A Case of Facial Nerve Palsy


Medical Student Clinical Pearl by Livia Clarke

 

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. M McGraw

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ A Case of a Facial Nerve Palsy

 


Case 

A 45-year-old male presents to the Emergency Department with muscle paralysis of the left side of his face. That morning, he experienced some difficulty eating his breakfast and noticed that the left side of his face was immobile when looking in the mirror. He is also experiencing paresthesia of the left side of his face. He is an otherwise healthy individual with no past medical history and not taking any medications.

On examination, he is vitally stable and in no apparent distress. He has left sided facial paralysis involving the upper and lower portions of the face, suggesting impairment of cranial nerve VII, as well as paresthesia. The rest of the cranial nerve exam is normal. Upper and lower extremity muscle tone and strength are normal. Sensation is normal. Cerebellar testing with finger-to-nose, heel-to-shin, and rapid alternating movements is normal. Gait is normal.


Differential Diagnosis of Facial Nerve Palsy (1,3)

  • Peripheral Causes:
    • Lyme disease
    • Otitis media
    • Ramsey Hunt syndrome
    • Guillain-Barre syndrome
    • Cholesteatoma or tumor of parotid gland
    • Bell’s Palsy
    • Leukemia
  • Central causes:
    • MS
    • Neoplasm
    • Stroke

Bell’s Palsy

Bell’s Palsy is a common idiopathic condition that results from the peripheral paralysis of the seventh cranial nerve causing unilateral facial paralysis4. It is thought to be caused from inflammation causing compression of the facial nerve at the geniculate ganglion3,4. The exact cause of this inflammation is unknown, but suspected causes include viral infections such as Herpes simplex virus1.

 

Figure 1: Anatomy of the facial nerve (American Family Physician)

 

Patients often present with sudden onset (over several hours and up to 72 hours) of unilateral facial paralysis that involves the upper and lower face1,4. Commonly patients cannot close the affected eyelid, experience eyebrow sagging, loss of the nasolabial fold, and drooping of the affected corner of the mouth1,4. Patients may also experience impairment in taste and decreased tearing of the eye1,4.

 

Figure 2: Presentation of a left Bell’s Palsy. A) Inability to raise left eyebrow. B) & C) Inability to close left eye or raise left corner of mouth (UptoDate).

 

The involvement of both upper and lower portions of the face is important because facial weakness originating from central causes (i.e., stroke, tumor) results in a pattern of facial weakness restricted to the lower region of the face that spares the forehead3.

Figure 3: (A) a facial nerve lesion. (B) a supranuclear lesion with forehead sparing (American Family Physician).

The risk of Bell’s Palsy is three times greater during pregnancy, with the highest risk in the third trimester and during the first week postpartum. Hypertension has also been associated with an increased risk in some studies1. Other risk factors include diabetes, preeclampsia and obesity4.


Diagnosis

Bell’s Palsy is a diagnosis of exclusion and is diagnosed clinically1. If there are atypical features, the patient should be evaluated for central causes. During the assessment of a patient presenting with Bell’s Palsy it is important to assess for a patient’s ability to completely close the affected eye.


Treatment

In most cases, Bell’s Palsy will resolve without treatment4. Oral corticosteroids are often prescribed to reduce the inflammation of the facial nerve. Prednisone 60-80 mg/day for one week is recommended2. Often an antiviral will also be prescribed, but its effectiveness is not proven. Valacyclovir 1000mg three times daily for one week or acyclovir 400mg five times daily for 20 days are popular choices for those with severe symptoms2. If the patient is unable to completely close the affected eye, they must be cautioned to apply hydrating solutions (i.e. artificial tears) during waking hours as well as artificial tears ointment and taping the eyelid shut during sleep to prevent corneal injury5.


Prognosis 

Bell’s Palsy has a favorable prognosis. Approximately 70% of patients will completely recover without treatment by 3-6 months2. With glucocorticoid treatment, 80-85% of patient are expected to completely recover2. 7-15% of patients will experience recurrent Bell’s Palsy either on the same or opposite side2.


Case Continued 

The patient’s symptoms were classic for Bell’s palsy, and he did not have any atypical features. He was provided a prescription of an oral corticosteroid and an antiviral and discharged home.


References

  1. Hatzenbuehler, J., & Pulling, T. J. (2011). Diagnosis and Management of Osteomyelitis.American Family Physician84(9), 1027–1033.
  2. Chiappini, E., Mastrangelo, G., & Lazzeri, S. (2016). A Case of Acute Osteomyelitis: An Update on Diagnosis and Treatment.International Journal of Environmental Research and Public Health13(6), 539.
  3. Yuschak, E., Chase, S., Haq, F., & Vandever, C. (2019). Demographics and Length of Stay for Osteomyelitis in Opioid Drug Users: A Unique Population with High Healthcare Costs.Cureus11(3), e4339.
  4. Calhoun, J. H., & Manring, M. M. (2005). Adult Osteomyelitis.Infectious Disease Clinics of North America19(4), 765–786.
  5. Hogan, A., Heppert, V. G., & Suda, A. J. (2013). Osteomyelitis.Archives of Orthopaedic and Trauma Surgery133(9), 1183–1196.
  6. Pichichero, M. E., & Friesen, H. A. (1982). Polymicrobial Osteomyelitis: Report of Three Cases and Review of the Literature.Clinical Infectious Diseases4(1), 86–96.
  7. Momodu, I.I., & Savaliya, V. Osteomyelitis. ]. StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan. Updated 2023 May 31.
  8. Arnold, S. R., Elias, D., Buckingham, S. C., Thomas, E. D., Novais, E., Arkader, A., & Howard, C. (2006). Changing Patterns of Acute Hematogenous Osteomyelitis and Septic Arthritis: Emergence of Community-associated Methicillin-resistant Staphylococcus aureus.Journal of Pediatric Orthopaedics26(6), 703–708.
  9. Parikh, M. P., Octaria, R., & Kainer, M. A. (2020). Methicillin-Resistant Staphylococcus aureus Bloodstream Infections and Injection Drug Use, Tennessee, USA, 2015-2017.Emerging Infectious Diseases26(3), 446–453.
  10. Best, K., Hussien, S., Malik, A., Patel, S., & Michael, M. B. (2022). Suprapubic Osteomyelitis in an Intravenous Drug User: A Case Report. InCureus (Vol. 14, Issue 1, pp. e21312–e21312).
  11. Lauri, C., Tamminga, M., Glaudemans, A. W. J. M., Juárez Orozco, L. E., Erba, P. A., Jutte, P. C., Lipsky, B. A., IJzerman, M. J., Signore, A., & Slart, R. H. J. A. (2017). Detection of Osteomyelitis in the Diabetic Foot by Imaging Techniques: A Systematic Review and Meta-analysis Comparing MRI, White Blood Cell Scintigraphy, and FDG-PET.Diabetes Care40(8), 1111–1120.
  12. Schirò, S., Foreman, S. C., Bucknor, M., Chin, C. T., Joseph, G. B., & Link, T. M. (2020). Diagnostic Performance of CT-Guided Bone Biopsies in Patients with Suspected Osteomyelitis of the Appendicular and Axial Skeleton with a Focus on Clinical and Technical Factors Associated with Positive Microbiology Culture Results.Journal of Vascular and Interventional Radiology31(3), 464–472.
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Serum Sickness-Like Reaction


Medical Student Pearl by Nicole Barry1 & Laura Harkness2

1. B.Sc., M.A., MD Candidate, Class of 2024, Memorial University

2.B.Sc., MD Candidate, Class of 2025, Dalhousie University

Reviewed by Dr. M McGraw & Dr. M Kovalik

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Serum Sickness-Like Reaction  NBarry & LHarkness

 


Case Overview 

History of Presenting Illness

A 5-year-old male arrives at the emergency department (ED) with his mother who is concerned her son is having an allergic reaction. She reported that the week prior, he presented to his family doctor’s office with general malaise and productive cough. He tested positive for Group A Streptococcal infection and was started on amoxicillin. The day prior to arriving at the ED, he developed a purpuric urticarial rash that covered his trunk and extremities which continued to progress. He complained of bilateral ankle pain and fatigue. The patient had no past medical history, was not on any other medications, his family history was unremarkable, and had no known allergies. There was no recent change in diet or environmental exposures.

Physical Exam

The patient had a temperature of 38.3 degrees. All other vital signs were normal. On exam, his gait was antalgic. His trunk and extremities had multiple large, erythematous, annular plaques. The lesions were pruritic, non-blistering, and non-photo sensitive (see Figure 1). His lips were erythematous, and cheeks appeared flush. His mucous membranes were spared. Head and neck exam was otherwise unremarkable. His ankles were swollen bilaterally, limited range of motion in all directions and non-tender to palpation. His knees were also swollen bilaterally, non-tender, positive patellar tap test. Wrist did not show signs of swelling, restricted motion, or pain.

Investigations

Based on the wheal-like rash, Lyme disease, Vasculitis and Kawasaki were ruled out. Reactive arthritis was unlikely with a lack of family history. Throat swab was collected to rule out post-streptococcal glomerulonephritis. Based on the age of the child, further blood work was held while throat swab was analyzed as to not cause distress. Renal function, CPR and Lyme anti-bodies may be indicated if the child was otherwise unwell with high degree of suspicious of a more severe diagnosis.

Diagnosis

Given the presentation, you consider serum sickness-like reaction as a diagnosis. You consult dermatology for their opinion.

The dermatologist on call confirms the diagnosis as serum sickness-like reaction.

 

Figure 1. Drug-induced urticaria in a pediatric patient (CincinattiChildren’s.org).


Serum Sickness-Like Reaction

Serum sickness was originally named due to the compilation of symptoms following injection of horse serum for treatment of scarlet fever and diphtheria1. Traditionally, the term serum sickness should be reserved for those reactions following a heterologous or chimeric protein therapeutic.

Other, similar acute inflammatory presentations are referred to as serum sickness-like reactions (SSLR), and classically present with a characteristic rash, fever, malaise, and polyarthralgia or polyarthritis one to two weeks after exposure to a causative agent2. If a patient has previously been exposed to the causative agent, the reaction may occur sooner. Serum sickness-like reaction is a type of hypersensitivity reaction following the administration of a substance, including vaccines or other medicines. Common antibiotics shown to result in SSLR are cefaclor, amoxicillin, and trimethoprim-sulfamethoxazole3-5. Serum sickness-like reaction is also highly associated with certain non-steroidal anti-inflammatory drugs, anti-cancer agents, and biologics4.  Serum sickness-like reaction can also occur following certain infections, particularly streptococcal infection, and hepatitis B6,7.

Normally self-limiting, SSLR most often subsides within weeks after discontinuing the responsible agent8. Onset of symptoms of SSLR is tri-phasic, with the first peak at day 5 post exposure, second peak at day 7 and third at day 1010. Although most seen in adults, SSRL are an increasingly common etiology of acute arthritis in children9,10.

The differential diagnosis for such reactions can include, but is not limited to:

  • Autoimmune diseases, including systemic lupus erythematosus, reactive arthritis.
  • Drug reactions, such as drug reaction with eosinophilia and systemic symptoms, Stevens-Johnson syndrome, drug-induced sweet syndrome.
  • Infectious diseases, including Epstein-Barr virus, Lyme disease, erythema multiforme, disseminated meningococcemia.
  • Vasculitis, including IgA vasculitis (Henoch-Schoenlein purpura), hypersensitivity vasculitis.


Diagnosis

The diagnosis of SSLR is typically based on the characteristic compilation of symptoms, including the typical urticarial-like lesions, arthralgias, with or without fever, secondary to, most commonly, drug exposure11. It’s important to rule out Steven-Johnson Syndrome/Toxic Epidermal Necrolysis in both pediatric and adult populations with lack of mucous membrane involvement8.


Pathophysiology

Serum sickness-like reaction is a Coombs type III/immune complex mediated hypersensitivity reaction. The formation of antigen-antibodies complexes, involving an antigen and coinciding antibody, are required for the reaction to occur. The immune complex formation of serum sickness is mediated by C3 and C5a complement proteins which recruit mast cells and neutrophils to release histamines resulting in vascular permeability (Figure 2). Normally excreted by phagocytes, they are unable to clear these complexes due to the overwhelming number of complexes formed or the under performance of the mononuclear phagocyte system. These immune complexes target certain organs in the body—why they target some and not others are not well understood. Typically, they will target joint spaces, presumed to be due to the fenestrations into the synovial fluid. Once deposited in areas of the body, these complexes will activate an inflammatory response12.

Figure 2. Type III immune complex mediated hypersensitivity mechanism of serum sickness.

 


Treatment

Serum sickness-like reactions resolve when the agent responsible is discontinued and cleared from the patient’s system. Most patients do not require additional treatment. Symptoms typically subside within two to three weeks, but in some cases may linger for up to three months. If required, arthralgias and fever can be treated with non-steroidal anti-inflammatory and analgesic medications11. For patients with severe symptoms, glucocorticoid medications can be prescribed. Intravenous immunoglobulin may be indicated for worsening or unresolving symptoms. Outcomes of serum sickness and SSLR are good, and prolongation of symptoms more than 40 days is uncommon10. Offending drug should be avoided in the future. In situations where the causative agent cannot be discontinued, treatment is highly dependent on the drug in question, and should be based on a case-by-case basis13.


Case Conclusion

While in the ED, the dermatologist on call recommended to discontinue the amoxicillin that the patient was taking for Group A Strep. Supportive measures were also recommended, as well as analgesics or NSAIDs for symptom management. The dermatologist agreed to follow up with this patient in the subsequent days to ensure resolution of symptoms and whether future treatment was needed.


References

  1. von Pirquet CF, Schick B. (Die Serumkrankheit). Serum Sickness, Schick B (Ed), Williams & Wilkins, Leipzig 1905 (translation Baltimore 1951).
  2. Vincent C, Revillard JP. Antibody response to horse gamma-globulin in recipients of renal allografts: relationship with transplant crises and transplant survival. Transplantation 1977; 24:141.
  3. Clark BM, Kotti GH, Shah AD, Conger NG. Severe serum sickness reaction to oral and intramuscular penicillin. Pharmacotherapy 2006; 26:705.
  4. Brucculeri M, Charlton M, Serur D. Serum sickness-like reaction associated with cefazolin. BMC Clin Pharmacol 2006; 6:3.
  5. Stricker BH, Tijssen JG. Serum sickness-like reactions to cefaclor. J Clin Epidemiol 1992; 45:1177.
  6. Hengge UR, Scharf RE, Kroon FP, Pfeffer K. Severe serum sickness following pneumococcal vaccination in an AIDS patient. Int J STD AIDS 2006; 17:210.
  7. Liang, Jake T. “Hepatitis B: the virus and disease.” (2009): S13-S21.
  8. Wener, Mark H., N. F. Adkinson Jr, and A. M. Feldweg. “Serum sickness and serum sickness-like reactions.” UpToDate. Wolters Kluwer Health, Philadelphia, PA (2013).
  9. Yorulmaz A, Akın F, Sert A, et al. Demographic and clinical characteristics of patients with serum sickness-like reaction. Clin Rheumatol 2018; 37:1389.
  10. Kunnamo I, Kallio P, Pelkonen P, Viander M. Serum-sickness-like disease is a common cause of acute arthritis in children. Acta Paediatr Scand 1986; 75:964.
  11. Del Pozzo-Magaña, Blanca R., and Alejandro Lazo-Langner. “Serum sickness-like reaction in children: review of the literature.” Dermatology 7 (2019): 106-111.
  12. Tolpinrud WL, Bunick CG, King BA. Serum sickness-like reaction: histopathology and case report. J Am Acad Dermatol 2011; 65:e83.
  13.  Bayraktar F, Akinci B, Demirkan F, et al. Serum sickness-like reactions associated with type III insulin allergy responding to plasmapheresis. Diabet Med 2009; 26:659.
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EM Journal Club – The BUCKLED Trial

Presenter: Dr. Casey Jones (RCPSC EM PGY1)
Host: Dr. David Lewis 


Ultrasonography or radiography for suspected pediatric distal forearm fractures

Snelling et al., for the BUCKLED trial group

NEJM, 2023; 388:2049-2057.


PICO

  • Research Question: Is ultrasonography non-inferior to X-ray with respect to ..
  • Population: Children and adolescents between 5–15 years old presenting to an ED with an isolated, acute, clinically non-deformed distal forearm injury
  • Intervention: Randomization to either POCUS by a trained ED practitioner or radiography for injury evaluation
  • Comparison: POCUS vs Radiography
  • Outcome: Self-reported physical function of affected arm at 28 days

 

Background

  • Forearm fractures represent 40-50% of all childhood fractures
  • Distal third of forearm accounts for ~75% forearm fractures and 20-25% of all pediatric fractures
  • Most fractures are buckle fractures, treated conservatively with a wrist splint
  • Other pediatric fracture patterns include greenstick, Monteggia, Galeazzi, and Salter-Harris fractures
  • POCUS for distal forearm fractures is accurate, timely, and confers no radiation.
  • Ultrasonography may be more accessible in low and middle-income countries.
  • Is POCUS just as good as x-ray in diagnosing distal forearm fractures in pediatric patients?

 

Methods

  • Bedside Ultrasound Conducted in Kids with Distal Upper Limb Fractures in the Emergency Department (BUCKLED) trial
  • Study Design: Multi-center, open-label, noninferiority, randomized controlled trial
  • Setting: Four centers in Queensland, Australia (large tertiary pediatric hospital, two large mixed academic hospitals with dedicated pediatric treatment areas within their emergency departments, and one mixed hospital without a dedicated pediatric treatment area)
  • Inclusion criteria
    • Age 5-15
    • Distal forearm injury requiring radiological evaluation
    • Ability to follow up (distance from centre, telephone, internet access)
  • Exclusion criteria – many, but namely:
    • Obvious angulation
    • Injury sustained >48 hr prior to presentation
    • Compound / open fracture, neurovascular compromise, known bone disease
    • Suspicion of non-accidental injury, additional injuries
  • Imaging modalities
    • X-Ray – minimum 2 views performed by radiography. Classified by treating clinician (not radiologist) into either: no fracture, buckle fracture, other fracture
    • POCUS – 6-view forearm POCUS protocol with assessment of secondary signs (Snelling et al., 2020, BMJ)

 

  • POCUS credentialling
    • Scans in the study were done by either: nurse practitioner, physiotherapist, or emergency physician
    • Training course – 2 hour simulated course with lectures and staged learning (scanning)
    • 3 proctored scans on actual patients
    • Logbook of total 20 patients with a mix of at least 10 buckle and cortical breach fractures, then image interpretation quiz
  • Outcome measures:

  • Statistical analysis

    • Assumed true between-group difference in PROMIS score of 0 at 4 weeks, with noninferiority margin of 5 points (chosen by experts from trial group)
    • Power: 300 participant enrollment  outcome data for 224 participants (112 per group)  90% power with one-sided alpha of 0.025
    • Primary outcome of PROMIS score at 4 weeks was analyzed for noninferiority of ultrasonography to radiography
    • Primary analysis was with linear regression modeling to assess noninferiority of POCUS to radiography

Results

  • Participant characteristics (Table 1)
    • Well randomized groups for ultrasound and radiography (n=135 each group)
  • Primary outcome:
    • PROMIS (physical function score) at four weeks showed no difference between ultrasonography and radiography

  • Secondary outcomes:
    • No difference in physical function scores at week 1 or 8 between POCUS/X-ray
    • Parent / caregiver-reported satisfaction (5-point likert scale) appeared to be greater in POCUS group vs X-ray at 4 weeks (0.19 points) and 8 weeks (0.20 points)
    • Patients in POCUS group had shorter length of stay in the ED (median difference: 15 minutes), and shorter treatment time (median difference: 28 minutes) versus X-ray group
    • No substantial difference between groups in number of follow-up radiography films obtained up to week 8

 

Authors Discussion and Conclusions

  • The authors show that point-of-care ultrasound can be used as an initial diagnostic test in distal forearm injury in pediatric patients, with XR reserved for features suggestive of a diagnosis that leads to casting and follow-up (i.e. POCUS best suited for diagnosing buckle fractures)
  • Reduced initial radiography at initial ED presentation, especially in patients with buckle fracture or no fracture.
  • A diverse group of health care practitioners (physicians, nurse practitioners, physiotherapists) were trained to use ultrasound for this purpose
  • “The present randomized trial examined the feasibility, safety, acceptability, and timeliness of using an ultrasonography-first approach to the diagnosis of clinically non-angulated distal forearm injury in children and adolescents who presented to the emergency department.”

Discussion at journal club

Strengths

  • Well powered trial to study their question of non-inferiority of POCUS to XR
  • Feasible approach to imaging distal radius, and transferrable to many health professions
  • Showed that simple fractures can be initially imaged with POCUS only

Weaknesses

  • Children with features of a more concerning fracture (i.e. anything more than a buckle) received x-ray anyway (122 films were obtained in POCUS group vs 375 in XR group)
    • To that end, does this study show that POCUS may only be appropriate for simple fractures?

Bottom Line

This was a well-designed and executed study by this group in Australia. This method of diagnosing distal forearm injuries would be helpful in rural or resource-limited settings that don’t have readily accessible X-ray. I will certainly be using this more at the bedside in children with this injury pattern!


Further Reading

Quick Take NEJM Video

View the author’s webinar here

 

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Pancreatic Pseudocysts: An Uncommon Cause of Painless Jaundice


Medical Student Clinical Pearl by Thomas Camp

 

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. J Vonkeman

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ Pancreatic Pseudocysts: An Uncommon Cause of Painless Jaundice

 


Introduction

It’s 6:30 pm on a Monday evening, and a 52-year-old man presents to the ER with overt jaundice. He says that he’s been feeling great and that he only came in because his coworkers have been teasing him about his changing skin colour.


History and Physical

The patient reports that his skin has been turning yellow for the past week. He denies abdominal pain, nausea, vomiting, weight loss, fever, and fatigue. He also denies any pruritus, bruising, gastrointestinal bleeding, abdominal distension, or mental status changes. On further questioning, he reveals that his stool was pale this morning and that his urine has been unusually dark. Last year he was admitted to hospital for acute pancreatitis, which was thought to be induced by heavy alcohol consumption.

He is unaware of any other medical conditions and does not take any regular medications or herbal supplements. The patient denies any alcohol consumption since his previous admission, any history of IV drug use, and any history of international travel or blood transfusions. He smokes two packs of cigarettes per and there is an extensive family history of gastric cancer.

Physical examination reveals a thin, overtly jaundiced man with scleral icterus and a strong scent of tobacco. His lungs are clear, and his heart sounds are normal. His abdomen is soft and nontender, and there is no evidence of organomegaly or extra hepatic manifestations of liver disease (Figure 1). Ultrasound reveals a distended gallbladder and biliary tree without stones.


Approach to Jaundice

Jaundice is the result of excessive bilirubin levels in the blood, and bilirubin is a product of heme catabolism.2 The differential diagnosis for jaundice is broad but, conceptually, can be divided into pre-hepatic, intra-hepatic, and post-hepatic causes (Figure 2).3

  • Pre-hepatic jaundice is the result of excessive unconjugated bilirubin production, which overwhelms the liver’s ability to conjugate it for excretion. Hemolysis is the most common cause of pre-hepatic jaundice.
  • Intra-hepatic jaundice is the result of either decreased bilirubin uptake or impaired bilirubin conjugation within the liver’s hepatocytes,4 leading to impaired secretion in the bile. Common causes include viral hepatitis, drug toxicity, alcoholic hepatitis, and any of the many conditions leading to cirrhosis.
  • Post-hepatic jaundice is the result of biliary obstruction, which impairs the flow of bile into the duodenum. Gallstones and cancer are the most common cause, but pancreatic pseudocysts, primary sclerosing cholangitis, and bile duct strictures are also possible etiologies.

The distention of the biliary tree, the presence of acholic stools, and dark urine suggests post-hepatic jaundice in this patient.  These are characteristic findings of post-hepatic jaundice because the lack of bilirubin entering the duodenum results in pale stools, and at the same time conjugated bilirubin is water soluble, giving urine a dark colour.3 His age, sex, smoking status, and family history are also significant risk factors for pancreatic cancer, which commonly presents with jaundice.5

 


Work Up

Laboratory investigations reveal conjugated hyperbilirubinemia with a large increase in ALP and a mild increase in ALT. This is a cholestatic pattern of liver injury, which is characterized by a fourfold or greater increase in ALP and absent or mild elevations in the aminotransferases.6,7 In contrast, a hepatocellular pattern of liver injury is characterized by elevated aminotransferases and normal or mildly elevated ALP.6,7

INR and albumin levels are normal, suggesting that synthetic liver function is preserved. Normal hemoglobin levels (that are also stable when compared to the patient’s historical baseline) help exclude hemolysis from the differential. Elevated lipase is worrying for pancreatic cancer but could be explained by obstruction of the pancreatic duct by another cause, for example, gallstones not appreciated on ultrasound.

An urgent CT scan is ordered, and the radiologist comments that there is a complex cystic mass arising from the head of the pancreas that is causing obstruction of the common bile and pancreatic ducts. He notes that underlying malignancy cannot be excluded, and endoscopic retrograde cholangiopancreatography (ERCP) is recommended for further investigation. The patient is referred to gastroenterology and discharged home.


Conclusion 

A week later, ERCP confirms that the mass is in fact a pancreatic pseudocyst. Pancreatic pseudocysts are collections of fluid with a well-defined wall that lack the epithelium required to be classified as true cysts. Classically, they form after an episode of acute pancreatitis, but they are also seen in chronic pancreatitis, in obstruction of the pancreatic duct, and after pancreatic trauma.8 The cyst is drained endoscopically, a technique that is now considered preferable to a percutaneous approach due to its excellent rates of resolution (82-94%).9 The patient’s jaundice resolves over the following weeks and repeat laboratory investigations normalize within two months.


Key Points

  • Categorizing jaundice as pre-hepatic, intra-hepatic, or post-hepatic can provide a useful framework for formulating a differential diagnosis.
  • A fourfold or greater increase in ALP with mild or no elevation in the aminotransferases is characteristic of post-hepatic jaundice.
  • Consider pancreatic pseudocysts in patients presenting with post-hepatic jaundice, especially if they have a recent history of acute pancreatitis.

References

  1. Scott L Friedman M. Clinical manifestations and diagnosis of alcohol-associated fatty liver disease and cirrhosis. In: Post TW, ed. UpToDate. Wolters Kluwer; 2023. https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-alcohol-associated-fatty-liver-disease-and-cirrhosis
  2. John S, Pratt DS. Jaundice. In: Loscalzo J, Fauci A, Kasper D, Hauser S, Longo D, Jameson JL, eds. Harrison’s Principles of Internal Medicine, 21e. McGraw-Hill Education; 2022. http://accessmedicine.mhmedical.com/content.aspx?aid=1197684641
  3. Beckingham IJ, Ryder SD. ABC of diseases of liver, pancreas, and biliary system. Investigation of liver  and biliary disease. BMJ. 2001;322(7277):33-36. doi:10.1136/bmj.322.7277.33
  4. Wolkoff AW. The Hyperbilirubinemias. In: Loscalzo J, Fauci A, Kasper D, Hauser S, Longo D, Jameson JL, eds. Harrison’s Principles of Internal Medicine, 21e. McGraw-Hill Education; 2022. http://accessmedicine.mhmedical.com/content.aspx?aid=1190492793
  5. Freelove R, Walling AD. Pancreatic cancer: Diagnosis and management. Am Fam Physician. 2006;73(3).
  6. Moseley RH. EVALUATION OF ABNORMAL LIVER FUNCTION TESTS. Medical Clinics of North America. 1996;80(5):887-906. doi:https://doi.org/10.1016/S0025-7125(05)70472-7
  7. Bethea ED, Pratt DS. Evaluation of Liver Function. In: Loscalzo J, Fauci A, Kasper D, Hauser S, Longo D, Jameson JL, eds. Harrison’s Principles of Internal Medicine, 21e. McGraw-Hill Education; 2022. http://accessmedicine.mhmedical.com/content.aspx?aid=1190492731
  8. Habashi S, Draganov P V. Pancreatic pseudocyst. World J Gastroenterol. 2009;15(1):38-47. doi:10.3748/wjg.15.38
  9. Piraka C, Chen YK. Pseudocyst Drainage: ERCP and EUS Approaches. Tech Gastrointest Endosc. 2007;9(3). doi:10.1016/j.tgie.2007.05.002
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A Case of Spaghetti Wrist: Approach to an Extensive Volar Forearm Laceration in the ED


Medical Student Clinical Pearl by Krystal Stewart

 

 

MD Candidate, Class of 2024

Dalhousie University

Reviewed by Dr. F MacKay

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ A Case of Spaghetti Wrist: Approach to an Extensive Volar Forearm Laceration in the ED

 


Case Presentation

A 13-year-old male presents to the Emergency Department by ambulance, with a deep laceration to his distal volar forearm. The injury occurred at a friend’s house, after tripping on a bong with the shattered glass lacerating his left wrist. The patient was intoxicated by cannabis at the time of arrival and experienced bouts of age regression while attempting to assess and treat him. He is otherwise healthy, with no significant past medical history and is not taking any regular medications. This was an isolated injury; no other lacerations were found on the body, and blood loss at the site of injury was well controlled by the time of arrival at the ED.

On physical examination, pertinent findings consist of the ulnar arterial pulse not being palpable, no sensation throughout the ulnar nerve distribution of the hand, and the flexor carpi ulnaris tendon is visibly torn. Capillary refill was normal, with perfusion being provided solely by the radial artery – which remains intact. Motor examination of the hand was difficult to assess due to patient’s intoxicated state and pain level. The patient felt he was unable to move his hand but was able to wiggle his thumb and index finger.

The on-call plastic surgeon was consulted to assess the defect. The wound was washed out with saline and briefly explored under local anesthetic by the surgeon. Subsequently, the wound was closed with simple interrupted sutures and a volar slab splint was placed on the hand and forearm for temporary stability. The patient was admitted overnight to the pediatric floor to await further exploration in the OR and reparation of the ulnar artery, ulnar nerve, and several flexor tendons.


Anatomical Context

Figure 1: Carpal tunnel anatomy of the volar wrist.1


Clinical Approach

A deep laceration of the distal volar forearm may otherwise be known as the “spaghetti wrist,” due to the number of potential structures that could require repair, including tendons, nerves, and vessels. This term came about from the appearance of lacerated tendons overlying the red background of muscle.2 There lacks a unified classification system for this term in the literature, thus defining a volar forearm laceration and its level of severity as a spaghetti wrist injury is more subjective – with an arbitrary sum of structures lacerated.3

First begin by assessing the patient for hemodynamic instability, if bleeding – apply direct pressure, if it continues a temporary tourniquet may be needed.2 It is important to evaluate for hemorrhagic shock and resuscitation prior to assessment of the hand.2

Vascular status of the hand can be assessed with capillary refill or Doppler ultrasound to each fingertip.2 If the hand is considered well perfused and bleeding is well controlled, surgical exploration can be delayed, as it will take several days for cut tendons, nerves, and vessels to retract.2 If there is concern for arterial laceration, palpation for radial and ulnar pulses would be valuable.

The next important assessment is a focused sensory and motor examination of the hand. Lightly touch at the three sensory areas that represent the cutaneous radial, median ulnar innervation of the hand as demonstrated in Figures 2 and 3.2 Evaluating the extrinsic and intrinsic hand muscle innervation requires a focused motor examination, as demonstrated in Figure 4.2 Have the patient demonstrate a series of hand gestures, the “OK” sign using the index finger and the thumb represents the muscles innervated by the median nerve.2 By abducting the digits, this represents the muscles innervated by the ulnar nerve.2 Lastly, demonstrating a “thumbs up” sign represents the muscles innervated by the radial nerve.2 If there is lack of sensation at a particular sensory distribution and/or lack of ability to demonstrate those representative hand gestures for extrinsic and intrinsic muscle innervation, it should be noted that the associated nerve(s) may be damaged.

To evaluate for any associated injuries to bone, muscle, tendon or ligament, gentle manipulation and palpation is required, along with assessing passive and active range of motion.2 It may also be valuable to assess if there is any ulnar or radial deviation of the wrist.2

 

 

Figure 2: Cutaneous innervation of the volar hand.2

 

Figure 3: Cutaneous innervation of the dorsal hand.2

 

Figure 4: Motor examination of the hand. I: Median nerve, II: Ulnar nerve, III: Radial nerve.2


Management 

Important information to gather on clinical history include the use of anticoagulants, diagnosis of advanced liver disease or diabetes. As the former two impair hemostasis, and the latter may impair wound healing.2 Broad spectrum IV antibiotics may be warranted if the wound is largely contaminated or extensive in size.2 There is a potential risk of contracting tetanus based on the mechanism of injury, thus it is important that the patient has tetanus prophylaxis.2,4An X-ray of the hand and forearm may be necessary if suspicion of a bony fracture.

A consult should be sent to the Plastic Surgery service for further management, including surgical exploration and reparation of any lacerated nerves, tendons, and vessels. These structures begin to retract after injury; thus, it is important that reparation is done within two weeks of injury. If plastic surgeon on call is planning to see the patient in clinic, have the forearm and wrist dorsally splinted at the position of safe immobilisation – wrist in 0-30 degree of extension, MCP joints in 70-90 degrees of flexion and IP joints in full extension.5,6 Once the repair is completed and appropriate hand immobilization has been achieved, the patient should see a designated occupational hand therapist for further patient education and hand rehabilitation.


Prognosis 

The road to recovery largely depends on the patient’s willingness to undergo post-operative rehabilitation and adhere to the regimens set forth by the surgeon and the occupational hand therapist. Age and smoking status may also impact neurologic recovery.5 Nerve regrowth from the site of laceration is a slow process, with approximately 1 mm in growth daily.5 Recovery tends to be functional, with less emphasis on perfection. Ulnar innervation tends to be less predictable in regrowth of intrinsic muscles.5 Possible long-term sequelae include stiffness, neuropathic pain, and cold intolerance.5


Key Points

  • If the hand is de-vascularized, immediate emergency surgery is essential.5
  • If the injury was self-inflicted, a consult to psychiatry is recommended once medically cleared.5
  • Negative prognostic factors include increasing age, low education level, presence of a crush injury.7

Complications

With complex volar forearm lacerations there is the risk of developing acute compartment syndrome post-injury. Diagnosis of acute compartment syndrome is achieved clinically, with signs of swollen and taut muscle compartment(s), pain out of proportion to the injury, or severe pain with passive digital extension.2 Neurological deficits present as a late feature of the syndrome, including paresthesia, paresis and then paralysis.2 Paresthesia is an indicative feature of early nerve ischemia.2 The intra-compartmental absolute pressure may also be measured if suspicious of compartment syndrome – an emergent forearm fasciotomy should be done if greater than or equal to 30 mmHg.2

Post-operative complications may include major deformity of hand due to clawing, ‘anesthetic hands,’ as well as neuromas – being the most cited complication.3 The former two are most likely due to the initial injury rather than a complication from the surgery itself.3 The term ‘clawing’ refers to an ulnar nerve palsy, where the hand will resemble that of a claw hand.8

 


Conclusion

While the Spaghetti Wrist terminology does not have a severity scale, it is intuitively known to be an emergent case with the need for prompt management. Whether the cause of injury was accidental or self-inflicted, the same steps must be taken to ensure that the function of the hand can be salvaged – as the impact on the patient’s physical function and psychological health could be enormous if not managed correctly.


References

  1. Hansen JT, Netter FH. Netter’s Clinical Anatomy. 2nd Philadelphia, PA: Saunders/Elsevier; 2010.
  2. Thai JN, Pacheco JA, Margolis DS, et al. Evidence-based Comprehensive Approach to Forearm Arterial Laceration.West J Emerg Med. 2015;16(7):1127-1134. doi:10.5811/westjem.2015.10.28327
  3. Koshy K, Prakash R, Luckiewicz A, Alamouti R, Nikkhah D. An Extensive Volar Forearm Laceration – The Spaghetti Wrist: A Systematic Review.JPRAS Open. 2018;18:1-17. Published 2018 Jul 11. doi:10.1016/j.jpra.2018.06.003
  4. Bae C, Bourget D. Tetanus. In:StatPearls. Treasure Island (FL): StatPearls Publishing; August 19, 2022.
  5. Meals CG, Chang J. Ten Tips to Simplify the Spaghetti Wrist.Plast Reconstr Surg Glob Open. 2018;6(12):e1971. Published 2018 Dec 12. doi:10.1097/GOX.0000000000001971
  6. Dobson P, Taylor R, Dunkin C. Safe splinting in hand surgery.Ann R Coll Surg Engl. 2011;93(1):94. doi:10.1308/003588411×12851639108033
  7. De M, Singhal M, Naalla R, Dave A. Identification of Prognostic Factors in Spaghetti Wrist Injuries.J Hand Surg Asian Pac Vol. 2021;26(4):588-598. doi:10.1142/S2424835521500569
  8. Lane R, Nallamothu SV. Claw Hand. In:StatPearls. Treasure Island (FL): StatPearls Publishing; January 8, 2023.
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An EM Approach to Syncope in Adults

 

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

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/

 

 

 

 

 

 

 

 

 

 

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EM Grand Rounds: Practical Points in Aboriginal Health

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