An interesting derm case in the ED: Mycosis Fungoides

Mycosis Fungoides: A Medical Student Clinical Pearl

 

Nicholas Relja, B.Sc.(Hon), M.Sc.
Dalhousie Medicine New Brunswick
M.D. Candidate, Class of 2022

All case histories are illustrative and not based on any individual

Reviewed by Dr. Devon Webster

Copyedited by Dr. Mandy Peach

Case

A 55-year-old male presented to the ED after concerned family brought him in due to ongoing generalized weakness lasting approximately one month. On inspection he had erythematous, scaly, ulcerative lesions covering his entire body with only facial sparing. He mentioned burning-like pain originating from his ulcerative lesions. He had been previously diagnosed with T-cell lymphoma 30 years ago and had gone through multiple rounds of chemo and radiation therapy since that time.

Picture from: Denis D, Beneton N, Laribi K, Maillard H (2019). Management of mycosis fungoides-type cutaneous T-cell lymphoma (MF-CTCL): focus on chlormethine gel. Cancer Management and Research. Vol 11: 2241-2251

Differential for itchy, erythematous rash:

Condition
Atopic dermatitis
Contact dermatitis
Drug eruptions
Erythrodermic psoriasis
Psoriasis
Sezary syndrome
Various lymphomas

 

When reviewing the patient’s past medical history you see they were previously diagnosed with Mycosis Fungoides – a rare cutaneous form of T-cell lymphoma.

Epidemiology

Mycosis fungoides has an incidence of approximately 6 cases per million per year in the United States. It is more common in adults over 50 years of age, with a male to female ratio of 2:1. The disease is also more common amongst the Black population than in Caucasians or Asians.8,9

Etiology

The exact cause of mycosis fungoides is not known; however, there a variety of mechanisms that have been postulated:2

• Genetic and epigenetic abnormalities.3,4
• Environmental and occupational exposure to noxious substances and chemicals.5
• Human T-lymphotropic virus Type 1 – a suspected infection-type etiology.6
• Cytokines such as IL-2 and IL-4 due to their increased presence in patients with mycosis fungoides and Sezary syndrome.7

 

There are three stages of mycosis fungoides and therefore clinical presentation will vary depending on the stage of disease:

Patch stage: Erythematous, or brownish scaly patch, which may show some atrophy. It is possible to have one or multiple lesions develop in areas such as the gluteal region or on the proximal thighs. The likeness of this stage has been compared to “small-plaque” or “large plaque” parapsoriasis; however, the plaques are actually not plaques but patches instead.10

Plaque stage: This is the second stage – lesions will be larger, more numerous and will show infiltration. The lesions appear annular, are raised and have well-defined edges as well as asymmetry in terms of their distribution. Face and scalp involvement can also be seen starting at this stage.11

Tumor stage: The final stage – erythematous-purplish papules or nodules of larger diameter.12

There are other clinical variants of mycosis fungoides, but they are not as common, and some are quite rare.

Sezary syndrome:
In advanced form of the mycosis fungoides, Sezary syndrome may be present. This syndrome involves erythroderma with pruritus, lymphadenopathy and atypical circulating lymphocytes (referred to as Sezary or Lutzner cells).13

Evaluation in the ED

A detailed history and physical exam including checking for lymphadenopathy (most commonly cervical nodes) and organomegaly14,15 in addition to documenting the rash characteristics.

Labs: CBC, liver function tests, LDH

Radiological tests: depends on extent of lymphadenopathy and organomegaly. Can do a CXR in the ED for lung involvement, but otherwise advanced imaging can be decided upon by specialist consultant and may include CT, US, PET or MRI.

Biopsy: lymph nodes and rash – by consultants

Treatment and Management – refer to your friendly neighborhood dermatologist.

Early stage:

Treatment options include topical therapies such as corticosteroids and other agents, UV therapy, local radiation and systemic immunosuppressants 15,16,17.

Advanced Stage:

Treatment for the advanced stages of mycosis fungoides are directed at disease control and symptom relief. Localized radiation, targeted immunotherapy or chemotherapy. 15, 18

Prognosis

The prognosis of mycosis fungoides is variable but in general as the stage gets more advanced and with patients over the age of 60, the prognosis becomes poorer. Other poor prognostic factors include increased LDH, tumor distribution and organ involvement.2

Case Conclusion

The patient seen in hospital by the dermatologist on call and was deemed to be in the plaque stage. He was admitted due to the advancing course and and inability to manage his symptoms from home. Further care will involve palliation and a focus on quality of life.

 

References:

  1. Olisova, O. Y. et al. [Current possibilities of the differential diagnosis of plaque parapsoriasis and the early stages of mycosis fungoides]. Arkh. Patol. 81, 9–17 (2019).
  2. Lim, H. L. J. et al. Epidemiology and prognostic factors for mycosis fungoides and Sézary syndrome in a multi-ethnic Asian cohort: a 12-year review. J. Eur. Acad. Dermatol. Venereol. JEADV 33, 1513–1521 (2019).
  3. Bergallo, M. et al. DNA from Human Polyomaviruses, MWPyV, HPyV6, HPyV7, HPyV9 and HPyV12 in Cutaneous T-cell Lymphomas. Anticancer Res. 38, 4111–4114 (2018).
  4. Väisänen, E. et al. Cutavirus DNA in Malignant and Nonmalignant Skin of Cutaneous T-Cell Lymphoma and Organ Transplant Patients but Not of Healthy Adults. Clin. Infect. Dis. Off. Publ. Infect. Dis. Soc. Am. 68, 1904–1910 (2019).
  5. Slodownik, D., Moshe, S., Sprecher, E. & Goldberg, I. Occupational mycosis fungoides – a case series. Int. J. Dermatol. 56, 733–737 (2017).
  6. Blaizot, R., Ouattara, E., Fauconneau, A., Beylot-Barry, M. & Pham-Ledard, A. Infectious events and associated risk factors in mycosis fungoides/Sézary syndrome: a retrospective cohort study. Br. J. Dermatol. 179, 1322–1328 (2018).
  7. Fujii, K. New Therapies and Immunological Findings in Cutaneous T-Cell Lymphoma. Front. Oncol. 8, 198 (2018).
  8. Amorim, G. M., Niemeyer-Corbellini, J. P., Quintella, D. C., Cuzzi, T. & Ramos-E-Silva, M. Clinical and epidemiological profile of patients with early stage mycosis fungoides. An. Bras. Dermatol. 93, 546–552 (2018).
  9. Amorim, G. M., Niemeyer-Corbellini, J. P., Quintella, D. C., Cuzzi, T. & Ramos-E-Silva, M. Hypopigmented mycosis fungoides: a 20-case retrospective series. Int. J. Dermatol. 57, 306–312 (2018).
  10. Pimpinelli, N. et al. Defining early mycosis fungoides. J. Am. Acad. Dermatol. 53, 1053–1063 (2005).
  11. Burg, G., Dummer, R., Nestle, F. O., Doebbeling, U. & Haeffner, A. Cutaneous lymphomas consist of a spectrum of nosologically different entities including mycosis fungoides and small plaque parapsoriasis. Arch. Dermatol. 132, 567–572 (1996).
  12. Keehn, C. A., Belongie, I. P., Shistik, G., Fenske, N. A. & Glass, L. F. The diagnosis, staging, and treatment options for mycosis fungoides. Cancer Control J. Moffitt Cancer Cent. 14, 102–111 (2007).
  13. Lopez, A. T., Bates, S. & Geskin, L. Current Status of HDAC Inhibitors in Cutaneous T-cell Lymphoma. Am. J. Clin. Dermatol. 19, 805–819 (2018).
  14. Prince, H. M. & Querfeld, C. Integrating novel systemic therapies for the treatment of mycosis fungoides and Sézary syndrome. Best Pract. Res. Clin. Haematol. 31, 322–335 (2018).
  15. Wain, T., Venning, V. L., Consuegra, G., Fernandez-Peñas, P. & Wells, J. Management of cutaneous T-cell lymphomas: Established and emergent therapies. Australas. J. Dermatol. 60, 200–208 (2019).
  16. Dairi, M., Dadban, A., Arnault, J.-P., Lok, C. & Chaby, G. Localized mycosis fungoides treated with laser-assisted photodynamic therapy: a case series. Clin. Exp. Dermatol. 44, 930–932 (2019).
  17. Photiou, L., van der Weyden, C., McCormack, C. & Miles Prince, H. Systemic Treatment Options for Advanced-Stage Mycosis Fungoides and Sézary Syndrome. Curr. Oncol. Rep. 20, 32 (2018).
  18. Alpdogan, O., Kartan, S., Johnson, W., Sokol, K. & Porcu, P. Systemic therapy of cutaneous T-cell lymphoma (CTCL). Chin. Clin. Oncol. 8, 10 (2019).

 

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Well, that’s a pain – in the lower back: A case of back pain in the ED

Lower Back Pain: Medical Student Clinical Pearl

Grace Dao, CC4

MD Candidate

Class of 2021

Case Presentation

Mr. Payne Bach is a 54 yo male who presents to the emergency department via EMS with lower back pain.
He reports that he hurt his back this afternoon when he was picking up a heavy, antique chair. Immediately, he felt something “give out” in his back and reports a sharp 10/10 central lower back pain that radiates unilaterally to the left side. It did not radiate down his legs. He was unable to ambulate due to the pain and called EMS.

He received 975 mg Acetaminophen in the ambulance which did not alleviate his pain. Mr. Bach reports that before picking up the chair he was feeling well. He denies any history of back pain or activities of back overuse. He denies any history of trauma or injury to his back recently or in the past. In the emergency department he reports his pain remains at 10/10 and cannot sit up or move in bed due to the pain.

He denies any change in sensation or pain to his legs. He denies any change in sensation to his perineum or any bowel incontinence. He has not urinated since the incident. Incidentally when reviewing a past medical history he reports an unintentional weight loss of 15 lbs in the last 2 months. He denies any history of a prior cancer diagnosis. On review of systems he denies history of cough, fevers, night sweats, hematochezia or gross hematuria. Mr. Bach has a 20 pack year smoking history.

Mr. Bach had difficulty with the physical exam due to pain. He appeared very distressed. All vital signs were within normal limits. An order for IV opiods was ordered and he was reassessed 30 minutes later.

Physical exam

Inspection: there were no obvious deformities of the back, no scarring or bruising or abrasions. Mr. Bach continued to look uncomfortable but was no longer in any acute distress.
Palpation: Mr. Bach was tender to palpation over L4-5. There was tenderness to palpation of the paraspinal muscles at the same level.
ROM: Mr. Bach was very hesitant to move, thus, it was difficult to assess his range of motion.
Neuro: Reflexes at the knee and ankle were normal. Babinski was negative. Normal sensation throughout all dermatomes. 5/5 strength on flexion/extension at the hip, knee and ankle.
Special tests: Straight leg raise and Lasegue’s test were negative.

Back Pain

Back pain is an extremely common condition. It is estimated that 70-85% of people will experience back pain at some point in their life1. A recent study out of an emergency department in Halifax, found that 3.17% of patients presented with to the emergency department with a complaint of lower back pain2. Back pain is within the top 5 reasons for primary care visits3. The differential diagnosis for lower back pain ranges from mechanical lower back pain to critical conditions that need to be recognized 4. Due to its prevalence and potentially sinister causes it is important to have an evidence-based approach to lower back pain.

 

To Image or Not to Image-That is the Question

Choosing Wisely Canada has put out recommendations for both Family and Emergency physicians with regards to low back pain. For family medicine the recommendation is “don’t do imaging for lower-back pain unless red flags are present” 5. It has been found that imagining those without red flags before 6 weeks does not improve outcomes.5

Similarly, for emergency medicine the recommendation is “don’t order lumbosacral (low back) spinal imaging in patients with non-traumatic low back pain who have no red flags/pathologic indicators.”6

Red flags 6:

Cauda Equina Syndrome
Severe worsening pain, especially at night
Significant trauma
Weight loss
History of Cancer
Fever
Night sweats
Steroid use
IV drug use
First episode of back pain in age > 50, especially concerning if age > 65
Widespread neurological signs (loss of sensation, loss of motor function, loss of reflexes in the legs)

 

It is also important to remember that not all red flags are created equal and to include clinical judgement in the decision making process.8 A systematic review examining the predictive value of commonly assessed red flags found that for fracture older age, prolonged steroid use, severe trauma, and contusion/abrasion increased the probability of fracture to 10-33%, and if multiple red flags are present fracture risk increases to 42-90%.

When considering red flags that increase risk of malignancy, previous history of malignancy increased risk 7-33%; while older age, unexplained weight loss, and failure to improve after one month all were found to have post-test probabilities of less than 3% when predicting malignancy risk8.

Back to our case

Mr. Bach has red flags for both fracture and malignancy:

Severe, worsening pain
Age > 50
Weight loss

XRs of the lumbar spine were ordered and indicated several compression fractures, with one area suspicious for a metastatic lesion. Follow CT spine was ordered and confirmed metastatic disease. Mr. Bach was admitted to hospital for pain control, physiotherapy and a malignancy work up.

 

References
1. Andersson, G. B. (1999). Epidemiological features of chronic low-back pain. Lancet 354(9178):581-585. doi:10.1016/S0140-6736(99)01312-4
2. Edwards, J., Hayden, J., Asbridge, M., & Magee, K. (2018). The prevalence of low back pain in the emergency department: A descriptive study set in the Charles V. Keating Emergency and Trauma Centre, Halifax, Nova Scotia, Canada. BMC Musculoskeletal Disorders, 19(1), 306. https://doi.org/10.1186/s12891-018-2237-x
3. Finley, C. R., Chan, D. S., Garrison, S., Korownyk, C., Kolber, M. R., Campbell, S., Eurich, D. T., Lindblad, A. J., Vandermeer, B., & Allan, G. M. (2018). What are the most common conditions in primary care? Systematic review. Canadian family physician Medecin de famille canadien, 64(11), 832–840.
4. Patel, A.T., & Ogle, A.A. (2000). Diagnosis and management of acute low back pain. Am Fam Physician 61(6):1779-1790.
5. College of Family Physicians of Canada. Choosing Wisely Canada. Thirteen Things Physicians and Patients should question. July, 2019. Retrieved from: https://choosingwiselycanada.org/family-medicine/
6. Canadian Association of Emergency Physicians. Choosing Wisely Canada. Ten things Physicians and Patients Should Question. July, 2019. Retreived from: https://choosingwiselycanada.org/emergency-medicine/
7. Toward Optimized Practice (TOP). (2011). Guideline for the evidence-informed primary care Management of Low Back Pain. Retrieved from: https://portal.cfpc.ca/resourcesdocs/uploadedFiles/Directories/Committees_List/Low_Back_Pain_Guidelines_Oct19.pdf
8. Downie, A., Williams, C. M., Henschke, N., Hancock, M. J., Ostelo, R. W. J. G., de Vet, H. C. W., Macaskill, P., Irwig, L., van Tulder, M. W., Koes, B. W., & Maher, C. G. (2013). Red flags to screen for malignancy and fracture in patients with low back pain: Systematic review. BMJ, 347.

Copyedited by Dr. Mandy Peach

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Detection of Foreign Bodies in Soft Tissue – A PoCUS-Guided Approach

 

Medical Student Clinical Pearl

Sophia Miao, CC4

MD Candidate, Class of 2021

Dalhousie University

 

Reviewed & Edited by Dr David Lewis (@e_med_doc)

All case histories are illustrative and not based on any individual.


 

Case Report

A 33-year-old woman presents to the ED with pain and swelling over the third digit of her right hand.  One week prior to this, she had shattered a jar and a small glass splinter lodged into her finger.  This was promptly removed at home, and the puncture wound healed without intervention.

She presented to the emergency room 7 days later with new pain and swelling surrounding the initial puncture wound.  There is no significant past medical history and most recent Td booster was given 2 years ago.  On examination, there was some mild erythema, swelling, and tenderness on palpation of the lateral aspect of the middle phalanx of the right hand.  She is otherwise well.  You wonder about the possibility of a retained foreign body.


 

PoCUS-Guided Approach to the Detection of Foreign Bodies in Soft Tissue

Foreign bodies in soft tissue are a common complaint in the emergency department, with open wounds comprising 5.7 million (or 4.5% of total) visits to the ED in 2010.[1]  Foreign bodies were found in up to 15% of wounds.[2]  If retained, complications of these include allergic reaction, inflammation, delayed wound healing, damage to adjacent tissue structures, neurovascular damage, tetanus, and infectious complications including cellulitis, necrotizing fasciitis, synovitis, and abscess formation.[3],[4]  Proper detection, and subsequent removal, of retained foreign bodies is therefore essential to evaluate the wound and prevent associated complications.

Diagnosis of a retained FB requires a high index of suspicion.  Clinical suspicion should be raised when there is a compelling history and physical exam.  The latter may include signs of inflammation and/or infection, including warmth, swelling, erythema, tenderness, abscess formation, and discharging wound).[5],[6]

Conventional radiography is known to commonly miss radiolucent materials such as wood and plastic.  It has been shown that plain radiographs have only a 7.4% sensitivity in the detection of wood foreign bodies.5  Remarkably, even glass – a radiopaque material – has been demonstrated to have been missed in up to 35% of x-ray film studies.[7]  There is increasingly compelling evidence for the clinical usefulness and accuracy of bedside ultrasonography in the detection of soft-tissue foreign bodies.  It has been shown to have a specificity of 92% (95% CI = 88%-95%) and sensitivity ranging from 83.3% to 100%.[8],[9]


PoCUS Technique

Probe selection: the use of a high-frequency ultrasound probe is recommended.  This allows for greater axial resolution at the expense of less penetration, which is suitable for the detection of small foreign bodies, as they typically lodge in superficial tissues.[10]

If the wound is open, a transparent covering such as a Tegaderm or probe cover can be used to cover either the wound or probe before scanning.[11]

Medium: standard technique for assessment of soft-tissue structures by ultrasound involves the use of a standoff pad or gel mound.  However, this is not always possible due to the irregular curvature of extremities such as fingers and feet, which may result in poor contact between the probe and skin, decreased field of view, and patient discomfort.  A water-bath technique can circumvent this and has been shown to be superior in such cases.[12]

Method: the area of interest should be scanned in both longitudinal and transverse planes.  Foreign bodies are best detected when the transducer aligns with the longitudinal axis of the foreign body, and therefore revealing the span of the object.[13]  As foreign bodies tend to embed less than 2 cm below the surface of the skin, the depth of field should remain superficial in order to avoid false positives.

US Probe: Ultrasound Water Bath for Distal Extremity Evaluation

 


Findings

Ultrasonography and plain film findings of foreign bodies in soft tissue are summarized in the table below.

Table 1. Ultrasound and x-ray findings of foreign bodies.6,[14],[15],[16]

Material Ultrasound findings X-ray findings
Wood Hyperechoic; may become isoechoic with surrounding tissue as it denatures over time

Posterior acoustic shadowing

Radiolucent, often undetectable
Glass Hyperechoic, bright

Posterior acoustic shadowing

± Posterior comet tail reverberation, diffuse beam scattering

Radiopaque
Plastic Hyperechoic

Posterior acoustic shadowing

Radiolucent, often undetectable
Metal Hyperechoic, bright

Posterior acoustic shadowing

± Posterior comet tail reverberation

Radiopaque

 

Foreign bodies may also display a straight or regular contour.6

 

Image 1 – Wood splinter in volar aspect digit, mildly hyperechoic, surrounding hypoechoic halo, irregular acoustic shadowing

Image 2 – Plastic FB, within tendon sheath, volar aspect digit, brightly hyperechoic, long axis

Image 3 – Plastic FB, within tendon sheath, volar aspect digit, brightly hyperechoic, short axis

 

Image 4 – Glass FB – brightly echogenic, posterior reverberation, FB long axis

 

Image 5 – Metal FB – brightly echogenic, posterior reverberation, FB long axis

 

 

It is important to note that the acoustic shadowing may be complete or partial, as this is dependent on the angle of sonography and foreign body material.[17]  It is also possible to see a hypoechoic halo around the FB, which may be suggest edema, abscess formation, granulation tissue, or other inflammatory process.[18]  As the inflammatory reaction develops, the halo effect becomes more apparent; therefore the foreign body is therefore best visualized by PoCUS several days after the initial injury.6


PoCUS-Guided Foreign Body Removal

There are several options for removal of a foreign body with PoCUS:[19]

  1. Needle localization. Once the foreign body has been identified on PoCUS, a hollow injection needle can be inserted under ultrasound guidance and local anesthetic is delivered through this.  This can be done in either the transverse or longitudinal plane.  The ultrasound probe is then removed, and an incision is made along the needle.  Through the incision site, tweezers or forceps can be used to remove the foreign body.
  2. Real-time ultrasound-guided extraction. This technique is similar to the needle localization method. However, rather than removing the transducer following the needle insertion, the entire procedure is done under direct ultrasound visualization.  The probe is held in the longitudinal plane to visualize both the forceps and the foreign body during the extraction process.

 

There is a risk of obscuring the view of the foreign body on ultrasound with air as a result of the incision itself or through anesthetic delivery.  Saline may be used to irrigate and therefore mitigate the issue.19

The patient’s tetanus status should be verified and updated, if required.  Antibiotic therapy may also be provided, should the risk of infection justify it.


Limitations

There is the possibility of false positives.  Foreign bodies must be differentiated from other hyperechoic body structures, including ossified cartilage, sesamoid bones, scar tissue, gas bubbles, and intermuscular fascia.14  Visualization is therefore important in both longitudinal and transverse planes, as well as comparison with the opposite side.  Acoustic shadowing, hypoechoic halo, and posterior comet tails, if present, can also be indicative of a FB rather than organic body tissue.

Traumatic air injection as a result of penetrating injury can create a scatter artifact on ultrasound, which can be misinterpreted as an acoustic shadow associated with a foreign body.  To differentiate this from a true acoustic shadow, pressure may be applied through the transducer to displace the scatter artifact.6

As is commonplace with all emergency ultrasonography, limitations also include the technical skill of the operator.[20]  A foreign body may also be too small to be detectable by ultrasound.  It is therefore important to remember that a negative scan does not necessarily rule out the possibility of a retained foreign body, and the history and physical examination must be considered in conjunction with the ultrasound findings.

 


 

References

[1] National Center for Health Statistics. Emergency Department Visits. Available from: http://www.cdc.gov/nchs/fastats/emergency-department.htm.

[2] Steele MT, Tran LV, Watson WA, Muelleman RL. Retained glass foreign bodies in wounds: predictive value of wound characteristics, patient perception, and wound exploration. Am J Emerg Med. 1998 Nov;16(7):627-30. DOI: 10.1016/s0735-6757(98)90161-9. PMID: 9827733.

[3] Skinner EJ, Morrison CA. Wound Foreign Body Removal. In:StatPearls. Treasure Island (FL): StatPearls Publishing; 2020. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554447/.

[4] Ebrahimi A, Radmanesh M, Rabiei S, Kavoussi H. Surgical removal of neglected soft tissue foreign bodies by needle-guided technique. Iran J Otorhinolaryngol. 2013 Winter;25(70):29-36. PMID: 24303416; PMCID: PMC3846242.

[5] Levine MR, Gorman SM, Young CF, Courtney DM. Clinical characteristics and management of wound foreign bodies in the ED. Am J Emerg Med. 2008 Oct;26(8):918-22. DOI: 10.1016/j.ajem.2007.11.026. PMID: 18926353.

[6] Atkinson P, Bowra J, Harris T, Jarman B, Lewis D. Point of Care Ultrasound for Emergency Medicine and Resuscitation. Oxford, United Kingdom: Oxford University Press; 2019. DOI: 10.1093/med/9780198777540.001.0001.

[7] Kaiser, C. William MD; Slowick, Timothy MBA; Spurling, Kathleen Pfeifer RN, JD; Friedman, Sissie MA. Retained Foreign Bodies, The Journal of Trauma: Injury, Infection, and Critical Care: July 1997 – Volume 43 – Issue 1 – p 107-111.

[8] Davis J, Czerniski B, Au A, Adhikari S, Farrell I, Fields JM. Diagnostic Accuracy of Ultrasonography in Retained Soft Tissue Foreign Bodies: A Systematic Review and Meta-analysis. Acad Emerg Med. 2015 Jul;22(7):777-87. DOI: 10.1111/acem.12714. Epub 2015 Jun 25. PMID: 26111545.

[9] Atkinson P, Madan R, Kendall R, Fraser J, Lewis D. Detection of soft tissue foreign bodies by nurse practitioner-performed ultrasound. Crit Ultrasound J. 2014 Jan 29;6(1):2. DOI: 10.1186/2036-7902-6-2. PMID: 24476553; PMCID: PMC3922659.

[10] Dean AJ, Gronczewski CA, Costantino TG. Technique for emergency medicine bedside ultrasound identification of a radiolucent foreign body. The Journal of Emergency Medicine. 2003;24(3):303–8. DOI: 10.1016/S0736-4679(02)00765-5.

[11] Chen KC, Lin AC, Chong CF, Wang TL. An overview of point-of-care ultrasound for soft tissue and musculoskeletal applications in the emergency department. J Intensive Care. 2016 Aug 15;4:55. DOI: 10.1186/s40560-016-0173-0. PMID: 27529031; PMCID: PMC4983782.

[12] Krishnamurthy R, Yoo JH, Thapa M, Callahan MJ. Water-bath method for sonographic evaluation of superficial structures of the extremities in children. Pediatr Radiol. 2013 Mar;43 Suppl 1:S41-7. DOI: 10.1007/s00247-012-2592-y. Epub 2013 Mar 12. PMID: 23478918.

[13] Rooks VJ, Shiels WE 3rd, Murakami JW. Soft tissue foreign bodies: A training manual for sonographic diagnosis and guided removal. J Clin Ultrasound. 2020 Jul;48(6):330-336. DOI: 10.1002/jcu.22856. Epub 2020 May 8. PMID: 32385865.

[14] Mohammadi A, Ghasemi-Rad M, Khodabakhsh M. Non-opaque soft tissue foreign body: sonographic findings. BMC Med Imaging. 2011 Apr 10;11:9. DOI: 10.1186/1471-2342-11-9. PMID: 21477360; PMCID: PMC3079678.

[15] Lewis D, Jivraj A, Atkinson P, Jarman R. My patient is injured: identifying foreign bodies with ultrasound. Ultrasound. 2015 Aug;23(3):174-80. DOI: 10.1177/1742271X15579950. Epub 2015 Mar 26. PMID: 27433254; PMCID: PMC4760591.

[16] Campbell EA, Wilbert CD. Foreign Body Imaging. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470294/.

[17] Anderson MA, Newmeyer WL 3rd, Kilgore ES Jr. Diagnosis and treatment of retained foreign bodies in the hand. Am J Surg. 1982 Jul;144(1):63-7. DOI: 10.1016/0002-9610(82)90603-1. PMID: 7091533.

[18] Little CM, Parker MG, Callowich MC, Sartori JC. The ultrasonic detection of soft tissue foreign bodies. Invest Radiol. 1986 Mar;21(3):275-7. DOI: 10.1097/00004424-198603000-00014. PMID: 3514541.

[19] Paziana K, Fields JM, Rotte M, Au A, Ku B. Soft tissue foreign body removal technique using portable ultrasonography. Wilderness Environ Med. 2012 Dec;23(4):343-8. DOI: 10.1016/j.wem.2012.04.006. Epub 2012 Jul 25. PMID: 22835803.

[20] Pinto A, Pinto F, Faggian A, Rubini G, Caranci F, Macarini L, Genovese EA, Brunese L. Sources of error in emergency ultrasonography. Crit Ultrasound J. 2013 Jul 15;5 Suppl 1(Suppl 1):S1. DOI: 10.1186/2036-7902-5-S1-S1. Epub 2013 Jul 15. PMID: 23902656; PMCID: PMC3711733.

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Periorbital Inflammation – Red Eye – Red Flags

 

Medical Student Clinical Pearl

Alysha Roberts

MD Candidate, Class of 2021

Dalhousie University

@aeroberts_21

Reviewed & Edited by Dr David Lewis (@e_med_doc)

All case histories are illustrative and not based on any individual.


Case

A 40 year old male presents to the emergency department with a red, swollen eye. Without a known trigger, he had a one day history of progressive pain, erythema, and edema surrounding his left eye. He denied any fever or chills or visual changes, or headache. A thorough review of systems was negative, except for a complaint of worsening pain with extraocular movement.

On exam, he was afebrile and his vital signs were within normal limits. His visual acuity was normal, and pupils were equal and reactive to light. Extraocular movements were intact but associated with worsening pain. The periorbital tissue was erythematous, edematous, and hot to touch. Examination is limited by the severity of the patient’s swelling. Figure 1 illustrates an example of a patient with severe, unilateral eyelid swelling and erythema.

You suspect periorbital cellulitis.

Figure 1. Unilateral eyelid edema. Retrieved from https://www.merckmanuals.com/professional/eye-disorders/orbital-diseases/preseptal-and-orbital-cellulitis


 

Periorbital Versus Orbital Cellulitis

Periorbital cellulitis, commonly referred to as pre-septal cellulitis, is an infection of the skin and soft tissue surrounding the orbit. Most commonly, it is the result of an infection spreading from the sinuses or from local trauma.1,2 It presents as a unilateral swelling of the eye-lid. Both periorbital and orbital cellulitis are most commonly caused by Staphylococcus Aureus and Streptococcus Pneumoniae. It is important to distinguish periorbital from orbital cellulitis, which is an infection of the orbit itself extending beyond the orbital septum. Orbital cellulitis is a sight-threatening emergency, and urgent imaging should be acquired in addition to consultation with ophthalmology or otolaryngology.3 Other complications of orbital cellulitis include orbital or subperiosteal abscess, and cavernous sinus thrombosis. Figure 2 illustrates the difference between periorbital (preseptal) and orbital cellulitis, as well as its complications.

Figure 2. Orbital anatomy and potential complications from orbital cellulitis. Retrieved from https://www.merckmanuals.com/professional/eye-disorders/orbital-diseases/preseptal-and-orbital-cellulitis

Any patient with unilateral eyelid edema should be evaluated for red flags of orbital cellulitis, given its potential seriousness. Red flag signs and symptoms include:3,4

  • Painful or restricted extraocular movements
  • Reduced visual acuity
  • Relevant afferent pupillary defect
  • Diplopia
  • Proptosis
  • Chemosis
  • Severe headache

 

Differential Diagnosis

Other considerations for the differential diagnosis in a unilateral, swollen red eye include:5

  • Periorbital ecchymosis due to blunt trauma
  • Contact dermatitis secondary to local irritant
  • Atopic dermatitis due to allergic sensitivity
  • Orbital tumors

 

Risk Factors

Risk factors for periorbital and orbital cellulitis include:6

  • Sinusitis
  • Dental infection
  • Insect bite
  • Trauma

 

Periorbital cellulitis is most commonly caused by an insect bite in children, and trauma in adults. Comparatively, orbital cellulitis is most often the result of trauma in children, and sinusitis in adults.


 

Diagnostic Investigations

Patients who are febrile or appear unwell should have early initiation of IV antibiotics following blood cultures. Though periorbital cellulitis is a clinical diagnosis, if there is suspicion for orbital cellulitis a CT scan of the orbits and sinuses is the gold standard. Positive findings include inflammation of extraocular muscles, anterior globe displacement, and fat stranding. Inflammation of the sinuses should not be used to differentiate periorbital from orbital cellulitis, as up to 41% of cases of periorbital cellulitis may have CT evidence of sinusitis. Figure 3 displays a labelled CT image with common findings in orbital cellulitis.7

 

Figure 3. Orbital CT image with labels. Retrieved from https://ctscanmachines.blogspot.com/2018/07/ct-scan-of-periorbital-cellulitis.html

In addition to CT imaging, there may be a role for point of care ultrasound (PoCUS) in the diagnosis and management of periorbital and orbital cellulitis. However, research is currently lacking on whether its use may avoid the need for further diagnostic imaging.8 Findings from pediatric emergency medicine suggest that orbital ultrasound may be preferred in evaluating young patients who are unable to cooperate with a thorough physical examination.9 One important application of orbital PoCUS is in the assessment of orbital abscesses. Subperiosteal abscesses may complicate more than 50% of cases of orbital cellulitis, and are not reliably detected by CT.10 Additionally, orbital ultrasound may be an appropriate alternative in settings where advanced imaging is not available, in order to guide early initiation of antibiotics.

Orbital Abscess from – The PoCUS Atlas


 


 

Treatment Best Practices  

Antibiotic choice should be guided by local susceptibility guidelines. An appropriate choice would cover S. aureus, S. pyogenes, and anaerobes.11,12 In this case, we initiated intravenous ceftriaxone and metronidazole while awaiting CT results.

The following therapeutic guidelines are from Bugs and Drugs – It is recommended that that guidelines for therapy are accessed directly from their website or from other reputable sources.

Periorbital Cellulitis

 

Orbital Cellulitis

From Bug and Drugs

 


Case Conclusion

Given this patient’s complaint of increased pain with extraocular movement, a CT orbit was performed. Fortunately, there were no signs of orbital cellulitis. The patient was treated with IV ceftriaxone and metronidazole and scheduled to return to the emergency department the next day for re-evaluation and consideration of step-down to oral antibiotics.


Summary

Orbital cellulitis is a serious condition that should be carefully distinguished from periorbital cellulitis. On history, clinicians should ensure they inquire about recent sinus or dental infections, trauma to the orbit, or possible insect bites. Physical exam should carefully assess for signs of orbital cellulitis, including proptosis, chemosis, and limited extraocular movements. Any positive red flag or clinical suspicion warrants a CT scan of the orbits and sinuses to exclude orbital cellulitis.


Further Reading

Great photo article in Canadian Family Physician

Management algorithm

Patient Information Leaflet

 

 


 

References

  1. Preseptal and Orbital Cellulitis – Eye Disorders – Merck Manuals Professional Edition. (n.d.).Retrieved January 12, 2021, from https://www.merckmanuals.com/professional/eye-disorders/orbital-diseases/preseptal-and-orbital-cellulitis
  2. Lightning Learning: Orbital Cellulitis — #EM3: East Midlands Emergency Medicine Educational Media. (n.d.). Retrieved January 12, 2021, from https://em3.org.uk/foamed/7/5/2019/lightning-learning-orbital-cellulitis
  3. Periorbital cellulitis — entsho.com. (n.d.). Retrieved January 12, 2021, from https://entsho.com/periorbital-cellulitis
  4. Distinguishing Periorbital from Orbital Cellulitis. (2003). American Family Physician, 67(6), 1349.
  5. Differential Diagnosis of the Swollen Red Eyelid – American Family Physician. (n.d.). Retrieved January 12, 2021, from https://www.aafp.org/afp/2015/0715/p106.html
  6. Risk factors of preseptal and orbital cellulitis – PubMed. (n.d.). Retrieved January 12, 2021, from https://pubmed.ncbi.nlm.nih.gov/19149979/
  7. Ct Scan Of Periorbital Cellulitis – ct scan machine. (n.d.). Retrieved January 12, 2021, from https://ctscanmachines.blogspot.com/2018/07/ct-scan-of-periorbital-cellulitis.html
  8. Kang, T. L., Seif, D., Chilstrom, M., & Mailhot, T. (2014). Ocular ultrasound identifies early orbital cellulitis. Western Journal of Emergency Medicine, 15(4), 394. https://doi.org/10.5811/westjem.2014.4.22007
  9. Seguin, J., Le, C.-K., Fischer, J. W., Tessaro, M. O., & Berant, R. (2019). Ocular Point-of-Care Ultrasound in the Pediatric Emergency Department. Pediatric Emergency Care, 35(3), E53–E58. https://doi.org/10.1097/PEC.0000000000001762
  10. Derr, C., & Shah, A. (2012). Bedside ultrasound in the diagnosis of orbital cellulitis and orbital abscess. Emergency Radiology, 19(3), 265–267. https://doi.org/10.1007/s10140-011-0993-0
  11. Orbital Cellulitis – StatPearls – NCBI Bookshelf. (n.d.). Retrieved January 12, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK507901/
  12. Periorbital Cellulitis – StatPearls – NCBI Bookshelf. (n.d.). Retrieved January 12, 2021, from https://www.ncbi.nlm.nih.gov/books/NBK470408/
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A case of cholecystitis

Medical Student Clinical Pearl

Alana Jewell

M.D. Candidate, Class of 2022

Memorial University Faculty of Medicine

Reviewed & Edited by Dr. Mandy Peach

All case histories are illustrative and not based on any individual.

 

Case Presentation

A 70-year-old gentleman presented with four days of right upper abdominal pain radiating to the LUQ with nausea + vomiting, anorexia, flatulence, and bloating. Patient has PMHx of Crohn’s disease with a history of small bowel obstruction (SBO) and multiple surgeries. He felt these symptoms were like his SBO but he continued to have normal bowel movements. He had a similar episode a few months ago after eating fast food, but did not seek care for.

You suspect cholecystitis.

 

Differential Diagnosis

Can’t miss diagnoses for atraumatic abdominal pain 4:

ruptured AAA
pancreatitis
cholangitis
mesenteric ischemia
obstruction
perforated viscus
complicated diverticulitis
ruptured ectopic pregnancy

Differential for RUQ pain :

hepatitis
biliary colic
cholecystitis
cholangitis
pancreatitis
pneumonia
pleural effusion
pulmonary embolism

 

There is no single exam finding or laboratory test that has the ability to rule out acute cholecystitis5.

 

A combination of clinical evaluation, laboratory values, and diagnostic imaging are key to differentiate abdominal pain and make a diagnosis.

 

Cholecystitis

Cholecystitis is defined as inflammation of the gallbladder, typically caused by persistent stone obstruction in the cystic duct.

Acute cholecystitis (AC): Stone obstruction leads to bile trapping, increased intraluminal pressure, and an acute inflammatory process, typically presenting with RUQ pain, leukocytosis, and fever1.

Chronic cholecystitis: defined as recurrence of these events and is associated with fibrosis and mucosal atrophy2.

Acalculous cholecystitis: consider in chronically debilitated patients, classically elderly patients in ICU on total parental nutrition after sustained trauma or significant burn injury11.

Ascending (or acute) cholangitis: an important complication of cholecystitis – a serious bacterial infection of the common bile duct. It presents with Charcot’s triad of fever, jaundice, and abdominal pain2.

 

Acute cholecystitis is diagnosed and graded on severity by using the Tokyo Guidelines3.

 

 

 

Gallstones (which cause 95% of acute cholecystitis) are common in Western society, with about 10% of people affected, and 80% of those affected being asymptomatic1,3. The risk of pain or complications is 1-4% per year2.

 

Risk factors for cholesterol gallstones (the most common type) 2:

increased age
female gender
pregnancy
parity
race
high calorie
low fibre diet
low activity
obesity

 

 

 Clinical Presentation and findings

Clinical presentation varies with severity.

On history, a patient may have anorexia, emesis, fever, nausea, and RUQ pain.  On examination, guarding, Murphy’s sign (pain upon deep inspiration while palpating RUQ), rebound tenderness, abdominal rigidity, and RUQ tenderness may be seen2. Patients may describe a history of biliary colic, but with the presenting episode being more severe and longer in duration.

Mild-moderate cases have RUQ pain, fever, leukocytosis, and may have a palpable mass in the RUQ2. The most severe patients may have jaundice and, if have a secondary bacterial infection, could have signs of sepsis.

 

Case Continued

 

Physical Exam

Patient was tender to light palpation over RUQ and epigastric region. No rigidity, rebound tenderness, or guarding was noted.

Bloodwork

  • Elevated WBC with neutrophilic shift
  • C reactive protein > 250
  • Normal lipase, liver enzymes and renal function.

The most common laboratory findings in acute cholecystitis are an increased CRP and leukocytosis2.

 

This patient requires imaging to confirm the suspected diagnosis.

 

Diagnostic Imaging

Ultrasound

Ultrasound is the first-choice modality for imaging of AC. It is easily available in any emergency department, cost-effective, and minimally invasive3. Ultrasound findings can include5,6,9, as seen below 6.

 GB wall thickening > 3.5 mm
pericholecystic fluid
biliary sludge
gallstones
sonographic Murphy sign

 

If an ultrasound is positive, there is no need for further testing.

If negative, a CT should be ordered to exclude other diagnoses2,7.

 

CT findings for AC may include 3,6 as seen below 2:

thickening of GB wall
enlargement of GB
gallstones in GB neck or cystic duct
fluid accumulation around GB
pericholecystic fat stranding

 

Many gallstones are not radiopaque and may be missed on CT7

 

Management

Assessment with Tokyo Guideline diagnostic criteria can be used every 6-12 hours until a diagnosis is clear if initially uncertain, and to check severity until surgical management8.

In the Emergency Department, a patient is best managed with supportive care.

IV fluids,
NPO
Analgesia (NSAIDs are first-line treatment for AC. If ineffective, opioids are second line2. )

 

Secondary infection can result from bile stasis. Empiric antibiotics may be started against E. coli, Klebsiella, and Enterococcus5.

Definitive treatment for AC is cholecystectomy, with the gold standard being done laparoscopically (lap-C)2,7. Having a lap-C within 24-72 hours of symptom onset is recommended to decrease complication rates. If left unoperated for more than 72 hours chronic inflammation may occur, potentially complicating the surgery1. If a patient is ineligible for surgery, percutaneous cholecystostomy (gallbladder drainage) may be performed7.

 

Case Conclusion

Formal ultrasound found a hydropic gallbladder with pericholecystic fluid, thickened wall, and stranding. Cholecystitis was diagnosed. The patient was given analgesia and covered with ceftriaxone and metronidazole10. He went on to have an uncomplicated lap cholecystectomy.

 

References

  1. Indar, Adrian A, and Beckingham, Ian J. “Acute Cholecystitis.” BMJ, vol. 325, no. 7365, 2002, pp. 639–643.
  2. Wilkins, Thad, MD, MBA, et al. “Gallbladder Dysfunction: Cholecystitis, Choledocholithiasis, Cholangitis, and Biliary Dyskinesia.” Primary Care, vol. 44, no. 4, 2017, pp. 575–597.
  3. Yokoe, Masamichi, et al. “Tokyo Guidelines 2018: Diagnostic Criteria and Severity Grading of Acute Cholecystitis (with Videos).” Journal of Hepato-Biliary-Pancreatic Sciences, vol. 25, no. 1, 2018, pp. 41–54.
  4. Anjum, Omar, et al. “Ottawa’s Clerkship Guide to Emergency Medicine.” Department of Emergency Medicine, University of Ottawa, Mar. 2018.
  5. Jain, Ashika, et al. “History, Physical Examination, Laboratory Testing, and Emergency Department Ultrasonography for the Diagnosis of Acute Cholecystitis.” Academic Emergency Medicine, vol. 24, no. 3, 2017, pp. 281–297.
  6. Chawla, Ashish, et al. “Imaging of Acute Cholecystitis and Cholecystitis-Associated Complications in the Emergency Setting.” Singapore Medical Journal, vol. 56, no. 8, 2015, pp. 438–444.
  7. Bagla, Prabhava, et al. “Management of Acute Cholecystitis.” Current Opinion in Infectious Diseases, vol. 29, no. 5, 2016, pp. 508–513.
  8. Mayumi, Toshihiko, et al. “Tokyo Guidelines 2018: Management Bundles for Acute Cholangitis and Cholecystitis.” Journal of Hepato-Biliary-Pancreatic Sciences, vol. 25, no. 1, 2018, pp. 96–100.
  9. Flemming, Lewis & Henneberry (2017). PoCUS – Measurements and Quick Reference http://sjrhem.ca/pocus-measurements-quick-reference/
  10. Bugs & Drugs Medical App
  11. Forsythe (2016). Cholecystitis. First Aid for the Emergency Medicine Boards, Third Edition: Abdominal and Gastrointestinal Emergencies. McGraw-Hill Education. China.

 

 

 

 

 

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A Case of Ectopic Pregnancy

 

Medical Student Clinical Pearl – December 2020

Marisa O’Brien

@mbob58

MD Candidate, Class of 2021

Memorial University of Newfoundland

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual

 


Case Report

A 36-year-old G2P1 female presented to the Emergency Department following a pre-syncopal episode at work. The patient noted a sudden onset of significant abdominal cramping, nausea, and vaginal bleeding with clots that morning followed by an episode of lightheadedness while sitting at her desk. The patient denied any loss of consciousness, no dyspnea, no chest pain, no palpitations, and no fevers/chills. She had no known allergies and no current medications. She was a non-smoker and denied any alcohol or drug usage.

The patient’s past medical history was significant for recent treatment with methotrexate for an ectopic pregnancy eight days prior. The patient had a history of amenorrhea for 7 weeks and a serum β-hCG of 302 mlU/mL at that time. A transvaginal ultrasound was performed at 8 weeks for abdominal pain and light spotting which revealed an IUD in situ with no evidence of an intrauterine pregnancy. An early ectopic pregnancy was diagnosed and the patient was consented to receive medical management with methotrexate. She was followed up with serial β-hCG’s which gradually, but slowly, trended down to 110 mIU/ml by day 6. The patient noted slight abdominal cramping and PV bleeding following the methotrexate however this had settled after 3 days with no ongoing symptoms until today.

On initial assessment, the patient appeared well, no acute distress, and all vital signs were stable.  The abdominal exam revealed bowel sounds present in all four quadrants and the abdomen was tympanic to percussion. On palpation the abdomen was soft and nondistended with LLQ and suprapubic tenderness however, no guarding or rebound tenderness was appreciated.

Initial investigations included a CBC, β-hCG, PT & PTT, type and screen, urinalysis, EKG, & POCUS.

 


Definition

An ectopic pregnancy occurs when a fertilized egg implants at a site other then the endometrium of the uterus, most commonly the fallopian tubes. They often present as vaginal bleeding and/or abdominal pain in the setting of a positive β-hCG.1

A critical complication is a ruptured ectopic pregnancy which occurs by erosion through the tissue the zygote has implanted in resulting in intraabdominal bleeding from the exposed vessel and possible hypovolemic shock.2 Rupture should be suspected in patients presenting with hemodynamic instability including syncope, hypotension, and tachycardia. However, young healthy females may appear vitally stable initially due to compensatory mechanisms. Additional physical exam findings suggestive of a ruptured ectopic pregnancy include severe abdominal pain with guarding or rebound tenderness and abdominal distention. Pain may radiate to the shoulder due to irritation of the diaphragm from blood in the peritoneal cavity.1,3

 


Risk factors for ectopic pregnancy4

  • Previous ectopic pregnancy
  • Prior fallopian tube surgery
  • Previous pelvic or abdominal surgery
  • Sexually transmitted infections
  • Pelvic inflammatory disease
  • Endometriosis
  • Cigarette smoking
  • Maternal age > 35 years
  • History of infertility
  • Assisted reproductive technology (IVF)

 

 


Differential diagnosis for vaginal bleeding in early pregnancy1:

  • Physiologic
  • Spontaneous abortion
  • Cervical, vaginal, or uterine pathology
  • Subchorionic hematoma
  • Heterotopic pregnancy
  • Gestational trophoblastic disease

 


Sonography

According to the discriminatory zones, an intrauterine pregnancy is expected to be visualized on a transvaginal ultrasound at β-hCG levels of 1500 – 2000 mlU/mL and on a transabdominal ultrasound at levels of 4000 – 6500 mlU/mL.5

Gestational Age Β-hCG range (mlU/mL)
<1 week 5 – 50
1-2 weeks 50 – 500
2-3 weeks 100 – 5000
3-4 weeks 500 – 10,000
4-5 weeks 1000 – 50,000
5-6 weeks 10,000 – 100,000
6-8 weeks 15,000 – 200,000
8-12 weeks 10,000 – 100,000

Table 1: Estimated β-hCG levels in relation to gestational age.3

In the first trimester of a normal pregnancy, the serum β-hCG should increase by ≥ 53% every 48 hrs until 41 days of gestation.1,3 Serum β-hCG will then continue to rise more slowly until approximately 10 weeks after which it will begin to decline until reaching a plateau. Serum β-hCG levels are noted to raise more slowly in an ectopic pregnancy, thus a slower rate of increase, plateau, or decline in serum β-hCG in the first 41 days suggests a possible miscarriage or ectopic pregnancy.1

Note on β-hCG Discriminatory Zones

The value of discriminatory zones in the emergency management of ectopic pregnancy is low, with many considering it unreliable and potentially dangerous. In short, a low β-hCG does not exclude an ectopic. This useful post provides a good summary on ectopic rule-out in the ED:

Rule Out Ectopic in the Emergency Department

 

An intrauterine pregnancy is confirmed by visualization of a gestational sac and a yolk sac within the uterus (juxtaposed to bladder).1 A gestational sac alone is not sufficient for diagnoses of an intrauterine pregnancy as it may be a pseudogestational sac formed by hormonal stimulation from an ectopic pregnancy.5 Additionally, if an intrauterine pregnancy is visualized, a heterotopic pregnancy should also be considered.1 The risk of heterotopic pregnancy when conceived normally is estimated to be 1 in 30,000.

Figure 1: Visualization of an intrauterine pregnancy on a transvaginal ultrasound.3

 

 

Structure Transvaginal Ultrasound Transabdominal Ultrasound
Gestational Sac 4.5-5 weeks 5.5-6 weeks
Yolk Sac 5-5.5 weeks 6-6.5 weeks
Fetal Pole 5.5-6 weeks 7 weeks
Cardiac Activity 6 weeks 7 weeks
Fetal Parts 8 weeks >8 weeks

Table 2: Ultrasound findings based on gestational age.5

 


Diagnosis of Ectopic Pregnancy

An ectopic pregnancy is suspected in all women with a positive pregnancy test when no intrauterine pregnancy is visualized on ultrasonography. A low β-hCG or declining β-hCG does not exclude an ectopic. Ultrasound findings of an ectopic pregnancy may include an extrauterine gestational sac or embryonic cardiac activity outside of the uterus, a complex adnexal mass, or intraperitoneal fluid.3

From emupdates.com

 


Management of Ectopic Pregnancy

Is the patient unstable?

  • If the patient is hemodynamically unstable (tachycardia or hypotension or pale or syncopal) then commence immediate resuscitation (IV Access, CBC, type & crossmatch,  iv fluids, transfusion, etc) and stat consult to ObGyn.

In stable patients

  • Consult ObGyn
  • The gold-standard of treatment for ectopic pregnancy is surgical management however, treatment options include expectant, or medical management.6 Medical management with methotrexate, a folic acid antagonist that inhibits DNA synthesis and cell production, has a higher success rate when initiated at lower β-hCG levels. Methotraxate is initiated if β-hCG is <5000 mlU/mL and is reserved for those with reliable follow up as β-hCG levels are required to be trended until they are undetectable. Individuals with renal disease, hepatic disease, active pulmonary disease, or immunodeficiencies are not candidates for methotrexate.3,7 Individuals who do not meet the criteria for medical management, are hemodynamically unstable, have failed methotrexate, or a ruptured ectopic is suspected, will receive surgical management.6

 


Case Report Continued

The patient was hemodynamically stable on presentation. Her vital signs were normal. As part of the initial assessment, PoCUS was used to further evaluate for the presence of free fluid in the abdomen or pelvis. Free fluid was identified in the RUQ in both Morrison’s pouch and surrounding the caudal tip of the liver. Intraperitoneal fluid was also seen in the LUQ in both the subphrenic and splenorenal spaces. Free fluid was also visualized in Douglas’ pouch in the pelvic view.

RUQ

LUQ

Pelvis

 

Throughout the PoCUS examination the patient remained well appearing, however she had become hypotensive with a blood pressure of 90/53 mmHg. Her initial bloodwork had come back at this time revealing a β-hCG of 32 mlU/mL and a Hgb of 67 g/L. The patient received 1g of TXA, and a 1L bolus of normal saline while PRBC’s were ordered. She was documented to be Rh+ thus, she did not require RhoGAM (anti-D immune globulin). An urgent consultation to Obstetrics and Gynecology was made following the visualization of intraabdominal fluid and the patient underwent an exploratory laparotomy shortly after.

 


Key Points

  • Ectopic pregnancy should be considered in the differential diagnosis of any female patient, of childbearing age, presenting with abdominal pain, syncope or shock
  • An Intrauterine contraceptive device does not exclude an ectopic
  • Unless a previous ultrasound has documented the presence of an intrauterine pregnancy, an empty uterus in a patient with a positive pregnancy test should be considered to be a possible ectopic until ruled out
  • An intrauterine pregnancy on ultrasound requires the following to be confirmed:
    • A gestational sac and a yolk sac, in the uterus which is juxtaposed to the bladder
    • or a gestational sac containing a normal fetal pole, in the uterus which is juxtaposed to the bladder
  • A low β-hCG or declining β-hCG does not exclude an ectopic
  • Medical management of ectopic pregnancy with methotrexate requires close follow-up. Failure can occur. Ruptured ectopic pregnancy can still occur.

 


Further Reading

Ectopic Pregnancy and Ruptured Ectopic: Pitfalls in Diagnosis

ED Rounds – Early Pregnancy

The Pregnant ED Patient – A Compendium of Pearls

 

 


References

  1. Tulandi, T. (2020, November 2). Ectopic pregnancy: Clinical manifestations and diagnosis. Retrieved from: https://www.uptodate.com/contents/ectopic-pregnancy-clinical-manifestations-and-diagnosis?search=ectopic%20pregnancy&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H1
  2. Toy, E.C., Simon, B.C., Takenaka, K.Y., Liu, T.H., & Rosh, A.J. (2017). Ectopic Pregnancy. Case Files Emergency Medicine. (4th, pp. 369-376). McGraw-Hill Education.
  3. Hang, B.S. (2016). Obstetrics and Gynecology. Tintinalli’s Emergency Medicine: A Comprehensive Guide. (8th, pp. 629-633). McGraw-Hill Education.
  4. The American College of Obstetricians and Gynecologists. (2018, February). Retrieved from: https://www.acog.org/womens-health/faqs/ectopic-pregnancy
  5. Leonard, N.J. (2019, January 23). The Pregnant Pelvic POCUS. EMRounds. Retrieved from: https://emrounds.org/the-pregnant-pelvic-pocus/
  6. Tulandi, T. (2020, March 31). Ectopic pregnancy: Choosing a treatment. Retrieved from: https://www.uptodate.com/contents/ectopic-pregnancy-choosing-a-treatment?search=ectopic%20pregnancy&topicRef=5407&source=see_link#H2976630177
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Small Bowel Obstruction & PoCUS

Small Bowel Obstruction & PoCUS – Medical Student Pearl

Patrick Rogers, Clinical Clerk (CC3)

Memorial University of Medicine Class of 2021

Reviewed by Dr. Kavish Chandra

Small bowel obstructions (SBO) are a common cause of acute abdominal pain in emergency departments across Canada. Diagnostic imaging plays a key role in the diagnosis and management of SBO as the history, clinical examination and laboratory investigations lack the sensitivity and specificity needed. Furthermore, diagnostic imaging may help differentiate SBO from other causes of abdominal pain (hernias, malignancies, intussusception, etc).

Historically, plain film abdominal radiography (AXR) has been an initial investigation in emergency departments when an SBO is suspected.  However, the current literature suggests that abdominal radiography is a relatively poor test for the diagnosis or exclusion of SBO when compared to other available modalities like US, CT, or MRI. In fact, multiple studies argue for the reduction of abdominal x-rays, especially when patients come in presenting with general abdominal tenderness. 1 Fortunately, there exists a compelling alternative: point of care ultrasound (PoCUS), and is being increasingly used as a first line investigation for SBO. 2

There are several reasons why physicians may start to choose PoCUS over traditional diagnostic modalities:

  • PoCUS avoids the radiation exposure that patients receive from cumulative plain films and abdominal CT’s. 3
  • PoCUS has been shown to reduce time to diagnosis and treatment in comparison to abdominal plain films. 3
  • PoCUS is more sensitive/specific modality when compared to abdominal plain film. 4
  • PoCUS allows for serial examination in the ED. 5
  • PoCUS may be rapidly available to centers with limited access to CT scanner. 6

The current evidence is highly favorable for the diagnostic efficacy of PoCUS in SBO. Here are the findings of peer-reviewed studies on the subject (published between 2013-2020):

  • PoCUS has high diagnostic accuracy and may also decrease time to diagnosis of SBO in comparison to other imaging modalities like CT and plain film.2
  • PoCUS has been found to have superior diagnostic accuracy for SBO in comparison to plain abdominal radiography. 4
  • PoCUS has been shown to be an accurate tool in the diagnosis of SBO with a consistently high sensitivity of 94-100% and specificity of 81-100%. 5
  • Current evidence suggests PoCUS is comparable in sensitivity and specificity to a CT scan when diagnosing SBO. 6
  • Ultrasound was found to be equivalent to CT in terms of diagnostic accuracy with a sensitivity of 92.31% (95% CI, 74.87% to 99.05%) and a specificity of 94.12% (95% CI, 71.31% to 99.85%) in the diagnosis of SBO. 7
  • In a study comparing XR, US, CT, and MRI, the abdominal x-ray was shown to be to be the least accurate imaging modality for the diagnosis of SBO. AXR’s were found to have a positive likelihood ratio of 1.64 (95% CI 1.07 to 2.52). In contrast, CT and MRI were both quite accurate in diagnosing SBO with positive likelihood ratios of 3.6 (95% CI = 2.3 to 5.4) and 6.77 (95% CI = 2.13 to 21.55). The use of ultrasound was found to have a positive likelihood ratio of 9.55 (95% CI = 2.16 to 42.21) and a negative likelihood ratio of 0.04 (95% CI = 0.01 to 0.13) for beside scans. 4

There are two major barriers identified in the literature that may prevent the effective use of PoCUS in the diagnosis of SBO. First, not every emergency physician has been trained on the use of PoCUS. Fortunately, two recent studies show that even minimally trained ED physicians can use it accurately. 8 Secondly, some surgeons have argued that PoCUS does not show the location of the obstruction accurately. This becomes a concern when the care team elects for surgical management of the patient’s SBO. However, recent evidence suggests that PoCUS may lead to quicker time to diagnosis and enteric tube insertion in conservative management. 8

Finally, how can learners use this technology? 5 Here are some specific sonographic findings to look for when evaluating a patient for SBO with US:

 

  • Dilatation of small bowel loops > 25 mm *
  • Altered intestinal peristalsis *
  • Increased thickness of the bowel wall
  • Intraperitoneal fluid accumulation

Figure 1. Dilatation of small bowel loops. Image courtesy Dr. Kavish Chandra

Figure 2. Altered intestinal peristalsis*. Image courtesy Dr. Kavish Chandra

Figure 3. – abnormal peristalsis “to and fro”9

References

  1. Denham G, Smith T, Daphne J, Sharmaine M, Evans T. 2020. Exploring the evidence-practice gap in the use of plain radiography for acute abdominal pain and intestinal obstruction: a systematic review and meta-analysis. International Journal of Evidence Based Healthcare. DOI: 10.1097/XEB.0000000000000218
  2. Guttman J, Stone M, Kimberly H, Rempell J. 2015. Point of care ultrasonography for the diagnosis of small bowel obstruction in the emergency department. CJEM. DOI: 10.2310/8000.2014.141382
  3. Flemming H, Lewis D. 2016. SBO- A New Focus for PoCUS. Saint John Regional Hospital Department of Emergency Medicine
  4. Taylor M, Lalani N. 2013. Adult small bowel obstruction. Academic Emergency Medicine. DOI: 10.1111/acem.12150
  5. Pourman A, Dimbil U, Shokoohi H. 2018. The accuracy of point of care ultrasound in detecting small bowel obstruction in emergency department. Emergency Medicine International. DOI: 10.1155/2018/3684081
  6. Gottlieb M, Peska, G, Pandurangadu A, Nakitende D, Takhar S, Seethala R. 2018. Utilization of ultrasound for the evaluation of small bowel obstruction: A systematic review and meta-analysis. The American Journal of Emergency Medicine. DOI: 10.1016/j.ajem.2017.07.085
  7. Tamburrini S, etal. 2019. Diagnostic accuracy of ultrasound in the diagnosis of small bowel obstruction. Diagnostics. DOI: 10.3390/diagnostics9030088
  8. Carpenter C. 2013. The end of X-Rays for suspected small bowel obstruction? Using evidence-based diagnostics to inform best practices in emergency medicine. Academic Emergency Medicine. https://doi.org/10.1111/acem.12143
  9. The PoCUS Atlas. https://www.thepocusatlas.com/bowel-gi

Copyedited by Dr. Mandy Peach

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Spontaneous Abortion

Medical Student Clinical Pearl

Miranda Lees, Clinical Clerk II

Dalhousie Medicine New Brunswick, Saint John

Reviewed by Dr. Mandy Peach

Case

A 21yo G3P1A1 female at 6 weeks gestation presented to the Emergency Department with an 8 hour history of vaginal bleeding and abdominal pain. The bleeding is a mixture of bright red and brown blood with no clots, and the abdominal pain is episodic cramping in her suprapubic region.

Her obstetrical history is significant for 2 prior pregnancies, the first of which was carried to term with an uncomplicated vaginal delivery, and the second of which had resulted in a spontaneous abortion at 6 weeks gestation. She is otherwise healthy. The patient noted with both prior pregnancies she had similar vaginal bleeding around 6-8 weeks gestation. She was given RhoGAM due to her Rh- blood type.

On assessment the patient appeared well with all vital signs within normal limits. On physical exam bowel sounds were present, the abdomen was tympanic to percussion, and pain on palpation was present in the patient’s suprapubic region.

 

Differential for life threatening causes of vaginal bleeding in pregnancy

<20 weeks gestation >20 weeks gestation
      ruptured ectopic pregnancy          placental abruption
       retained products of conception          placenta previa
       complication of termination          post partum hemorrhage

Other causes for vaginal bleeding to consider in pregnancy and in non-pregnant patients

Spontaneous abortion
Acute heavy menstrual bleeding
Genitourinary trauma
Uterine arteriovenous malformation
Ruptured ovarian cyst
Ovarian torsion
Pelvic Inflammatory Disease
Fibroids
Polyps
Foreign body
Coagulation disorder
Medication related
Gynecologic malignancy

 

Investigations

A βhCG was ordered to confirm pregnancy and bedside ultrasound was done to look for intrauterine pregnancy.

Transabdominal ultrasound showed the following:

The presence of a gestational sac within the uterus and a fetal heartbeat within the fetal pole confirmed a viable intrauterine pregnancy (IUP). The patient was diagnosed with threatened abortion.

 

Spontaneous Abortion-an overview

Spontaneous abortion is one of the most common complications of pregnancy, occurring in 17-22% of pregnancies2 and is defined as loss of pregnancy prior to 20 weeks gestation, occurring most often in the first trimester3. There are 3 primary causes: chromosomal abnormalities in the fetus, maternal anatomic abnormalities, and trauma.3

Risk factors for spontaneous abortion

age (below 20 and above 35)
moderate to severe bleeding (especially if passage of clots)
prior pregnancy loss
maternal comorbidities (DM, autoimmune conditions, obesity, thyroid disease)
infection (notably parvovirus, CMV and untreated syphilis)
teratogenic medications
maternal radiation exposure
maternal smoking
caffeine
alcohol use

 

Classification4

Missed abortion is characterized by an asymptomatic death of the fetus with a lack of contractions to push out the products of conception.5

Clinical presentation

Spontaneous abortion most commonly presents with vaginal bleeding and cramping, ranging from mild to severe1. However, most women with first-trimester bleeding will not undergo spontaneous abortion1. Bleeding associated with spontaneous abortion often involves passage of clots or fetal tissue, and the cramping can be constant or intermittent, often worse with passage of tissue1.

Diagnosis

Confirmation of spontaneous abortion requires pelvic ultrasound.

In patients with a prior ultrasound showing intrauterine pregnancy, diagnosis of spontaneous abortion can be made if a subsequent ultrasound shows no intrauterine pregnancy or a loss of previously-seen fetal heartbeat1.

In patients with a prior ultrasound showing intrauterine pregnancy with no fetal heartbeat, spontaneous abortion is diagnosed based on the following1:

  • A gestational sac >25mm in diameter containing no yolk sac or embryo
  • An embryo with crown rump length >7mm with no fetal cardiac activity
  • After pelvic ultrasound showing a gestational sac without a yolk sac, absence of embryo with a heartbeat in >2 weeks
  • After pelvic ultrasound showing a gestational sac with a yolk sac, absence of embryo with a heartbeat in >11 days

Case conclusion

The patient was treated with IM RhoGAM, a formal pelvic and transvaginal ultrasound was arranged for the next day, and she was discharged home. The follow-up ultrasound showed a gestational sac present in the uterus, an embryo with crown rump length of 8.1mm and the presence of a fetal heartbeat.

 

References

  1. Borhart D. Approach to the adult with vaginal bleeding in the Emergency Department. In: UptoDate, Hockberger R (Ed), UpToDate, Waltham, MA. (Accessed on October 8, 2020).
  2. Gracia C, Sammel M, Chittams J, Hummel A, Shaunik A, et al. Risk Factors for Spontaneous Abortion in Early Symptomatic First-Trimester Pregnancies. Obstetrics & Gynecology. 2005;106(5):993-999. doi 1097/01.AOG.0000183604.09922.e0.
  3. Prager, Mikes & Dalton. Pregnancy loss (miscarriage): Risk factors, etiology, clinical manisfestations, and diagnostic evaluation. In: UptoDate, Eckler (Ed), UptoDate, Waltham MA. (accessed Nov 28, 2020)
  4. Diaz. 2018. Types of Spontaneous Abortion. In: GrepMed. Image Based Medical Reference. https://www.grepmed.com/images/5425/classification-spontaneous-obstetrics-diagnosis-abortion-obgyn-types (Accessed Nov 28, 2020)
  5. Alves C, Rapp A. Spontaneous Abortion (Miscarriage) [Updated 2020 Jul 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560521/.

 

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Skin and Soft Tissue Infections: A PoCUS Guided Approach

Medical Student Clinical Pearl – November 2020

 

Robert Hanlon

@roberthanlon12

Year: 4
DMNB Class of 2021
 

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual

 


Case Report

A 25yr old male presents with a 3 day history of a red swollen foot following an insect bite. He has no past medical history. On examination there is some erythema and swelling on the dorsum of the left foot. Palpation is very tender.

You are aware of recommended guidelines that advise I&D for purulent infections and decide to proceed with the procedure. Despite trying to freeze the area with lidocaine, the procedure is still painful and no pus is drained. You point to the minimal serosanguinous exudate and sheepishly suggest to the patient that the I&D was successful and that a course of antibiotics will resolve this issue.


Skin and Soft Tissue Infections: A POCUS Guided Approach

Skin and soft tissue infections (SSTIs) have a variety of potential causes, ranging in severity from mild infections like cellulitis to abscess all the way to life-threatening causes like necrotizing fasciitis.1 SSTIs are commonly encountered in the emergency department, with cellulitis and abscesses being the two most common.2 It is important to be able to recognize SSTIs and provide appropriate treatment. Abscesses require invasive management, whereas cellulitis is treated with systemic therapies; therefore, it is important to be able distinguish the different between the two types. Doing so can be difficult because of the hidden nature of abscesses. However, ultrasound can be a useful tool in establishing the presence of an abscess. This article is a review of the clinical approach and treatment for SSTIs, focusing on cellulitis and abscesses, as well as the use of ultrasound in helping to establish the diagnosis.


Approach

Clinical suspicion is the initial step in the diagnosis of SSTIs. These infections have multiple causes; therefore, obtaining a detailed history is crucial. Information about immunocompromised state, place of residence, travel, any recent trauma or surgery, previous antimicrobial use, lifestyle, hobbies, and animal bites is essential to developing an adequate differential diagnosis.3

A good understanding of the normal skin flora and common infectious organisms is key to assessing SSTIs. The most commons organisms implicated in SSTIs are Staphylococcus aureus and Streptococcus species.4-6 Methicillin resistant S. aureus (MRSA) being an important strain that has increased in prevalence in the past 20 years. Risk factors such as presence of abscess, intravenous drug use, previous MRSA status, antibiotics within 8 weeks, diabetes mellitus, and previous hospital admission within the last year increase the likelihood of the infection being cause by MRSA.4-6

Physical examination findings are crucial for establishing the presence of an SSTI; the typical criteria are a superficial lesion with the classic inflammatory findings of redness (rubor), swelling (tumor), warmth (calor), and pain (dolor).1,2,7 An abscess is defined as a fluctuant mass of puss localized and buried within a tissue, organ, or potential space; however, clinically it can be hard to determine to presence of this mass.2,7 Other associated signs and symptoms, such as crepitus, bullae, and hemorrhage, may be present upon diagnosis or may develop later during the course.2,7 Due to overlapping clinical presentations of the different SSTIs, it can be difficult to differentiate between them.


Cellulitis – No Abscess
Cellulitis – Possible Abscess
Abscess
Early Abscess

Assessment with POCUS:

Due to the similarities between different SSTI cutaneous findings and their different treatments, it is important to establish if there is an abscess present. It was common, before the introduction of ultrasound, to perform a blind needle aspiration of the infected area in order to determine the presence/absence of an abscess.8,9 However, this subjects that patient to the risks of an invasive procedure as well as pain. On the other hand, treating infection with empiric antibiotics in the presence of an unknown abscess delays drainage and allows for potential worsening of the infection.8,9

A study by Tayal et al. demonstrated that the use of ultrasound was beneficial in patients who had both low and high pretest probability for needing incision and drainage. In patients suspected of having simple cellulitis (low pretest), ultrasound was used to change management in over half of participants; establishing the need for drainage due to imaging of a fluid collection. The opposite was true in the patients suspected of having an abscess (high pretest); the study found that ultrasound was able to determine that more than half of this group did not need drainage, because of the absence of a fluid collection on imaging.10 Other studies have had similar findings, but the percent change in management was slightly lower.11

A study by Barbic et al. demonstrated that POCUS provided a rapid, non-invasive, painless, and easily repeatable test, that distinguished between abscess and cellulitis in the vast majority of cases. Their analysis concluded that POCUS had a sensitivity of 96.2% and a specificity of 82.9% in diagnosing the presence of an abscess.12 They concluded that POCUS can accurately diagnose abscess in paediatric and adult populations and is likely superior to clinical examination.12


Cobblestones

Classic finding for cellulitis (but not specific to cellulitis). There will be hyperechoic lobules of subcutaneous fat surrounded by relatively hypoechoic inflammatory fluid.13

Cobblestone – Cellulitis

Purulent Fluid Collection

Classic finding for an abscess; have a rounded shape of anechoic or hypoechoic fluid collection, and there will be surrounding areas of cobblestones from the overlying cellulitis.13 As well, there should be no color flow if doppler is applied to the area (helping to distinguish from lymph node or vessel).14

Abscess – Anechoic Collection
Possible Abscess or Lymph Node? – This is a lymph node – see below
Colour flow differentiates lymph node from abscess

Necrotizing Fasciitis

Because you do not want to miss it! Findings via ‘STAFF’; subcutaneous thickening, air, and fascial fluid.14 Note, that ultrasound does not to exclude the diagnosis. Also need clinical correlation to increase suspicion of such a serious infection.15

Necrotizing Fasciitis – STAFF

Treatment:

According to The Infectious Diseases Society of America (2014) guidelines, management of SSTIs is differentiated based on the presence/absence of purulence (i.e. abscess/fluid collection). They recommend that all purulent infections be treated with incision and drainage, with more severe infections (signs of systemic involvement) being cultured with sensitivities in order to add antibiotics to the treatment.16 Otherwise, non-purulent infections are to be treated with systemic antibiotics; the severity of the infection determining the route and choice of agent.16

Antibiotic therapy, in addition to incision and drainage of a skin abscess, is suggested for patients with any of the following:17

  • Single abscess ≥2 cm or multiple abscesses
  • Large are of surrounding cellulitis
  • Patients with immunosuppression or other comorbidities
  • Signs of systemic involvement (fever > 38°C, hypotension, or tachycardia)
  • Poor clinical response to incision and drainage alone
  • Presence of an indwelling medical device
  • High risk for adverse outcomes with endocarditis (these include a history of infective endocarditis, presence of prosthetic valve or prosthetic perivalvular material, unrepaired congenital heart defect, or valvular dysfunction in a transplanted heart)
  • High risk for transmission of aureus to others (such as in athletes or military personnel)

 

Horizon Health’s local trends recommend the following (see guideline or Spectrum app for full details)

Severity of Infection

 

 

Antibiotic

Mild

Moderate

Severe

Cephalexin 500 – 1000mg PO q6h x 5 days

ceFAZolin 2 g IV q8h x 5 days

ceFAZolin 2 g IV q8h +/- Clindamycin 900 mg IV q8h

If true beta-lactam allergy

Cefuroxime 500 mg PO BID or TID x 5 days

Clindamycin 600-900 mg IV q8h x5 days

 

If MRSA suspected

Septra 800/160 mg or 1600/320 mg PO q12h x 5 days

Vancomycin 25-30 mg/kg IV once then 15mg/kg IV q8 to q12h x 5 days

ADD Vancomycin 25-30 mg/kg IV once then 15mg/kg IV q8 to q12h

 


Some research is suggesting that POCUS can take the assessment of abscesses one step-further and impact management based on the depth and size of the fluid collection seen in imaging. Russell et al. found that abscesses less than 0.4cm below the skin surface could be effectively treated without incision and drainage.18 Another study found that patients, with skin abscesses less than or equal to 5cm in diameter, treatment with oral antibiotics in combination with incision and drainage had improved short-term outcomes compared to those patients treated with the procedure alone.18 While as mentioned above, UpToDate, suggests that antibiotics be used in single abscess greater than 2 cm in size. As well, research has found that ultrasound guided incision and drainage provides lower failure rates (less recurrent infections or multiple incisions) compared to blind incision and drainage. Likely due to better visualization of the abscess and more adequate initial drainage.19


Limitations

There are some limitations to POCUS for SSTIs: ultrasound imaging and interpretation rely on the user’s ability to obtain high-quality images in order to assess whether an abscess is present. It is important for the user to be familiar with different findings on ultrasound to guide appropriate treatment. An abscess may appear hypoechoic, hyperechoic, or anechoic (depending on tissue contents), and usually has posterior acoustic enhancement.19 Determining if it is drainable can be difficult due to this variability in imaging, and it is also quite common for early abscesses to present like cellulitis with erythema, no fluctuance, and an ultrasound that is negative for a fluid collection.20 In cases of a suspected evolving abscess, sometimes referred to as a non-ripe abscess, supportive care, including warm compresses, pain control, and close follow-up, is recommended.20 The practitioner may treat this like cellulitis; however, the patient may return with perceived failure of therapy if discharge advice does not include the possibility of of an abscess forming over time.


Abscess examples from the SJ archives


References

  1. Moffarah AS, Al Mohajer M, Hurwitz BL, Armstrong DG. Skin and Soft Tissue Infections. Microbiol Spectr. 2016 Aug;4(4). doi: 10.1128/microbiolspec.DMIH2-0014-2015.

 

  1. Martinez, N. “Skin and Soft-Tissue Infections: Itʼs More Than Just Skin Deep.” Advanced Emergency Nursing Journal, vol. 42, no. 3, 2020, pp. 196–203.

 

  1. Cieri, B., Conway, E., Sellick, J., & Mergenhagen, K. (2019). Identification of risk factors for failure in patients with skin and soft tissue infections. The American Journal of Emergency Medicine, 37(1), 48-52.

 

  1. Borgundvaag, B., Ng, W., Rowe, B., Katz, K., Farrell, Brian, Guimont, Chantal, . . . Gregson, Dan. (2013). Prevalence of methicillin-resistant Staphylococcus aureus in skin and soft tissue infections in patients presenting to Canadian emergency departments. CJEM, 15(3), 141-160.

 

  1. Esposito, S., De Simone, G., Pan, A., Brambilla, P., Gattuso, G., Mastroianni, C., . . . Savalli, F. (2019). Epidemiology and Microbiology of Skin and Soft Tissue Infections: Preliminary Results of a National Registry. Journal of Chemotherapy (Florence), 31(1), 9-14.

 

  1. Stenstrom, R., Grafstein, E., Romney, M., Fahimi, J., Harris, D., Hunte, G., . . . Christenson, J. (2009). Prevalence of and risk factors for methicillin-resistant Staphylococcus aureus skin and soft tissue infection in a Canadian emergency department. CJEM, 11(5), 430-8.

 

  1. Spelman, D., Baddour, LM. (2020). Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Retrieved November 11, 2020. From: https://www.uptodate.com/contents/cellulitis-and-skin-abscess-epidemiology-microbiology-clinical-manifestations-and-diagnosis?search=abscess%20treatment&topicRef=110530&source=see_link#H2443336514

 

  1. Comer, Amanda B. “Point-of-Care Ultrasound for Skin and Soft Tissue Infections.” Advanced Emergency Nursing Journal, vol. 40, no. 4, 2018, pp. 296–303.

 

  1. Gaspari, R., Sanseverino, A., & Gleeson, T. (2019). Abscess Incision and Drainage With or Without Ultrasonography: A Randomized Controlled Trial. Annals of Emergency Medicine, 73(1), 1-7.

 

  1. Tayal, V., Hasan, N., Norton, H., & Tomaszewski, C. (2006). The Effect of Soft‐tissue Ultrasound on the Management of Cellulitis in the Emergency Department. Academic Emergency Medicine, 13(4), 384-388.

 

  1. Alsaawi, A., Alrajhi, K., Alshehri, A., Ababtain, A., & Alsolamy, S. (2017). Ultrasonography for the diagnosis of patients with clinically suspected skin and soft tissue infections: A systematic review of the literature. European Journal of Emergency Medicine, 24(3), 162-169.

 

  1. Barbic, D., Chenkin, J., Cho, D., Jelic, T., & Scheuermeyer, F. (2017). In patients presenting to the emergency department with skin and soft tissue infections what is the diagnostic accuracy of point-of-care ultrasonography for the diagnosis of abscess compared to the current standard of care? A systematic review and meta-analysis. BMJ Open, 7(1), E013688.

 

  1. Atkinson DP, Bowra J, Harris T, Jarman B, Lewis D, editors. Point of Care Ultrasound for Emergency Medicine and Resuscitation. Oxford University Press; 2019. pp. 140, 199-200.

 

  1. Gottlieb, M., Schmitz, G., Grock, A., & Mason, J. (2018). What to Do After You Cut: Recommendations for Abscess Management in the Emergency Setting. Annals of Emergency Medicine, 71(1), 31-33.

 

  1. Castleberg, E., Jenson, N., & Dinh, V. (2014). Diagnosis of necrotizing faciitis with bedside ultrasound: The STAFF Exam. The Western Journal of Emergency Medicine, 15(1), 111-113.

 

  1. Stevens, D., Bisno, A., Chambers, H., Dellinger, E., Goldstein, E., Gorbach, S., . . . Wade, J. (2014). Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America. Clinical Infectious Diseases : An Official Publication of the Infectious Diseases Society of America, 59(2), 147-159.

 

  1. Spelman, D., Baddour, LM. (2020). Cellulitis and skin abscess in adults: treatment. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Retrieved November 11, 2020. From: https://www.uptodate.com/contents/cellulitis-and-skin-abscess-in-adults-treatment?search=abscess%20treatment&topicRef=110529&source=see_link

 

  1. Russell, F., Rutz, M., Rood, L., Mcgee, J., & Sarmiento, E. (2020). Abscess Size and Depth on Ultrasound and Association with Treatment Failure without Drainage. The Western Journal of Emergency Medicine, 21(2), 336-342.

 

  1. Gaspari, R., Sanseverino, A., & Gleeson, T. (2019). Abscess Incision and Drainage With or Without Ultrasonography: A Randomized Controlled Trial. Annals of Emergency Medicine, 73(1), 1-7.

 

  1. Thornton J, Hellmich T. Evaluation and Management of Abscesses in the Emergency Department. Emergency Medicine Reports. 2017 May 1;38(10).
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A Case of Uveitis

Medical Student Clinical Pearl (RCP) October 2020

Ben McMullin, Clinical Clerk III

Dalhousie Medicine New Brunswick, Saint John

Reviewed by Dr. Mandy Peach

 

Case Presentation

A 40 year old female presented to the Emergency Department with a 5 day history of right sided eye pain. The pain came on insidiously and had gradually been worsening. She had gone to a walk in clinic 3 days prior to presenting to the ED, and was prescribed antibiotics. Her symptoms continued to worsen despite treatment.

In the emergency department, she denied any discharge, and claimed that her eye was not pruritic. She stated that her eye pain was photophobic, but denied any visual disturbances or changes. She did not have fever or chills.

On exam, she did not have any periorbital erythema or conjunctival injection. She did not have any discharge. Normal ocular movements were noted. Her pupils were equal and reactive to light. Her visual acuity was 20/20 in both eyes. Peripheral vision was normal bilaterally. On slit lamp exam, no foreign body or corneal abrasion was identified.

Ophthalmology was consulted emergently, and agreed to assess this patient the same day.

 

Differential Diagnosis

  • Conjunctivitis
  • Acute closed-angle glaucoma
  • Scleritis
  • Keratitis
  • Uveitis
  • Foreign body1

 

Definition

Uveitis refers to inflammation in the uvea, which is the middle portion of the eye. The uvea is made up of the iris and the ciliary body anteriorly, and the choroid posteriorly. Inflammation can be localized anteriorly, posteriorly, or can be generalized.1

Figure 1 : Anatomy of the eye. Rosenbaum, James. “Uveitis: etiology, clinical manifestations, and diagnosis” last modified August 31, 2020

Anterior uveitis can be acute or chronic, and the acute form is the most common form of uveitis. Posterior uveitis, affecting the retina and choroid, and intermediate uveitis, affecting the vitreous body, are less common.2 Uveitis can be classified by location, clinical course or side affected.

Table 1: Classification of uveitis. Muñoz-Fernández S, & Martín-Mola E. (2006). Uveitis. Best Practice & Research Clinical Rheumatology 2006; 20(3), 487-505.

 

Etiology

Approximately 30% of uveitis cases are idiopathic.1 However uveitis can be associated with many rheumatologic conditions such as spondylarthritis, juvenile idiopathic arthritis, psoriatic arthritis, as well as inflammatory bowel disease, multiple sclerosis, and sarcoidosis3. It can also arise from infectious sources such as cytomegalovirus, HSV, varicella zoster virus, lyme disease, syphilis, and tuberculosis, among others. Uveitis can also occur after trauma to the eye.1

 

Clinical Presentation

Anterior and posterior uveitis typically have different presentations.

In anterior inflammation, pain, photophobia, and redness are more commonly seen with a variation in the degree of vision loss (if any). On exam, one can see a ciliary flush where inflammation of the limbus results in redness next to the iris, but not in the periphery of the eye.

Figure 2:  Ciliary flush. https://commons.wikimedia.org/wiki/File:Ciliary-flush.jpg

Photophobia is consensual meaning shining a light in the unaffected eye causes pain in the affected eye due to pupillary constriction.7 On slit lamp examination one may see ‘cells and flare’ when looking at the anterior chamber  in the oblique view – the stereotypical ‘snowflakes in headlights’ appearance.

Figure 3: Cells and flare.http://blog.clinicalmonster.com/2017/08/22/bored-review-anterior-uveitis/cell-flare/

Precipitates or a hypopyon may also be seen.

 

Posterior inflammation is more subtle and can present with non specific vision changes such as flashers/floaters or decreased visual acuity, while pain is less frequently present.1

Visual loss is an important complication of uveitis and can be caused by cataracts, macular edema, epiretinal membrane, and glaucoma.4

 

 

Red Flags for Painful Red Eye

 The following signs and symptoms should prompt urgent referral to ophthalmology:

  • Severe eye pain
  • Vision loss or deficits
  • Loss of pupil reactivity
  • Corneal ulceration
  • Extraocular eye movement stiffness5

 

 

Management

 Uveitis is an ophthalmologic emergency which is vision threatening. Ophthalmological follow up within 24 hours is vital. Without prompt referral to an ophthalmologist for slit lamp examination and treatment, vision loss can be permanent.1

Topical corticosteroids such as prednisolone are often used in the initial management of uveitis. Immunomodulatory agents can also be used6 – both should be used in discussion with an ophthalmologist as inappropriate steroid use could lead to worsening infection or corneal ulceration7.

To help control pain from excessive constriction of the pupil, cycloplegic drops – like Homatropine (1 drop TID of 2‐5% solution) – can be used. Be aware the effects can last a few days.7

A workup for associated conditions is also reasonable, such as chest XR and serologic testing for commonly associated autoimmune and rheumatologic conditions. Screening for associated infections should also be considered.4

 

 

 References

  1. Rosenbaum, James. “Uveitis: etiology, clinical manifestations, and diagnosis” last modified August 31, 2020, https://www.uptodate.com/contents/uveitis-etiology-clinical-manifestations-and-diagnosis?search=uveitis&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H4
  2. Muñoz-Fernández S, & Martín-Mola E. (2006). Uveitis. Best Practice & Research Clinical Rheumatology 2006; 20(3), 487-505.
  3. Brown, H. (2010). Uveitis.Gp, , 34-35. Retrieved from http://ezproxy.library.dal.ca/login?url=https://www-proquest-com.ezproxy.library.dal.ca/docview/744242835?accountid=10406
  4. Dunn, James. Uveitis. Prim Care Clin Office Pract 2015; 42: 305-323.
  5. Dunlop AL, Wells JR. Approach to red eye for primary care practitioners. Prim Care Clin Office Pract 2015; 42: 267-284.
  6. Dupre AA & Wightman JM. (2018). Red and painful eye. In R. M. Walls (Ed.), Rosen’s Emergency Medicine: Concepts and Clinical Practice (9th, pp. 169-183). Philadelphia, PA: Elsevier Inc.
  7. Emergency Medicine Cases (2010). Nontraumatic Eye Emergencies. Retrieved from https://emergencymedicinecases.com/episode-9-nontraumatic-eye-emergencies/

 

Copyedited by Dr. Mandy Peach

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Non-emergent new onset, symptomatic, severe hyperglycemia

 

Medical Student Clinical Pearl – September 2020

 

Nick Quinn

Year: 4
DMNB Class of 2021

Reviewed and Edited by Dr. Stephen Hull (Endocrinologist) and Dr. David Lewis

 

All case histories are illustrative and not based on any individual


 

Case Report

A 64-year-old man present to the ED after noting a random blood glucose of 32 while at his daughter’s house that he checked with her point of care glucose monitoring. He reports a 6-week history of polyuria, polydipsia, and 15-pound weight loss over the past 4 weeks. He also reports refractory oral candidiasis infection for which he had seen his primary care provider about.

His past medical history is significant for only hypertension and benign prostatic hyperplasia, for which he takes hydrochlorothiazide and tamsulosin.

On exam, he is a mildly obese man with abdominal adiposity, he appears well but anxious, he is in no physical distress. He is alert, and oriented to person, place, and time, although at times seems mildly tangential. There is no jaundice, he is not diaphoretic, he appears to be perfusing well.

His GCS is 15, his heart rate 92 and regular, blood pressure is 116/72, his respiratory rate is 18, temperature is 36.8 degrees, and his oxygen saturation is 96% on room air, his glucose was 46 mmol/L.

His cardiac and respiratory exam are unremarkable. His abdomen is scaphoid, soft, non-tender, there is no guarding, rigidity, rebound tenderness, there are no masses felt, or signs of extra hepatic manifestations of liver disease. A fluid status exam reveals dry mucous membranes, dry axilla, normal skin turgor, and a normal capillary refill. In addition to a dry oropharynx, there is also leukoplakia present. His pupils are equal and reactive to light bilaterally, his strength and sensation is normal bilaterally in both his upper and lower limbs, there is no tremor present.

 


Initial Assessment

Initial survey of someone presenting with symptomatic hyperglycemia should be to rule out diabetic ketoacidosis (DKA), which occurs more commonly, though not exclusively in patients with type 1 diabetes, and hyperglycemia hyperosmolar state (HHS), which again occurs more commonly though not exclusively in patients with type 2 diabetes, both of which can be serious acute complications from diabetes and can cause a patient to become unstable. Initial primary survey should include an assessment to exclude precipitating causes of hyperglycemia including the I’s of DKA and HHS[1]:

 

  • Insulin deficiency (new onset T1DM, failure to take enough insulin)
  • Infection (PNA and UTI)
  • Ischemia or infarction (MI, CVA, Acute mesenteric ischemia)
  • Inflammation (pancreatitis, cholecystitis)
  • Intoxication (Alcohol, drugs)
  • Iatrogenesis (glucocorticoids, thiazides)

Despite the age of this symptomatic, severe hyperglycemic patient, late onset type 1 diabetes should remain on the differential. As such, a pertinent family history should be elucidated, which includes type 1 or type 2 diabetes, the age of diagnosis, and history of other autoimmune conditions. Similarly, noting the presence or absence of other markers of insulin resistance or metabolic syndrome are helpful to determine a diagnosis which would be more in keeping with a diagnosis of type 2 diabetes. Some of the signs of insulin resistance include:

  • Impaired glucose tolerance, impaired fasting glucose
  • Coronary artery disease
  • Metabolic syndrome (abdominal adiposity, low HDL, hypertriglyceridemia, hypertension, impaired fasting glucose)
  • Polycystic ovarian syndrome
  • Non-alcoholic fatty liver disease
  • Acanthosis nigricans

 

Classic presentation of hyperglycemia:

Most patients with hyperglycemia will be asymptomatic if their plasma glucose is in the mild range, however once plasma glucose rise above the renal threshold, patients can develop an osmotic diuresis, which can lead to the classic presentation of[1]:

  • Polyuria
  • Polydipsia
  • Polyphagia
  • Weight loss

 

The subsequent diuresis and dehydration may lead to a variety of other symptoms as well including tachycardia, lightheadedness, and weakness as a result of possible electrolyte abnormalities. As the degree of hyperglycemia worsens, subsequent dehydration and electrolyte abnormalities secondary to the osmotic diuresis may lead to additional symptoms including[2]:

 

  • Abdominal pain
  • Tachypnea (or Kussmaul’s respirations with acidosis)
  • Hypotension
  • Ketotic breath (fruity odor)
  • Marked tachycardia
  • Neurologic symptoms (seizures, focal weakness, lethargy, coma, death)

 


Acute Metabolic Decompensation Spectrum of Diabetes

Although occasionally understood as discrete entities, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) are conditions that exist at either ends of a spectrum of acute metabolic decompensation of diabetes that share a similar pathophysiology [3]. Both conditions are characterised by a decreased net effect of insulin, with concomitant dysregulation of certain hormones, including glucagon, catecholamines, and cortisol, as well as significant dehydration and electrolyte abnormalities [3]. At one end, DKA is characterized by complete lack of insulin due to absent pancreatic secretions or exogenous insulin, and results in acidosis and ketosis but lacks hyperosmolarity; at the other end, HHS is characterized by a hyperosmolar state without acidosis[4]. To appreciate these two mechanisms and their spectrum, it’s important to first understand the pathogenesis of type 1 and type 2 diabetes.

 

Type 1 diabetes is an autoimmune disease whereby the immune system produces autoantibodies against pancreatic beta cells, leading to their eventual destruction, and complete absence in the capacity for insulin production. As such, without exogenous administration of insulin and subsequent uptake of glucose by the cells, glucagon is secreted which results in increased gluconeogenesis and glycogenolysis [5]. The increased concentration of glucose in the blood results in a process of osmotic diuresis and eventual significant dehydration through loss of water and electrolytes [3]. Similarly, without insulin present for glucose uptake by cells, the process of lipolysis increases to form free fatty acids as a compensatory mechanism for energy production. These free fatty acids are taken up by the liver and formed into ketones to be used as an energy source. However, due to their low pKa, ketones cause the blood to become more acidic [4]. Attempts are made to buffer the ketoacidosis with hyperventilation, but it is eventually overwhelmed resulting in metabolic decompensation and metabolic acidosis – the resulting state is known as DKA[4].

 

The development of Types 2 diabetes occurs over a prolonged period of time which initially begins with insulin resistance, whereby the glucose transporters are less sensitive to insulin, and it becomes more difficult for glucose to enter the cell. Initially, the pancreas compensates by increasing insulin secretion to maintain normal levels of glucose uptake [5]. However, eventually, the pancreas is not able to meet the demands of the increasing insulin resistance, and blood glucose levels begin to rise – it is at this point where the pancreas beta cell mass begins to decline as it is no longer able to sustain the elevated levels of insulin production [5]. As this process continues, the pancreas beta cells are no longer able to compensate, and rapid rises in glucose will be seen. Eventually, this process will lead to severe reduction in beta cell mass and significant reductions in the capacity to produce insulin, leading to type 2 diabetes [5]. Because there is typically some degree of beta cell function maintained, the process of ketosis is typically avoided in acute situations that may precipitate metabolic decompensation [3]. The presence of some insulin inhibits the process of increased lipolysis and subsequent production of acid-promoting ketone bodies for energy sources during these acute metabolic decompensation scenarios. Nonetheless, the relative deficiency in insulin results in significant increases in blood glucose, which ultimately leads to both a hyperosmolar state as well as an osmotic diuresis and significant levels of dehydration, known as hyperglycemic hyperosmolar state[5].

 

Through this illustration of either complete or relative insulin deficiency and the resulting metabolic decompensation, it can be seen how physiologic characteristics between these extremes could be observed. Depending on the proportion of beta cell mass and function that is preserved, different levels of insulin secretion could be observed, resulting in a continuum between hyperglycemic ketoacidosis and hyperosmolar hyperglycemic states.


 

Investigations

Initial investigations of symptomatic hyperglycemia should include a basic metabolic profile, CBC, venous blood gas, additional electrolytes (for those who may be suspected of profound dehydration), ECG (acidemia may result in extracellular potassium shifts and demonstrate ECG changes consistent with hyperkalemia), and a urinalysis with culture and sensitivity[6].

 


Case Continued…

His plasma glucose was 43 mmol/L, his CBC was normal, his Na was 132, his K+ was 3.8, his Cl was 109 mmol/L, his BUN was 6 mmol/L, and his creatinine was 98 mmol/L. His serum osmolality was 294 mmol/L. Urine dipstick was negative for signs of infection, negative for ketones, and positive for glucose. The venous blood gas revealed a pH of 7.41, pCO2 of 43, his bicarb was 26. His ECG was normal sinus rhythm.

At this point, the working diagnosis was new onset type 2 diabetes with symptomatic severe hyperglycemia and mild dehydration. He did not have any significant alteration in his mental status nor did his serum osmolality meet criteria for hyperosmolar hyperglycemic state diagnosis – it was elevated, but not significantly. No precipitating event was identified.



 

Management

Management for DKA and HHS is centered around correcting intravascular volume depletion, correcting electrolyte abnormalities, and insulin replacement therapy. Many recommendations and protocols exist for individuals who present in DKA or HHS, however management and disposition of symptomatic, severe hyperglycemia is less clear from the emergency department perspective[8].

Due to the dehydration, intravenous normal saline (0.9%) for the first few hours is often used for fluid management in HHS, and then switching to ½ NS once the serum sodium normalizes [2]. Unless the patient is truly volume deplete, he may not require intravenous fluid resuscitation in this scenario and oral intake is likely adequate.

For symptomatic (catabolic – polydipsia, polyuria, unintentional weight loss) insulin is recommended as the initial treatment modality in all individuals, rather than an oral hypoglycemic agent such as metformin[2]. After insulin has been initiated, and if plasma glucose is well controlled in the near term, it may be possible to discontinue insulin therapy for some individuals and transition to oral hypoglycemic agents, however this decision would require careful follow-up and the involvement of either endocrinologists or general internists.

Insulin administration may be through subcutaneous injections, or through an intravenous line, depending on the severity of hyperglycemia. IV insulin infusion may be appropriate for DKA or HHS, however in the present case, starting a subcutaneous injection as part of a home insulin regimen while admitted or upon discharge would be appropriate, as starting an insulin infusion may delay discharge from hospital. Often, a plasma glucose target for hyperglycemia before discharge from the ED that would be appropriate is 20 mmol/L[8].

Once the plasma glucose has been normalized, the patient needs to continue on a diabetes management plan. It would be appropriate to involve endocrinologists or general internists for decisions in both the acute management as well as to plan follow up management. These specialists would be able to advise on some of the topics discussed above including diagnosis, treatment, management of complications, decisions on insulin administration, discussions with patients regarding the implications of their new diagnosis including lifestyle interventions, decisions around hypoglycemic agents, costs, recommended screening for complications, associated risks, among others. Similarly, the endocrinologist can recommend and facilitate the referral to a diabetes educator.

The Canadian Diabetes Association recommends a multifaceted treatment plans for newly diagnosed diabetes, including diabetes education, healthy behaviour intervention, and screening for complications[9]. A diabetes educator, along with other healthcare providers, can coordinate self-management education (SME). SME is defined as a systematic intervention that involves active participation by the individual in self–monitoring of health parameters and/or decision-making with the application of knowledge and skills acquired during education sessions[10]. There is a strong body of literature which suggests educational interventions that emphasize knowledge, emotional and behaviour support, coping strategies and self-management training can promote improved glycemic control at all ages[11]. Similarly, there is strong evidence to suggest that SME is associated with important clinical outcomes in people with diabetes including reductions in A1C levels, improvements in cardiovascular risk factors, and reductions in foot ulcerations, infections and amputations [11].

The Canadian Diabetes Association also recommend that anyone with evidence of metabolic decompensation (marked hyperglycemia, ketosis, or unintentional weight loss) and/or symptomatic hyperglycemia should be started immediately on a home insulin regime, regardless of A1C level [9].

Home insulin regimens

For an individual being discharged with a new diagnosis of type 2 diabetes, who was not previously on any antihyperglycemic agents, and has an indication for initiation of insulin such as the present case, an appropriate strategy would be to initiate either

  1. Basal insulin (with or without metformin)– 10 units of basal insulin at bedtime
  2. Basal-bolus – total daily dose of 0.3 to 0.5 units/kg; 40% of total daily dose as basal insulin, and 20% of total daily dose as bolus insulin 3 times per day using rapid-acting insulin[9].

For both approaches, patients can either self-titrate to a target fasting glucose of 4.0 to 7.0 mmol/L (or individualized target), or titration may be done in conjunction with a healthcare provider [9]. For self-titration, patients adjust their bedtime basal insulin by 1 unit every day until at target [9]. However, if using the ultra-long-acting basal insulins such as degludec, patients should adjust by 2 units every 3-4 days, or 4 units once a week until target is reached.

Lantus Dosing Calculator

Diabetes Canada – Insulin Prescription

Disposition

Discharging a patient on a new insulin regimen raises concerns for either non-adherence, improper dosing, and hypoglycemia. Despite not being in HHS or DKA, the new onset symptomatic severe hyperglycemia patient may require a brief admission to hospital if the risk of an adverse event occurring upon discharge is significant.


 

Discharge from the hospital with a new prescription for Insulin – The Evidence

One study from Chicago used an emergency department rapid acting protocol to determine if it would have an impact on degree of hyperglycemia, ED length of stay, and adverse events including hypoglycemia. They were trying to achieve the American Diabetes Association recommendation target blood glucose level of <10 mmol/L before discharge to expedite discharge from the ED[12]. They demonstrated the more aggressive ED protocol with rapid acting insulin did result in better glycemic control by an additional 5 mmol/L and a 36 hour reduction in hospital length of stay, but it did not affect ED length of stay[12]. The rate of hypoglycemia was 7.4%, suggesting the aggressive insulin protocol is not without risk and hypoglycemia should be considered as a potential risk when discharging someone on insulin for new onset diabetes[12].

Another study looked at the association between plasma glucose levels at time of discharge from the ED and 7-day adverse events including DKA/HHS, repeat ED visits, or admission to hospital amongst patients who had originally presented to ED with at least a plasma glucose level of 22 mmol/L. The found rates of return visits for hyperglycemia was 13%, hospitalization was 7%, and that of iatrogenic hypoglycemia was 2%[13]. They also concluded that an elevated discharge glucose level was not associated with increased risk of repeat ED visits or hospitalization within 7 days, and suggested the ED management should be focused on ensuring appropriate outpatient follow-up and treatment of long-term glycemic control instead of aiming for a “safe” glucose threshold before discharge[13]. A Canadian study trying to determine risk factors for repeat ED visits in patients presenting with hyperglycemia from any cause found that being on insulin was associated with an increased risk for repeat ED visits (OR 1.9) again supporting the idea that insulin regimens do pose a risk for complications and subsequent repeat ED visits[14].


 

Back to the case…

Generally, patients with HHS or DKA are admitted to hospital, however there are no recommendations for the symptomatic severe hyperglycemic patient and should be determined by a thorough clinical evaluation. When deciding the disposition for this type of patient, several important factors should be considered when deciding whether or not to discharge someone on insulin: the level of social support system at home; any informal care that could be provided through friends or family; his overall general capacity to adhere to the insulin regimen; whether or not he has a family doctor; his relative health literacy; and his socioeconomic status. Depending on these factors, someone may be at a high risk for hypoglycemia, HHS, or other metabolic derangements if they are unable to adhere to the insulin regimen.

The patient in the ED was felt to have a relatively low level of health literacy, and he lived on his own, and was of a lower SES. He had few other medical comorbidities and had difficulty understanding his current presentation, which we felt decreased his ability to manage his new onset type 2 diabetes with an insulin regimen. As such, the patient was consulted to family medicine and subsequently admitted to hospital where he could then be monitored and subsequently enrolled in the diabetes education program to receive adequate information on his new diagnosis and management approach. He was also started on an insulin infusion given his plasma glucose level of 43 mmol/L. Alternatively, if they patient was determined to be of low risk for HHS or hypoglycemia or other metabolic derangements from non-compliance, they could be discharged home on insulin and then instructed to follow-up with both their family doctor and attend the next diabetes education program[9].


 

Conclusion

  • DKA and HHS must be ruled out in the symptomatic hyperglycemic patient in the emergency department
  • DKA and HHS exist on a spectrum of acute metabolic decompensation complication of diabetes
  • Individuals with new onset symptomatic severe hyperglycemia consistent with type 2 diabetes should be started on insulin therapy
  • Consultation of endocrinology and diabetes education are critical components for the assessment and management plan for new onset symptomatic severe hyperglycemia
  • A careful assessment of a patient’s social situation should be undertaken to help guide the disposition of the new onset symptomatic severe hyperglycemic patient. This assessment should include a careful evaluation of the social history, and account for risks of hypoglycemia, or HHS.

 


Quick Reference Guide to Diabetes Management from Diabetes Canada

Healthcare provider tools from Diabetes Canada


References:

  1. Clerkship directors in emergency medicine. Hyperglycemia. Kenny Banh. November, 2019. Retrieved from: https://www.saem.org/cdem/education/online-education/m4-curriculum/group-m4-endocrine-electrolytes/hyperglycemia

 

  1. Initial management of blood glucose in adults with type 2 diabetes mellitus. Wexler, D; Nathan, D; Mulder, J. UpToDate. Topic updated August 7th, 2020. Retrieved from: https://www.uptodate.com/contents/initial-management-of-blood-glucose-in-adults-with-type-2-diabetes-mellitus#H26275125

 

  1. Gosmanov AR, Gosmanova EO, Kitabchi AE. Hyperglycemic crises: diabetic ketoacidosis (DKA), and hyperglycemic hyperosmolar state (HHS). InEndotext [Internet] 2018 May 17. MDText. com, Inc.

 

  1. Kitabchi AE, Umpierrez GE, Miles JM, Fisher JN. Hyperglycemic crises in adult patients with diabetes. Diabetes care. 2009 Jul 1;32(7):1335-43.

 

  1. Weir GC, Bonner-Weir S. Five stages of evolving beta-cell dysfunction during progression to diabetes. Diabetes. 2004 Dec 1;53(suppl 3):S16-21.

 

  1. Management of Hyperglycemic Crises in Patients With Diabetes. Abbas E. Kitabchi, Guillermo E. Umpierrez, Mary Beth Murphy, Eugene J. Barrett, Robert A. Kreisberg, John. Malone, Barry M. Wall. Diabetes Care Jan 2001, 24 (1) 131-153;

 

  1. Goguen, Jeannette, and Jeremy Gilbert. “Hyperglycemic emergencies in adults.”Canadian journal of diabetes42 (2018): S109-S114.

 

  1. EMOttawa. No thanks, I’m sweet enough: Nono-emergent hyperglycemia in the E. Rajiv Thavanathan, Seotember 27th, 2018. Retrieved from: https://emottawablog.com/2018/09/no-thanks-im-sweet-enough-non-emergent-hyperglycemia-in-the-ed/

 

  1. Lipsombe L, Booth G, Butalia S, Dasgupta K, et al.Diabetes Canada 2018 Clinical Practice Guidelines for the Prevention and Management of Diabetes in Canada: Pharmacologic Glycemic Management of Type 2 Diabetes in Adults. Can J Diabetes 2018;42(Suppl 1):S88-S103.

 

  1. Sherifali D, Berard LD, Gucciardi E, MacDonald B, MacNeill G. Diabetes Canada 2018 Clinical Practice Guidelines for the Prevention and Management of Diabetes in Canada: Self-management education and support. Canadian journal of diabetes. 2018 Apr 1;42:S36-41.

 

  1. Worswick J, Wayne SC, Bennett R, Fiander M, Mayhew A, Weir MC, Sullivan KJ, Grimshaw JM. Improving quality of care for persons with diabetes: an overview of systematic reviews-what does the evidence tell us?. Systematic reviews. 2013 Dec 1;2(1):26.

 

  1. Munoz, C., Villanueva, G., Fogg, L., Johnson, T., Hannold, K., Agruss, J., & Baldwin, D. (2011). Impact of a subcutaneous insulin protocol in the emergency department: Rush Emergency Department Hyperglycemia Intervention (REDHI).The Journal of Emergency Medicine,40(5), 493–8.

 

  1. Driver, B. E., Olives, T. D., Bischof, J. E., Salmen, M. R., & Miner, J. R. (2016). Discharge Glucose Is Not Associated With Short-Term Adverse Outcomes in Emergency Department Patients With Moderate to Severe??Hyperglycemia.Annals of Emergency Medicine,68(6), 697–705.e3.

 

  1. Yan, J. W., Gushulak, K. M., Columbus, M. P., van Aarsen, K., Hamelin, A. L., Wells, G. A., & Stiell, I. G. (2017). Risk factors for recurrent emergency department visits for hyperglycemia in patients with diabetes mellitus.International Journal of Emergency Medicine,10(1), 23.
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Wound Management in the ED: Absorbing the Literature – Case Study

 

A review of the principles of emergency wound management including detailed guide to suture material.

 

Medical Student Clinical Pearl – June 2020

Robert Hanlon

@roberthanlon12

Year: 4
DMNB Class of 2021

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual


 

Case Report

You are a third year clinical clerk asked to go see a patient and assess their injuries. A 28 year old female, who is sitting upright in bed and texting her friends, came into the Emergency department via ambulance with a laceration over her right forearm and wrist. EMT vital signs are as follows: BP 128/84, HR 106, RR 18, Temp 37.2, O2 Sats 99% on RA, GCS 15, and Blood glucose 6.4 mmol/L. She weighs 60 kg. The paramedics had wrapped her arm with gauze, which has a blood tinged color to it.

Crying Boy Laying Down With Injured Leg. Selective Focus On Shin.. Stock Photo, Picture And Royalty Free Image. Image 81697370.

What is your approach?


 

Emergency Wound Management

 

A – Ask yourself: is the patient stable or unstable?

  • Based on this patient’s vital signs and the fact that they seem calm and comfortable in bed, they are stable. The tachycardia noted in the vitals is likely due to pain/stress at the time collection and when taken again in the ED her heart rate is 78 and regular.
  • A critical wound (hemorrhage or arterial bleeding) will likely need immediate attention and the patient may be presenting with vital signs that suggest more instability (low BP, high HR, high RR, High Temp, low O2 Sats).
  • If the patient is stable and not exsanguinating, then a brief history and physical should be performed. 1,2 Obtain a brief history:

Arterial bleeding

 

 

B – Obtain a brief history:

Mechanism and timing of injury: The patient was carrying towels down the stairs to her pool, tripped and fell down 5 steps, landing on her right side and breaking through a glass panel on her deck. This occurred 45 minutes ago.

Potential for concurrent injuries based on mechanism: The patient denies any loss of consciousness or head trauma. Denies any pain besides the laceration and does not feel like she has broken any bones.

Functional status prior to injury: She had full range of movement and full sensation in her right arm, wrist, and hand prior to the injury.

Medical History: Patient denies any allergies, diabetes, renal disease, cardiac and vascular diseases, and no bleeding disorder. She is a healthy non-smoker, and her only medication is an OCP.

Tetanus Status: She is up-to-date with her immunizations and her last tetanus shot was 2 years ago.

 

C- Perform a Physical Exam:

Patient is a well-looking 28 year old female with no signs of distress. She is alert and oriented to person, place, and time. She has a bandage on her right forearm that has dried blood on it. She denies any numbness or tingling in her hand. There is no obvious deformity of the arm.

Remove bandage and assess wound: Patient has a 6 cm rounded laceration with the wound extending from the mid-wrist on the volar side to Lister’s tubercle on the dorsal side. It looks like you can see some tendons and muscle at the wound base, but they do not look injured. There is no sign of glass or other foreign bodies, no dead tissue, and the wound bed appears bloody. It has a slow stream of blood running out of it. The surround skin is pink and appears undamaged.

Assess for neurovascular compromise 3,4  : The wrist anatomy is complex and it is important to consider the underlying anatomy when deciding on how to test for injury. Also compare to the patients “normal” other side.

Test for motor function: patient is able to fully extend, flex, and deviate the wrist to both ulnar and radial sides. She is able to flex, extend, abduct, and adduct her thumb, and has no trouble with opposition. She has flexion at the PIP and DIP joints from D2 to D5. She is able to fully extend her fingers and perform abduction as well. Her strength is 5/5 for these movements as well.

Test for sensation: Patient has sensation to light-touch and pin-prick over her thenar eminence, distal aspect and dorsal aspect (proximal to PIP) of D2, D3, and radial half of D3 (testing for intact median nerve). As well as sensation over the radial aspect of the dorsal hand (Radial Nerve). With this injury you should not expect the ulnar nerve to be damaged, but you’re a studious clerk and testing reveals intact sensation.

Test for vascular compromise: You do not notice any pulsatile aspect to the bleeding, her skin is pink, warm, and has <3 seconds of capillary refill. You palpate strong radial pulses and are reassured that she has not injured this artery.

 

With this examination you are reassured that she has not injured any underlying structures (tendons, nerves, muscles, and vasculature). You tell the patient that despite a large cut, she is lucky that no serious damage was done.

 

D- Obtain Pain Control: Either local or regional anesthesia.

Luckily, you just finished your plastic surgery rotation and had plenty of experience drawing up local anesthetic. You also learned how to inject a wound while trying to minimize the patients pain. You were told to ALWAYS USE EPI and ALWAYS USE BICARB in your anesthetic solution.5 You draw up one 10 ml solutions (or 100mg) of Lidocaine 1% with epinephrine 1:100,000 buffered with 1 ml bicarbonate (1:10 ratio of bicarb to lidocaine). Maximum dose being 7mg/kg or 420 mg for this patient. You’re wondering if you might need more and realize that you could be getting close to the patient maximum dose; however, you remembered you could always dilute your solutions to double the amount of syringes and still have effective analgesia.5,6 You use a smaller gauge needle (27 or 30 gauge) as this helps to reduce the pain experienced by the patient.5 You let the patient sit for a while so the analgesia will be effective.

ED Rounds – EM and Hand Surgery – Dr Don Lalonde

Regional anesthesia of the hand

 

E – Irrigation and Cleansing:

You irrigation the wound with copious amounts of tap water (or saline). Again, you notice no foreign bodies or signs of infection. You position the patient lying down in bed and cleanse the skin around the wound with chlorhexidine swabs to prep the surface for wound closure.1,3,7,8

Note: Debridement of jagged, dead, or highly contaminated tissue may be necessary in order to promote wound healing and provide an optimal surface for closure and cosmetic effect.3

 

F- Wound Closure with Sutures:

When you were gathering your supplies you realized there were many options for sutures, so you decided to ask your attending. They recommended a non-absorbable either 4-0 or 5-0 Nylon suture and to use a simple interrupted technique. You closed the wound and the edges approximated well. You, your patient, attending are all happy with the result. The patient is discharged with follow-up for suture removal in 7 days.

Wound Closure Resources

 

Useful Patient Information Reference from the ACS

 


 

Suture Types: To absorb or not to absorb?

 

Typical emergency department suture choice is a monofilament non-absorbable suture, this is due to ease of handling, knot security (does not easily break), and emergency texts report a lower rate of infections.1,2,3 There is also the need for suture removal, which requires follow-up and a second look at how the wound is healing. Absorbable sutures are usually harder to handle and tying knots can be tricky due to ease of breaking, especially with smaller sized sutures. Much of the emergency texts cite an increase in rates of infection with absorbable sutures as a reason not to choose them. However, evidence suggests that there is no significant difference in rates of infections or clinical outcome.9-12 Literature does point towards higher rates of tissue reactivity (inflammation associated with placing of suture) with absorbable sutures.12 Really selection of sutures comes down to wound factors (location and tension requirements), patient factors (need for follow-up, compliance, etc.), as well as physician preference. See tables for types and recommended use.

 


 

References:

  1. Busse, Brittany, and SpringerLink. Wound Management in Urgent Care. 1st Ed. 2016.. ed. Cham: Springer International : Imprint: Springer, 2016. Web.
  2. Cydulka, Rita K. Tintinalli’s Emergency Medicine Manual. 8th ed. New York: McGraw-Hill Education, 2018. Print.
  3. Reichman, Eric F. Reichman’s Emergency Medicine Procedures. McGraw Hill Professional, 2018.
  4. Janis, Jeffrey E. Essentials of plastic surgery. CRC Press, 2014.
  5. Strazar, A. Robert, Peter G. Leynes, and Donald H. Lalonde. “Minimizing the Pain of Local Anesthesia Injection.” Plastic and Reconstructive Surgery3 (2013): 675-84. Web.
  6. Lalonde, Donald H. ““Hole-in-One” Local Anesthesia for Wide-Awake Carpal Tunnel Surgery.”Plastic and Reconstructive Surgery 5 (2010): 1642-644. Web.
  7. Deboard, Ryan H, Dawn F Rondeau, Christopher S Kang, Alfredo Sabbaj, and John G Mcmanus. “Principles of Basic Wound Evaluation and Management in the Emergency Department.”Emergency Medicine Clinics of North America 1 (2007): 23-39. Web.
  8. Forsch, Randall T. “Essentials of Skin Laceration Repair.” American Family Physician8 (2008): 945-51. Web.
  9. Kharwadkar, N., S. Naique, and P.J.A Molitor. “Prospective Randomized Trial Comparing Absorbable and Non-absorbable Sutures in Open Carpal Tunnel Release.” Journal of Hand Surgery1 (2005): 92-95. Web.
  10. Xu, Utku, Bin, Xu, Utku, Bo, Wang, Utku, Liwei, Chen, Utku, Chunqiu, Yilmaz, Utku, Tonguç, Zheng, Utku, Wenyan, and He, Utku, Bin. “Absorbable Versus Nonabsorbable Sutures for Skin Closure: A Meta-analysis of Randomized Controlled Trials.” Annals of Plastic Surgery5 (2016): 598-606. Web.
  11. Sheik-Ali, Sharaf, and Wilfried Guets. “Absorbable vs Non Absorbable Sutures for Wound Closure. Systematic Review of Systematic Reviews.” IDEAS Working Paper Series from RePEc(2018): IDEAS Working Paper Series from RePEc, 2018. Web.
  12. deLemos, D. (2018). Closure of minor skin wounds with sutures. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. Retrieved July 3rd, 2020. Source
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