Category Archives: Clinical Pearl

A Case of Boerhaave Syndrome

Posted on by

Medical Student Clinical Pearl by Jillian Allan

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. R Goss

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ JAllan A Case of Boerhaave Syndrome

 

Case Presentation

44-year-old male presents to the ER with a 5-hour history of retrosternal chest pain and recent onset shortness of breath. He was out drinking the previous night and has been profusely vomiting since 5am.

Differential Diagnosis

A variety of conditions may present in this fashion:

  • GERD/Gastritis/ Esophagitis/Gastric ulcer
  • Pneumothorax
  • Aortic dissection
  • Acute pancreatitis
  • ACS/MI
  • Cannabis hyperemesis syndrome
  • Esophageal rupture

History and Physical

Upon arrival to the ER, he is hemodynamically unstable: tachycardic (125), hypotensive (90/58) and febrile (38.2 C). His O2 sats are 86% on RA. He has no history of gastroesophageal reflux or other relevant medical conditions. He does not use cannabis.

On examination, his abdomen is soft, he is tender in the left upper quadrant and diffusely across his chest wall. Breath sounds are decreased on the leftIn addition, he has bilateral supraclavicular crepitus on palpation and a positive Hamman’s crunch (mediastinal crackling, synchronous with the heartbeat) on auscultation. His neck is becoming increasingly distended, and you have noticed a change in phonation since his arrival.

Etiology 

Boerhaaves syndrome is most commonly caused by profuse vomiting but can also be the result of anything that increases esophageal pressure such as weightlifting, seizures, abdominal trauma, locally invasive cancers/infections, childbirth, or compressed air injuries.7

Pathophysiology 

  • Esophageal perforations are classified into 3 groups:
    • Cervical esophagus: can present with neck tenderness, dysphagia, or dysphonia
    • Thoracic esophagus: presents with severe back pain, pleuritic, chest or epigastric pain, inability to lie supine. Most common area for perforation.
    • Intra-abdominal esophagus: Peritonitis

 

  • Severity of perforation tends to depend on the location of rupture, with intrathoracic esophageal ruptures leading to more devastating outcomes.
    • Intrathoracic rupture results in contamination of the thoracic cavity with gastric contents, which can lead to chemical mediastinitis, infection and mediastinal necrosis.6
    • Barogenic rupture of the cervical esophagus has a more benign course, as the spread of contamination to the mediastinum is slow and attachments of the esophagus to the prevertebral fascia limit the lateral dissemination of esophageal flora.6

Evaluation

  • Diagnosis is established through a computed tomography (CT) scan of the chest or contrast enhanced esophagram. Contrast should be water soluble (gastrografin) to avoid mediastinal contamination with barium contrast.
    • CT: Findings suggestive of esophageal rupture include esophageal wall edema and thickening, peri-esophageal fluid, mediastinal widening, and free air/fluid within the pleural spaces, retroperitoneum, or lesser sac.6
    • Radiography: Plain films may also demonstrate air in the soft tissues of the prevertebral space. Other indications can include pleural effusion, hydropneumothorax, mediastinal widening or subdiaphragmatic air.6 While thoracic and cervical radiography can aid in diagnosis, they cannot exclude or confirm esophageal rupture and should not routinely be performed to diagnose this condition. However, a plain radiograph may be performed, and mediastinal air found incidentally when the diagnosis had not been suspected.
    • Esophagram: Reveals the location and extent of perforation of the esophagus by the extravasation of the contrast medium.6
  • Endoscopy should be performed with caution due to the risk of further esophageal damage.

Case Continued

Laboratory results showed elevated leucocytes at 12.9 x 109/L (normal 4.5-11.5) and an elevated C-reactive protein level but were otherwise unremarkable.

An erect chest radiograph and urgent CT was done, which showed the “V” sign of Naclerio, a V shaped collection of air along the mediastinum and diaphragm, indicating pneumomediastinum (Fig.1a).2 An urgent contrast CT confirmed the radiograph findings, showing pneumomediastinum and left hydropneumothorax (Fig. 1b).2

 

Figure 1. Boerhaave syndrome in a 44-year-old man. (A) Chest radiograph showing Naclerio’s V sign, demonstrating air outlining the mediastinal borders (arrows), indicating pneumomediastinum. (B) Chest CT showing pneumomediastinum and left hydropneumothorax.2

  

Esophageal perforation was confirmed with a contrast esophagram, which showed leakage from the lower esophageal sphincter into the left pleural space.

 

Figure 2. Contrast esophagram showing esophageal rupture at lower esophageal sphincter with leakage into the left pleural space.1

Treatment and Management

  • Mainstay of treatment includes volume resuscitation, broad-spectrum antibiotic coverage, and surgical evaluation.
  • 3 treatments options: conservative, endoscopic, or surgical
    • Conservative: typically reserved for small or contained ruptures.
    • Endoscopic: stent placement to prevent fistula formations or seal esophageal leaks.
    • Surgical: primary esophageal repair via open thoracotomy vs VATS (video-assisted thoracoscopic surgery) with fundic reinforcement- which is the gold standard of treatment if within 24 hours.7

Case Conclusion

The patient underwent an emergency VATS procedure which revealed a small tear in the lower esophagus, which was successfully repaired with sutures and a pleural patch. The patient made an uneventful recovery and was discharged on postoperative day 6.

Summary of Key Points

References

  1. Calvin S.H. Ng, Wilfred L.M. Mui and Anthony P.C. Yim. Barogenic esophageal rupture: Boerhaave Syndrome. CAN J SURG December 01, 2006 49 (6) 438-439;
  2. Chew, Fatt Yang; Yang, Su-Tso. Boerhaave Syndrome. CMAJ 2021 September 27;193:E1499. doi:10.1503/cmaj.202893.
  3. Kassem MM, Wallen JM. Esophageal Perforation And Tears. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532298/
  4. Kukuruza K, Aboeed A. Subcutaneous Emphysema. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK542192/
  5. Rawla P, Devasahayam J. Mallory Weiss Syndrome. [Updated 2022 Oct 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538190/
  6. Triadafilopoulos, G. Boerhaave Syndrome: Effort rupture of the esophagus. In: UpToDate, Waltham, MA. (Accessed on October 29th, 2022).
  7. Turner AR, Turner SD. Boerhaave Syndrome. [Updated 2021 Dec 15]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430808/
Continue Reading

Ultrasound in Tonsillitis – Submandibular Approach (Transcutaneous)

Posted on by

PoCUS Clinical Pearl by Dr. Rawan Makhdom

DalEM PoCUS Fellow

Reviewed by Dr. D Lewis

Copy Edited by Dr. D Lewis

Pdf Download: EMSJ RMakhdom Ultrasound in Tonsillitis – Submandibular Approach

Case

A 33-year-old gentleman presents to the ED with a history of fever and sore throat for the past week.

Seven days ago, he was diagnosed with tonsillitis and started on Amoxicillin but showed no clinical improvement.

Three days ago, his antibiotic was changed to Azithromycin.

At his present visit, he is febrile with a complaint of sore throat and muffled voice.

 

 

 

Background

Tonsillitis is an infection or inflammation of the tonsils. The tonsils are areas of lymph tissue on both sides of the throat, above and behind the tongue. They are part of the immune system, which helps the body fight infection. Tonsillitis is usually self-limiting, with most patients recovering within 4 to 10 days. Tonsillitis is usually viral, but can be bacterial e.g., strep throat and in rare cases, a fungus or a parasite can cause tonsillitis. The main symptoms of tonsillitis are a sore throat, and swollen tonsils. Symptoms may also include a fever, a congested or runny nose, swollen lymph nodes, a headache, and trouble swallowing.

 

Figure 1: Normal vs Inflamed Tonsils. (Mayoclinichealthsystem.org)

 

  • Peritonsillar Abscess (PTA) is one of the most common deep neck space infection
  • PTA is a potentially life-threatening complication if not treated.
  • Blind aspiration can lead to eroding or extending of the pus into the deep tissues of the neck, carotid sheath, or posterior mediastinum.

 

Can PoCUS help?

  • The ability of clinicians to reliably differentiate PTA from peritonsillar cellulitis (PTC) by physical examination alone is limited. (2)
  • Both conditions can have overlapping clinical presentations and findings; however, these 2 conditions have very different treatment regimens.
  • Blind needle aspiration is the typical method of choice to diagnosis a PTA, has also been found unreliable with a reported false-negative rate of 10% to 24% (2)
  • So, POCUS can help to differentiate and can also help with needle aspiration!

 

Endocavity Approach (Intraoral)

Figure 2: Ultrasound of Normal Tonsil using Endocavity Approach. (Google images)

 

Technique:

  • The probe is placed into the mouth against the affected tonsil to visualize any adjacent collection.
  • The transducer should be covered with either a condom or a finger from a sterile glove filled with ultrasound gel.
  • A topical anesthesia can be applied (spray) to the oropharynx prior to the examination.

Advantages:

  • It can aid the efficacy and safety of aspiration by localizing the area of pus and visualizing the relationship of the abscess to the carotid artery.

Disadvantages:

  • Not all EM providers have access to an endocavity probe.
  • The patient may also have trismus or difficulty opening their mouth wide enough to accommodate the endocavity probe.
  • Some patients simply cannot tolerate the oral ultrasound.

 

Submandibular Approach (Transcutaneous)

 

Technique:

  • Curvilinear/ linear probe was placed under the patient’s mandible.
  • Marker toward the patient’s ear.
  • Fanned to locate the tonsils.
  • Transverse plane/longitudinal plane (1,5).


Figure 3: Submandibular Approach for Scanning Tonsils using High Frequency Probe. (Brown Emergency Medicine brownemblog.com)

 

Endocavity vs Submandibular Approach

Comparing the two different techniques, intraoral had a sensitivity and specificity of 91% and 75% while transcervical (TCU) had a sensitivity and specificity of 80% and 81% (4).

 

PTA PoCUS Pearl

  • When there is doubt, evaluate the contralateral side.
  • Locate the internal jugular vein and carotid artery and fan the transducer cephalad.
  • with the tonsil appearing laterally and adjacent to the hyperechoic oropharyngeal space.
  • Ask the patient to swallow.
  • Using color Doppler can help identify vascular flow from the internal carotid as well as inflamed tonsillar tissue.
  • As most PTAs are superior and posteriorly located, these will appear deep on transcutaneous views.

 

Figure 4: Ultrasound of PTA using Linear Probe. (SJRHEM)

 

Figure 5: Ultrasound of PTA using Curvilinear Probe. (SJRHEM)

 

Figure 6: Another Ultrasound of PTA using Linear Probe. (SJRHEM)

 

References

  1. Mathew Lecuyer “What is that hot potato voice? POUCS for the PTA” 3 May, 2019. http://brownemblog.com/blogposts/2019/4/24/ptaultrasound
  2. Michael Secko MD a, et al. “Think Ultrasound First for Peritonsillar Swelling.” The American Journal of Emergency Medicine, 23 Jan. 2015. sciencedirect.com/science/article/abs/pii/S0735675715000339.
  3. Matti Sievert, et “the value of transcutaneous ultrasound in the diagnosis of tonsillar abscess: A retrospective analysis” 6 Dec, 2021. https://www.sciencedirect.com/science/article/abs/pii/S0385814621001279
  4. Daniel J. Kim MD a ,et “Test Charcteristics of ultrasound for the diagnosis of peritonsillar abscess: A systematic review and meta-analysis” 10 Jan, 2023. https://onlinelibrary.wiley.com/doi/full/10.1111/acem.14660
  5. Hiroshi Hori, MD, et “The effectiveness of transcutaneous cervical ultrasonography for diagnosing peritonsillar abscess in patient complaining of sorethroat” 22 Jan, 2021. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7796778/
Continue Reading

A Meeting with the Curb: Review of Lip Laceration Repair

Posted on by

Medical Student Pearl by Nick Ellingwood

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. B Ramrattan

Copy Edited by Dr. J Vonkeman

Pdf Download:  EMSJ NEllingwood Review of Lip Laceration Repair

Case Presentation

A 68-year-old female presents to the ED with facial trauma. She tells you that she was walking in a parking lot trying to remember where she parked when she suddenly tripped over a curb and scraped her face on the asphalt. She remembers the event and did not lose consciousness. She denies any nausea/vomiting, headache, or blurry vision. She arrived at the ED by EMS who say that her GCS has remained 15. She tells you that she is a healthy individual other than her diabetes for which she takes Metformin and Ozempic. She does not smoke or drink alcohol. She tells you numerous times during your history that she is very worried about her lip injury and how it will look after it heals.

On exam, she is alert and oriented to person, place, and time. She has an abrasion over her nasal bridge and a laceration at the midline of her lower lip which is approximately 1.5cm deep extending all the way through the vermillion. Her upper right incisor is chipped. She is tender over her nasal bone. Her pupils are equal and reactive, and she has normal extra-ocular movements. She has normal facial sensation and strength and there is symmetrical rise of the uvula. There is no battle sign, hemotympanum, or periorbital bruising. You quickly test her sensation and strength is all her extremities which is normal.

Figure 1: Similar lip laceration as the patient in this case. (Benjamincousinsmd.com)

Associated Injuries

Before repairing a lip laceration, associated injuries must be considered. Common associated injuries include dental fractures, LeFort fractures, nasal bone fractures and jaw fractures.1 Much less common, but can’t miss, associated injuries include intracranial bleed, basal skull fracture, or orbital floor fractures.

Impression/Plan

Given that she is older than 65 years old, you can’t rule out a head injury based of the Canadian CT Head Rule. However, given the mild mechanism of injury and the lack of signs/symptoms of intracranial pathology you decide to forego a CT head and turn your attention to the lip laceration.

Background

When repairing a lip laceration, extra vigilance is needed to ensure proper cosmetic appearance and to preserve the functionality of the lips. It is often one of first facial features people look at when talking to someone and therefore, minimal scarring and good aesthetic are often very important to patients presenting with these lacerations. The lips are also important in tactile sensation, phonation, and mastication.

Evaluation

Lip lacerations are almost always repaired with primary closure because of the difference in aesthetic outcome between primary and secondary closure. Secondary closure may be appropriate in patients with a delayed presentation, signs of infection (erythema, drainage of pus), or contamination in the wound.1 Evaluation of the laceration includes location, length, depth, involvement of the vermillion border and presence of contamination or foreign bodies. Make sure to examine the internal and external lip as partial thickness without vermillion border involvement could be managed conservatively.

Figure 2: Anatomy of the superficial and deep structures of the lips (UpToDate, 2023)1

Anesthesia

Local anesthesia is often avoided in lip lacerations as it can cause swelling which will contort the laceration making it more difficult to maximize the cosmetic appearance. In young children, conscious sedation is needed as they will not stay still for the repair even if they are anesthetized. In adults, infraorbital nerve blocks are used for upper lips lacerations and mental nerve block are used for lower lip lacerations. These nerve blocks provide excellent anesthesia and the landmarking for these blocks are relatively simple. The supraorbital foramen, infraorbital foramen and mental foramen are lined up in a midsagittal plane (See figure 3). Another way to landmark the mental foramen is to find the midpoint between the alveolar crest of the second premolar and the inferior border of the mandible.2 When the mental foramen is located, inject 2-3cc of 1% lidocaine with epinephrine and bicarbonate approximately 1cm under the skin towards the mental nerve. If your laceration is at the midline, then bilateral mental nerve blocks will be needed. Next, wait 15-20 minutes to allow for the anesthetic to take full effect before starting the repair.

Figure 3: Anatomical location of the supraorbital foramen, infraorbital foramen, and mental foramen. (Can J Anesth/J Can Anesth 56, 704–706 (2009).)2

Laceration Repair

Once the laceration is fully anesthetized, you can irrigate the wound and thoroughly examine the laceration. You need to rule out any foreign bodies in the lip through palpation as teeth fragment may not be initially visualized. If in doubt, a lateral XRay may rule out any teeth fragments in the lips as they are radiopaque. You may need to get an extra set of hands to help evert the lip when closing the inner lip portion of the laceration. The most important suture in this repair is the suture at the vermillion border as lining up the vermillion border perfectly will yield the best cosmetic result.3,4Some clinicians prefer to close the inner and outer fibrofatty junction before the vermillion border, whereas some will put their first suture at the vermillion border before closing the deeper tissues. After these steps, you simply need to bring the rest of the lacerations back together. Most clinicians will use either 4-0 or 5-0 absorbable sutures for their deep sutures then 5-0 or 6-0 absorbable sutures for the superficial sutures depending on the anticipated tension on the wound when closed.

Aftercare

The main considerations for aftercare of wounds are tetanus, prophylactic antibiotics, and follow-up.

  • A tetanus booster should be given to patients who are unsure as to when their last dose was or if it has been greater than 5 years since their last Tdap.
  • The evidence of prophylactic antibiotic treatment for lip lacerations is lacking. One study by Steele et al showed that there may be a benefit to prophylactic antibiotics in full thickness lip lacerations such as our case, but their results were not statistically significant.5 The face in general is such a highly vascularized area that if the patient is healthy and not taking any immunosuppressants medications, then the risk of infection is low, and antibiotics are not needed. Irrigation with salt water 2-3x/day is sufficient.
  • Lastly, simple lip lacerations that were repaired in the ED with satisfactory results don’t need Plastics follow-up. If the lip is quite disfigured and you are worried about the cosmetic results, then these patients should be seen by Plastics either in the ED or within 24 hours. Follow-up after several days or more should be avoided as the laceration will already be in the healing stage. This would make any revision and/or alteration to cosmetic results difficult.

References

  1. Hollander, J., & Weinberger, L. (2022, September). Assessment and management of lip lacerations. UpToDate.
  2. Tsui, B.C.H. Ultrasound imaging to localize foramina for superficial trigeminal nerve block. Can J Anesth/J Can Anesth 56, 704–706 (2009).
  3. Espinosa MC, Hohman MH, Sivam S. Oral and Maxillofacial Surgery, Facial Laceration Repair. [Updated 2023 May 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-.
  4. Armstrong, B. Denise. “LACERATIONS OF THE MOUTH.” Emergency medicine clinics of North America 18.3 (2000): 471–480. Web.
  5. Steele, Mark T et al. “Prophylactic Penicillin for Intraoral Wounds.” Annals of emergency medicine 18.8 (1989): 847–852. Web

 

Continue Reading

Approach to Foot Radiographs

Posted on by

Resident Pearl by Dr. Sarah Belbraouet

Diagnostic Radiology PGY2

Dalhousie University

Reviewed by Dr. R Goss

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ SBelraouet An Approach to Foot Radiographs

Foot XRs in the ED

Foot Radiographs are often requested in the emergency department. Indicated in cases of trauma, infection, or pain for instance, it is essential to have an efficient and structured approach to reading these studies.

Using a consistent approach to any radiograph is key to overcoming common pitfalls and blind spots in imaging. This resident clinical pearl will provide a systematic approach that can be molded into personal preferences (1).

1. Adequacy (2)

A standard foot radiograph includes an AP or anteroposterior view (also called DP view or dorsoplantar), a lateral view and an oblique view.

  • AP view: all metatarsal bones should be appropriately visible.
  • Oblique view: taken with a 30-40 degree medial angulation of the foot.
  • Lateral view: includes a projection of the ankle. Here, the base of the 1st, 2nd and 3rd metatarsal should align with the three cuneiforms.

 

 Figure 1: Foot series

 

Figure 2: Foot Anatomy

2. Soft Tissue

Assess for soft tissue swelling and/or effusion; these findings can guide you to an underlying pathology (i.e.: fracture).

3. Bone (1)

Outline the cortex of each bone to assess for fractures.

  • Beware that subtle and frequently missed fractures usually occur at the base of the metatarsal bones.
  • An unattached bone may represent a bone fragment, an avulsion fracture, or an accessory ossicle in which case, could be normal variant anatomy.

4. Cartilage and Joints (2)

Always look out for a Lisfranc injury located at the Lisfranc joint complex which is best seen on the AP and oblique views. The Lisfranc ligament stabilizes the foot therefore, a missed injury can lead to great damage to the foot cartilage. Arthritis and collapse of the arch are complications of a missed Lisfranc injury.

  • The Lisfranc ligament complex consists of a dorsal, interosseous, and plantar ligament (see Figure 3).
  • The medial borders of the 2nd metatarsal and 2nd cuneiform, also named intermediate cuneiform, should be aligned on the AP view. The medial border of the 3rd metatarsal and 3rd cuneiform should align on the oblique view.
  • If there is any disruption or widening of the 1st-2nd metatarsal space, a Lisfranc injury should be suspected.
  • This injury typically results from an axial load to a plantarflexed foot or a crush injury.

 

Figure 3: The Lisfranc ligament complex. Red: Dorsal ligament, Blue: Interosseous ligament, Green: Plantar ligament (6)

 

Examine the midtarsal joints for good alignment to assess for appropriate integrity of the corresponding ligaments.

 

Figure 4: Midtarsal joints (5)

 

5. Additional View Needed?

  • Weight bearing foot AP or lateral view if a Lisfranc injury is suspected. Some institutions will acquire a foot CT instead as it is more sensitive for this type of injury and could also unveil subtle findings that would be missed on a plain radiograph.
  • Os calcis view if there is suspicion for a calcaneal fracture.
    • Around 60% of tarsal bone fractures are associated with the calcaneus.

The Bohler’s angle is used on plain radiographs to assess the presence and severity of these fractures. This angle is measured on the lateral view and results from an initial line drawn from the highest point of the anterior process of the calcaneus and the posterior articular facet (line 1) followed by a line joining the highest point of the posterior articular facet with the calcaneal tuberosity as shown in figure 5. A normal Bohler’s angle ranges between 20 and 40 degrees, any value below should raise suspicion for a calcaneal fracture.

 

Figure 5: Bohler’s angle (6)

 

Pitfall

Apophysis of the proximal 5th metatarsal: Appears from age 10 and 12 in girls and boys, respectively and generally fuses within 2-4 years. This apophysis is located laterally and oriented parallel to the shaft as seen in Figure 6. Do not mistake this with an avulsion fracture or an os peroneum (accessory bone) which are often oriented transversally.

 

Figure 6 : Apophysis of the proximal 5th metatarsal (4)

Figure 7 : Avulsion fracture of the 5th metatarsal (9)

 

Bottom Line

Foot radiographs are often utilized in clinical practice and especially in the emergency department. Research shows that having a systematic approach improves the diagnosis accuracy and therefore can reduce the incidence of inappropriate management of foot injuries (8).

 

References

  1. https://radiopaedia.org/articles/foot-radiograph-an-approach
  2. https://www.aliem.com/emrad-foot-x-ray/
  3. https://www.researchgate.net/figure/Oblique-radiographs-of-a-Lisfranc-injury-and-normal-right-foot-The-rotation-and-loss-of_fig1_262265287
  4. https://radiopaedia.org/articles/apophysis-of-the-proximal-5th-metatarsal?lang=us
  5. https://radiopaedia.org/articles/midtarsal-joint?lang=us
  6. https://radiopaedia.org/articles/bohler-angle-2?lang=us
  7. https://radiologyassistant.nl/musculoskeletal/wrist/foot-1#foot-case-1-distortion
  8. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1964112/
  9. https://www.mdedge.com/familymedicine/article/100121/pain/twisted-ankle

Continue Reading

A Case of Bilateral Internuclear Ophthalmoplegia (INO)

Posted on by

 

Resident Pearl by Dr. Saly Halawa 

iFMEM PGY2

Dalhousie University

Reviewed by Dr. B Ramrattan

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Bilateral INO SHalawa

 

Case Presentation

A 42yo male presents to the Emergency Department with abrupt onset right-sided facial numbness and double vision. His facial numbness quickly improved but he continued to have diplopia and gait ataxia. He denied headache, nausea or photophonophobia. The patient had a history of sickle cell disease and diabetes. His medications included hydroxyurea and insulin. On physical examination, he was unable to adduct his eyes bilaterally on lateral gaze with abducting nystagmus. His power, tone, reflex, and sensation were all normal.

Internuclear Ophthalmoplegia (INO)

Internuclear ophthalmoplegia (INO) is a neurologic condition characterized by impaired control of conjugate eye movements (1). It is caused by a lesion of the medial longitudinal fasciculus (MLF) in the brainstem. The MLF is the pathway containing internuclear neurons connecting cranial nerve nuclei that control conjugate eye movements. These include the nucleus of the abducens nerve (CN VI) in the pons and the contralateral nucleus of the oculomotor nerve (CN III) in the midbrain supplying the medial rectus (1). Together CNIII and CN VI allow for adduction and abduction of the eye, respectively. For instance, interneurons of CNVI on one side project across the midline to the contralateral MLF which ascends to CNIII to control the medial rectus on that side, allowing the lateral and medial rectus to move the eyes together (1). In this way, the MLF coordinates eye movements between both eyes allowing for conjugate gaze. Patients with INO have an adduction deficit on the ipsilateral side with associated contralateral nystagmus of the abducting eye.

INO is named with respect to the side of the adduction deficit, which is the side of the MLF lesion. A R sided INO is due to a lesion of the R MLF. Patients may also present with bilateral INO as in the case presented here.

 

Figure 1: Adduction Defects produced by Internuclear Ophthalmoplegia (1)

Patients with INO often experience horizontal diplopia due to dysconjugate gaze or they may report vertical-oblique diplopia due to associated skew deviation (1). Patients may also present with difficulty in tracking fast-moving objects as a result of a mismatch in saccadic movements between the eyes.

Differential

The differential diagnosis for INO is broad (1). The most common causes of bilateral INO include multiple sclerosis in younger patients, often younger than 50 yrs old, or due to brainstem infarction in older patients. Other causes of INO include infection, toxicity to medications including amitriptyline, benzodiazepines or ethanol, chiari malformations or trauma. In the present case, bilateral INO was the first presentation of MS due to demyelination of the MLF.

Prognosis

Prognostically, INO symptoms do improve over time, often resolving spontaneously after an average of 2 months, but up to 12 months (2). Associated neurologic symptoms such as vertigo, ataxia, sensory or speech deficits are poor prognosticating factors. Those with cerebrovascular etiology have less favorable recovery as well.

Figure 2: Internuclear Ophthalmoplegia caused by lesion at the Medial Longitudinal Fasciculus (4)

Video link: https://www.youtube.com/watch?v=eL3_6yYJdUA&ab_channel=MoranCORE

 

Case Conclusion

CT angiography of the brain demonstrated no evidence of acute infarction. MRI showed periventricular white matter hyperintensities which was also seen in the corpus callosum, suspicious for multiple sclerosis. He was given a five-day trial of methylprednisolone.

Bottom Line

Though uncommon, internuclear ophthalmoplegia points to a brainstem lesion with a wide variety of causes. Multiple sclerosis should be suspected in a young patient presenting with bilateral INO.

References

  1. Toral M, Haugsdal J, Wall M. Internuclear Ophthalmoplegia. EyeRounds.org. posted June 8, 2017; Available from: http://EyeRounds.org/cases/252-internuclear-ophthalmoplegia.htm
  2. Eggenberger E, et al. Prognosis of ischemic internuclear ophthalmoplegia. Ophthalmology. 2002; 109(9):1676-8.
  3.  https://www.youtube.com/watch?v=eL3_6yYJdUA&ab_channel=MoranCORE
  4. https://sketchymedicine.com/2013/12/internuclear-opthalmoplegia/

Continue Reading

Understanding Urachal Anomalies

Posted on by

 

Medical Student Pearl by Alexander MacPherson

MD Candidate, Class of 2024

Dalhousie University New Brunswick

Reviewed by Dr. B Ramrattan

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Understanding Urachal Anomalies by AMacpherson

 

Case Presentation

17-year-old male presents to the emergency room with what he tells you is a pop bottle amount pus-like fluid discharging from his belly button. He appears well and said that this has happened before, but it was never in this amount. He and his family members are, however, concerned as to what may be causing this unusual presentation. Patient denies any past abdominal surgeries or piercings.

Physical Exam

  • Vitals: HR 70, BP 118/78, RR 14, T 37.3°C
  • Tenderness in the periumbilical region
  • Discharge of whitish, mucus-like liquid.
  • Red, dome shaped swelling at centre of umbilicus.

Differential Diagnosis [1]

  1. Urachal anomaly
  2. Abscess
  3. Benign lesion (hamartomas, pyogenic granulomas etc.)
  4. Primary malignancy (urachal adenoma, melanoma, squamous cell carcinoma and basal cell carcinoma).
  5. Metastatic lesion
  6. Omphalitis

Common Clinical Findings of Urachal Anomalies [1]

Urachal anomalies when found in children typically present with:

  • Umbilical drainage
  • Abdominal pain
  • Abnormal appearance of the umbilicus, with a palpable mass
  • Infection
  • Incidental finding

Urachal anomalies when found in adulthood typically present with:

  • Hematuria
  • Pain
  • Dysuria
  • Incidentally

Investigations

  • The primary investigation for a urachal anomaly is through Imaging.
    • Most urachal remnants are diagnosed via abdominal ultrasonography.
    • CT abdomen, MR abdomen and Voiding Cystourethrography (VCUG) are also used to detect and diagnose urachal anomalies and to confirm that there are no associated genitourinary tract abnormalities. [1,2].
  • Our patient received an ultrasound and went on for a CT abdomen to confirm the diagnosis of urachal cyst.

Treatment

  • Surgical resection seems to be the most definitive way to manage and prevent the return of symptoms. It is also important to note that adults presenting with urachal anomalies are at a considerable progressive risk for cancer and if not removed should undergo routine screening.
  • Early removal of urachal remnants at first diagnosis are deemed to be best at preventing future morbidity by some studies, while others recommend that children who are experiencing asymptomatic lesions do not benefit from prophylactic excision [1,2,3]
  • Our patient was referred to general surgery and the urachal cyst was excised.

Background on Urachal Anomalies

During embryologic development the allantois has a connection to the apex of the fetal bladder. This connection is called the urachus and allows for fetal bladder emptying [4]. In a normally developing fetus, the bladder descends into the pelvis. This decent of the bladder stretches the urachus and its lumen is eventually obliterated. The now obliterated urachus is a fibrous cord that is called the median umbilical ligament and continues to be connected to the umbilicus and the bladder. This process, like any other, can be disrupted [5].

The disruption can be divided into several urachal anomalies based on the amount of and where the residual tissue is located (Figure 1):

  1. Patent urachus: A complete failure of closure of the lumen forming a tubular connection between the bladder and umbilicus. Allows for urine to drain through the umbilicus.
  2. Bladder diverticulum: Extra tissue present at the bladder end but does not continue to the umbilicus.
  3. Umbilical polyp: Extra tissue and patency at the umbilical end that does not continue to the bladder.
  4. Urachal cyst: An area of patency in between the bladder and umbilicus that does not communicate with either [1,4].

Figure 1. Urachal anomaly types. Accessed from UpToDate [6]

An Important Note on Malignancy

  • Although there have been no reports of urachal adenocarcinoma in the urachal anomalies resected from children a longitudinal study by Ashley et al (2007) found that 51% of those resected from adults showed evidence of malignancy. It was also determined that age >55 and hematuria were the strongest predictors for malignancy [2].
  • A comprehensive review performed by Gleason et al (2013) however determined that urachal anomalies are more common that previously reported and that the number needed to excise to prevent one case of urachal adenocarcinoma was 5,721 [3]

References

  1. Palazzi, D. L., & Brandt, M. L. (2021, August 27).Care of the umbilicus and management of umbilical disorders. UpToDate. Retrieved April 16, 2022, from https://www.uptodate.com/contents/care-of-the-umbilicus-and-management-of-umbilical-disorders
  2. Ashley RA, Inman BA, Routh JC, Rohlinger AL, Husmann DA, Kramer SA. Urachal anomalies: a longitudinal study of urachal remnants in children and adults. J Urol. 2007 Oct;178(4 Pt 2):1615-8. doi: 10.1016/j.juro.2007.03.194. Epub 2007 Aug 16. PMID: 17707039.
  3. Gleason JM, Bowlin PR, Bagli DJ, Lorenzo AJ, Hassouna T, Koyle MA, Farhat WA. A comprehensive review of pediatric urachal anomalies and predictive analysis for adult urachal adenocarcinoma. J Urol. 2015 Feb;193(2):632-6. doi: 10.1016/j.juro.2014.09.004. Epub 2014 Sep 16. PMID: 25219697.
  4. Briggs KB, Rentea RM. Patent Urachus. [Updated 2021 Jun 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557723/
  5. Naiditch, Jessica A.; Radhakrishnan, Jayant; Chin, Anthony C.(2013). Current diagnosis and management of urachal remnants. Journal of Pediatric Surgery, 48(10), 2148–2152.        doi:10.1016/j.jpedsurg.2013.02.069
  6. Retrieved from: https://www.uptodate.com/contents/image?imageKey=PEDS%2F79324&topicKey=PEDS%2F5009&search=urachal+cyst+infection&rank=1%7E150&source=see_link

Continue Reading

Could it be Kawasaki Disease?

Posted on by

 

Medical Student Pearl by Farhad Hossain

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. M McGraw

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Could it be Kawasaki Disease FHossain

 

 

 

Case Presentation

A 6-year-old female presents to the Emergency Department with a history of a fever over 5 days. She had initially visited the ED a few days ago, where croup was suspected, and she was administered a dose of dexamethasone with minimal improvement. On the day she was brought in for the second time her fever had peaked. Her mom reports increased fatigue and decreased PO intake over the duration, as well as rash.

On physical exam vitals were stable aside from an elevated temperature. Mucosal changes were observed inside her mouth and on her tongue, a non-pruritic rash was present over most of her body, and she had enlarged cervical nodes and an otitis media of the right ear. Further examination showed no pharyngitis, no conjunctivitis, lungs were clear, and heart sounds were normal.

Aside from previous croup and infections, she is otherwise healthy.

Labs yielded elevated CRP and WCC.

Given the clinical picture you consider Kawasaki Disease.

Kawasaki Disease

Kawasaki disease (KD) is an acute systemic vasculitis that mostly affects small and medium size vessels.1-3 It is typically self-limited and usually presents in those under the age of 5.1 Kawasaki disease is now the most common cause of acquired heart disease in children in developed countries due involvement of the coronary arteries.4,5 There are no pathognomonic tests, so diagnosis is dependent on key clinical signs and exclusion of other diagnoses on the differential. A differential can include the following:

  • Scarlett fever
  • Peritonsillar abscess
  • Group A Strep
  • Rheumatic fever
  • Measles

Etiology and Pathophysiology

While several theories have been proposed to explain the cause of KD, none have been definitively proven. Evidence suggests that genetic factors increase the predisposition of KD as siblings are more likely develop it than the general population, as well as those of Japanese descent.3,4 The trigger for the disease has also been believed to be some viral or bacterial antigen that enters the body through mucosal surfaces such as the lung as roughly 40% of children diagnosed with KD tested positive for a viral pathogen.1-4 Various cytokines and immune cascades lead to myocarditis and arteritis, eventually this may cause weak spot in the vessel that predisposes the formation of aneurysms.2,4

Diagnosis

The diagnosis of KD is clinical and requires the presence of fever that has persisted for 5 or more days that is not better explained by another cause and 4/5 of the following:1,3-6

  • Extremity changes such as erythema of the palms/soles and desquamation of the fingers/toes
  • An erythematous rash that is commonly a maculopapular eruption, but urticarial and multiforme-like rashes have been seen. The rash is usually diffuse and affects the trunk and extremities.
  • Bilateral bulbar conjunctival injection with uveitis often observed.
  • Changes to the oral mucosa include erythema, fissuring, strawberry tongue (erythema and prominent fungiform papillae), and diffuse erythema of the oral mucosa.
  • Cervical adenopathy is usually unilateral and confined to the anterior cervical triangle but is the least common clinical finding observed.

Patients can meet the definition of typical or classical KD, but those who do not meet the set criteria can be diagnosed with incomplete KD based off of clinical, laboratory, and echocardiographic findings.6 The following figure shows the evaluation of suspected KD:6

Figure 1: Algorithm for the evaluation of typical Kawasaki Disease. Figure obtained from UpToDate.

 

Aside from measuring CRP, additional lab findings are assessed in those with incomplete KD. The evaluation of suspected incomplete KD is shown in the below figure:1

 

Figure 2: Algorithm for the evaluation incomplete Kawasaki Disease. Figure obtained from McCrindle et al.

People with either complete or incomplete KD should receive an echocardiogram to assess for coronary artery aneurysm in the acute phase of the disease, as well as other cardiac abnormalities.1 It is common for initial echocardiography to be normal, but it does establish a baseline for sequential scans.

Treatment

Treatment for KD should be initiated immediately if clinical criteria are met. It is treated with intravenous immunoglobulin (IVIG) and high dose aspirin.1-6 The maximum dose of IVIG is 2 g/kg and it has been shown that increasing dose (up 2 kg/kg) reduces risk of CA aneurysms and duration of fever.1,5 Aspirin, usually 30 to 100 mg/day divided into 4 doses, modifies the risk in KD leading to lower risk of thrombosis.1,3,5 Studies have demonstrated that combining IVIG with corticosteroids has better effect on reducing coronary artery abnormalities in those who are refractory to initial therapy.1,4 Disease modifying anti-rheumatic drugs and antibodies have been used to treat KD, but there is not enough evidence to recommend their use as treatment.3 Patients often start seeing improvements in 36 to 48 hours. Long term management depends on the patient and the risk of coronary events reaches a peak at 5 to 6 weeks after the acute phase.

Case Conclusion

The patient was started on amoxicillin 500 mg tid down in the Emergency Department for the otitis of the right ear and within 12 hours showed improvement. It was determined she met 3 of 5 criteria for KD along with the fever that persisted for 5 days, so an echocardiogram was ordered. Upon review of the echocardiogram there were no findings suggestive of KD. The patient was discharged with a script of amoxicillin and instructed to follow up with her family doctor if conditions worsen.

References

  1. McCrindle BW, Rowley AH, Newburger JW, et al. Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease: A Scientific Statement for Health Professionals From the American Heart Association. Circulation. 2017;135(17). doi:10.1161/CIR.0000000000000484
  2. Noval Rivas M, Arditi M. Kawasaki disease: pathophysiology and insights from mouse models. Nat Rev Rheumatol. 2020;16(7):391-405. doi:10.1038/s41584-020-0426-0
  3. Ramphul K, Mejias SG. Kawasaki disease: a comprehensive review. Arch Med Sci Atheroscler Dis. 2018;3(1):41-45. doi:10.5114/amsad.2018.74522
  4. Owens AM, Plewa MC. Kawasaki Disease. In: StatPearls. StatPearls Publishing; 2023. Accessed March 30, 2023. http://www.ncbi.nlm.nih.gov/books/NBK537163/
  5. Galuppo J, Kowker A, Rolfs J, Nicholas J, Schmidt E. Kawasaki disease: Shedding light on a mysterious diagnosis. J Am Acad Physician Assist. 2020;33(7):18-22. doi:10.1097/01.JAA.0000668792.41976.f2
  6. Sundel R. Kawasaki disease: Clinical features and diagnosis. Post TW, ed. UpToDate.Waltham, MA: UpToDate Inc. UpToDate.com (Accessed on March 30, 2023)

Continue Reading

An EM Approach to Syncope in Adults

Posted on by

 

Medical Student Pearl

Samarth Fageria

Med 3

Memorial University of Newfoundland Class of 2024

Reviewed by Dr. J Gross

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ An EM Approach to Syncope by SFargeria

 

Case

A 60-year-old male presented to the ED after experiencing recurrent episodes of syncope. The first episode occurred at a convenience store in an upright position. He denied prodrome and exertional activity at the time of syncope. After a transient loss of consciousness, he woke up confused with urinary incontinence. He felt nauseous and had emesis in the ambulance on the way to ED. He had two more episodes of syncope over the span of two hours. On assessment in the ED, he endorsed a past history of light-headedness preceded by laughing and holding his breath. He denied dyspnea and chest pain. He had no significant past medical history. There was no family history of cardiovascular disease and syncope, and social history was unremarkable.

 

On examination, he was alert and oriented. He had a minor laceration on his forehead from the fall. His respiratory and cardiovascular exams were unremarkable, neurological exam was normal. In the ED, his blood work was unremarkable. He was placed on telemetry when he had two more episodes of syncope. The monitor showed 20-second-long sinus pauses corresponding with the syncopal episodes. Cardiology was consulted and he was temporarily placed on intermittent transcutaneous pacing.

 

 

Differential Diagnosis of Syncope2

True Syncope

1. Reflex (autonomic hypersensitivity)

  • Vasovagal, carotid sinus hypersensitivity, situational

2. Orthostatic hypotension

  • Volume depletion, autonomic failure

3. Cardiac

  • Valvular (aortic stenosis, mitral stenosis), dysrhythmias (bradyarrhythmia, ventricular tachyarrhythmia, supraventricular tachyarrhythmia), mechanical (pacemaker dysfunction), cardiomyopathy, infiltrative (eg. hemochromatosis, sarcoidosis, amyloidosis), acute MI, ARVC, cardiac tamponade, acute aortic dissection

Other Causes

1. Medication/ Drug-induced

  • Anti-hypertensives, QT prolonging meds, insulin, alcohol, anti-depressants, anti-glycemic agents, diuretics, anti-anginal agents, etc

2. Transient Loss of Consciousness (TLOC)

    • Traumatic brain injury, seizure disorders, intoxications, hindbrain TIA, conversion disorders and metabolic abnormalities

 

Background

Syncope is defined as a brief, sudden, transient loss of consciousness due to cerebral hypoperfusion1. The three broad categories of syncope are reflex, orthostatic and cardiac syncope. The most common cause of cardiac syncope includes dysrhythmias1. A good past medical history of cardiovascular disease is important as it is 85-94% sensitive and 64-83% specific in predicting a cardiac etiology of syncope1.

Diagnostic Workup

Diagnostic workup for syncope requires a thorough history, physical exam, and a 12-lead ECG. Cardiac monitoring is necessary in patients that present to ER with an acute presentation of syncope, and a strong suspicion for cardiac etiology2. History should consist of identifying high-risk features that warrant a prompt cardiology consult2. A detailed HPI should consist of asking about an absence of a prodrome, exertional or supine syncope, concomitant trauma, past medical history of cardiovascular disease and family history of sudden cardiac death (<50 years)2. Low-risk features include presence of a prodrome, specific triggers (eg. dehydration, stress, laughter), syncope while upright and the absence of cardiovascular disease2. Vital signs and a cardiac exam should be completed2. If cardiac causes of syncope cannot be ruled out on first assessment, a 12-lead ECG should be placed to assess for dysrhythmias or conduction disease, and serial troponin values should be collected2.

 

Though there are multiple clinical decision rules for syncope, the following have been externally validated: Evaluation of Guidelines in Syncope Study (EGSYS), San Francisco Syncope Rule and Osservatorio Epidemiologico sulla Sincope nel Lazio (OESIL)1. Patients that are stratified as high risk require admission for further evaluation. EGSYS predicts the probability of cardiac syncope at two years based on abnormal ECG findings (eg. BBB, sinus bradycardia), heart disease (eg. ischemic, structural), palpitations before syncope, as well exertional and positional syncope, symptoms of prodrome (nausea/vomiting) and predisposing/precipitating factors1. An admission is warranted if the patient scores a three or higher as there is a 21% mortality risk at two years1. The OESIL risk score estimates a 1-year all-cause mortality in patients presenting with syncope1. The factors include age (>65), history of cardiovascular disease, lack of prodrome and abnormal ECG characteristics (eg. BBB, AV conduction disorders and hypertrophy)1. Admission is warranted for one or more variables1. The Canadian Syncope Risk Score can be used in patients presenting to ER with syncope to predict a 30-day serious adverse events2.  It consists of factors such as abnormal QRS axis, corrected QT interval >480 ms, elevated troponin (>99th percentile of normal population) and ED diagnosis based on evaluation to stratify patients into risk categories: very low (-3 to -2), low (-1 to 0), medium (1 to 3), high (4 to 5) and very high (6 to 11)2.

The Canadian Journal of Cardiology recommends a disposition algorithm for patients presenting to ER with syncope that is based on history of a serious medical condition and high-risk features3. Figure 1 illustrates an approach to disposition from the ER. Patients that have an unclear etiology and intermediate risk should be considered for an urgent cardiology assessment.

 

Figure 1: A disposition plan for patients presenting to the ER with syncope (Canadian Cardiovascular Society 2020).

Best Practice for Treatment

Given the benign course, treatment for vasovagal syncope is based on lifestyle modification, education and reassurance2. Lifestyle modification consists of educating patients on identifying and managing prodromes early and managing triggers (eg. dehydration, defecation, micturition, laughing, coughing and crowded environments)2.

Treatment for orthostatic syncope also relies on lifestyle modification, education and reassurance2. Lifestyle modification consists of re-adjusting diuretics, ACE-inhibitors, angiotensin receptor blockers, calcium channel and beta blockers to ensure optimal blood pressure and hydration control2.

Managing cardiac syncope requires addressing the underlying etiology through antiarrhythmic medications (eg. tachyarrhythmias), cardiac pacing (eg. bradyarrhythmias), catheter-directed ablation and ICD insertion1. Cardiac pacemaker therapy is indicated for patients that have intermittent sinus node disease if correlation is identified between sinus pauses on ECG and syncope3. Selected patients that are diagnosed with the bradycardia-tachycardia form of sick sinus syndrome, can benefit from a percutaneous cardiac ablative technique3.  Dual-chamber pacing is recommended for patients with sinus node dysfunction provided there is an increased risk of AV block4.

Case continued

The patient was admitted and had no further asystole after receiving atropine and intermittent transcutaneous pacing. He was accepted for a dual-chamber pacemaker insertion and was discharged with the diagnosis of syncope with sinus arrest and vagal overtones.

Take Home Points

  1. Patients presenting to the ER with new-onset syncope require a thorough history and physical exam to rule out cardiogenic causes.
  2. Validated clinical decision-making tools can be helpful to supplement clinical judgement for assessing the risk of a future cardiac event, identifying the need for a cardiology consult and creating a disposition plan.

References

  1. Runser LA, Gauer RL, Houser A. Syncope: Evaluation and Differential Diagnosis. Am Fam Physician. 2017;95(5):303-312. https://www.aafp.org/pubs/afp/issues/2017/0301/p303.html#:~:text=A%20standardized%20approach%20to%20syncope,%2C%20physical%20examination%2C%20and%20electrocardiography
  2. UpToDate. www.uptodate.com. https://www.uptodate.com/contents/syncope-in-adults-clinical-manifestations-and-initial-diagnostic-evaluation
  3. Sandhu RK, Raj SR, et al. Canadian Cardiovascular Society Clinical Practice Update on the Assessment and Management of Syncope. Can J Cardiol. 2020;36(8):1167-1177. doi:10.1016/j.cjca.2019.12.023 https://www.onlinecjc.ca/article/S0828-282X(19)31549-1/fulltext
  4. Brignole M, Moya A, de Lange FJ, et al. 2018 ESC Guidelines for the diagnosis and management of syncope. Eur Heart J. 2018;39(21):1883-1948. doi:10.1093/eurheartj/ehy037https://academic.oup.com/eurheartj/article/39/21/1883/4939241?login=false
  5. Dakkak W, Doukky R. Sick Sinus Syndrome. In: StatPearls. Treasure Island (FL): StatPearls Publishing; July 18, 2022. https://www.ncbi.nlm.nih.gov/books/NBK470599/

Continue Reading

Under pressure: Anorectal abscesses… to drain or not to drain?

Posted on by

Resident Clinical Pearl

Victoria Landry

iFMEM R3

Reviewed by Dr. J Mekwan

Copy Edited by Dr. J Vonkeman

PDF Download: EMSJ Anorectal Abscess by VLandry

Case

A 57yo male presents to the emergency department with complaints of a lump near his rectum and pain with sitting which developed over the past week. He is afebrile with normal vital signs. He tells you that about 6 months ago this same thing occurred and drainage was attempted in the ED but was unsuccessful. A colorectal surgeon subsequently drained it successfully under local anesthetic in clinic later the same day. He has had no recurrence of symptoms until the past week. He smokes and has hypertension controlled with medication but is otherwise healthy.

He denies pain with defecation and has not had any rectal bleeding nor changes in bowel habits. He feels otherwise well and denies fevers or chills.

On exam you find a tender firm mass in the subcutaneous tissue lateral to his rectum on the left side. There is minimal overlying erythema and no fluctuance.

Key Point #1: Always do a Digital Rectal Exam

  • Palpate in all directions to localize area of tenderness1
  • Should be unremarkable after you get past the anal verge2 – if tenderness, mass, induration past anal verge, do a CT scan to assess for deeper abscess

You think back to your perirectal anatomy and recall the spaces where abscesses can develop.

Figure 1: Transverse anorectal anatomy3

Figure 2: Longitudinal anorectal anatomy3

 

  Perianal Ischiorectal Intersphincteric Supralevator Postanal
Incidence 40-45% 20-25% 20-25% <5% 5-10%
Location Outside anal verge, red, swollen, fluctuant, easily palpable at anal verge Between rectum and ischial tuberosity, outside sphincters, palpable through rectal wall or lateral to anal verge on buttocks Lower rectum, between sphincters, inferior to levator ani (tender indurated mass in rectum) Above levator ani (tender indurated mass in rectum) Posterior to rectum, Deep to external sphincter, inferior to levator ani
Symptoms Painful perianal mass Buttock pain Rectal fullness, throbbing, worse with defecation Perianal and buttock pain Rectal fullness and pain near coccyx
Fever, ↑WBC No Possibly Possibly Yes Yes
Fistula formation ++ + +++ +++ –
ED I&D Yes Possibly: I&D/needle aspiration only if abscess is superficial and fluctuant No No:

Consult surgery for urgent drainage

 No

Table 1: Types of abscesses3

** caution as mass may be bigger/deeper than anticipated – prudent to defer to surgery for their expertise

Figure 3: Anorectal abscess locations4

Key Point #2: Get a CT scan to define the abscess for any of the following2

  • Unable to see the abscess superficially
  • Patient is unable to tolerate the DRE due to significant pain
  • Induration, bogginess or tenderness in the supralevator space (above the sphincter muscle)
  • If the extent of the abscess is uncertain4

Note: can use POCUS to evaluate location of abscess, but caution against false reassurance as to extent/depth, and safer to rely on palpable fluctuant mass to determine if I&D is safe

 

Figure 4: Perianal abscess on CT1

Management5

  • Simple, isolated, fluctuant perianal abscess4
    • Bedside I&D
    • Goal is to relieve the pus under pressure2
  • Ischiorectal abscess2
    • Can consider I&D only if superficial, but prudent to get a CT first
    • Consult surgery for their expertise
  • Intersphincteric, Supralevator, Postanal
    • CT to define the abscess
    • Consult surgery

Key Point #3: Err on the side of caution

Only do I&D in the ED if the following criteria are met3 [3]

  • Perianal abscess (+/- ischiorectal) is small and superficial
  • Patient
    • Is Well-appearing
    • Is Cooperative
    • Has no complicating factors (DM, immune compromise etc.)

Incision and Drainage of simple perianal abscess2

  • Local anesthetic – lidocaine with epinephrine
    • Infiltrate superficial skin where you will poke with needle
    • occasionally procedural sedation is needed3
  • Needle poke +/- aspiration (18guage) or pinpoint incision over painful region to localize purulent pocket4
  • Inject more local anesthetic2
  • Enlarge the incision
    • Make incision as close to anal verge as possible to minimize the length of any potential fistula2,5,6
    • Cruciate (with trimming of the flaps) or elliptical incision over fluctuant part of abscess is preferred over a linear incision to keep incision open and draining without painful packing2
    • If linear only, will need packing to prevent premature closure
    • Note: loop drainage technique not recommended for I&D in the ED7
  • Break up loculations with finger (increased tactile feedback and better control) or hemostat +/- irrigation with saline7
  • Cover with bulky dressing4
  • Ideally, close follow up until complete healing (up to 8wks) to monitor for recurrence and for fistula formation5
  • Uncomplicated perianal abscesses do not require antibiotics after successful drainage2.

Figure 5: Cruciate incision4

Instruct the patient to WASH8

  • W – warm water sitz baths 5-10min BID-QID PRN, with Epsom salts (start the day after I&D)
    • Water >40°C helps decrease anal canal pressure
  • A – analgesics (NSAIDs, topical 1-2% lidocaine gel)
  • S – stool softeners (PEG, senna)
  • H – high fiber diet +/- fiber supplement
  • Uncomplicated perianal abscesses do not require antibiotics after successful drainage2.

Indications for antibiotics (+/- tetanus +/- admission to hospital with surgical consult)4

  • Surrounding cellulitis
  • Immune compromise
  • Valvular heart disease
  • Diabetes
  • Systemic symptoms (Fever, ill appearing, leukocytosis)
  • Elderly

Note: Send off a wound culture before giving antibiotics

Antibiotic choice5:

  • Systemic: piperacillin-tazobactam
  • Oral: Amoxicillin-clavulanate or Metronidazole + ciprofloxacin

A word on fistulas

  • Fistulas are a connection between two epithelium-lined surfaces, characterized by persistent or recurrent anal drainage. They are seen in Crohn’s, TB, cancer, FB reactions, and as a complication of anorectal abscesses. Treatment is surgical3
  • ~50% of anorectal abscesses form a fistula overtime2
  • Suggest surgical consultation after drainage of perianal abscess as fistula formation is common4
  • Fistulas may be missed on CT scan; MRI is more sensitive for diagnosis2     

Take home points: 

  1. Always do a rectal exam as part of the initial evaluation
  2. Have a low threshold to get a CT scan to define the abscess
  3. Reserve I&D in the ED for perianal abscesses that are visible, superficial and fluctuant

References

  1. Farah, Jennifer, Mason, Jessica, and Werner, Jessie, “Perirectal Abscess & Pilonidal Cyst.” [Online]. Available: https://www.emrap.org/episode/gastro/perirectal
  2. Jhun, Paul and Cologne, Kyle, “Anorectal Infections,” HIPPO EMRAP, vol. 15, no. 9, pp. 17–18, Sep. 2015.
  3. Parrillo, “Anorectal Emergencies,” presented at the EMRAP, Temple University Hospital EM Residency, Feb. 2004. [Online]. Available: https://www.emrap.org/episode/september2004/anorectal
  4. Berberian J.G., & Burgess B.E. Tintinalli J.E., & Ma O, & Yealy D.M., & Meckler G.D., & Stapczynski J, & Cline D.M., & Thomas S.H.(Eds.), “Anorectal disorders,” in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e, McGraw Hill, 2020. [Online]. Available: https://accessmedicine-mhmedical-com.ezproxy.library.dal.ca/content.aspx?bookid=2353&sectionid=219642697
  5. Streitz Matthew, Long Brit, “Anorectal Disease,” in CorePendium, Burbank, CA: CorePendium, LLC, 2022. [Online]. Available: https://www.emrap.org/corependium/chapter/reclLjrt5HvPGSIDv/Anorectal-Disease#h.d78nqbylr3x
  6. Bleday, Ronald, Perianal and perirectal abscess. uptodate.com, 2022. [Online]. Available: https://www.uptodate.com/contents/perianal-and-perirectal-abscess
  7. Cavanaugh, Megan and Ormon, Rob, “Anorectal Disorders.” [Online]. Available: https://www.emrap.org/episode/april2011/anorectal
  8. Lipp, Chris, “Anorectal Disorders.” [Online]. Available: https://canadiem.org/crackcast-e096-anorectal-disorders/

 

 

 

 

 

 

 

 

 

 

Continue Reading

Unvexing the VExUS Score – An Overview

Posted on by

Unvexing the VExUS Score – An Overview

 

PoCUS Clinical Pearl

Dr Steven Chen

DalEM PoCUS Elective

PGY2 Internal Medicine, University of Toronto

Reviewed: Dr David Lewis

Copyedited: Dr David Lewis

Introduction:

The pursuit of a rapid and objective measure of volume status has always been a vexing problem for clinicians as proper fluid management is pivotal for patient outcomes. In recent years, there has been increased attention towards the concept of “fluid-responsive” as liberal fluid boluses can often be associated with poor outcomes as a result of systemic congestion. 1

In the POCUS community, while Inferior Vena Cava (IVC) measurements have promise in assessing central venous pressure, the subsequent translation towards “volume responsiveness” has been met with many other limitations. For one, it did not account for venous congestion at other organ levels such as the pulmonary, renal, or hepatic systems. 2,3

Venous excess ultrasound (VExUS) is a growing bedside ultrasound-based approach that aims to provide a more comprehensive assessment of venous congestion. This was initially described by Beaubien-Souligny et al. (2020) from a post-hoc analysis correlating ultrasound grading parameters with risk in development of AKI in cardiac surgery patients.4 The protocol serves to assess multiple sites of venous congestion, including the IVC, hepatic veins, portal veins and intrarenal veins. By assessing congestion in these multiple sites, the VExUS score has gained attraction in providing a more comprehensive assessment of systemic congestion. 4,5

View Acquisition:

The VExUS protocol is composed of four main components outlined below:

  • IVC diameter
  • Hepatic Vein Doppler Assessment
  • Hepatic Portal Vein Doppler Assessment
  • Intrarenal Vein Doppler Assessment

This can be performed using either the curvilinear probe (preferred) or the phased array probe. The patient should be positioned flat and supine on the bed to acquire the views. The table below depicts some suggested views where larger regions of the veins may be accessible for pulse wave doppler gating in reference to standardized sonography protocols. 6,7

Note: Reviewing the basics of pulse wave doppler will be needed prior to completing VExUS scans (not covered in this article).

 

 

 

 

 

Interpretation:

Interpretation of the VExUS grading system is well summarized in diagram below (sourced from POCUS1018) and takes some practice to differentiate normal from abnormal waveforms. Pulse wave doppler assessment is pursued only if the inferior vena cava is found plethoric, defined as greater or equal to 2cm. 4,5

Each of the hepatic, portal and renal veins are subsequently examined and classified as normal, mildly congested, or severely congested. The VExUS system has four grades: Grade 0 represents no congestion in any organ, Grade 1 represents only mild congestive findings, Grade 2 represents severe congestive findings in only one organ, and Grade 3 represents severe congestive findings in at least two out of three organ systems. 4,5

Source: POCUS1018

Some sample waveforms are shown below with comments to help with distinguishing normal from abnormal waveforms.

 

Evidence:

VExUS has also been shown to be reliable and reproducible, with good interobserver agreement in trained individuals and correlation with other measures of volume status such as central venous pressure.4,5 As the technique is growing in the POCUS literature, below is a table summarizing several recent studies exploring its application across numerous settings.

Study Purpose Results
Beaubien-Souligny W, et al. (2020)4

 

Post-hoc analysis of a single centre prospective study in 145 patients

 

 

 

 Initial model of VExUS grading system looking at association in development of AKI in cardiac surgery population Association with subsequent AKI:

 

HR: 3.69 CI 1.65–8.24 p = 0.001;

+LR: 6.37 CI 2.19–18.50 when detected at ICU admission, which outperformed central venous pressure measurements

 
Bhardwaj V, et al. (2020)9

 

Prospective cohort study of 30 patients in ICU setting

 

 Prospective study on application of VExUS scoring on staging of AKI in patients with cardiorenal syndrome Resolution of AKI injury significantly correlated with improvement in VExUS grade (p 0.003).

 

There was significant association between changes in VExUS grade and fluid balance (p value 0.006).
Varudo R, et al. (2022)10

 

Case report of ICU patient with hyponatremia

 Application of VExUS in case report as rapid tool to help with volume status assessment in patient with complex hyponatremia Overall VExUS grade 2, prompting strategy for diuresis with improvement
Rolston D, et al. (2022)11

 

Observational study of 150 septic patients in single centre

 VExUS score performed on ED septic patients prior to receiving fluids with chart review done to determine if there is association with poorer outcomes Composite outcome (mortality, ICU admission or rapid response activation):

 

VExUS score of 0: 31.6% of patients

VExUS score of 1: 47.6% of patients

VExUS score >1: 67.7% of patients

(p: 0.0015)
Guinot, PG, et al. (2022)12

Prospective observational study of 81 ICU patients started on loop diuretic therapy

 Evaluation of multiple scores to predict appropriate diuretic-induced fluid depletion (portal pulsatility index, renal venous impedance index, VExUS) Baseline portal pulsatility index and renal venous impedance index were found to be superior predictors compared to VExUS.

 

The baseline VExUS score (AUC of 0.66 CI95% 0.53–0.79, p = 0.012) was poorly predictive of appropriate response to diuretic-induced fluid depletion.
Menéndez‐Suso JJ, et al. (2023)13

 

Cross-sectional pilot study of 33 children in pediatric ICU setting

 Association of VExUS score with CVP in pediatric ICU VExUS score severity was strongly associated with CVP (p<0.001) in critically ill children.
Longino A, et al. (2023)14

 

Prospective validation study in 56 critically ill patients

 Validation looking at association of VExUS grade with right atrial pressure. VExUS had a favorable AUC for prediction of a RAP ≥ 12 mmHg (0.99, 95% CI 0.96-1) compared to IVC

diameter (0.79, 95% CI 0.65–0.92).

Pitfalls:

It should be kept in mind that numerous factors may affect interpretation of VExUS gradings.

For the IVC component, increased intra-abdominal pressure can affect measurements independently of the pressure in the right atrium or may be affected by chronic pulmonary hypertension. The hepatic vein may not show significant changes even in severe tricuspid regurgitation if the right atrium can still expand and contract normally. In thin healthy people and those with arteriovenous malformations, the portal vein can have a pulsatile flow without venous congestion. It is also important to note that for patients with underlying disease renal or liver parenchymal disease, venous doppler recordings may be less reliable. 3-5

Outside of physiologic factors, another limitation is the need for adequate training and familiarity in performing and interpreting the technique. While VExUS is fairly well protocolized, it requires proficiency with pulse wave doppler to perform accurately. As with any new technique, there is a risk of variability in technique and interpretation. To avoid misinterpretation, it is important to consider repeat tracings to ensure consistency of results and to consider findings within the overall clinical context of the patient.

Bottom line:

VExUS is a non-invasive ultrasound method for assessing venous congestion across multiple organ systems. While there are several physiologic limitations and results need to be used in adjunct with the clinical picture, studies have shown promise for VExUS to be incorporated as part of a physician’s toolkit to help with clinical decision making. 3-5

References

  1. Atkinson P, Bowra J, Milne J, Lewis D, Lambert M, Jarman B, Noble VE, Lamprecht H, Harris T, Connolly J, Kessler R. International Federation for Emergency Medicine Consensus Statement: Sonography in hypotension and cardiac arrest (SHoC): An international consensus on the use of point of care ultrasound for undifferentiated hypotension and during cardiac arrest. Canadian Journal of Emergency Medicine. 2017 Nov;19(6):459-70.
  2. Corl KA, George NR, Romanoff J, Levinson AT, Chheng DB, Merchant RC, Levy MM, Napoli AM. Inferior vena cava collapsibility detects fluid responsiveness among spontaneously breathing critically-ill patients. Journal of critical care. 2017 Oct 1;41:130-7.
  3. Koratala A, Reisinger N. Venous excess doppler ultrasound for the nephrologist: Pearls and pitfalls. Kidney Medicine. 2022 May 19:100482.
  4. Beaubien-Souligny W, Rola P, Haycock K, Bouchard J, Lamarche Y, Spiegel R, Denault AY. Quantifying systemic congestion with point-of-care ultrasound: development of the venous excess ultrasound grading system. The Ultrasound Journal. 2020 Dec;12:1-2.
  5. Rola P, Miralles-Aguiar F, Argaiz E, Beaubien-Souligny W, Haycock K, Karimov T, Dinh VA, Spiegel R. Clinical applications of the venous excess ultrasound (VExUS) score: conceptual review and case series. The Ultrasound Journal. 2021 Dec;13(1):1-0.
  6. Mattoon JS, Berry CR, Nyland TG. Abdominal ultrasound scanning techniques. Small Animal Diagnostic Ultrasound-E-Book. 2014 Dec 2;94(6):93-112.
  7. Standardized method of abdominal ultrasound [Internet]. Japanese society of sonographers. [cited 2023Apr12]. Available from: https://www.jss.org/english/standard/abdominal.html#Longitudinal%20scanning_2
  8. Dinh V. POCUS101 Vexus ultrasound score–fluid overload and venous congestion assessment.
  9. Bhardwaj V, Vikneswaran G, Rola P, Raju S, Bhat RS, Jayakumar A, Alva A. Combination of inferior vena cava diameter, hepatic venous flow, and portal vein pulsatility index: venous excess ultrasound score (VExUS score) in predicting acute kidney injury in patients with cardiorenal syndrome: a prospective cohort study. Indian journal of critical care medicine: peer-reviewed, official publication of Indian Society of Critical Care Medicine. 2020 Sep;24(9):783.
  10. Varudo R, Pimenta I, Blanco JB, Gonzalez FA. Use of Venous Excess UltraSound (VExUS) score in hyponatraemia management in critically ill patient. BMJ Case Reports CP. 2022 Feb 1;15(2):e246995.
  11. Rolston D, Li T, Huang H, Johnson A, van Loveren K, Kearney E, Pettit D, Haverty J, Nelson M, Cohen A. 204 A Higher Initial VExUS Score Is Associated With Inferior Outcomes in Septic Emergency Department Patients. Annals of Emergency Medicine. 2021 Oct 1;78(4):S82.
  12. Guinot PG, Bahr PA, Andrei S, Popescu BA, Caruso V, Mertes PM, Berthoud V, Nguyen M, Bouhemad B. Doppler study of portal vein and renal venous velocity predict the appropriate fluid response to diuretic in ICU: a prospective observational echocardiographic evaluation. Critical Care. 2022 Dec;26(1):1-1.
  13. Menéndez‐Suso JJ, Rodríguez‐Álvarez D, Sánchez‐Martín M. Feasibility and Utility of the Venous Excess Ultrasound Score to Detect and Grade Central Venous Pressure Elevation in Critically Ill Children. Journal of Ultrasound in Medicine. 2023 Jan;42(1):211-20.
  14. Longino A, Martin K, Leyba K, Siegel G, Gill E, Douglas I, Burke J. Prospective Validation of the Venous Excess Ultrasound “(VExUS)” Score.

Downloadable Format

Download (PDF, 530KB)

Continue Reading

Approach to Inguinal and Femoral Hernias in the Emergency Department

Posted on by

Medical Student Pearl

Julia Short

Med 2

DMNB Class of 2025

Reviewed by Dr D Lewis

Copy Edited by Dr. J Vonkeman

PDF Download: EMSJ Approach to Inguinal and Femoral Hernias in the ED by JShort

Case

A 52-year-old male patient presents in the ER with a lump in their right groin. The lump protrudes when they cough and when laying on their left side, although it re-enters the abdomen on its own. You wonder if it could be a femoral or an inguinal hernia, and how to go about differentiating between the two.

Introduction

A hernia is defined as an organ, or part of an organ, that protrudes through the body wall in which it is normally contained. The etiology of a hernia can be due to congenital anatomical malformations or from acquired weakening of the body wall tissues. There are various subtypes of abdominal hernias, while groin hernias consist of inguinal and femoral hernias. Throughout their lifetime, males have a 27 to 43% chance of developing a groin hernia, while females have a 3 to 6% lifetime prevalence1. Although it is much more likely that a groin hernia is inguinal in nature (they account for 96% of groin hernias), it is clinically useful to identify and distinguish between the types of groin hernias. Additionally, there are important clinical features that must not be overlooked when characterizing a groin hernia.

Distinguishing inguinal from femoral hernias

An important landmark in determining the hernia origin is the inguinal ligament. Inguinal hernias protrude superior to the inguinal ligament, while femoral hernias present inferior to the inguinal ligament (Figure 1). This is because femoral hernias protrude from the femoral ring, located medial to the femoral vein. As a result, in males, femoral hernias will never course into the scrotum. Femoral hernias also present more lateral than inguinal hernias and may be difficult to differentiate from lymph nodes. Although they account for only 3% of all groin hernias, 40% of femoral hernias present as urgent due to bowel strangulation or incarceration1. Females are more likely to develop femoral hernias, while males are more likely to develop inguinal hernias.

Figure 1. Groin anatomy © 2023 UpToDate7

Distinguishing between direct and indirect inguinal hernias

Direct inguinal hernias originate medially, near the pubic tubercle and external inguinal ring. They protrude through Hesselbach’s triangle as a result of weakness in the floor of the inguinal canal. On exam, a bulge near the external (superficial) inguinal ring is suggestive of a direct inguinal hernia. In contrast, indirect inguinal hernias protrude near the midpoint of the inguinal ligament, at the internal (deep) inguinal ring (Figure 2). In males and females respectively, the internal inguinal ring is where the spermatic cord and round ligament exit the abdomen. A bulge in this area therefore suggests an indirect inguinal hernia. This type of hernia is the most common in all ages and sexes, accounting for approximately two thirds of all inguinal hernias2. In males, the indirect hernia often courses into the scrotum, which can be palpated if the patient strains or coughs. In contrast, it is rare for a direct hernia to course into the scrotum.

Figure 2. Anatomical comparison of direct and indirect inguinal hernias © 2020 Dr. Vaibhav Kapoor8

Clinical Approach

General considerations for investigating groin hernias include assessing the symptoms at presentation as well as any “red flag” physical findings. Patients commonly complain of dull or heavy types of discomfort when straining, which resolves when straining stops. Most groin hernias occur on the right side. Common physical findings include a bulge in the groin, which can indicate the type of hernia based on location relative to the inguinal ligament (Figure 3). However, in female or obese patients, the layers of abdominal wall may make the hernia more difficult to locate. In these cases, ultrasound or other imaging is needed to detect hernias. Clinicians should also determine if the hernia is reducible, or if the herniated bowel can be returned to the abdominal cavity when moderate pressure is applied externally.

Figure 3. Locations of femoral and inguinal hernias on examination © 2023 UpToDate7

 

Physical examination has a 76 to 92% sensitivity and 96% specificity for diagnosing groin hernias, although imaging may also be required1,2. Nausea, vomiting, fever, moderate-to-severe abdominal pain, localized tenderness, or bloating may indicate more sinister pathology such as bowel incarceration (when the hernia contents cannot return to the abdominal cavity), strangulation (when the blood supply to the involved bowel section is compromised) or necrosis.

Figure 5. CT images of A) femoral hernia (courtesy of Chris O’Donnell9 and B) inguinal hernia (courtesy of Erik Ranschaert10)

Management

Uncomplicated or asymptomatic hernias in males can be monitored through watchful waiting. Surgical repair is a definitive treatment for inguinal hernias and should be considered for symptomatic or complex hernias. If repair is needed for an uncomplicated inguinal hernia, a laparoscopic repair is recommended. Watchful waiting is not recommended for femoral hernias – these patients should have a laparoscopic repair (when anatomically feasible).

Manual reduction of the hernia can be performed by following the GPS Taxis technique. Taxis is a non-invasive technique for manual reduction of incarcerated tissues in a hernia to the original compartment5. “GPS” is an acronym to remind clinicians to be gentle, be prepared, and be safe when performing taxis5. Conscious sedation with intravenous diazepam and morphine is recommended for the procedure. Consider having an anesthetist present for the procedure if the patient is frail. Provide appropriate early resuscitation by monitoring vital signs, administering oxygen therapy and establishing IV access. Place the patient in Trendelenburg position. Begin the GPS Taxis technique by palpating the fascial defect around the base of the hernia and gently manipulating hernia contents back into the abdominal cavity. Use gentle manipulation pressure over 5-10 minutes until a gurgling sound is heard (indicating successful reduction of bowel).

 

Taxis guided by ultrasound may increase success rates for reduction.

https://sjrhem.ca/taxis-reduction-of-inguinal-hernia/

Figure 4. Colourized clip demonstrating PoCUS assisted Taxis reduction of an inguinal hernia11

 

It should be noted that the major contraindication to performing GPS Taxis is bowel strangulation within the hernia. A rare but serious complication of manual reduction is reduction en masse, when a loop of bowel remains incarcerated at the neck of the hernia after manual reduction6. This can lead to early strangulation, intestinal necrosis, sepsis, organ failure and death. Femoral hernias and indirect inguinal hernias are at higher risk of reduction en masse from manual reduction attempts.

References:

  1. UpToDate – Classification, clinical features, and diagnosis of inguinal and femoral hernias in adults
  2. Hammoud M, Gerken J. Inguinal hernia. StatPearls. 2022 Aug 15.
  3. UpToDate – Overview of treatment for inguinal and femoral hernia in adults
  4. Bates’ Guide to Physical Examination and History Taking, 12th ed. (pdf). Chapter 13: Male Genitalia and Hernias
  5. Pawlak M, East B, de Beaux AC. Algorithm for management of an incarcerated inguinal hernia in the emergency settings with manual reduction. Taxis, the technique and its safety. Hernia, 25, 1253-1258. 2021 May 25.
  6. Yatawatta A. Reduction en masse of inguinal hernia: a review of a rare and potentially fatal complication following reduction of inguinal hernia. BMJ Case Rep. 2017 Aug 7.
  7. UpToDate – Classification, clinical features, and diagnosis of inguinal and femoral hernias in adults
  8. Kapoor, V. Difference between and inguinal and umbilical hernia. 2020. Retrieved from: https://www.drvaibhavkapoor.com/difference-between-inguinal-and-umbilical-hernia.html
  9. Patel, MS. Femoral hernia. Radiopaedia. 2022 Dec 28. Retrieved from: https://radiopaedia.org/articles/femoral-hernia
  10. Fahrenhorst-Jones, T. Inguinal hernia. Radiopaedia. 2022 Apr 12. Retrieved from: https://radiopaedia.org/articles/inguinal-hernia
  11. PoCUS assisted Taxis reduction of an inguinal hernia. Video obtained courtesy of Dr. David Lewis.

Continue Reading

Headaches and Herpes Zoster

Posted on by

Headache and Herpes Zoster

Medical Student Pearl

 

James Tang

Dalhousie University Class of 2023

Reviewed by: Dr. Erin Slaunwhite

Copyedited by: Dr. Janeske Vonkeman

Case

Mr. H is a 57 yo gentleman who presents to the ED complaining of a 3-day history of headache. He describes a progressive worsening of a constant dull ache unilaterally above his left eye. It’s currently a 4-5/10 in severity and does not radiate. He has not had any nausea or vomiting, and no phonophobia but asks you to dim the lights in the room if that’s possible. He has no previous history of the same. He has not noticed any shooting pains associated with eating or drinking cold foods/liquids. He denies any associated autonomic symptoms on that side. Mr. H tells you he’s tried Tylenol and Advil at home and although it seemed to help a bit initially, the pain has continued to worsen over the last couple of days. He hasn’t noted any changes in the severity of his headache with physical activity.

Mr. H has no relevant past medical history and does not take any regular medications. He enjoys drinking 1-2 beers on the weekends, does not use cannabis, and has never used any other recreational drugs.

On physical exam, Mr. H appears his stated age and appears quite tanned from his job in construction. His vital signs are within normal limits. On close inspection, you make note of an area of erythematous macules and papules forming on his left forehead and extending 1-2 cm above and below his scalp line. The area is mildly tender to touch. His cranial nerve exam was otherwise normal. His remaining neuro exam, as well as head and neck, cardiac, respiratory, and abdominal exams were all normal.

A general approach to primary headache – Tension TIC TAC TOE

The International Headache Society (IHS) outlines specific diagnostic criteria for headache disorders within their International Classification of Headache Disorders (ICHD 3rd edition).1 Below is an abbreviated summary of the select common diagnoses that the ICHD discusses in much greater detail2-5:

Danger signs – features suggestive of secondary headache (e.g. space-occupying lesion, sub-arachnoid hemorrhage, cervical artery dissection, giant cell arteritis, infection, trauma, etc)2,4,5:

  • Systemic symptoms including fever, weight loss, progressive N/V
  • Neoplasm history
  • Neurologic deficit (including confusion, weakness, vision loss, numbness, impaired alertness, side locked headache)
  • Onset is sudden or abrupt (thunderclap)
  • Older age (> 50 yo)
  • Pattern change from previous headaches
  • Positional headache
  • Precipitated by Valsalva or exertion
  • Papilledema
  • Progressive headache and atypical presentations
  • Pregnancy or puerperium
  • Post-traumatic onset of headache
  • Pathology of the immune system such as HIV

Patients with danger signs suggestive of secondary headache should be considered for imaging. If a primary headache is suspected but imaging is performed for no other reason than reassurance, it can be detrimental to the patient if the results return incidental findings (e.g. vascular lesion) likely unrelated to the headache.

But our patient’s presentation doesn’t really seem to fit into any of these categories…

Herpes Zoster

In immunocompetent individuals, the diagnosis of herpes zoster is based solely on the clinical presentation: unilateral, usually painful vesicular eruption with a well-defined dermatomal distribution (see Figure 1). Prodromal symptoms include malaise, headache, photophobia, abnormal skin sensations, and occasionally fever. These symptoms may occur one to five days before the appearance of the rash. Age is the most important risk factor for the development of herpes zoster. A dramatic increase in the age-specific incidence of herpes zoster begins at approximately 50 years of age with 40% occur in people at least 60 years of age.6 It is estimated that approximately 50% of persons who live to 85 years of age will have had an episode of herpes zoster.6

Figure 1. Vesicular eruption in keeping with herpes zoster ophthalmicus with a crusted skin rash following the V1 dermatomal distribution and does not cross midline.7

Antiviral therapy is the first-line treatment and should be initiated within 72 hours of rash onset to increase the rate of healing, decrease the duration of acute herpes zoster, and decrease severity and pain. Ideally, initiation of antiviral therapy should be started during the pre-eruptive phase of herpes zoster, but often the diagnosis can only be confidently made once the distinctive rash presents.

See Table below for antiviral doses9:

Pain management

For acute herpes zoster, mild to moderate pain may be controlled with acetaminophen and/or nonsteroidal anti-inflammatory drugs. For those with moderate pain not responding to acetaminophen and nonsteroidal anti-inflammatory drugs, a short course of a short acting opioid such as hydromorphone or morphine could be considered or a course of corticosteroids. If the pain does not rapidly respond to opioid analgesics or if opioids are not tolerated, the addition of an adjunctive therapy should be considered including nortriptyline, gabapentin, or pregabalin. Despite these adjunctive therapies not having been extensively studied in patients with acute herpes zoster pain, they have evidence for other forms of nerve-type pain.8 The addition of corticosteroids to acyclovir decreases the pain of acute herpes zoster and speeds lesion healing and return to daily activities. Combination therapy with corticosteroids and antivirals should be considered in older patients with no contraindications.8

Theoretical models suggest that reducing pain during the acute phase of herpes zoster may stop the initiation of the mechanisms that cause chronic pain, thus reducing the risk of postherpetic neuralgia.8

 

Postherpetic neuralgia

Postherpetic neuralgia is the most common complication of herpes zoster.9 It occurs in ~30% of patients older than 80 years and ~20% of patients 60 to 65 years; it is rare in patients younger than 50 years.6 Postherpetic neuralgia may persist from 30 days to more than 6 months after the lesions have healed, and most cases resolve spontaneously.9 Although antiviral medications slow the production of the virus and decrease the viral load in the dorsal root ganglia, evidence showing that these medications alter the incidence and course of postherpetic neuralgia is inconsistent.8 The major risk factors for postherpetic neuralgia are older age, greater acute pain, and greater rash severity.8

Case conclusion

Mr. H’s headache did not fit into any specific category of headache as is often the case. Although he did meet the criteria for certain danger signs (e.g. age >50), imaging was forgone due to the finding of an erythematous maculopapular rash over his forehead. Mr. H’s rash followed the dermatomal distribution of the ophthalmic branch of the trigeminal nerve and was highly suspicious of an early herpes zoster outbreak.

The patient was given a prescription for valacyclovir to take for 7 days with instructions to seek care if lesions break out close to his eye or his pain becomes unmanageable with over-the-counter analgesia. Herpes zoster opthalmicus can be a sight-threatening condition that requires close ophthalmology follow up if there is any concern of lesions near or in the eye or the patient has clinical signs or symptoms. Mr H inquired about getting the shingles vaccine and was advised to follow up with his family doctor to arrange this following resolution of his rash.

Key Takeaways

  • Have a structured approach to understanding the different classes of primary headaches
  • Know the danger signs that could be suggestive of a secondary headache
  • Clinical judgement should be prioritized in determining who to image
  • Herpes zoster is a clinical diagnosis in immunocompetent individuals
  • Appropriate pain management of acute herpes zoster and vaccination can help prevent chronic pain syndromes

 

References

  1. The International Classification of Headache Disorders – ICHD-3. Accessed June 24, 2022. https://ichd-3.org/
  2. Evaluation of Acute Headaches in Adults. Accessed June 24, 2022. https://www.aafp.org/pubs/afp/issues/2001/0215/p685.html
  3. Primary care management of headache in adults Clinical Practice Guideline | September 2016 2 nd Edition. Published online 2016.
  4. Ponka D, Kirlew M. Top 10 differential diagnoses in family medicine: Headache. Can Fam Physician. 2007;53(10):1733. Accessed June 24, 2022. /pmc/articles/PMC2231438/
  5. Do TP, Remmers A, Schytz HW, et al. Red and orange flags for secondary headaches in clinical practice: SNNOOP10 list. Neurology. 2019;92(3):134-144. doi:10.1212/WNL.0000000000006697
  6. Epidemiology, clinical manifestations, and diagnosis of herpes zoster – UpToDate. Accessed June 24, 2022. https://www.uptodate.com/contents/epidemiology-clinical-manifestations-and-diagnosis-of-herpes-zoster
  7. Darren Shu JT, Ghosh N, Ghosh S. Herpes zoster ophthalmicus. BMJ : British Medical Journal (Online). 2019;364. doi: https://doi.org/10.1136/bmj.k5234.
  8. Herpes Zoster and Postherpetic Neuralgia: Prevention and Management. Accessed June 24, 2022. https://www.aafp.org/pubs/afp/issues/2011/0615/p1432.html
  9. Clinical Overview of Herpes Zoster (Shingles) | CDC. Accessed June 24, 2022. https://www.cdc.gov/shingles/hcp/clinical-overview.html
Continue Reading