Tag Archives: stroke

Journal Club – IV TNK compared with tPA for Acute Ischemic Stroke in Canada

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Presenter: Dr. Rhiannan Pinnell (FRCPC-EM R1)

Host: Dr. Paul Atkinson

Article:

Research Question/PICO

  • Research Question
    • “The aim of the Alteplase compared to Tenecteplase (AcT) trial was to determine whether intravenous tenecteplase, at a dose of 0·25 mg/kg, is non-inferior to alteplase in all patients presenting early after acute ischaemic stroke who meet standard of care criteria for intravenous thrombolysis.”
  • Population:
    • Patients >18year presenting to stroke center within 4.5h of symptom onset with disabling acute ischemic stroke
  • Intervention
    • TNK at a dose of 0.25mg/kg
  • Comparison
    • Standard dose alteplase
  • Outcome:
    • “Excellent neurological outcome” as measured by the proportion of patients with a mRS of 0-1 at 90-120 days

Background

  • There are 2 mainstays of treatment for ischemic stroke – thrombolysis and endovascular therapy (EVT).
    • Thrombolytics are “clot buster” medications, whereas EVT is an interventional radiology procedure which physically removes the clot
  • The major thrombolytic used since the 90s has been alteplase or tPa.
  • Current guidelines indicate that within 6 hrs since onset of disabling stroke, consider thrombolysis (disabling) and/or EVT. Strongly recommended for <4.5h as long as there are no standard lytic contraindications.
    • Per Canadian stroke best practices, median door to needle time <30 min, 90% should be less than 60 min.
  • There are 2 issues with tPA
    • First, there is a fair bit of debate surrounding both the quality of evidence and the efficacy of this treatment. Throughout the numerous trials, some have been neutral and others have been stopped early due to increased harm/bleeding compared to placebo. The current practice is based mostly on ECASS-3 (2008) and NINDS 2 (1995) and there are some concerns around the fragility indices and baseline imbalance in stroke severity.
    • Also, tPA must be given as an infusion as the half life is only 5-10 mins.
  • What is new?
    • Tenecteplase has a higher fibrin specificity and longer half life so it can be given as a single dose.
    • Currently preferred for MI, given as 5 tier weight-based system which works out to around 0.5-0.55mg/kg.
  • Prior phase 2 studies of TNK for ischemic stroke have found that 0.25mg/kg probably best dose. Phase 3 studies have found that TNK at 0.4mg/kg is not superior to standard alteplase.
  • To date, there have been no phase 3 comparisons between 0.25 and standard alteplase.

Methods

  • Design:
    • Prospective multicentre RCT at 22 Canadian stroke centers (both regional and EVT capable).
    • Open label for treatment, outcome mRS was taken over the phone by a blinded evaluator.
    • Non-inferiority, with subsequent superiority calculations.
    • Used “minimal sufficient balance” algorithm to balance allocation by site.
  • Funding: Funded by Canadian Institutes of Health Research & Alberta Strategy for Patient Oriented Research Support Unit.
  • Population:
    • Inclusion
      • 18+ w/ ischemic stroke, presenting within 4.5h. Could be eligible for EVT but did not have to be.
    • Exclusion
      • Standard contraindications for IV thrombolysis (ICH, etc.)
    • Intervention/procedures:
      • Alteplase – 0.9mg/kg IV to max of 90, w 10% bolus in 1 min, rest over 1 hr
      • TNK – bolus of 0.25mg/kg
    • Outcomes
      • Primary
        • mRS 0-1 at 90-120 days
      • Secondary
        • mRS 0-2 at 90-120
        • EQ-VAS and EQ-5D-5L 90-120
        • Door to needle
        • Proportion given EVT
        • Recanalization at angiogram
        • Baseline CT to arterial puncture time
        • Cognition assessment
        • Length of stay in hospital
        • Discharge destination
        • Safety: sICH, orolingual angio-edema, extracranial bleeding requiring transfusion (within 24h of thrombolysis). 90 day all cause mortalit
    •  Statistics
      • Non-inferiority was established if the lower 95% CI of in TNK group was more than -5%
      • Sample size 1600 for 90% power assuming 35% in tPA and 38% in TNK group have mRS 0-1
      • Intention to treat analysis

Results

  • Sample
    • Size: 1577. 0.6% lost to follow up.
    • Baseline characteristics (No statistical calculations reported for baseline differences)
      • Median age 74y, 48% female.
      • Baseline NIHSS 10 in alteplase group, 9 in TNK group
      • 93-94% at comprehensive stroke centre
      • 32% got EVT
      • Times (min in TNK vs alteplase group)
        • Symptom onset to hospital arrival: 82 vs 83
        • Symptom onset to randomization:121 vs 123
        • Door to CT 15 vs 16
        • Symptom onset to needle 128 vs131
        • Door to needle 36 vs 37
        • CT to arterial puncture 60 vs 58,
        • Puncture to reperfusion 31 vs 27
      • Median follow up at 97 days
    • Results
      • Primary:
        • 90-120 day mRS 0-1 36.9% of patients who received TNK, 34.8% of those who received alteplase.
        • Unadjusted risk difference ****** Lower bound 95% CI of difference of rate of primary outcomes (-2.6-6.9) >-5%, so non-inferior.
        • No difference based on subgroup – e.g. age, sex, NIHSS, large vessel occlusion (defined as internal carotid artery, M1 segment middle cerebral artery (MCA) occlusion, or functional M1 MCA, occlusion (ie, all ipsilateral M2-MCA segments)), etc.
      • Secondary:
        • No significant difference in any secondary outcomes or in safety outcomes in either intention to treat or per protocol analysis.

Authors conclusions

  • “The AcT trial provides robust empirical evidence that tenecteplase is comparable to alteplase in patients presenting with acute ischaemic stroke, with similar function, quality of life, and safety outcomes. Given the ease of administration of tenecteplase compared with alteplase, these results provide a compelling rationale to support switching the standard-of-care intravenous thrombolytic agent for acute ischaemic stroke from alteplase to tenecteplase at a dose of 0·25 mg/kg.”

Discussion at Journal Club

Strengths

  • ED focus
  • Large size, multi center. Involved a range of types of hospitals, from community to academic.
  • RCT with what appears to be good randomization (although no statistics were reported regarding the success of randomization).
  • Excellent per protocol analysis (800/806, 762/771) and very low loss to follow up.

Weakness

  • Conception: Is there an issue surrounding the fundamental comparison to alteplase, since this is so debated? We had some debates about this, and whether there should have been a control group who did not receive a lytic, but concluded that this would probably have been impossible from an ethics board perspective.
  • Baseline values: Numerically slightly more patients with baseline NIHSS <8 (40.5%) in TNK group vs alteplase (38.4%)
  • Methods:
    • This was an open label study. Although the authors did blind the outcome assessors, they did not blind the patients. This still has a risk of exaggerating results, as the Rankin scale has inter-rater variability.
    • There are many secondary outcomes used, which is sometimes seen as scavenging for statistical significance. In this non-inferiority trial, however, it may be a benefit as they are looking for any possible dangers.
    • There may be some issues with using the Rankin score as dichotomous – e.g. there a large difference between “requires some assistance” and “bedridden”
    • There was no subgroup analysis looking at the impact of EVT.

Bottom line

  • This is a well performed study and has good internal validity. It opens up another alternative for stroke treatment – but, based on a non-inferiority trial, TNK wouldn’t be considered a mandatory alternative yet. What it does provide is the opportunity to conduct future studies that could show it to be superior.
  • TNK might also improve treatment timelines (e.g. giving a dose right before going to EVT), as well as permit patients to be lysed and immediately transported with EMS (as currently there are barriers surrounding running the infusion during transport).

 

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Bell’s Palsy or Stroke?

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Bell’s Palsy or Stroke? A Medical Student Clinical Pearl

Alicia Synette, Med III

Class of 2022 MUN

Reviewed by Dr. Jeremy Gross

Copyedited by Dr. Mandy Peach

Case

A 48M presented to the Emergency Department with right sided facial droop and altered facial sensation for two days.

He woke up one morning and described the right side of his face as feeling “saggy”. At this time, he assumed that he had slept funny. The facial droop progressed that day until it became noticeable by his wife. Two days later, he decided to go to the ER when his symptoms did not resolve. At this time, he described altered sensation at the right side of the face and tongue, which he compared to the feeling of local anesthetic after dental work. His smile was “crooked”, he was unable to purse his lips, and he could not completely close his right eye. The affected eye was also red and irritated. Taste and hearing were unchanged. Review of systems was otherwise unremarkable.

PMH: T2DM, HTN, hyperlipidemia

Medications: Ramipril, Fenofibrate, Janumet, Rosuvastatin, ASA, Lantus, Humalog

On exam, he appeared well, he was afebrile, and vital signs were stable. Pupils were equal and reactive to light. Conjunctival injection was present at the right eye with increased tearing. Mild facial droop was apparent. The right eyelid was droopy and he was unable to keep it closed against resistance. Facial movements on the right side were also weak (smile, purse lips, puff cheeks, close eyes tight), however, weakness of the forehead muscles could not be appreciated when asked to raise his eyebrows. Sensation to light touch was altered at V1. Pinprick touch was normal. There was no deviation of the tongue. He had 5/5 strength and normal sensation bilaterally at the extremities. Normal rapid alternating movements and normal heel to shin test. Normal hearing bilaterally and no hyperacusis.

Accessed from grepmed – https://www.grepmed.com/

Differential Diagnosis for Facial Nerve Palsy

Table 1: differential diagnosis for facial nerve palsy.6

Investigations

Lab results were unremarkable aside from an elevated random blood glucose. HbA1C level from one month prior to the ER visit was 11.1%.

CBC – LKC 8.2, Hgb 137, PLT 213

Electrolytes – Na 140, K 3.9, Cl 103

Glucose (random) 9.9

Urea 5.4, Ca+ 2.45, Mg 0.87, TSH 1.33

CT head showed no evidence of mass lesion, hemorrhage, hydrocephalus, subacute or chronic infarct.

 

Bell’s Palsy

Bell’s palsy is an isolated CNVII (facial nerve) paresis/paralysis as a result of acute inflammation and/or edema of the nerve. The onset is typically acute and progresses within hours, and while the cause is unknown, it is thought that the most likely etiology is viral (HSV, CMV, EBV).5

 

The facial nerve innervates the facial muscles, therefore, CNVII palsy presents with sudden onset unilateral facial paralysis, which can include: 1

  • Eyebrow sagging.
  • Inability to close the eye.
  • Disappearance of the nasolabial fold.
  • Drooping at the affected corner of the mouth, which is drawn to the unaffected side.2

 

CNVII also innervates the lacrimal glands, salivary glands, stapedius muscle, and taste fibres on the tongue, therefore, other associated features can include:1

  • Decreased tearing.
  • Hyperacusis
  • Loss of taste sensation on the anterior 2/3 of the tongue. 2

Figure 1: Anatomy of the facial nerve. 6

 

Risk Factors5

  • Pregnancy
  • Severe pre-eclampsia
  • Obesity
  • Hypertension
  • Diabetes
  • Upper respiratory illnesses

House-Brackmann Classification

The House-Brackmann classification seen below is used to determine severity of facial nerve dysfunction and has prognostic value. The lower the grade, the more likely a patient is to make a full recovery.7

Table 2: House-Brackmann classification of facial nerve dysfunction.3

 

Diagnosis

Diagnosis of Bell’s Palsy is considered a clinical diagnosis so there is no gold standard test, however, other causes of facial nerve palsies tend to have associated features and can be ruled out clinically. Most significantly, it is important to rule out life-threatening central lesions, such as ischemic/hemorrhagic stroke.4

Central vs. Peripheral Lesions

Central lesions – result in forehead sparing, as the facial nerve is innervated by ipsilateral and contralateral fibres from the motor cortex. Patients with forehead sparing need a head CT to rule out a central cause such as a stroke or mass!5

Peripheral lesions – the lesion is below the nucleus, and all the fibres innervating the facial nerve will be affected. Results in no forehead sparing.5

Figure 2: facial nerve lesion vs. supranuclear lesion with forehead sparing. 6

Other pertinent findings on history can include: rashes, arthralgias, or fevers, exposure to ticks (Lyme disease), and vesicular eruption (Ramsay Hunt Syndrome). In addition to a full cranial nerve and peripheral nerve exam, physical examination should involve assessment of the ear, tympanic membrane, and parotid gland for signs of AOM, cholesteatoma, or parotid tumor.6

Further investigations6

  • Lyme serology: if clinical suspicion for Lyme disease
  • Head CT: gradual onset of symptoms or forehead sparing
  • Neurology referral: bilateral palsies or no improvement

 

Treatment

Corticosteroids +/- antiviral is the choice of treatment for Bell’s Palsy. Studies have demonstrated that antivirals alone have no benefit, but in combination with corticosteroids there is a significantly increased benefit compared to corticosteroids alone. Patients should be started on corticosteroids within 72 hours of presentation for a course of at least 7 days. Physicians can also discuss with patients the potential benefit of adding an anti-viral.8

Eye care is an important consideration in these patients as a proportion will have incomplete eye closure, putting them at risk of corneal injury. Artificial tears during the day are recommended as well as taping the eyelid closed to prevent excessive dryness or trauma.9

With treatment, patients will see improvement within weeks and most experience full recovery within 3-4 months. 5

 

Case Conclusion

Our patient was started on valacyclovir 100mg TID x7 days and prednisone 60mg daily x 7 days for suspected Bell’s Palsy. Despite a normal CT, which helped to rule out central causes of facial paresis (stroke, subdural hematoma, brain tumor), the potential forehead sparing of the patient’s presentation presented concern for stroke. He was referred to Stroke Prevention Clinic and was seen the following day.

Neurology assessed the patient and appreciated that there was mild weakness in the forehead noted as a “reduction of wrinkles”, therefore, the diagnosis of Bell’s Palsy was confirmed. It was recommended that he continue the valacyclovir and prednisone course. It was also recommended that he patch the eye in the evenings and continue to use lubricating eye drops in the affected eye to prevent exposure keratitis.

Key Points

  1. Bell’s palsy results in unilateral facial nerve paresis/paralysis, without forehead sparing
  2. Associated symptoms may include: decreased tearing, hyperacusis, loss of taste
  3. No investigations are required; however, patients with true forehead sparing need a head CT as this finding is suggestive of a central lesion
  4. Patients with systemic symptoms, gradual onset, or bilateral symptoms should have further work-up
  5. Most cases will resolve in 3-4 months with treatment
  6. Treatment with corticosteroids +/- an antiviral for 7 days should be initiated within 72 hours of symptom onset

 

 

References

  1. Baugh, R., et al. 2013. Clinical Practice Guideline. Otolaryngology–Head and Neck Surgery, 149(3_suppl), pp.S1-S27. Retrieved from: https://journals.sagepub.com/doi/10.1177/0194599813505967?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed
  2. 2021. CRACKCast E105 – Brain and Cranial Nerve Disorders – CanadiEM. Retrieved from: https://canadiem.org/crackcast-e105-brain-cranial-nerve-disorders/
  3. House, J. and Brackmann, D., 1985. Facial Nerve Grading System. Otolaryngology–Head and Neck Surgery, 93(2), pp.146-147. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/3921901/
  4. McCaul, J., Cascarini, L., Godden, D., Coombes, D., Brennan, P. and Kerawala, C., 2014. Evidence based management of Bell’s palsy. British Journal of Oral and Maxillofacial Surgery, 52(5), pp.387-391. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/24685475/
  5. org.au. 2021. RACGP – A general practice approach to Bell’s palsy. Retrieved from: https://www.racgp.org.au/afp/2016/november/a-general-practice-approach-to-bell%E2%80%99s-palsy/#1
  6. Tiemstra JD, Khatkhate N. Bell’s palsy: diagnosis and management. Am Fam Physician. 2007 Oct 1;76(7):997-1002. PMID: 17956069. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/17956069/
  7. Yoo, M., et al. 2020. Evaluation of Factors Associated With Favorable Outcomes in Adults With Bell Palsy. JAMA Otolaryngology–Head & Neck Surgery, 146(3), p.256. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/31971554/
  8. Hato, N., et al. Efficacy of early treatment of Bell’s palsy with oral acyclovir and prednisolone. Otol Neurotol. 2003 Nov;24(6):948-51. Retrieved from: https://pubmed.ncbi.nlm.nih.gov/14600480/
  9. Ronthal, M. Greenstein, P. 2021. Bell’s palsy: Treatment and prognosis in adults. Retrieved from Uptodate October 26, 2021 from https://www.uptodate.com/contents/bells-palsy-pathogenesis-clinical-features-and-diagnosis-in-adults?search=bells%20palsy%20management&topicRef=5286&source=see_link

 

 

 

 

 

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EM Reflections – November 2019

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Thanks to Dr Paul Page for leading the discussions this month

Edited by Dr David Lewis 

Discussion Topics

  1. Popliteal Artery Thrombus

    • Closed loop communication is key to avoid possible poor outcomes with follow up
    • Relying on other specialties to arrange follow up with ED patients can result in error. Direct contact with specialty to arrange urgent follow up is the best approach
    • Also make sure patient is aware of plan

  1. Vertebral Artery Dissection / Thrombus

    • A thorough neurological exam and documentation is essential for vertigo presentation
    • Can’t walk, Can’t go home

  2. Elderly Delirium / Dementia with Sepsis

    • Majority of delirious patients are quiet and withdrawn, not hyperactive
    • For patients with dementia , get baseline functioning from family if possible

Popliteal Artery Thrombus

The full differential diagnosis should be considered in possible cases of DVT including Baker’s cyst, cellulitis, lymphedema, chronic venous insufficiency, superficial thrombophlebitis, popliteal venous or arterial aneurysm, peripheral vascular disease, enlarged lymph nodes compressing the veins, heterotopic ossification, hematoma, and muscle tears.

 

Ultrasound for Lower Extremity Deep Venous Thrombosis
Multidisciplinary Recommendations From the Society of Radiologists in Ultrasound Consensus Conference

It’s Not All Deep Vein Thrombosis: Sonography of the Painful Lower Extremity With Multimodality Correlation

 

Consultations and Referals

One of the most common ways for doctors to collaborate is through referral and consultation. Poor communication between referring physicians and consultants can lead to disruptions in care, delayed diagnoses, unnecessary testing, iatrogenic complications, and frustrated physicians and patients. Improving the referral-consultation process is one of the most effective ways of providing safer care and reducing the risk of medical-legal difficulties.

  • What is the question I want answered?
  • Who has the specialized knowledge and skill to answer it?
  • How urgent is the clinical situation?
  • Do I need advice from the consultant or would a transfer of care to the consultant be more appropriate in the specific circumstances?
  • Have all the appropriate steps been taken to this point?
  • Has the patient consented to the referral?

CMPA Guidance on Referrals

 

 

Vertebral Artery Dissection / Thrombus

See these SJRHEM Reflections post on the same subject:

EM Reflections – March 2017

EM Reflections – May 2019

 

and this post on the HINTS exam:

HINTS exam in Acute Vestibular Syndrome

 

 

 

 

Elderly Delirium / Dementia with Sepsis

The fluctuating presentation of delirium makes it difficult to recognize but we should be attentive to certain hallmarks, including alterations in attention and awareness and acute changes in cognition.  These can be associated with hallucinations or other perceptual disturbances.  Collateral information and family input can be critical in detecting changes from baseline function and cognition.  The more acute temporal course of delirium is important to distinguish from underlying dementia, which is itself one of the most important risk factors for delirium.  The most common presentation, the hypoactive form, is a quiet, subdued, withdrawn state.

The Seriousness of Deliriousness: Delirium in the ED

 

See this SJRHEM Rounds

ED Rounds – Delirium in the ED

 

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EM Reflections – May 2019

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Thanks to Dr Paul Page for leading the discussions this month

Edited by Dr David Lewis 

 

Discussion Topics

  1. Measles – Refresher
  2. Posterior Stroke – Beware of Mimics
  3. Missed Fracture – Distracting Injuries

 

Measles – Refresher

Measles has for many years been an infrequent diagnosis in our population. However falling herd immunity is resulting in cases presenting to Canadian ED’s.

Measles signs and symptoms appear around 10 to 14 days after exposure to the virus.

  • Fever
  • Dry cough
  • Runny nose
  • Sore throat
  • Conjunctivitis

 

Measles causes a red, blotchy (erythematous maculopapular) rash that usually appears first on the face and behind the ears, then spreads downward to the chest and back and finally to the feet. Koplick’s spots can appear 1-2 days before the rash. The rash appearance can be variable, discrete maculopapular or merging erythematous.

 

Visit emDocs.net for this great refresher on EMin5 – Measles

EM in 5: Measles

 

Posterior Stroke – Beware of Mimics

Stroke Mimics

  • Acute peripheral vestibular dysfunction (Don’t forget the HINTS exam)
  • Basilar migraine
  • Intracranial hemorrhage
  • SAH
  • Brain Tumour
  • Toxic or metabolic disturbances
  • Neuroinflammatory or chronic infectious disorders

Note that it is possible to be influenced by past experience with mimics, resulting in falsely diagnosing a mimic in the presence of a stroke.

Stroke Chameleons

Stroke chameleons are disorders that look like other disorders but are actually stroke syndromes

  • Bilateral thalamic ischaemia is such a disorder and may cause reduced consciousness level or a global amnesic syndrome
  • Bilateral occipital stroke may present as confusion or delirium
  • Infarcts limited to the medial vermis in medial posterior inferior cerebellar artery (PICA) territory usually cause a vertiginous syndrome that resembles peripheral vestibulopathy

A very useful BMJ review article on Posterior Stroke can be accessed here.

Be cautious of migraine diagnosis with history that is different to typical migraine presentation. Multiple visits should raise concerns. Importance of thorough neuro exam to find possible deficits that would raise suspicion for more serious pathology. In posterior stroke, special attention should be given to examining the visual fields.

 

Imaging in Stroke and TIA

See Rounds Presentation by Dr. Dylan Blacquiere (Neurologist)

Imaging Recommendations. Dr Jake Swan (Radiologist)

After meeting with Dr. Blacquiere and the ER Department regarding stroke management and SAH management, I’m recommending the following based on new literature and evolving management in “high risk” patients.

1) High risk TIA patients, such as those who had a profound motor / speech deficit that is resolving should have a CTA carotid / COW as well as their standard CT head.

2) SAH patients should have CT done prior to LP due to false positive LP rates.  If there is any question about vascular malformation / aneurysm, follow with a CTA. The CTA isn’t necessary for every headache patient, etc, just those with a positive bleed on the unenhanced CT.

 

The evidence is summarised in this recent paper – Imaging Recommendations for Acute Stroke and Transient Ischemic Attack Patients: A Joint Statement by the American Society of Neuroradiology, the American College of Radiology and the Society of NeuroInterventional Surgery

 

Missed Fracture – Distracting Injuries

Standard ATLS teaching, but this error still occurs……

Ensure a complete secondary survey is completed in all patients presenting with history of trauma.

Read the StatPearl Article and then do the MCQ test here

 

Trauma! Initial Assessment and Management

 

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EM Reflections – December 2017

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Thanks to Dr Joanna Middleton for leading the discussion this month and providing these tips and references.

Edited by Dr David Lewis 

 

Top tips from this month’s rounds:

Incomprehensible Patient – Delirium or Aphasia?

Pediatric Trauma

CME QUIZ

 

Take Home Points

  • Sudden onset language impairment should be assumed to be aphasia until proven otherwise
  • Aphasia is most commonly caused by CVA and usually has associated lateralising motor signs (but not always)
  • Aphasic patients will be able to perform non-verbal tasks normally
  • If in doubt involve telestroke / neurology early
  • Global aphasia can have a catastrophic outcome on quality of life. In selected patients, early thrombolysis can significantly improve prognosis.
  • The injuries sustained by children in chest trauma are frequently different from adults
  • Signs of shock in pediatric trauma can be subtle
  • Use evidence based guidelines e.g PECARN when considering CT for abdominal trauma
  • Elevated Tropinin or abnormal ECG suggest blunt cardiac injury

 

Incomprehensible Patient – Delirium or Aphasia?

Both can present with disorders of speech and language, however it is important to rapidly distinguish aphasia due to it’s association with stroke and the benefits of early thrombolysis.

Delirium, also known as acute confusional state, is an organically caused decline from a previously baseline level of mental function. It often has a fluctuating course, attentional deficits, and disorganization of behaviour including speech and language.

Aphasia is an impairment of language, affecting the production or comprehension of speech and the ability to read or write. Aphasia is always due to injury to the brain, most commonly from a stroke, but also trauma, tumour or infection.

 

The first tip here is to figure out how to describe the features of a patient’s language. How is the patient’s language produced and understood?

Are the words clearly enunciated (favoring aphasia) or slurred (favoring delirium)?

Is the patient’s speech grammatically correct (delirium) or lacking in appropriate syntax (aphasia)?

Is the patient’s prosody—or pattern of speech—fluent (delirium) or irregular (aphasia)?

Can the patient understand spoken language (delirium) or is there a major difficulty with following simple verbal/written commands (aphasia)?

Naming and repetition should also be assessed as part of any neurologic examination, but impairment in these modalities is not as useful in distinguishing delirium from aphasia.

The motor evaluation of inattention in a delirious patient involves testing for asterixis, either with arms and wrists fully extended or having the patient squeeze the fingers of the examiner (the “milk maid’s sign”). A delirious patient will struggle with these tasks, the extended hands may flap or the fingers may intermittently lose their grip. The aphasic patient, in contrast, may not have trouble with this.

Speak of the devil: Aphasia vs. delirium

 

Global Aphasia

  • Severe impairment of production, comprehension and repetition of language
  • Usually large CVA of left MCA
  • Usually associated with extensive perisylvian injury affecting both Broca’s and Wernicke’s areas
  • Usually accompanied by right hemiparesis and often a right visual field deficit (in right handed pt)
  • Patients with global aphasia can be shown to perform normally on nonverbal tasks such as picture matching, demonstrating they are not suffering from confusion or dementia

 

Stroke Thrombolysis – Indications and Contraindications Reminder

Patient Selection for Thrombolytic Therapy in AIS:

Inclusion criteria: Patients  >18 years of age with symptoms of AIS and a measurable neurological deficit with time of onset <4.5 h.

Exclusion criteria:

A. History

  • History of intracranial hemorrhage
  • Stroke, serious head injury or spinal trauma in the preceding 3 months
  • Recent major surgery, such as cardiac, thoracic, abdominal, or orthopedic in previous 14 days
  • Arterial puncture at a non-compressible site in the previous 7 days
  • Any other condition that could increase the risk of hemorrhage after rt-PA administration

B. Clinical

  • Symptoms suggestive of subarachnoid hemorrhage
  • Stroke symptoms due to another non-ischemic acute neurological condition such as seizure with post-ictal Todd’s paralysis or focal neurological signs due to severe hypo- or hyperglycemia
  • Hypertension refractory to antihypertensives such that target blood pressure <185/110 cannot be achieved
  • Suspected endocarditis

C. Laboratory

  • Blood glucose concentration below 2.7 mmol/L or above 22.2 mmol/L
  • Elevated activated partial-thromboplastin time (aPTT)
  • International Normalized Ratio (INR) greater than 1.7
  • Platelet count <100 x 109/L
  • Current use of direct thrombin inhibitors or direct factor Xa inhibitors with elevated insensitive global coagulation tests (aPTT for dabigatran, INR for rivaroxaban) or a quantitative test of drug activity (Hemoclot® for dabigatran, specific anti-factor Xa activity assays for rivaroxaban, apixaban and edoxaban). In this situation, endovascular treatment (thrombectomy) should be considered if patient eligible.

D. CT or MRI Findings

  • Any hemorrhage on brain CT or MRI
  • CT showing early signs of extensive infarction (hypodensity more 1/3 of cerebral hemisphere), or a score of less than 5 on the Alberta Stroke Program Early CT Score [ASPECTS], or MRI showing an infarct volume greater than 150 cc on diffusion-weighted imaging.

Relative contraindications for rt-PA therapy in AIS include the following:

  • Recent myocardial infarction with suspected pericarditis
  • Rapidly improving stroke symptoms
  • Pregnancy or post-partum period
  • Recent GI or urinary tract hemorrhage (within 21 days)

From Thrombosis Canada

Take Home Points

  • Sudden onset language impairment should be assumed to be aphasia until proven otherwise
  • Aphasia is most commonly caused by CVA and usually has associated lateralising motor signs (but not always)
  • Aphasic patients will be able to perform non-verbal tasks normally
  • If in doubt involve telestroke / neurology early
  • Global aphasia can have a catastrophic outcome on quality of life. In selected patients, early thrombolysis can significantly improve prognosis.

 

Pediatric Trauma

Some specific issues particular to pediatric trauma are highlighted:

Pediatric Chest Trauma

Children have compliant chests and thus sustain musculoskeletal thoracic injuries far less frequently (5% of traumas). However, due to this elasticity, the most common injury is a pulmonary contusion.

PITFALLS

Don’t expect traditional adult injury findings: Absence of chest tenderness, crepitus and flail chests does not preclude injury.

Bendy ribs – injury to internal organs with little external evidence

Lung contusions ~50% of chest trauma

Force transmitted to lung parenchyma – lung lacerations much less common <2%

 

Pediatric Abdominal Trauma

Beware: 20-30% of pediatric trauma patients with a “normal” abdominal exam will have significant abdominal injuries on imaging.

Any polytrauma patient with hemodynamic instability should be considered to have a serious abdominal injury until proven otherwise. Tachycardia primary reflex for kids in response to hypovolemia and it may be the only sign of shock.

HIGH RISK – Indications for CT

• History that suggests severe intra-abdominal injury e.g abrupt acceleration/deceleration, pedestrian vs vehicle, handlebar injury, fall from horse etc

• Concerning physical – tenderness, peritoneal signs, seatbelt sign or other bruising

• AST >200 or ALT >125

• Decreasing Hb or Hct

• Gross hematuria

• Positive FAST

PECARN 

The Pediatric Emergency Care Applied Research Network (PECARN) network derived a clinical prediction rule to identify children (median age, 11 years) with acute blunt torso trauma at very low risk for having intra-abdominal injuries (IAIs) that require acute intervention.

The prediction rule consisted of (in descending order of importance)

  • no evidence of abdominal wall trauma or seat belt sign
  • Glasgow Coma Scale score greater than 13
  • no abdominal tenderness
  • no evidence of thoracic wall trauma
  • no complaints of abdominal pain
  • no decreased breath sounds
  • no vomiting

The rule had a negative predictive value of 5,028 of 5,034 (99.9%; 95% confidence interval [CI] 99.7% to 100%), sensitivity of 197 of 203 (97%; 95% CI 94% to 99%), specificity of 5,028 of 11,841 (42.5%; 95% CI 41.6% to 43.4%), and negative likelihood ratio of 0.07 (95% CI 0.03 to 0.15).

Holmes JF et al. Identifying children at very low risk of clinically important blunt abdominal injuries. Ann Emerg Med 2013 Feb 4; [e-pub ahead of print]. (http://dx.doi.org/10.1016/j.annemergmed.2012.11.009)

 

Blunt Cardiac Injury

Largest pediatric case series of BCI – 184 patients – 95% had simple cardiac contusions. https://www.ncbi.nlm.nih.gov/pubmed/8577001

The clinical presentation of blunt cardiac injury varies. Mild injuries may present without objective findings, while some patients may have minor dysrhythmias.

A normal ECG and troponin I during the first 8 hours of hospital stay rules out blunt cardiac injury, and the negative predictive value of combining these 2 simple tests was 100%. https://www.ncbi.nlm.nih.gov/pubmed/12544898

 

Click image to link to full article

 

Traumatic Tricuspid Injuries

Location, location, location

RV posterior to sternum – blunt force elevates pressures resulting in rupture of chordae, papillary muscle injury or tear of leaflet

Most frequent associated injury:  pulmonary contusion

“The presence of a transient right bundle branch block in the setting of myocardial contusion is a described, but under-recognized occurrence.”

“Although an rsr’ in the right precordial leads may be normal in children, it’s combination with an abnormal frontal axis (“bifasicular block”) is always abnormal and suggest injury to the RV”

 

Episode 95 Pediatric Trauma

Take Home Points

  • The injuries sustained by children in chest trauma are frequently different from adults
  • Signs of shock in pediatric trauma can be subtle
  • Use evidence based guidelines e.g PECARN when considering CT for abdominal trauma
  • Elevated Tropinin or abnormal ECG suggest blunt cardiac injury

 

CME QUIZ

EM Reflections - Dec 17 - CME Quiz

EM Reflections – Dec 17 – CME Quiz

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ED Rounds – May 2016

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Imaging Decisions in Vascular Disease

Presented by Dr. Dylan Blacquiere (Neurologist)

 

 

Download (PDF, 11.39MB)

 

New Imaging Recommendations. Dr Jake Swan (Radiologist)

After meeting with Dr. Blacquiere and the ER department regarding stroke management and SAH management, I’m recommending the following based on new literature and evolving management in “high risk” patients.

1) High risk TIA patients, such as those who had a profound motor / speech deficit that is resolving should have a CTA carotid / COW as well as their standard CT head.

2) SAH patients should have CT done prior to LP due to false positive LP rates.  If there is any question about vascular malformation / aneurysm, follow with a CTA. The CTA isn’t necessary for every headache patient, etc, just those with a positive bleed on the unenhanced CT.

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