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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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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Whose Line is it Anyway? – PoCUS in a Patient with Dyspnea

Medical Student Clinical Pearl – March 2020

Nguyet (Na) Nguyen

MD 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

ID: 60 y/o M with dyspnea presenting to the ED late evening

HPI: Patient complained of increasing SOB starting the morning on day of presentation, with a worsening 3 days of non-productive cough. No chest pain or other cardiac features. No complaint suggestive of URTI or GI illness. Patient was given Atrovent and Ventolin en route by EMS, and was allegedly moving more air into his lungs after this intervention. Patient reports no ankle swelling, paroxysmal nocturnal dyspnea, but reports using 2 pillows to elevate himself when sleeping. Patient reports no fever, unexplained weight loss or fatigue.

Past medical history includes chronic back pain, DM, atrial fibrillation, peripheral DM-related ulcers, chronic kidney disease, BPH, colon cancer with hepatic metastases. Past surgical history significant for 5x CABG, liver and colon resection.

His medications are amitriptyline 10mg PO qhs, acetaminophen 650mg PO BID, dutasteride 0.5mg PO daily, ferrous sulfate 300mg PO daily, furosemide 40mg PO BID, metformin 500mg BID, pantoprazole 40mg PO BID, pregabalin 150mg PO BID, primidone 125mg PO daily, rosuvastatin 40mg PO qhs, rivaroxaban 15mg PO daily.

He has a distant 10 pack-years smoking history, drinks alcohol occasionally, and does not use recreational drugs. The patient lives with his wife in their own home.

Physical exam: Patient was markedly pale, non-diaphoretic, in tripod position with increased work of breathing. His temperature was 36.9, regular pulse rate at 105, respiratory rate 22, oxygen saturation 90% on room air and a nebulizer mask through which he was receiving aerosolized Atrovent and Ventolin. His BP was 125/78mmHg.

Cardiovascular exam revealed distant S1S2 in a chest with no visible deformity. His JVD was at the level of the sternal angle, there was no pedal edema bilateral. Capillary refill was 3 seconds bilateral at the thumbs. Percussion revealed no focal dullness, however on auscultation, basal crackles were heard more prominently in the right lung base, though also present on the left. There were also wheezes noted in the upper lobes heard in the anterior chest. Abdomen was soft, non-distended, non-tender. Neurological exam unremarkable.

Investigations: ECG showed sinus tachycardia with a LBBB, bloods drawn for routine labs, VBG, lactate, CXR ordered.

Differential diagnosis: AECOPD vs congestive heart failure.

PoCUS (Arrival Time + 10 mins): B-lines were observed in both lungs when a curvilinear probe was placed over different areas of the anterior chest. A small pleural effusion was also noted at the bottom of the right lung. B-lines represent increased fluid in an area of the lung, and given different clinical contexts maye represent pulmonary edema, pneumonia, or pulmonary contusion. In this case the most likely explanation for bilateral diffuse B-Lines is CHF and Pulmonary Edema. 

Working Diagnosis (Arrival Time + 10 mins): CHF and Pulmonary Edema

Management (Arrival Time + 15 mins): Pending transfer fo CXR and results of investigations the patient was treated with intravenous diuretics. He passed 500mls of urine and his symptoms improved considerably.

 

Investigations Results (Arrival Time + 45 mins): leukocytes 6.4, hemoglobin 83, platelet 165, sodium 140, potassium 5/0, chloride 101, creatinine 120, urea 11.7, glucose 17.0. Venous blood gas showed pH 7.31, pCO2 555, HCO3- 28 and lactate 2.7.

CXR (Arrival Time + 45 mins):

CXR was similar to above, this image is from: https://radiopaedia.org/cases/acute-pulmonary-oedema-6

 

Final impression: Congestive heart failure


What are B Lines?

These are the ultrasound equivalent of Kerley-B lines often reported on chest X-ray, which indicate edema in the lungs. For an exam to be positive (i.e indicative of pathology), one needs to see a minimum of 3 B-lines per view. B-lines look like flashlight beams traveling undisrupted down the entire ultrasound screen, as seen in the images above obtained during the exam.

These need to be distinguished from other artifacts such as ‘A-lines’ and ‘comet tails’. A-lines are seen in normal lungs. These are ‘repetitive reverberation’ artifacts of the normal pleura in motion. (Figure 1)(1)

‘Comet tails’- reported first by Lichenstein et al. in 1998 (although he was describing B-Lines in this paper) (Figure 2) (1), are ‘short, hypoechoic artifacts’ that only descend vertically partially down the screen. These are normal lung artifacts. This paper explains “a common misunderstanding in lung ultrasound” nomenclature that stems from Lichtenstein’s original paper.

Download pdf

 

From: https://www.mdedge.com/emergencymedicine/article/96697/imaging/emergency- ultrasound-lung-assessment

 


More on Comet Tails Artifact in this post from LitFL:

Comet tail artefact

 


 

Protocols

There are multiple protocols that guide the ultrasound technique (4) , some of which are:

  • Lichenstein et al (1998): longitudinal scans of anterior and lateral chest walls of patients in semi- recumbent position. Positive test defined as bilateral multiple B-lines diffuse anterolateral or lateral. The protocol had reported sensitivity (true positive) of 100%, and specificity (true negative) 92% for cardiogenic pulmonary edema. Blue Protocol (2015)
  • Liteplo et al (2008): anterior and lateral chest walls with patient supine: each chest divided into 4 zones (anterior, lateral, upper and lower). Positive test: pathologic pattern found in >1 zone on each side, with both sides involved.
  • Volpicelli et al. (2008): longitudinal scans of supine patients with chest divided into 11 areas (3 anterior R, 3 lateral R, 2 anterior L, 3 lateral L) to obtain score 0-11. Scores strongly correlated with radiologic and BNP (lab marker of CHF) at presentation.

 

 


 

What is the Evidence?

Al Deeb et al. conducted a systematic review and analysis of prospective cohort and prospective case-control studies in the ED, IDU, inpatient wards and prehospital settings (n = 1075). This was published in Acad Emerg Med (2014), which reported a sensitivity of 94.1% for using B-lines to diagnosis acute cardiogenic pulmonary edema (ACPE), and a specificity of 92.4% for patients with a moderate- high pretest probability for ACPE.

The SIMEU Multicenter study reported in 2015 reported a significantly higher accuracy (97% sensitivity and 97.4% specificity) with an approach incorporating lung ultrasound (LUS) in differentiating acute decompensated heart failure (ADHF) and non-cardiac causes of acute dyspnea, compared to approaches using the initial clinical workup (past medical history, history of presenting illness, physical examination, ECG, ABG), chest X-ray alone and natriuretic peptides.

Martindale et al. reported in 2016 (Academic Emergency Medicine) high positive likelihood ratio of pulmonary edema observed on lung ultrasound and low negative likelihood ratio of B-line pattern on lung US in affirming the presence of acute heart failure, after a systematic review and analysis of 57 prospective and cross-sectional studies (n = 1,918).

A useful Systematic Review “Emergency department ultrasound for the detection of B-lines in the early diagnosis of acute decompensated heart failure: a systematic review and meta-analysis ” from McGivery et al from SJRHEM (7), was published in 2018.


 

Learning Point

For a patient presenting to the ER with dyspnea, using PoCUS to observe 3 or more B-lines in two bilateral lung zones +/- pleural effusion can rapidly guide an accurate diagnosis of acute congestive heart failure.


 

References

  1. Taylor, T., Meer, J., Beck, S. Emerg Med. (2015) https://www.mdedge.com/emergencymedicine/article/96697/imaging/emergency- ultrasound-lung-assessment Last accessed Feb 29, 2020
  2. Lee, FCY, Jenssen, C., Dietrich, CF Med Ultrason (2018); 20(3): 379-384
  3. Ang SH. & Andrus P Curr Cardiol Rev. 2012 May; 8(2): 123-136https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3406272/
  4. Al. Deeb M., Barbic S., Featherstone R., Dankoff J., Barbic D. Acad Emerg Med 2014 Aug; 21(8): 843-52 https://www.ncbi.nlm.nih.gov/pubmed/25176151
  5. Pivetta E et al. Chest. 2015 Jul; 148(1): 202-210 https://www.ncbi.nlm.nih.gov/m/pubmed/25654562/
  6. Martindale JL, Wakai A, Collins SP, Levy PD, Diercks D, Hiestand BC, Fermann GJ, deSouza I, Sinert R, Acad Emerg Med. 2016 Mar; 23(3): 223-242 https://www.ncbi.nlm.nih.gov/pubmed/26910112
  7. McGivery K, Atkinson P, Lewis D, et al. Emergency department ultrasound for the detection of B-lines in the early diagnosis of acute decompensated heart failure: a systematic review and meta-analysis. CJEM. 2018;20(3):343‐352. doi:10.1017/cem.2018.27

 

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Acute Kidney Injury

Medical Student Clinical Pearl – January 2020

Carine Nzirorera

 

Faculty of Medicine
Dalhousie University
CC3
Class of 2021

Carine Nzirorera- ResearchGate

 

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual


 

Acute kidney injury (AKI) is defined as an abrupt decrease in kidney function and is classified based on changes in serum creatinine level, reduction of urine output, and need for renal replacement therapy [1]. The Kidney Disease: Improving Global Outcomes (KDIGO) is the most preferred definition and staging system. According to KDIGO guidelines AKI is define as an 1) increase in serum creatinine by ≥0.3 mg/dL (≥26.5 µmol/L) within 48 hours, or 2) an increase in serum creatinine ≥ 1.5 fold from baseline within 7 days, or 3) urine output <0.5 mL/kg/hour for 6 hours [2].

KDIGO staging criteria [2]

Stage 1 an increase of serum creatinine level of 1.5 to 1.9 times baseline, OR increase in serum creatinine by ≥0.3mg/dL (≥26.5 µmol/L) OR a urine output less than 0.5 mL/kg/hour for 6 to 12 hours.

Stage 2 an increase of serum creatinine level of 2 to 2.9 times baseline OR a urine output less than 0.5 mL/kg/hour for more than 12 hours.

Stage 3 an increase of serum creatinine level of greater than 3 times baseline OR increase in serum creatinine to ≥4.0 mg/dL (≥353.6 µmol/L), OR a urine output less than 0.3 mL/kg/hour for ≥24 hours OR anuria output ≥12 hours OR initiation of renal replacement therapy such as dialysis.


 

Case Presentation

69y male with a history of kidney stones had experienced 1 week of hematuria, 1 month of bilateral flank pain and unintentional 20 lbs weight loss over 2 months. Patient was scheduled for a CT scan of his urinary tract and was urgently sent to emergency department after his creatinine levels were found to be severely elevated (2300 µmol/L).

Patient had a 20 year history of kidney stones and previous abdominal CT scans showed small stones in both kidneys =/< 2mm. Patient was afebrile, had no dysuria or increased frequency but complained of difficulty initiating urination and noticed a reduction of the stream even when his bladder felt full. Patient noted no vomiting, diarrhea or decrease in fluid and food intake. Patient had a positive family history of bladder cancer and was a smoker for 30+ years.


 

Etiology

Causes of acute kidney injury are organized based on located of the insult (Table 1) [1]. Causes related to decrease in renal perfusion are classified as prerenal injury. Decrease renal perfusion is seen in sepsis due to decreased arterial pressure from systemic vasodilation; intravascular volume depletion from vomiting, diarrhea or overuse of diuretics can also reduce circulation to the kidneys [1]. Lastly drugs like nonsteroidal anti-inflammatory drugs (NSAIDs) and angiotensin-converting enzyme (ACE) inhibitor can lower intraglomerular pressure causing reduced glomerular filtration rate. NSAIDs and calcineurin inhibitors constrict afferent (or preglomerular) arterioles while ACE inhibitors and angiotensin receptor blockers dilate efferent (or postglomerular) arterioles [3].

Direct renal damage to glomeruli, tubules, interstitium or vasculature are classified as Renal injury. Nephritides can be caused by infection (viral, bacterial, and fungal), medication (antibiotics, antivirals, protein pump inhibitors) toxins (ethylene glycol, aminoglycoside, rhabdomyolysis) or are secondary to conditions like hypertension, prolonged hypotension, lupus, diabetes mellitus and vasculitis.

Impaired drainage of urine distal to the kidneys due to obstruction of the urinary tract is classified as Postrenal cause of acute kidney injury.  Common causes of obstruction are kidney stones, injury, prostate, cervical or bladder cancer.

Previously 70% of community acquired cases of acute kidney injury are classified as prerenal causes [4], a more recent study found 55% of community acquired acute kidney injury were renal disease, 35% pre-renal disease and 10% were postrenal [5].

 


 

Clinical Presentation, History and Physical Exam

Clinical presentation of acute kidney injury varies with severity and varies with prerenal, renal and postrenal causes (Table 2). Patients with mild to moderate acute kidney injury are usually asymptomatic and identifiable by laboratory testing. Severe cases would present with vomiting, confusion, fatigue, anorexia, nausea, weight gain or edema [6]. Decline in mental status, asterixis or neurologic symptoms can be indicative of uremic encephalopathy, anemia or bleeding caused by uremic platelet dysfunction [1].

History and physical exam should determine cause of the kidney injury. Screening questions should be used to determine renal perfusion, any potential source of renal injury and any symptoms suggestive of obstructive uropathy (Table 2). Decreased renal perfusion can be assumed from a history of gastrointestinal illness, poor oral intake, use of diuretics, NSAIDs or ACE inhibitors [1,7]. Past medical history of diabetes mellitus, cardiac or liver disease can also indicate reduced renal perfusion [1,7]. Source of renal injury can be screen by assessing current medication for recent antibiotics, antiviral and protein pump inhibitors use, inquiring about past medical history of systemic illnesses such as lupus, viral, bacterial, or fungal infection or symptoms of infection such as rash, arthralgias, fatigue, and hematuria [1,7]. Postrenal cause can be determined from a history of gross hematuria, difficulty urinating, urgency or hesitancy to urinate or a history of kidney stones or bladder, prostate or cervical cancer [1,7].

 


 

Case continued

Blood work

  • CBC: elevated leukocytes (13.5) decreased erythrocytes (3.32), decreased hemoglobin (97), decreased Hematocrit (0.304) normal MCV
  • INR (1.2) APTT (44.3)
  • Liver function test were normal
  • Creatinine (2300)
  • Venous blood gas: decreased pH (7.17), decreased bicarbonate (13), pCO2 (36) and lactate (1.9 )
  • Electrolytes: elevated potassium (7.9), decreased sodium (131), decreased chloride (93), elevated glucose (10.7)

Figure 1. ECG of patient showing Sinus Rhythm and peaked T waves in V2, V3, and V4, an early manifestation of hyperkalemia. Other manifestations (not demonstrated here) include prolonged PR segment, loss of P wave, bizarre QRS complexes and sine wave.

 

PoCUS Imaging

Figure 2. Ultrasound imaging showing moderate hydronephrosis, areas of anechoic fluid indicated by red arrows.

CT Imaging

Figure 3. A) Pelvic CT showing bladder with diffuse wall thickening with a posterior globular neoplasm. B) Pelvic CT showing bladder with calculi within the neoplasm. C) Abdominal CT showing moderate bilateral hydronephrosis.

 

Diagnosis

It was determined that the cause of the acute kidney injury was diffuse thickening of the bladder wall causing obstruction of the ureterovesical junctions (Figure 3A and B). This resulted in bilateral moderate hydronephrosis (Figure 2 and 3C). Additionally, previous CBC reports showed the patient had chronic anemia likely from an underlying chronic kidney disease. This affected EPO production and resulted in decreased erythrocytes production from bone marrow.  With reduce erythrocytes, hemoglobin and hematocrit levels were also decreased. The acute kidney injury resulted in elevated creatinine level, leading to hyperkalemia and metabolic acidosis.

Management

Patient was admitted and fluid resuscitated. To correct his hyperkalemia patient was given 5 to 10 units of regular insulin and dextrose 50% intravenously to shift potassium out of circulation and into the cells. Calcium gluconate (10 mL of 10% solution infused over 5 mins) was given to reduce risk of arrhythmias.

To treat his bilateral hydronephrosis patient was sent to interventional radiology for placement of percutaneous nephrostomy tube. Follow up surgery will be needed to clear the ureters and biopsy of the bladder will be needed to determine treatment for the growth.  Depending on the remaining kidney function after treatment of the acute kidney injury the patient may require dialysis.


 

References

  1. Rahman, Mahboob, Fariha Shad, and Michael C. Smith. “Acute kidney injury: a guide to diagnosis and management.” American family physician 86.7 (2012): 631-639.
  2. KDIGO Clinical Practice Guideline for Acute Kidney Injury, Kidney Int Suppl. 2012;2(Suppl 1):8
  3. Erdbruegger Uta, Okausa Mark. “Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in adults”. Uptodate (2019)
  4. Kaufman J, Dhakal M, Patel B, Hamburger R. Community-acquired acute renal failure. American Journal of Kidney Disease 2 (1991): 191–198.
  5. Obialo CI, Okonofua EC, Tayade AS, Riley LJ. Epidemiology of de novo acute renal failure in hospitalized African Americans: Comparing community‐acquired vs hospital‐acquired disease. Archives of Internal Medicine 160.9 (2000): 1309– 13.
  6. Meyer TW, Hostetter TH. Uremia. New England Journal of Medicine 357.13 (2007): 1316–1325.
  7. Mesropian, Paul Der, et al. “Community‐acquired acute kidney injury: A challenge and opportunity for primary care in kidney health.” Nephrology 21.9 (2016): 729-735.

 

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PoCUS in Pericardial Effusion

Medical Student Clinical Pearl – October 2019

 

Alex Pupek

Faculty of Medicine
Dalhousie University
CC4
Class of 2020

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual


Case

A 70F with a history of bladder CA, HTN and 4.9cm AAA presented to the Emergency Department (ED) and was Triaged as Level 3 with a chief complaint of generalized weakness. Initial assessment was significant for hypotension and low-grade fever with dysuria elicited on history; she was started on Ceftriaxone with a working diagnosis of urosepsis. Bloodwork and imaging studies were sent to rule out other potential sources of infection.

She had a mild leukocytosis of 12.4, pH of 7.23 and a lactate of 5.0. Point-of-care urinalysis was unremarkable. The chest x-ray revealed an enlarged cardiothoracic ratio of 0.62 compared to 0.46 ten months previously, concerning for a pericardial effusion.

Upon reassessment, the patient appeared unwell with slight mottling to the skin, cool extremities and tenuous blood pressure; point of care ultrasound revealed a large pericardial effusion.  Interventional cardiology was paged; the patient was moved to the trauma area and an emergent pericardiocentesis was performed: 360cc of bloody fluid was removed. The pericardial drain was left in situ.

Post-procedure bloodwork included a troponin of 216 and CK of 204. The patient was admitted to the Cardiac Care Unit and discharged within a week’s time.

 


Pericardial Effusions and The Role of Point-of-Care Ultrasound (POCUS)

The normal pericardial sac contains up to 50 mL of plasma ultrafiltrate [1]. Any disease affecting the pericardium can contribute to the accumulation of fluid beyond 50mL, termed a pericardial effusion. The most commonly identified causes of pericardial effusions include malignancy and infection (Table 1).

 

Table 1 – UpToDate, 2019 – Diagnosis and Treatment of Pericardial Effusions


 

Evaluation of the pericardium with point-of-care ultrasound includes one of four standard views: parasternal long axis, parasternal short axis, subxiphoid and apical (Figure 1). A pericardial effusion appears as an anechoic stripe or accumulation surrounding the heart. Larger effusions may completely surround the heart while smaller fluid collections form only a thin stripe layering out posteriorly with gravity. Seen most commonly post-cardiac surgery, pericardial effusions may be loculated and compress only a portion of the heart. [1,2] (Table 2)

Figure 1[1]


Table 2 [2]


 

Both the pericardial fat pad and pleural effusions can be mistaken for pericardial effusions. The parasternal long-axis view is most helpful to accurately define the effusion with the descending aorta, posterior to the mitral valve and left atrium, serving as a landmark: the posterior pericardial reflection is located anterior to this structure. Fluid anterior to the posterior pericardial wall is pericardial, whereas a pleural effusion will lie posterior. The pericardial fat pad is an isolated dark area with bright speckles, located anteriorly; unlike fluid, it is not gravity dependent. Rather than competing with the cardiac chambers for space within the pericardial sac, the fat pad moves synchronously with the myocardium throughout the cardiac cycle. [1,2] (Figure 2)

Figure 2[1]


A pericardial effusion discovered on POCUS in the ED may be mistaken for tamponade, leading to inappropriate and invasive management in the form of pericardiocentesis.[2]

Patient tolerance of pericardial effusions depends on the rate by which they accumulate. As little as 150-200 mL of rapidly accumulating effusion can cause tamponade whereas much larger amounts of slowly accumulating fluid can be well tolerated. Pericardial effusions formed gradually are accommodated by adaptations in pericardial compliance. A tamponade physiology is reached once the intrapericardial pressure overcomes the pericardial stretch limit.[2] (Figure 3)

Figure 3[2]


The core echocardiographic findings of pericardial tamponade consist of:

  • a pericardial effusion
  • diastolic right ventricular collapse (high specificity)
  • systolic right atrial collapse (earliest sign)
  • a plethoric inferior vena cava with minimal respiratory variation (high sensitivity)
  • exaggerated respiratory cycle changes in mitral and tricuspid valve in-flow velocities as a surrogate for pulsus paradoxus

In the unstable patient with clinical and echocardiographic findings of tamponade, an emergent pericardiocentesis is indicated.[2]

A retrospective cohort study of non-trauma emergency department patients with large pericardial effusions or tamponade, ultimately undergoing pericardiocentesis, found that effusions identified by POCUS in the ED rather than incidentally or by other means saw a decreased time to drainage procedures, (11.3 vs 70.2 hours, p=0.055).[3]

Point of care ultrasound is a valuable tool during the initial evaluation of the undifferentiated hypotensive emergency department patient but should be interpreted judiciously and within clinical context to avoid unnecessary emergency procedures.


Additional Images

From GrepMed


 

echocardiogram-pericardial-tamponade-alternans-effusion

 


References

  1. Goodman, A., Perera, P., Mailhot, T., & Mandavia, D. (2012). The role of bedside ultrasound in the diagnosis of pericardial effusion and cardiac tamponade. Journal of emergencies, trauma, and shock, 5(1), 72.
  2. Alerhand, S., & Carter, J. M. (2019). What echocardiographic findings suggest a pericardial effusion is causing tamponade?. The American journal of emergency medicine, 37(2), 321-326.
  3. Alpert, E. A., Amit, U., Guranda, L., Mahagna, R., Grossman, S. A., & Bentancur, A. (2017). Emergency department point-of-care ultrasonography improves time to pericardiocentesis for clinically significant effusions. Clinical and experimental emergency medicine, 4(3), 128.

 

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Hemiplegic Migraine

Medical Student Clinical Pearl – January 2020

Alyssa BeLong, B.Sc.(Hon)

Dalhousie Medicine New Brunswick

M.D. Candidate, Class of 2021

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual


Case Presentation

A 45-year-old female presented with sudden-onset left-sided vision loss, right arm paralysis and auditory changes 24 hours ago. She subsequently developed a throbbing pain (6/10) behind her left eye which radiated over her scalp, with a sensation of water dripping down the back of her neck. Her symptoms resolved within 30 minutes except for ongoing headache and photophobia.


Differential Diagnosis

A variety of conditions may present with transient unilateral weakness or hemiplegia: (4)

  • Hemiplegic Migraine
  • Transient Ischemic Attack (TIA): Typically present with sudden onset of all symptoms rather than progression from one to another. A TIA is also less likely to present with headache, nausea, photophobia, phonophobia.
  • Brain Tumor: Typically present as progressive rather than transient neurologic symptoms.
  • Epilepsy with Post-Ictal Paralysis: Would expect paroxysmal symptoms at time of onset or change in level of consciousness as well as post-ictal confusion. Duration of symptoms also makes this unlikely.
  • Stroke-like Migraine Attacks After Radiation Therapy (SMART)
  • Other possible but rare/unlikely diagnoses include headache and neurologic deficits with cerebrospinal fluid lymphocytosis (HaNDL), CNS infection, Sturge-Weber syndrome as well as certain inherited disorders and metabolic disturbances.

Case Continued – History and Physical Exam

Clarification of visual field disturbance revealed a left homonymous hemianopia rather than loss of vision in the left eye. There was no change in speech or facial droop. There were no precipitating events and there were no alleviating or aggravating factors. The patient noted herself to be particularly stressed lately. She was otherwise healthy with a past medical history of migraines without aura many years prior. Family history was negative for thromboembolic events, she was not taking any medications and had no history of smoking or substance use.

On physical exam, the patient appeared well with all vital signs within normal limits. Cranial nerve exam was unremarkable apart from ongoing photophobia in her left eye. There was normal motor, strength, sensation, tone and reflexes bilaterally. There was no evidence of gait disturbance or dysdiadochokinesia.


Migraine Overview

Migraines typically present as severe episodic headaches often accompanied by photophobia, phonophobia and/or nausea, however presence of an aura can yield a variety of presentations. Migraines are currently thought to be neurologic in origin, although the exact pathophysiology remains unknown (2). Migraines were previously thought to be due to vascular changes, with vasodilation causing headache and vasoconstriction causing aura, however this theory is no longer viable (2).

Migraines affect 17% of women and 6% of men, with an overall prevalence of 12% (2). Migraines typically flow through four phases (2):

  1. Prodrome: Change in affect or vegetative symptoms 24-48hrs prior to onset of headache.
  2. Aura: Focal neurologic symptoms, including visual, sensory, language or motor disturbance.
  3. Headache: Often unilateral but can be bilateral, typically throbbing or pulsatile in quality, frequently accompanied by photophobia, phonophobia, nausea or vomiting.
  4. Postdrome: Sudden movement may trigger transient pain in location of the resolved headache.

While many types of migraines exist, 75% of migraines do not have an aura (2). Some patients also experience aura without headache. Factors thought to be involved in precipitation of migraine include stress, menstruation, fasting, weather, nitrates, wine and visual triggers (2, 3).  

Hemiplegic Migraine

  1. At least two attacks fulfilling criteria B and C
  2. Aura consisting of both of the following:
    1. Fully reversible motor weakness
    2. Fully reversible visual, sensory and/or speech/language symptoms
  3. At least two of the following four characteristics:
    1. At least one aura symptom spreads gradually over ≥5 minutes, and/or two or more symptoms occur in succession
    2. Each individual non-motor aura symptom lasts 5 to 60 minutes, and motor symptoms last <72 hours
    3. At least one aura symptom is unilateral
    4. The aura is accompanied, or followed within 60 minutes, by headache
  4. Not better accounted for by another ICHD-3 diagnosis, and transient ischemic attack and stroke have been excluded

Familial hemiplegic migraine requires one first or second degree relative to meet the above criteria for hemiplegic migraine. Sporadic hemiplegic migraine encompasses those who do not meet familial criteria. (4, 5).

  1.  

Treatment

Treatment of acute migraine in the emergency department follows similar principles to abortive management in an outpatient setting (6):

Abortive Agents

  • Triptans
    • Sumatriptan 6mg SC
  • Antiemetics / Dopamine Receptor Blockers
    • Metoclopramide 10mg IV, Prochlorperazine 10mg IV or Chlorpromazine 0.1mg/kg IV up to 25mg IV)
    • Diphenhydramine: given with parenteral antiemetics to prevent akathisia or dystonia. 12.5-25mg IV (q1h up to two doses)
  • Dihydroergotamine 1mg IV + Metoclopramide 10mg IV can be given if Metoclopramide monotherapy is ineffective.
  • Dexamethasone 10-25mg IV (or IM): Recommended in conjunction with the above treatments to lower risk of early headache recurrence.

In general, hemiplegic migraines can be treated the same as typical migraine with aura (4). Triptans and ergotamine are currently contraindicated due to their effect on vasoconstriction and theoretical risk of ischemic events, although this recommendation may change with evolving theory of migraine pathophysiology (4, 7).

Opioids are not recommended as first-line therapy and should not be routinely used in the acute management of migraine (6, 8).  


Case Continued – Treatment

The following medications were given in the emergency department:

  1. 10mg Metoclopramide IV
  2. 1mg Benztropine IV (for prevention of dystonia)
  3. 10mg Dexamethasone IV

Case Conclusion

The patient’s headache resolved with IV medications. She was advised to take it easy and consider scaling back on her shifts at work – a significant source of her stress. The patient was very pleased with her treatment and was discharged home.


Sources

  1. Donnelly K (2011). Homonymous Hemianopsia. In: Kreutzer J.S., DeLuca J., Caplan B. (eds) Encyclopedia of Clinical Neuropsychology. Springer, New York, NY. DOI: https://doi.org/10.1007/978-0-387-79948-3_739
  2. Cutrer F. Pathophysiology, clinical manifestations, and diagnosis of migraine in adults. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
  3. Martin VT, Behbehani MM (2001). Toward a rational understanding of migraine trigger factors. Medical Clinics of North America 85(4):911.
  4. Robertson C. Hemiplegic Migraine. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
  5. Headache Classification Committee of the International Headache Society (IHS) (2013). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia 33(9):629-808. DOI: 10.1177/0333102413485658
  6. Smith J. Acute Treatment of Migraine in Adults. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
  7. Russell MB, Ducros A (2011). Sporadic and familial hemiplegic migraine: pathophysiological mechanisms, clinical characteristics, diagnosis, and management. Lancet Neurology 10(5):457-70. DOI: 10.1016/S1474-4422(11)70048-5
  8. Friedman BW, West J, Vinson DR, Minen MT, Restivo A, Gallagher EJ (2015). Current management of migraine in US emergency departments: an analysis of the National Hospital Ambulatory Medical Care Survey. Cephalalgia 35(4):301.
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Tardive Dyskinesia in an Emergency Setting

Medical Student Clinical Pearl – October 2019

Faith Moore

Faculty of Medicine
Dalhousie University
CC3
Class of 2021

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual



Case

A 48-year-old female was brought to the emergency department by EMS after developing dystonia that morning, a couple hours earlier, following a restless night. The dystonia had begun affecting her arms, torso and buccal region, but eventually moved to also involve her legs. She had a history of recurrent tardive dyskinesia for the past 20 years since taking stelazine and developing tardive dystonia. She was switched to olanzopine after developing dystonia and stayed on it until two months ago. Her citalopram and clozapam dosing had been increased two weeks ago, and she had also started Gingko biloba extract two weeks ago. She had started Nuplazid 3 days ago.

Upon exam she was diaphoretic with no other abnormal findings other than dystonia affecting the entire body.


Tardive Dyskinesia

Pathophysiology

    • Tardive dyskinesia is a hyperkinetic movement disorder that is associated with the use of dopamine receptor-blocking medications.1 The exact mechanism is under debate, but the main hypotheses include an exaggerated response by dopamine receptors due to a chronic dopamine blockade, oxidative stress, gamma-aminobutyric acid (GABA) depletion, cholinergic deficiency, altered synaptic plasticity, neurotoxicity and defective neuroadaptive signaling. 2 The most accepted theory of the mechanism is that the chronic dopamine blockade caused by the dopamine receptor-blocking medications results in a hypersensitivity of the receptors, specifically at the basal ganglia. 1
    • The medications that are known to have the possibility to cause tardive dyskinesia include antipsychotic drugs, anticholinergic agents (ex. Procyclidine), antidepressants, antiemetics (ex. Metoclopramide), anticonvulsants, antihistamines, decongestants (ex. pseudoephedrine and phenylephrine), antimalarials, antiparkinson agents, anxiolytics, biogenic amines, mood stabilizers and stimulants.1

Who is most at risk?

    • The medications that are the most common culprits are first- and second-generation antipsychotics and metoclopramide. The incidence of tardive dyskinesia from chronic first-generation antipsychotic exposure is 5-6% 3, and is 4% for second generation antipsychotics 4. There is no prospective research on chronic metoclopramide use and the risk for tardive dyskinesia at this point and time5, but a study in the UK in 1985 showed 1 case of tardive dyskinesia for every 35 000 prescriptions6.
      • Most prominent risk factors
        • Old age5
        • Chronic exposure5
        • Patients who develop extrapyramidal symptoms while on antipsychotic drugs.7

Signs and Symptoms

      • Repetitive involuntary body movements that may involve the face, tongue, eyes, arms, torso and legs

Diagnosis

    • The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) classifies tardive dyskinesia as “involuntary movements (lasting at least a few weeks) generally of the tongue, lower face and jaw, and extremities (but sometimes involving the pharyngeal, diaphragmatic, or trunk muscles), developing in association with the use of a neuroleptic medication for at least a few months” and that persists for at least one month after the medication is stopped.8

Differential Diagnosis

    • Acute dyskinesia
    • Akathisia
    • Parkinsonism and tremor
    • Perioral tremor
    • Stereotypies and mannerisms
    • Spontaneous or idiopathic dyskinesias
    • Isolated dystonia
    • Primary movement disorders
    • Chorea from systemic causes 9

Key Questions for History and Physical

    • Are the movements voluntary?
    • Is there an accompanied feeling of restlessness?
      • If yes, might point towards akathisia.
    • When did these movements began?
    • What is the body distribution of the involuntary movements?
    • Are there any extrapyramidal signs and symptoms?
    • Are there any associated features?
    • Have there been any drug changes in the past few months?

 

Management in the Emergency Department

    • First line treatment of tardive dyskinesia generally begins with discontinuation of the offending drug. In the emergency department this should be done after consulting with the treating physician. These patients are often being treated for psychiatric disorder and the treatment of the psychiatric disorder must be balanced with the risk of tardive dyskinesia. It may be appropriate to switch from a first generation antipsychotic medication to a second generation antipsychotic generation medication.
    • If the symptoms of tardive dyskinesia need to be treated, like in our case with this patient, there are various drugs that can be tried.
    • Tetrabenazine is considered first line.10
      • Suggested doses of 12.5-25 mg starting daily dose with a 25-200 mg/day dose range.10
    • Other treatment options
      • Dextromethorphan11
        • In a recent case study patients took under 1mg/kg, not exceeding 42 mg/day.11
        • This was recommended by a local neurologist here at the Saint John Regional Hospital.
      • Valbenazine 12
        • Suggested dose of 40 mg UID, increasing to 80 mg UID after one week.12
      • Amantadine10
        • Suggested dose of 100 mg starting daily dose with a dose range of 100-300 mg/day 10
      • Benzodiazepines12
        • Clonazepam initiated at 0.5 mg and titrated by 0.5 mg increments every 5 days to response up to a maximum dose of 3-4 mg/day. 12
      • Diphenhydramine suggested dose of 25-50 mg IV13
      • Botulinum toxin injections12
    • Commonly used treatments lacking evidence of efficacy
      • Benztropine10

Drug Starting Dose Recommendations Dose Range
1st Line
Tetrabenazine 12.5-25 mg UID 25-200 mg UID
Other options
Dextromethorphan Under 1 mg/kg Not exceeding 42 mg UID
Valbenazine 40 mg UID Increase to 80 mg after 1 week
Amantadine 100 mg UID 100-300 mg UID
Clonazepam 0.5 mg 0.5-4.0 mg UID
Diphenhydramine 25 mg IV 25-50 mg IV
Botulinum toxin injection local injection to treat specific painful dystonia resistant to systemic therapy

 


Case Continued

The patient was given 2mg of Benztropine IV with no effect. Twenty minutes later he was then given 1mg of Ativan SL with no effect. Thirty minutes later the patient was given 150 mg Benadryl IV, and some improvement was then witnessed, the patient was allowed to sleep and was discharged approximately 5 hours after his arrival with no symptoms.


External Resources

Treatment strategies for dystonia

Diagnosis & Treatment of Dystonia


References

  1. Cornett EM, Novitch M, Kaye AD, Kata V, Kaye AM. Medication-Induced Tardive Dyskinesia: A Review and Update.Ochsner J. 2017 Summer;17(2):162-174. Review. PubMed PMID: 28638290; PubMed Central PMCID: PMC5472076.
  2. Kulkarni SK, Naidu PS. Pathophysiology and drug therapy of tardive dyskinesia: current concepts and future perspectives.Drugs Today (Barc). 2003 Jan;39(1):19-49. Review. PubMed PMID: 12669107.
  3. Glazer WM.Review of incidence studies of tardive dyskinesia associated with typical antipsychotics. J Clin Psychiatry. 2000;61 Suppl 4:15-20.  PubMed PMID: 10739326.
  4. Correll CU, Schenk EM.Tardive dyskinesia and new antipsychotics. Curr Opin Psychiatry. 2008 Mar;21(2):151-6. doi: 10.1097/YCO.0b013e3282f53132.  PubMed PMID: 18332662.
  5. Rao AS, Camilleri M.Review article: metoclopramide and tardive dyskinesia.Aliment Pharmacol Ther. 2010 Jan;31(1):11-9. doi: 10.1111/j.1365-2036.2009.04189.x.  PubMed PMID: 19886950.
  6. Bateman DN, Rawlins MD, Simpson JM.Extrapyramidal reactions with metoclopramide. Br Med J (Clin Res Ed). 1985 Oct 5;291(6500):930-2. doi: 10.1136/bmj.291.6500.930. PubMed PMID: 3929968; PubMed Central PMCID: PMC1417247
  7. Novick D, Haro JM, Bertsch J, Haddad PM.Incidence of extrapyramidal symptoms and tardive dyskinesia in schizophrenia: thirty-six-month results from the European schizophrenia outpatient health outcomes study. J Clin Psychopharmacol. 2010 Oct;30(5):531-40. doi: 10.1097/JCP.0b013e3181f14098. PubMed PMID: 20814320.
  1. American Psychiatric Association, Medication-induced movement disorders and other adverse effects of medication, Diagnostic and Statistical Manual of Mental Disorders, fifth edition, American Psychiatric Association, 2013.
  2. Tarsy D, Deik A. Tardive dyskinesia: Etiology, risk factors, clinical features, and diagnosis. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on September 9, 2019.)
  1. DynaMed [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No.T113751, Tardive Dyskinesia; [updated 2018 Nov 30, cited September 9, 2019]. Available from https://www.dynamed.com/topics/dmp~AN~T113751. Registration and login required.
  1. Kim J. (2014). Dextromethorphan for Tardive Dyskinesia. International Neuropsychiatric Disease Journal. 2. 136-140. 10.9734/INDJ/2014/7970.
  2. Tarsy D, Deik A. Tardive dyskinesia: Prevention, prognosis, and treatment. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on September 9, 2019.)
  1. Buttaravoli P, Leffler SM. Chapter 1 – dystonic drug reaction. 2012:1-3. doi:https://doi.org/10.1016/B978-0-323-07909-9.00001-5 “.
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Palpitations – A Paroxysmal Pearl

Palpitations – A Paroxysmal Pearl

Medical Student Clinical Pearl

Scott Fenwick

Class of 2021

Faculty of Medicine
Dalhousie University

Reviewed and Edited by Dr. David Lewis


Case Presentation:

A 49-year-old female presented with palpitations for the past 2 hours. She had two similar episodes in the last 2 weeks, both of which resolved within 1-2 minutes. She had no other symptoms. She was otherwise healthy, with no past medical history. She was a non-smoke and non-drinker who leads an active lifestyle. She denied weight loss, diarrhea, and heat intolerance.

On physical exam, she was tachycardic at 130bpm with an irregularly irregular pulse. She did not display any tremor or diaphoresis. On auscultation, S1 and S2 were audible, with no murmurs or extra sounds. Respiratory and abdominal exams were unremarkable.


What to ask on History?

Common Symptoms: palpitations, tachycardia, fatigue, weakness, dizziness, light-headedness, reduced exercise capacity, mild dyspnea, and polyuria. It is essential to know when exactly the symptoms started. AF that presents before 48 hours can be safely rhythm controlled without anticoagulation.(1)

Severe/Secondary Symptoms: angina, dyspnea at rest, presyncope and, uncommonly, syncope. Embolic events and heart failure can be severe complications of AF.

Past Medical History: cardiovascular or cerebrovascular disease, diabetes, hypertension, COPD, obstructive sleep apnea, and hyperthyroidism.


What to look for On Examination?

ABCs and vitals: particularly pulse rate and rhythm.

General Assessment: look for signs of thyroid disease, PE, pulmonary disease, alcohol withdrawal, and signs of liver disease from excessive alcohol ingestion.

CVS: precordial scars from prior cardiac surgery, JVP, peripheral edema, and auscultation for murmurs or additional sounds that might suggest valvular AF. There is often an apical-radial pulse deficit where not every apical beat has an associated radial beat due to lack of left ventricular stroke volume.(2)


Case Continued – Testing:

The patient was put on a cardiac monitor and an ECG was performed, demonstrating atrial fibrillation. There was also a right bundle branch block that was consistent with a previous ECG performed in 2017. Laboratory testing was unremarkable.

Depending on clinical suspicion, initial testing may include CBC, electrolytes, blood glucose, PT/INR, creatinine, BUN, TSH, cardiac enzymes, LFTs, and chest x-ray.2

See Basic ECG interpretation Pearl for a great guide to ECGs

Basic ECG Interpretation


 

Classifying Atrial Fibrillation:

AF is classically described as an irregularly irregular heartbeat, as can be observed from the variable RR intervals in the ECG above. In AF, there are no distinct P-waves due to the uncoordinated atrial activity. Broadly, AF can be divided into valvular and non-valvular subtypes. Non-valvular AF can be classified into the following categories:(1)

  • Paroxysmal – AF terminates spontaneously or with intervention within 7 days of onset.
  • Persistent – AF fails to terminate within 7 days of onset; often a progressive disease.
  • Long-Standing Persistent – AF has persisted for greater than 12 months.
  • Permanent – Joint decision between patient and provider to no longer pursue rhythm control.

AF commonly progresses from paroxysmal to persistent states. The above classification only refers to primary atrial fibrillation, not AF that is secondary to cardiac surgery, pericarditis, myocardial infarction, valvulopathy, hyperthyroidism, pulmonary embolism, pulmonary disease, or other reversible causes.

For persistent and permanent AF, the CHADS2 score can be used to estimate a patient’s 1-year risk of ischemic stroke without anticoagulation (0 = low risk, 1-2 = moderate risk, 3+ = high risk).(1)

Calculate it here

 

CAEP and CCS now recommend using the CHAD-65 Score to determine anticoagulation requirement.

 


 

Treatment

DC and chemical (e.g. procainamide) cardioversion are two well-described methods of treating uncomplicated AF. The goal of treatment is to return patients to NSR. Some important points about the two methods include:

  • DC cardioversion can be administered at an initial energy dose of 100J and increased up to 360J as needed.(2)
  • Procainamide is often given in doses of 15-18mg/kg, or more simply, 1g over 60 minutes. Average time to cardioversion is about 1 hour.(1)
  • DC cardioversion requires procedural sedation; whereas, chemical cardioversion does not.
  • In a recent RCT, combination therapy achieved NSR in 99% of patients; Attempting DC cardioversion first decreased length of hospital stay by 1.2 hours.(3)
  • Both therapies are generally well-tolerated by patients.

Case Continued – Treatment:

The patient was diagnosed with paroxysmal atrial fibrillation. The arrhythmia did not spontaneously resolve in the ED. DC and chemical cardioversion methods were considered and discussed with the patient. Direct Current (DC) cardioversion was performed under procedural sedation with propofol and fentanyl. Shocks of 100J and 200J were unsuccessful in converting the patient into normal sinus rhythm (NSR). A third shock at 300J was ultimately successful. The following ECG was obtained demonstrating NSR. As in the initial ECG, there is a RBBB present.

 

CHADS2 score was 0. Therefore anticoagulation or antithrombotic therapy not indicated.


 

Case Conclusion:

The patient was discharged home within 4 hours of arriving to hospital, anticoagulation was not prescribed. It is likely that she will experience AF again and require anticoagulation later in life.


 

References:

  1. January, C. T., Wann, L. S., Alpert, J. S., Calkins, H., Cigarroa, J. E., Cleveland, J. C., et al. (2014). 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: Executive summary. Journal of the American College of Cardiology, 64(21), 2246. doi:10.1016/j.jacc.2014.03.021
  2. Wakai, A., & Neill, J.O. (2003). Emergency management of atrial fibrillation. Postgrad Med J, 79(932), 313. doi:10.1136/pmj.79.932.313
  3. Scheuermeyer, F. X., Andolfatto, G., Christenson, J., Villa-Roel, C., & Rowe, B. (2019). A multicenter randomized trial to evaluate a chemical-first or electrical-first cardioversion strategy for patients with uncomplicated acute atrial fibrillation. Academic Emergency Medicine, 26(9), 969-981. doi:10.1111/acem.13669
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Approach to Resuscitation in Severe Calcium Channel Blocker Poisoning

Medical Student Clinical Pearl

J.L. Dobson

Faculty of Medicine
Memorial University of Newfoundland
M.D. Candidate 2020

Reviewed and Edited by Dr. Luke Taylor and Dr. David Lewis

and Liam Walsh. Pharmacist HHN


 

Introduction:

Calcium channel blockers (CCBs) have multiple clinical uses, including the management of hypertension, angina, and cardiac arrhythmias. [1] While CCBs are no longer the most widely prescribed antihypertensive as they were in the 1990s, their prevalence remains high. [2] This along with the existence of both immediate release and long-acting forms poses a challenge for the Emergency Physician faced with a case of CCB poisoning.

Physiology:

Myocardium in the sinoatrial and atrioventricular nodes uses the slow action potential created by calcium currents to conduct. CCBs act on this tissue by inhibiting this current, thus slowing conduction through the SA and AV nodes. This results in a decreased heart rate, prolonged PR intervals, and lengthened refractory periods through the AV node. Conversely, they also inhibit calcium flow in smooth muscle, resulting in coronary and peripheral artery dilation. This ultimately provides the mechanism for reflex tachycardia, increased AV conduction, and improved myocardial contractility. [3]

Adverse reactions to the physiological effects of CCBs include vasodilatory effects (peripheral edema, headache, palpitations), gastrointestinal effects (nausea, diarrhea, constipation), and negative inotropic effects (hypotension, bradycardia). [4]


 

Case Report:

A 80-year-old male is brought in to Trauma by ambulance with hypotension, bradycardia, and an altered level of consciousness. Report from EMS reveals the patient called about half an hour prior stating that he had taken medications in an attempt to commit suicide. Upon arrival, the pt was alert and oriented, and endorsed taking an unknown quantity of clonazepam and citalopram, and a deficit of up to four grams of Diltiazem was noted from his medications. He denied further substance use. Though initially stable, the patient deteriorated rapidly upon arrival to the emergency department.

In the Emergency Department, initial vitals revealed a BP of 88/68, P of 52 bpm and SPO2 of 93% on RA and a BG of 15. As such nasal prongs were placed and she was immediately given atropine as well as push dose epinephrine. Within ten minutes, there was further decline in mental status of the patient corresponding to a blood pressure of 83/61 and a heart rate persisting in the low 40s bpm. He was successively given further epinephrine, atropine and calcium chloride while toxicology was contacted. Despite recurrent doses of epinephrine and atropine, the patient remained profoundly hypotensive and bradycardic. Insulin (Humulin R) and dextrose were started at 0.5U/kg/hr with a 1U/kg bolus. This infusion was titrated up every thirty minutes with minimal improvement in vitals. At this point, remaining bradycardic at 37bpm, intralipid therapy was deemed necessary and so a bolus of 105mL was given. Having received epinephrine bolus along with a 0.2mcg/kg/hr infusion, maximum dose of atropine, 3g of Calcium chloride, with minimal clinical improvement cardiac pacing was initiated. Once good electrical and mechanical capture were achieved the patient underwent and RSI with ketamine and rocuronium. Once stabilized, he was transferred to ICU for further management. In ICU, the patient had a transvenous pacemaker floated successfully followed by a transitioning off the epinephrine to norepinephrine and vasopressin. Intralipid infusion was started and the insulin and glucose therapy was titrated up to a maximum of 4U/kg/hr. The patient unfortunately did not tolerate whole bowel irrigation. Despite the critical nature of their condition, the patient did slowly improve and pressors were weaned.


 

Discussion:

History & Primary Survey

This patient experienced negative inotropic effects of the extended release calcium channel blocker, resulting in cardiogenic shock. Ingestion of more than 5-10 times the usual dose of CCB results in severe intoxication: this patient was thought to have consumed four grams of Diltiazem, over eleven times the maximum recommended dose. [5] While any CCB can result in hypotension, knowledge of which CCB was taken is useful to set expectations for the patient’s progression: unlike dihydropyridine-type CCBs which would more likely present with reflex tachycardia, non-dihydropyridine CCBs like verapamil and diltiazem result in bradycardia. [6] Another crucial point in the primary survey is that, due to the neuroprotective effects of CCBs, mental status may initially be preserved until cerebral perfusion is severely affected. [5]

Initial Resuscitation

While the patient may initially be able to maintain their airway, mental status and vitals may deteriorate rapidly. [5] It is important to note that like any critical ill patient,  intubation may result in a further drop in heart rate and blood pressure via vagal stimulation. It is crucial to have adequate resuscitation prior to intubation. IV crystalloid fluids , IV atropine (up to three 1mg doses), as well as push dose epinephrine are interventions that can be used quickly at bedside to maintain circulation and heart rate while further investigations and treatments can be organized. [5,8]


Specific Treatments

For a severe CCB poisoning in which hypotension is refractory to IV fluids and atropine, all of the following treatments should be administered simultaneously. If the severity is milder, these treatments should be approached in a stepwise fashion, progressing to the next if the preceding treatment is ineffective. [5]

IV Calcium salt:

As a first line recommendation, a calcium chloride bolus (10-20mL 10%) followed by a continuous infusion (0.5 mEq Ca2+/kg/hr) or the equivalent of calcium gluconate is recommended, though often ineffective. [5] Mortality has been shown to be reduced with its administration, and hypercalcemia occurs only rarely. [7] [8]

IV Insulin with dextrose:

High-dose insulin therapy (1 u/kg bolus and 0.5 u/kg/hr infusion up to 10 u/kg/hr) has been shown to be safe and effective at improving hemodynamics, though response is delayed for 30-60 minutes. [5,7] It should be used with calcium and a vasopressor in the presence of myocardial dysfunction. [8] Blood glucose levels should be monitored every 15-30 minutes for hypoglycemia, and 50mL boluses of dextrose (D50W) given accordingly to maintain levels above 8.25 mM. [5] Hypokalemia is another risk of insulin therapy, therefore electrolytes should be monitored every 30 minutes and 20 mEq of potassium chloride given if needed. [5,7]

IV Vasopressor:

Administration of IV epinephrine has shown improvement in cardiac output. [7,8] In the setting of severe CCB poisoning, doses as high as 150mcg per minute of epinephrine may be needed. It is suggested to start the infusion at 2mcg per minute and titrate up to a systolic blood pressure of 100 mmHg, or a MAP of 65 mmHg. [5] These higher doses may result in a large improvement in patient MAP with minimal change in heart rate.

IV Lipid emulsion therapy:

If the patient is refractory to first-line treatments above, or upon consultation with medical toxicology centre, IV lipid emulsion therapy may be recommended. [8] Most commonly, this is given as a bolus of 1.5 mL/kg of 20% lipid emulsion, repeated up to every three minutes for three total boluses. An infusion of 0.25-0.5 mL/kg/minute may be started. [5] Complications of this treatment are still being studied.

Other considerations:

Studies most often show improvement of hemodynamics and no adverse effects with temporary cardiac pacing for bradycardia refractory to first-line treatments. [7,8] Extracorporeal membrane oxygenation may also be necessary if the patient is near cardiac arrest and remains refractory to previous treatments. [8] Dialysis provides no benefit. [5]

Decontamination:

If the patient is asymptomatic and/or hemodynamically stable, 50g of activated charcoal should be given. In the case of ingestion of extended-release CCBs, whole bowel irrigation should be performed regardless of the presence of symptoms. An asymptomatic patient should be monitored for 6-8 hours for immediate release and 24 hours for extended release forms. [5,8]

Investigations:

ECG may reveal PR interval prolongation due to CCB actions on the SA and AV nodes. Frequent blood glucose measurements are crucial to monitor for the effects of insulin treatment and the need for glucose replacement. Serum electrolytes, notably potassium levels, must be assessed for developed hypokalemia secondary to insulin treatment.



Conclusion:

We present a case and review the physiology of a severe calcium channel blocker poisoning. Key considerations in managing a CCB poisoning include specific dosage and form, initial resuscitation with a low threshold for intubation, fluids, and atropine. Further treatments will be required based on severity, such as intravenous calcium, insulin with dextrose, and lipid emulsion therapy, all of which should be initiated promptly if there is concern for massive over dose and patient declining. Other considerations include the need for further vasopressors and temporary cardiac pacing.

 


FIGURE: Society of Critical Care Medicine key recommendations for management of CCB poisoning. Source: “Experts consensus recommendations for the management of calcium channel blocker poisoning in adults.” Crit Care Med. 2017;45(3):e306-e315. DOI: 10.1097/CCM.0000000000002087


 

References:

[1] Elliott, WJ & Ram,CV. J Clin Hypertens (Greenwich). 2011;13:687–689.

[2] Eisenberg, MJ; Brox, A. & Bestawros, AN. Am J Med. 2004;116(1):35-42.

[3] Singh, BN; Hecht, HS; Nademanee, K. & Chew, CYC. Progress in Cardiovascular Diseases. 1982;15(2):103-132.

[4] Russell, RP. Hypertension. 1988;11(3):II42-44.

[5] Barrueto, F. “Calcium channel blocker poisoning.” UpToDate. 2019.

[6] Hofer, CA; Smith, JL & Tenholder, MF. Am J Med. 1993;95(4):431.

[7] St-Onge, M; Dubé, PA; Gosselin, S; Guimont, C; Godwin, J; Archambault, PM; Chauny, JM; Frenette, AJ; Darveau, M; Le Sage, N; Poitras, J; Provencher, J; Juurlink, DN & Blais, R. Clin Toxicol (Phila). 2014;52(9):926.

[8] St-Onge, M; Anseeuw, K; Cantrell, FL; Gilchrist, IC; Hantson, P; Bailey, B; Lavergne, V; Gosselin, S; Kerns, W; Laliberté, M; Lavonas, EJ; Juurlink, DN; Muscedere, J; Yang, CC; Sinuff, T; Rieder, M & Mégarbane, B. “Experts consensus recommendations for the management of calcium channel blocker poisoning in adults.” Crit Care Med. 2017;45(3):e306-e315.

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