Helbig H, Bogdahn U, Gamulescu A, Schlachetzki F. The retrobulbar “spot sign” as a discriminator between vasculitic and thrombo-embolic affections of the retinal blood supply. Ultraschall Med. 2012 Dec;33(7):E263-E267. doi: 10.1055/s-0032-1312925. Epub 2012 Sep 21. PMID: 23023446.
  • Nedelmann, Matt et al. “Retrobulbar Spot Sign Predicts Thrombolytic Treatment Effects and Etiology in Central Retinal Artery Occlusion” American Heart Association (AHA). Stroke. 2015;46:2322–2324
  • Smith, Austin T et al. “Using the Retrobulbar Spot Sign to Assist in Diagnosis and Management of Central Retinal Artery Occlusions.” Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine vol. 39,1 (2020): 197-202. doi:10.1002/jum.15073

By |2024-01-28T21:19:20-08:00Jan 29, 2024|Ophthalmology, SAEM Clinical Images, Ultrasound|

SAEM Clinical Images Series: A Rare Case of Purpura

An 88-year-old female presented to the ER with a chief complaint of cough, vague abdominal pain, and a rash. The patient stated that she was started on Cipro eyedrops 1 or 2 days prior to presentation for a possible eye infection. A day prior to presentation she developed a purple purpuric rash on her lower extremities that gradually progressed up her legs, and was present on her buttocks thighs, and lower legs. It was not on her palms or soles. She had no mucous membrane involvement. She lives alone. The nursing home called EMS given the patient’s severe and progressive rash and the fact that the patient was feeling unwell. She had no fever, vomiting, foreign travel, other new drug exposure, or other complaints.

GI: Abdomen is mildly diffusely tender without guarding or rebound.

Skin: There are scattered petechiae and purpura on her lower extremities, thighs, and buttocks. They are somewhat raised, non-blanching, not itchy, and non-tender. They are most prominent on her buttocks and dependent areas of her body.

WBC: 7.8 with normal differential

Platelets: 423

Comprehensive metabolic panel (CMP): normal kidney function and electrolytes

ESR: 125 mm/hour

CRP: 89 mg/L

Urinalysis (UA): >9,8000 bacteria, nitrite positive

This patient’s history and physical are consistent with Henoch-Schönlein purpura (IgA Vasculitis).

Common triggers include infection, drugs, and autoimmune.

Take-Home Points

  • Consider IgA vasculitis, even in an older patient.
  • Ciprofloxacin has been documented as a cause of IgA vasculitis.
  • Steroids and NSAIDs are the treatment of choice, and this condition usually improves with time.

  • Gamboa F, Rivera JM, Gómez Mateos JM, Gomez-Gras E. Ciprofloxacin-induced Henoch-Schönlein purpura. Ann Pharmacother. 1995 Jan;29(1):84. doi: 10.1177/106002809502900119. PMID: 7711355.
  • Gkoufa A, Sakellariou S, Katsoulas N, Georgakopoulou VE, Lazaris A, Cholongitas E. Henoch-Schönlein purpura associated with ciprofloxacin. Dermatol Ther. 2021 Jan;34(1):e14591. doi: 10.1111/dth.14591. Epub 2020 Dec 3. PMID: 33244823.

SAEM Clinical Images Series: Fever with Rash


A 40-year-old male, tailor by occupation, was brought to the Emergency Department with complaints of high-grade fever for the past 11 days. Fever was documented to be 102°F and was not associated with any chills or rigors. The patient also complained of shortness of breath for one week associated with a dry cough, as well as an altered sensorium for one day. The patient during his hospital stay developed ARDS and was on mechanical ventilation for 20 days. He was then extubated and discharged after 27 days.

Skin: Multiple eschars on knee, foot, and lower chest.

Complete Blood Count: WBC 31,000; Plt 12,000

BUN: 215 mmol/L

Creatinine: 2.5 mmol/L

Liver Function Tests: AST 192 IU/L; ALP 591 IU/L

Blood PCR for Scrub Typhus was found to be positive.

Scrub typhus is often diagnosed clinically based on exposure to endemic regions and its characteristic eschar, which usually appears on the lower extremities, axillae, or genital region. [1,2] Still, diagnosis can be tricky, and similar eschars can be caused by spider bites, Mediterranean spotted fever, Queensland tick typhus, African tick-bite fever, and anthrax. [3] Scrub typhus is a potentially fatal mite-borne rickettsial infection caused by Orientia tsutsugamushi. It is endemic to the Asia–Pacific region, which has an estimated 1 million instances per year. Those affected may have headaches, myalgias, hearing loss, and rash, in addition to fever. Encephalitis, hepatitis, and pulmonary and cardiac involvement can occur. [1,2]

Early empiric treatment with Doxycycline is life-saving.

Take-Home Points

  • Consider Scrub Typhus in a patient presenting with eschars.
  • Early empiric treatment with Doxycycline is life-saving.
  • Botelho-Nevers E, Raoult D. Fever of unknown origin due to rickettsioses. Infect Dis Clin North Am. 2007 Dec;21(4):997-1011, ix. doi: 10.1016/j.idc.2007.08.002. PMID: 18061086.
  • Hendershot EF, Sexton DJ. Scrub typhus and rickettsial diseases in international travelers: a review. Curr Infect Dis Rep. 2009 Jan;11(1):66-72. doi: 10.1007/s11908-009-0010-x. PMID: 19094827.
  • Shiao CC, Lin SY. Eschar: a clue to scrub typhus. CMAJ. 2011 Oct 18;183(15):E1152. doi: 10.1503/cmaj.101929. Epub 2011 Sep 12. PMID: 21911554; PMCID: PMC3193135.

SAEM Clinical Images Series: Post-Vaccination Rash


A 42-year old Bengali man with a history of hyperlipidemia presented to the Emergency Department with facial swelling, diffuse rash, renal insufficiency and proteinuria after receiving his COVID-19 vaccine (Moderna) booster dose. There were no adverse events with the first two doses of the vaccine except for mild transient sore throat and cough after the 2nd dose. Within a few hours after the booster dose, the patient noted a pruritic rash initially on his scalp, that then spread to his torso associated with facial swelling, fever, and chills. He presented to his primary care physician three days later. At that time, laboratory workup showed proteinuria, elevated C-reactive protein (65.2), and an elevated serum creatinine (2.84 mg/dl). He was advised to go to the Emergency Department.

General: He was in no distress; his vital signs were normal.

Skin: While the facial swelling had improved, the rash had progressed to involve the entire body. There were multiple skin lesions with raised borders, and central clearing (Figures 1 and 2); no mucosal involvement was noted.

The rest of his physical exam including lung, cardiac, gastrointestinal, and neurological examinations were normal.

Laboratory workup in the ED revealed resolution of proteinuria with serum creatinine returning to normal baseline value (0.89 mg/dl).

The patient’s rash is a classic erythema multiforme (EM) rash. The mRNA COVID-19 vaccine is a lipid nano particle-encapsulated, nucleoside-modified mRNA vaccine that encodes the perfusion spike glycoprotein of the SARS-CoV-2 virus. Local reactions include mild to moderate pain at the injection site, and systemic effects including fatigue, fever, and headache, commonly appearing within 2-5 days after the second dose. Erythema multiforme has been reported as a cutaneous reaction after the COVID-19 mRNA vaccine. As per the vaccine adverse event reporting system (VAERS) from the Centers for Disease Control and Prevention, to date, there have been 284 reported cases of EM after the Moderna COVID-19 vaccine and 500 cases reported after the Pfizer vaccine. The exact pathogenesis of EM after the vaccine is unclear. This delayed hypersensitivity reaction is likely from sensitization to a vaccine component. It appears to be a T-cell mediated response making CD4+ helper T-1 cells, release of gamma-interferon, and then recruitment of auto-reactive T-cells. It should be differentiated from immediate IgE-mediated hypersensitivity reactions such as flushing, urticaria, angioedema, and hypotension that usually appear within minutes of administering the vaccine.

While immediate hypersensitivity is a contraindication for further doses, erythema multiforme and other such delayed manifestations should not discourage the use of additional COVID-19 mRNA doses if appropriate.

Take-Home Points

  • Erythema multiforme is a delayed hypersensitive reaction that may occur after COVID-19 mRNA vaccine.
  • This type of delayed hypersensitivity reaction, likely from sensitization to vaccine component, is not a contraindication to further COVID-19 boosters.

  • Su JR, Haber P, Ng CS, Marquez PL, Dores GM, Perez-Vilar S, Cano MV. Erythema multiforme, Stevens Johnson syndrome, and toxic epidermal necrolysis reported after vaccination, 1999-2017. Vaccine. 2020 Feb 11;38(7):1746-1752. doi: 10.1016/j.vaccine.2019.12.028. Epub 2019 Dec 20. PMID: 31870573; PMCID: PMC7008074.
  • Vaccine Adverse Events Reporting System [Internet]. CDC. 2022. Available from:

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