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Understanding Urachal Anomalies

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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

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Could it be Kawasaki Disease?

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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)

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An EM Approach to Syncope in Adults

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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/

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Approach to Inguinal and Femoral Hernias in the Emergency Department

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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.

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Headaches and Herpes Zoster

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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
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