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., https://doi.org/10.1097/aog.0000000000004240.
  • 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., https://doi.org/10.1056/nejmcp0900696.
  • 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., https://doi.org/10.1016/s0090-8258(88)80009-x.

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

High sensitivity cardiac troponins for ED chest pain evaluation (2022 ACC pathway)

How do we best use high-sensitivity cardiac troponin (hs-cTn) to risk stratify patients with symptoms concerning for an acute myocardial infarction (AMI)? The 2022 American College of Cardiology (ACC) pathway provides timely guidance [1]. We help you translate this to your clinical practice, by illustrating with a case. Time to know your hs-cTn better.

Take-to-work points

  • When interpreting the hs-cTn, you can use either of the following pathways to optimize both accuracy and patient throughput:
    • European Society of Cardiology (ESC) 2020 0/1 hour or 0/2 hour pathway
    • High-Sensitivity Troponin in the Evaluation of Patients With Acute Coronary Syndrome (High-STEACS)
  • These clinical decision pathways utilizing hs-cTn are complicated to calculate on your own.
    • Encourage your ED to set up an algorithm that you can follow based on your laboratory’s assay.
    • Otherwise, apply a simplified approach. When patients present with <6 hours of symptoms, they are low risk if the 0- and 3-hour troponin levels are less than the 99th percentile upper reference limit (URL).
  • Low-risk patients do not routinely require stress testing in the ED.
  • Intermediate-risk patients may be further stratified based on recent stress testing or coronary angiogram findings plus a modified HEART or Emergency Department Assessment of Chest Pain (EDACS) score.

Applying the 2022 ACC guideline

Before delving into the specifics of the hs-cTn pathways, start with the ECG. The ACC 2022 pathway has a section dedicated to ECGs in ischemia [1], and FOAMcast has a great visual summary.

The 2022 ACC pathway [1] endorses clinical decision pathways that:

  • Use hs-cTn AND
  • Enable rapid rule-out using very low hs-cTn values (far below the 99th percentile) on arrival, or a very small change (delta) between 2 hs-cTn values.

Examples of such pathways include [2]:

  • The ESC 0/1 hour pathway, where hs-cTn is obtained on arrival, and if needed, 1 hour later.
  • The ESC 0/2 hour pathway, where hs-cTn is obtained on arrival, and if needed, 2 hours later.
  • The High STEACS pathway, where hs-cTn is obtained on arrival, and if needed, 3 hours later.

These clinical decision pathways take advantage of the diagnostic power of the delta hs-cTn value, resulting in higher sensitivity for AMI (99%) [3], more patients being able to be ruled-out for AMI [4], and more patients being discharged home with a shorter ED length of stay [5]. This contrasts traditional risk-stratification approaches, which compare hs-cTn values solely to the 99th percentile upper reference limit.

  • Note: Using the pathways and using a single hs-cTn result are not mutually exclusive concepts. Clinical decision pathways DO allow us to rule out AMI with a single hs-cTn value in some instances. An example is if the patient has a very low value (e.g., below limit of detection) AND the chest pain onset is >3 hours ago AND the ECG is non-ischemic.

Let’s apply the ESC 2020 0/1 hour pathway [2], with some modifications based on the 2022 ACC guidelines [1]:

high sensitivity cardiac troponin hs-cTn risk stratification

Figure 1. Stratification of patients for AMI based on high sensitivity troponin testing and the ESC 0/1 hour pathway (second hs-cTn drawn 1 hour after the initial hs-cTn test)

Notice how numbers are replaced with values A, B, C, D and E. That’s because these values are assay specific. You (or someone in your department) needs to know which assay your ED has, and use the appropriate values for that assay. Examples of cutoffs:

Figure 2: Assay-based cutoffs for different high sensitivity cardiac troponin tests from the 2022 ACC guideline [1] (Limit of quantification, LoQ)

One concept that cuts across all assays is the limit of quantification (LoQ). That’s the lowest hs-cTn value that can be reliably reported as a number for that assay. In the risk stratification pathway (figure 1), value E is often the LoQ, or an optimized threshold slightly above the LoQ.

Case #1

A 52-year-old woman presents with vague heaviness over the left side of the chest that does not radiate elsewhere. She does not recall clearly how it started, and it has been persistent for 5 hours. Its intensity does not change with walking or changes in posture. There are no associated symptoms such as diaphoresis, breathlessness, vomiting, fever, cough, or leg swelling.

She has hypertension and hyperlipidemia treated with lifestyle modification. She does not smoke. There is no family history of heart disease. She has no other recent illnesses or travel history.

On examination, her vital signs are normal. Heart sounds are dual with no murmurs and breath sounds are equal bilaterally. Pulses are well felt in all four limbs. There is no lower limb swelling or tenderness.

A 12-lead electrocardiogram (ECG) and chest x-ray (CXR) are unremarkable. The hs-cTn level on arrival is below the limit of quantification (LoQ).

Because the patient’s chest pain started >3 hours ago and she has a non-ischemic ECG, the initial hs-cTn is below LoQ already stratifies her as a LOW-RISK patient for AMI by the pathway. She does not need a repeat hs-cTn test. Caveat: Patients with known coronary artery disease might still have considerable risk for AMI even with this constellation of findings, requiring clinical judgment beyond this pathway [6].

Also do not forget that you still need to address other important potential causes of chest pain:

  • Aortic dissection appears unlikely, given the lack of suggestive features on history or physical examination. The onset was gradual with no radiation to the back or abdomen, and no features of distal ischemia such as neurological or pulse deficits. The CXR did not show any abnormalities consistent with a dissection.
  • Pulmonary embolism (PE) appears unlikely. She would be low risk by gestalt or structured scoring systems (Wells or revised Geneva), and a negative D-dimer would essentially rule out pulmonary embolism here. Note that the PE rule-out criteria do not help in this case, because she is >50 years old.

Thankfully, most patients will be low risk after walking through the above. What’s the disposition and follow-up plan for them? In short, less is more. As long as your clinical judgment concurs with a low-risk stratification, you should send the patient home with chest pain advice, return precautions, and recommendations to follow-up with their primary care provider within 30 days for optimal management of cardiovascular risk factors. You do not have to routinely order stress testing from the ED! This is endorsed in the 2022 ACC pathway [1] and the 2021 AHA chest pain guidelines [7].

The high-risk category

High-risk category hs-cTn values in the ESC 2020 0/1 hour pathway or high STEACS pathway come in 2 types:

  • A high absolute value
  • A high delta between two hs-cTn samples, which is suggestive of the rise or fall seen in AMI

Those values are assay- and pathway-specific, so you’ll need to find out more about your local assay. These in the high-risk category are usually admitted to the hospital to assess for AMI as well as other causes of troponin elevation.

What if you have a patient with intermediate findings?

Case #2

A 66-year-old man with hypertension, hyperlipidemia, diabetes mellitus, and chronic renal failure presents with poorly localized central chest discomfort while trying to sleep. It started 2 hours ago. The discomfort has a burning character, though he has never been diagnosed with reflux before.

His vital signs and physical exam are unremarkable other than an arteriovenous fistula on his left arm for hemodialysis. His ECG shows left ventricular hypertrophy.

The first hs-cTn results in the intermediate range on your assay-specific cutoff for the ESC 2020 pathway or high-STEACS pathway.

The first step is to repeat hs-cTn testing in 3-6 hours. Those with a significant change in hs-cTn (e.g., ≥ value D in the ESC 2020 pathway) will be diagnosed with acute myocardial infarction or acute myocardial injury (e.g., as seen in heart failure, arrhythmias, or sepsis).

How about those with no significant change? The ACC now endorses that these intermediate-risk patients can be considered for discharge with rapid follow-up, if 1 of these 4 criteria are met:

  1. Invasive or CT coronary angiogram <2 years ago without coronary plaque
  2. Stress test <1 year ago without ischemia
  3. Modified HEART score (where troponin is excluded) ≤3 [MDCalc] or EDACS<16 [MDCalc]
  4. Chronic elevations in hs-cTn similar to previously measured levels

Patients who do not meet these criteria above should get some form of additional evaluation such as non-invasive testing, such as a CT coronary angiogram, myocardial perfusion imaging, or stress echocardiography. If not, consider cardiology consultation or admission, or at least a shared decision-making with the patient for an expedited outpatient workup with the understanding that this group has a 30-day rate of death or MI ranging from 5% to 22% [1, 8, 9].

You repeat a hs-cTn 3 hours later and it remains unchanged. The patient has no previous stress testing or coronary angiogram, and he is not low risk by HEART or EDACS scoring.

You thus consult the cardiologist, who recommends to admit the patient to the hospital for further observation and evaluation.

References

  1. Writing Committee, Kontos MC, de Lemos JA, et al. 2022 ACC Expert Consensus Decision Pathway on the Evaluation and Disposition of Acute Chest Pain in the Emergency Department: A Report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. 2022;80(20):1925-1960. doi:10.1016/j.jacc.2022.08.750
  2. Collet JP, Thiele H, Barbato E, et al. 2020 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation [published correction appears in Eur Heart J. 2021 May 14;42(19):1908] [published correction appears in Eur Heart J. 2021 May 14;42(19):1925] [published correction appears in Eur Heart J. 2021 May 13;:]. Eur Heart J. 2021;42(14):1289-1367. doi:10.1093/eurheartj/ehaa575
  3. Burgos LM, Trivi M, Costabel JP. Performance of the European Society of Cardiology 0/1-hour algorithm in the diagnosis of myocardial infarction with high-sensitivity cardiac troponin: Systematic review and meta-analysis [published online ahead of print, 2020 Jun 29]. Eur Heart J Acute Cardiovasc Care. 2020;2048872620935399. doi:10.1177/2048872620935399
  4. Badertscher P, Boeddinghaus J, Twerenbold R, et al. Direct Comparison of the 0/1h and 0/3h Algorithms for Early Rule-Out of Acute Myocardial Infarction. Circulation. 2018;137(23):2536-2538. doi:10.1161/CIRCULATIONAHA.118.034260
  5. Chew DP, Lambrakis K, Blyth A, et al. A Randomized Trial of a 1-Hour Troponin T Protocol in Suspected Acute Coronary Syndromes: The Rapid Assessment of Possible Acute Coronary Syndrome in the Emergency Department With High-Sensitivity Troponin T Study (RAPID-TnT) [published correction appears in Circulation. 2021 Jun 22;143(25):e1118]. Circulation. 2019;140(19):1543-1556. doi:10.1161/CIRCULATIONAHA.119.042891
  6. Ashburn NP, Snavely AC, O’Neill JC, et al. Performance of the European Society of Cardiology 0/1-Hour Algorithm With High-Sensitivity Cardiac Troponin T Among Patients With Known Coronary Artery Disease. JAMA Cardiol. 2023;8(4):347-356. doi:10.1001/jamacardio.2023.0031
  7. Gulati M, Levy PD, Mukherjee D, et al. 2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines [published correction appears in Circulation. 2021 Nov 30;144(22):e455]. Circulation. 2021;144(22):e368-e454. doi:10.1161/CIR.0000000000001029
  8. Mueller C, Giannitsis E, Christ M, et al. Multicenter Evaluation of a 0-Hour/1-Hour Algorithm in the Diagnosis of Myocardial Infarction With High-Sensitivity Cardiac Troponin T. Ann Emerg Med. 2016;68(1):76-87.e4. doi:10.1016/j.annemergmed.2015.11.013
  9. Twerenbold R, Neumann JT, Sörensen NA, et al. Prospective Validation of the 0/1-h Algorithm for Early Diagnosis of Myocardial Infarction. J Am Coll Cardiol. 2018;72(6):620-632. doi:10.1016/j.jacc.2018.05.040

Featured image adapted from Adobe Firefly

ALiEM AIR Series | Toxicology Module

AIR series toxicology 2023 module

 

Welcome to the AIR Toxicology Module! After carefully reviewing all relevant posts in the past 12 months from the top 50 sites of the Digital Impact Factor [1], the ALiEM AIR Team is proud to present the highest quality online content related to related to toxicology in the Emergency Department. 8 blog posts met our standard of online excellence and were approved for residency training by the AIR Series Board. More specifically, we identified 3 AIR and 5 Honorable Mentions. We recommend programs give 4 hours of III credit for this module.

AIR Stamp of Approval and Honorable Mentions

In an effort to truly emphasize the highest quality posts, we have 2 subsets of recommended resources. The AIR stamp of approval is awarded only to posts scoring above a strict scoring cut-off of ≥30 points (out of 35 total), based on our scoring instrument. The other subset is for “Honorable Mention” posts. These posts have been flagged by and agreed upon by AIR Board members as worthwhile, accurate, unbiased, and appropriately referenced despite an average score.

Take the AIR Toxicology Module at ALiEMU

 

Interested in taking the AIR quiz for fun or asynchronous (Individualized Interactive Instruction) credit? Please go to the above link. You will need to create a free, 1-time login account.

Highlighted Quality Posts: Toxicology

Blog/PodcastArticle TitleAuthor(s)DateAIR/HM
EM OttawaBuprenorphine: A guide for ED providersMax Zworth, MD and Rebecca Seliga, MDMar 9, 2023AIR
EMCritAlcohol withdrawalJosh Farkas, MDMar 29, 2023AIR
ALIEMPhenobarbital as 1st line medication for alcohol withdrawal: have you switched from benzodiazepines yet?Alex Rogers MD, J.D. Cambron DOJun 1, 2023AIR
EM DocsN-acetylcysteine for Acetaminophen ToxicityEric Sabatini Regueira, MD and Ann-Jeannette Geib, MD Aug 3, 2023HM
EM DocsMethylene blueQuinton Nannet, MD and Christine Murphy, MDDec 27, 2022HM
EM DocsAcute organophosphate toxicityDaniel Escobar, MD and Ann-Jeannette Geib, MDJun 7, 2023HM
Core EMUpdates in high dose insulin and euglycemia therapy for the treatment of b-adrenergic receptor and calcium channel antagonist overdoseWilliam Plowe, MDMar 28, 2022HM
EM OttawaCBRNE and HAZMAT: Be preparedPatrick Fisk, MDJan 19, 2023HM

(AIR = Approved Instructional Resource; HM = Honorable Mention)

 

If you have any questions or comments on the AIR series, or this AIR module, please contact us!

 

Reference

  1. Lin M, Phipps M, Chan TM, et al. Digital Impact Factor: A Quality Index for Educational Blogs and Podcasts in Emergency Medicine and Critical Care. Ann Emerg Med. 2023;82(1):55-65. doi:10.1016/j.annemergmed.2023.02.011, PMID 36967275

 

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

vision

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 https://doi.org/10.1161/STROKEAHA.115.009839
  • 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

eschar

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.

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