>EM Reflections – June 2020

Thanks to Dr Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis 


Discussion Topics

  1. Antiviral Toxicity

    • Always adjust dosing in patients with renal impairment
  2. Necrotising Fasciitis

    • Difficult clinical diagnosis
    • Should be on the differential for all soft tissue infections
    • Delayed definitive care always results in poor outcomes
  3. Epidural Abscess

    • Thorough detailed neurological examination required
    • Isolated leg weakness is rare in Stroke
    • Progressive development of symproms and mixed UMN/LMN signs suggests spinal cord compression.

 


Antiviral Toxicity

Case

A 70yr old male presents with a typical zoster rash in the left L1 dermatome. He has a past medical history of chronic renal insufficiency. He is started on Valacyclovir 1000mg TID. He represents 3 days later with hallucinations including a feeling that he was occupying a dead body. What is the differential diagnosis?


 

Varicella Zoster Encephalitis vs Valacyclovir Toxicity

VZV and antiviral toxicity can present with similar symptoms

Two main risk factors increase the risk for VZV

  • age greater than 50 years old
  • immunocompromised due to reduced T cell-mediated immunity

The main risk factor for antiviral toxicity is renal insufficiency

Differentiation

  • Timing
    • Toxicity presents within 1-3 days of starting drug (vs 1-2 weeks)

 

  • Symptoms – both can present with confusion and altered LOC
    • Encephalitis – fever, HA, seizures, more likely with Trigeminal nerve (V1) or disseminated zoster
    • Toxicity – Visual hallucinations, dysphasia, tremor/myoclonus
    • Toxicity – Cotard’s syndrome…

Cotard’s Syndrome

“le délire des négations”

(delirium of negation)

https://en.wikipedia.org/wiki/Cotard_delusion

  • Described in 1880 by neurologist Jules Cotard
    • “patient usually denies their own existence, the existence of a certain body part, or the existence of a portion of their body”
  • Seen in schizophrenia, psychosis and…
  • ….acyclovir toxicity (felt to be due to metabolite CMMB (9-carboxymethoxymethylguanine) crossing BBB)

Further Reading

Varicella Zoster Encephalitis case report and outline

Valacyclovir Toxicity case report and outline

Cotard’s Syndrome

Drug Dosing in Chronic Kidney Disease

 

 

 


Necrotising Soft Tissue Infections (NSTI)

Case

A 28yr old female presents pain, redness and swelling over the right thigh. She has a past medical history of type 2 diabetes. She is managed as an outpatient with intravenous ceftriaxone q24hrs. Her symptoms failed to respond on follow up. What is the concern now? Are there any red flags? What condition needs to be considered in patients with soft tissue infections that fail to respond to antibiotics?


NSTI first described by Hippocrates 5th century BC

“[m]any were attacked by the erysipelas all over the body when the exciting cause was a trivial accident…flesh, sinews, and bones fell away in large quantities…there were many deaths.”

 

Necrotizing fasciitis is characterized by rapid destruction of tissue, systemic toxicity, and, if not treated aggressively, gross morbidity and mortality. Early diagnosis and aggressive surgical treatment reduces risk; however, it is often difficult to diagnose NF, and sometimes patients are treated for simple cellulitis until they rapidly deteriorate.

Infection typically spreads along the muscle fascia due to its relatively poor blood supply; muscle tissue is initially spared because of its generous blood supply.

Infection requires inoculation of the pathogen into the subcutaneous tissue or via hematogenous spread.

Classification

  • Type 1 – polymicrobial – older/diabetics/EtOH/IC/PVD
  • Type 2 – monomicrobial – usually group A beta-hemolytic strep (often hematogenous) – healthy people of all ages

Early signs and symptoms of NSTI are often identical to those seen with cellulitis or abscesses potentially making the correct diagnosis difficult

‘Classic’ Signs / Symptoms

(1) the presence of bullae
(2) skin ecchymosis that precedes skin necrosis
(3) crepitus
(4) cutaneous anesthesia
(5) pain out of proportion to examination
(6) edema that extends beyond the skin erythema
(7) systemic toxicity
(8) progression of infection despite antibiotic therapy or rapid progression

First 4 are “hard” signs

  • Erythema (without sharp margins; 72 percent)
  • Edema that extends beyond the visible erythema (75 percent)
  • Severe pain (out of proportion to exam findings in some cases; 72 percent)
  • Fever (60 percent)
  • Crepitus (50 percent)
  • Skin bullae, necrosis, or ecchymosis (38 percent)

Streaking lymphangitis favours the diagnosis of cellulitis over necrotizing fasciitis

Diagnosis

  • There is no set of clinical findings, lab test results and even imaging that can definitively rule out necrotizing fasciitis
    • “Surgical exploration is the only way to establish the diagnosis of necrotizing infection”.
    • “Surgical exploration should not be delayed when there is clinical suspicion for a necrotizing infection while awaiting results of radiographic imaging other diagnostic information”
  • But what if you really aren’t sure?  Or if you get pushback?
  • CT is probably the best test – esp Type 1 (gas forming)
    • Findings – gas, fluid collections, tissue enhancement, inflammatory fascial changes
  • Finger test…
    • “After local anesthesia, make a 2-3 cm incision in the skin large enough to insert your index finger down to the deep fascia. Lack of bleeding and/or “dishwater pus” in the wound are very suggestive of NSTI. Gently probe the tissues with your finger down to the deep fascia. If the deep tissues dissect easily with minimal resistance, the finger test is + and NSTI can be ruled in.”  (emergencymedicinecases.com)
  • But what about PoCUS????

PoCUS

Diagnosis of Necrotizing Faciitis with Bedside Ultrasound: the STAFF Exam

Findings – “STAFF”

ST – subcutaneous thickening
A – air
FF – fascial fluid

Ultrasound video demonstrating Subcutaneous Thickening, Air, and Fascial Fluid (STAFF).

 

Soft tissue ultrasound findings are significantly different when compared to normal soft tissue ultrasound

Bottom Line: Limited data, but basically PoCUS is not sufficient to rule-in or rule out, but might be helpful in raising suspicion level for necrotising fasciitis for physicians who routinely scan all soft tissue infections.

 

LRINF Score

The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) Score: A Tool for Distinguishing Necrotizing Fasciitis From Other Soft Tissue Infections

Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) Score.  2004, retrospective – score >6 negative predictive value of 96.0% and a positive predictive value of 92%.

 

A validation study looking only at patients with pathology-confirmed necrotizing fasciitis showed that a LRINEC score cutoff of 6 points for necrotizing fasciitis only had a sensitivity of 59.2% and a specificity of 83.8%, yielding a PPV of 37.9% and NPV of 92.5%. However, the study did show that severe cellulitis had a LRINEC Sscore ≥ 6 points only 16.2% of the time.  Therefore, the available evidence suggests that the LRINEC score should not be used to rule-out NSTI.

Bottom Line: Doesn’t rule-out…… or rule-in

 

Suggested Algorithm – UpToDate

 

EM Cases Review

BCE 69 Necrotizing Fasciitis

 

Further Reading

Necrotizing fasciitis – Can Fam Physician. 2009 Oct; 55(10): 981–987.

 


Epidural Abscess

Case

A 40yr old female presents with left leg weakness. She has a complex recent past medical history including recently diagnosed pneumonia, previous renal colic and type 2 diabetes. Could this be a stroke? What are the other causes of leg weakness? How does the examination differentiate UMN from LMN lesions? When considering a diagnosis of epidural abscess what investigation is required? How soon should it be performed?


Only 4% of Strokes present with isolated or predominant leg weakness. (Brain. 1994 Apr;117 ( Pt 2):347-54.
doi: 10.1093/brain/117.2.347)

Common mechanisms of weakness:

  • Upper motor neuron lesions (Stroke, Tumour, Spinal Cord Compression, etc)
  • Lower motor neuron lesions ( Neuropathy, Disc Prolapse, Spinal Cord Compression, etc)
  • Neuromuscular junction lesions (Myasthenia, etc)
  • Neuropathies (Guillain-Barre, etc)
  • Muscle (Myopathies, etc)

Full review on Muscle Weakness from the Merck Manual here

Weakness that becomes severe within minutes or less is usually caused by severe trauma or stroke; in stroke, weakness is usually unilateral and can be mild or severe. Sudden weakness, numbness, and severe pain localized to a limb are more likely caused by local arterial occlusion and limb ischemia, which can be differentiated by vascular assessment (eg, pulse, color, temperature, capillary refill, differences in Doppler-measured limb BPs). Spinal cord compression can also cause paralysis that evolves over minutes (but usually over hours or days) and is readily distinguished by incontinence and clinical findings of a discrete cord sensory and motor level.

Unilateral upper motor neuron signs (spasticity, hyperreflexia, extensor plantar response) and weakness involving an arm and a leg on the same side of the body: A contralateral hemispheric lesion, most often a stroke

Upper or lower motor neuron signs (or both) plus loss of sensation below a segmental spinal cord level and loss of bowel or bladder control (or both): A spinal cord lesion

 

Epidural Abscess

Spinal epidural abscess (SEA) is a severe pyogenic infection of the epidural space that leads to devastating neurological deficits and may be fatal. SEA is usually located in the thoracic and lumbar parts of the vertebral column and injures the spine by direct compression or local ischemia. Spinal injury may be prevented if surgical and medical interventions are implemented early. The diagnosis is difficult, because clinical symptoms are not specific and can mimic many benign conditions. The classical triad of symptoms includes back pain, fever and neurological deterioration.

Spinal Epidural Abscess: Common Symptoms of an Emergency Condition – A Case Report

 

  • 75% are a delayed diagnosis
    • Usually hematogenous spread, usually S. aureus
  • Diagnosis
    • CRP has an sensitivity of 85%, specificity of 50%
    • MRI is gold standard
    • CT with contrast 2nd choice

 

Further Reading

Spinal epidural abscess

Episode 26: Low Back Pain Emergencies

 

 

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