Tag Archives: neurology

An EM Approach to Syncope in Adults

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Medical Student Pearl

Samarth Fageria

Med 3

Memorial University of Newfoundland Class of 2024

Reviewed by Dr. J Gross

Copy Edited by Dr. J Vonkeman

Pdf Download: EMSJ An EM Approach to Syncope by SFargeria

 

Case

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

 

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

 

 

Differential Diagnosis of Syncope2

True Syncope

1. Reflex (autonomic hypersensitivity)

  • Vasovagal, carotid sinus hypersensitivity, situational

2. Orthostatic hypotension

  • Volume depletion, autonomic failure

3. Cardiac

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

Other Causes

1. Medication/ Drug-induced

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

2. Transient Loss of Consciousness (TLOC)

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

 

Background

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

Diagnostic Workup

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

 

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

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

 

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

Best Practice for Treatment

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

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

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

Case continued

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

Take Home Points

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

References

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

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EM Reflections – June 2020

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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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EM Reflections – May 2020

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Thanks to Dr Paul Page for leading the discussions this month

Edited by Dr David Lewis 

Discussion Topics

  1. Seizure disorder and safe discharge 

    • Consider risk factors for adverse outcome of discharge for all patients with recurrent seizure disorder
    • Use a checklist

  2. Competency and Capacity

    • Multidisciplinary consultation is paramount in deciding capacity
    • Special circumstances include vulnerable adults and pregnancy

  3. Testicular Torsion

    • Time = Testicle viability
    • Do not delay definitive management

Seizure disorder and safe discharge 

Case

A patient presents with recurrent seizures. They have a past medical history of schizophrenia and mental health delay. Following appropriate ED management with complete resolution of seizures and full recovery of the patient – what is the recommended disposition?

Seizure disorder is a common presentation to the Emergency Department. This EM Cases post provides an excellent summary for the ED approach to resolved seizures:

Ep 132 Emergency Approach to Resolved Seizures

 

ED approach to resolved seizures – Summary pdf

In this study – Ethanol withdrawal or low antiepileptic drug levels were implicated as contributing factors in 177 (49%) of patients. New‐onset seizures were thought to be present in 94 (26%) patients. Status epilepticus occurred in only 21 (6%) patients.

73% of patients were discharged.

 

 

 

Disposition

Most authors recommend admission for patients presenting with FIRST Seizure Episode. Patients with a past medical history of recurrent seizure disorder are more likely to be discharged than admitted.

However – this EBMedicine article cites an incidence of 19% seizure recurrence rate within 24 hours of presentation, which decreased to 9% if patients with alcohol related events or focal lesions on CT were excluded. They suggest, that at present, there is insufficient evidence to guide the decision to admit. They recommend this decision be tailored to the patient, taking into consideration the patient’s access to follow-up care and social risk factors (eg, alcoholism or lack of health insurance). Patients with comorbidities, including age > 60 years, known cardiovascular disease, history of cancer, or history of immunocompromise, should be considered for admission to the hospital.

 

Considerations For Safety On Discharge

Patients and their families should be counseled and instructed on basic safety measures to prevent complications (such as trauma) during seizures. For example, patients should be advised to avoid swimming or cycling following a seizure, at least until they have been reassessed by their neurologist and their antiepileptic therapy optimized, if needed. A particularly important point for seizure patients is education against driving. Although evidence remains controversial on this issue, there is general agreement that uncontrolled epileptic patients who drive are at risk for a motor vehicle crash, with potential injury or death to themselves and others. For this reason, most states do not allow these patients to drive unless they have been seizure-free on medications for 1 year. According to population survey data, 0.01% to 0.1% of all motor vehicle crashes are attributable to seizures

Competency and Capacity

Case

A young female patient with a history of polysubstance drug abuse presents with a psychotic episode. She refuses treatment. What are the competency and capacity implications? She is also pregnant. Does this change the the competency and capacity implications?

This LitFL post provides and excellent outline for Competency and Capacity in the ED:

Capacity and Competence

This article published by the RCPSC provides a useful outline from a Canadian perspective – with the following objectives.

  1. To clarify the role of decisional capacity in informed consent
  2. To discuss problems associated with decisional capacity and addiction

RCPSC – Decisional Capacity

 

 

Capacity in Pregnancy

Recommendations from the American College of Obstetricians and Gynecologists

On the basis of the principles outlined in this Committee Opinion, the American College of Obstetricians and Gynecologists (the College) makes the following recommendations:

  • Pregnancy is not an exception to the principle that a decisionally capable patient has the right to refuse treatment, even treatment needed to maintain life. Therefore, a decisionally capable pregnant woman’s decision to refuse recommended medical or surgical interventions should be respected.
  • The use of coercion is not only ethically impermissible but also medically inadvisable because of the realities of prognostic uncertainty and the limitations of medical knowledge. As such, it is never acceptable for obstetrician–gynecologists to attempt to influence patients toward a clinical decision using coercion. Obstetrician–gynecologists are discouraged in the strongest possible terms from the use of duress, manipulation, coercion, physical force, or threats, including threats to involve the courts or child protective services, to motivate women toward a specific clinical decision.
  • Eliciting the patient’s reasoning, lived experience, and values is critically important when engaging with a pregnant woman who refuses an intervention that the obstetrician–gynecologist judges to be medically indicated for her well-being, her fetus’s well-being, or both. Medical expertise is best applied when the physician strives to understand the context within which the patient is making her decision.
  • When working to reach a resolution with a patient who has refused medically recommended treatment, consideration should be given to the following factors: the reliability and validity of the evidence base, the severity of the prospective outcome, the degree of burden or risk placed on the patient, the extent to which the pregnant woman understands the potential gravity of the situation or the risk involved, and the degree of urgency that the case presents. Ultimately, however, the patient should be reassured that her wishes will be respected when treatment recommendations are refused.
  • Obstetrician–gynecologists are encouraged to resolve differences by using a team approach that recognizes the patient in the context of her life and beliefs and to consider seeking advice from ethics consultants when the clinician or the patient feels that this would help in conflict resolution.
  • The College opposes the use of coerced medical interventions for pregnant women, including the use of the courts to mandate medical interventions for unwilling patients. Principles of medical ethics support obstetrician–gynecologists’ refusal to participate in court-ordered interventions that violate their professional norms or their consciences. However, obstetrician–gynecologists should consider the potential legal or employment-related consequences of their refusal. Although in most cases such court orders give legal permission for but do not require obstetrician–gynecologists’ participation in forced medical interventions, obstetrician–gynecologists who find themselves in this situation should familiarize themselves with the specific circumstances of the case.
  • It is not ethically defensible to evoke conscience as a justification to attempt to coerce a patient into accepting care that she does not desire.
  • The College strongly discourages medical institutions from pursuing court-ordered interventions or taking action against obstetrician–gynecologists who refuse to perform them.
  • Resources and counseling should be made available to patients who experience an adverse outcome after refusing recommended treatment. Resources also should be established to support debriefing and counseling for health care professionals when adverse outcomes occur after a pregnant patient’s refusal of treatment.

Further Reading:

Ethically Justified Clinically Comprehensive Guidelines for the Management of the Depressed Pregnant Patient

How Do I Determine if My Patient has Decision-Making Capacity?

 

Testicular Torsion

Case

A 12 year old boy presents with scrotal discomfort in the early hours of the morning. The department is very busy and the waiting time to be seen is 4 hours. What triage category is this presenting complaint? If a diagnosis of torsion is considered, how quickly should definitive management be initiated?

Ramachandra et al. demonstrated through multivariate analysis of the factors associated with testicular salvage, that duration of symptoms of less than 6 h was a significant predictor of testicular salvage. They found that the median duration of pain was significantly longer in patients who underwent orchiectomy versus orchidopexy. Similar findings were seen with respect to time to operating room from initial presentation. They concluded that time to presentation is in fact the most important factor in determining salvageability of the testicle in testicular torsion. If surgical exploration is delayed, testicular atrophy will occur by 6 to 8 h, with necrosis ensuing within 8 to 10 h of initial presentation. Salvage rates of over 90% are seen when surgical exploration is performed within 6 h of the onset of symptoms, decreasing to 50% when symptoms last beyond 12 h. The chance of testicular salvage is less than 10%, when symptoms have been present for over 24 h

Factors influencing rate of testicular salvage in acute testicular torsion at a tertiary pediatric center.

Ramachandra P, Palazzi KL, Holmes NM, Marietti S

West J Emerg Med. 2015 Jan; 16(1):190-4.

[PubMed]

 

 

This study (Howe et al). confirmed the relationship between duration of torsion and testicle viability and also found a relationship between the degree of torsion

 

 

AAFP Review of Testicular Torsion: Diagnosis, Evaluation, and Management

 

 

 

 

 

 

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Hemiplegic Migraine

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Medical Student Clinical Pearl – January 2020

Alyssa BeLong, B.Sc.(Hon)

Dalhousie Medicine New Brunswick

M.D. Candidate, Class of 2021

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual

Case Presentation

A 45-year-old female presented with sudden-onset left-sided vision loss, right arm paralysis and auditory changes 24 hours ago. She subsequently developed a throbbing pain (6/10) behind her left eye which radiated over her scalp, with a sensation of water dripping down the back of her neck. Her symptoms resolved within 30 minutes except for ongoing headache and photophobia.

Differential Diagnosis

A variety of conditions may present with transient unilateral weakness or hemiplegia: (4)

  • Hemiplegic Migraine
  • Transient Ischemic Attack (TIA): Typically present with sudden onset of all symptoms rather than progression from one to another. A TIA is also less likely to present with headache, nausea, photophobia, phonophobia.
  • Brain Tumor: Typically present as progressive rather than transient neurologic symptoms.
  • Epilepsy with Post-Ictal Paralysis: Would expect paroxysmal symptoms at time of onset or change in level of consciousness as well as post-ictal confusion. Duration of symptoms also makes this unlikely.
  • Stroke-like Migraine Attacks After Radiation Therapy (SMART)
  • Other possible but rare/unlikely diagnoses include headache and neurologic deficits with cerebrospinal fluid lymphocytosis (HaNDL), CNS infection, Sturge-Weber syndrome as well as certain inherited disorders and metabolic disturbances.

Case Continued – History and Physical Exam

Clarification of visual field disturbance revealed a left homonymous hemianopia rather than loss of vision in the left eye. There was no change in speech or facial droop. There were no precipitating events and there were no alleviating or aggravating factors. The patient noted herself to be particularly stressed lately. She was otherwise healthy with a past medical history of migraines without aura many years prior. Family history was negative for thromboembolic events, she was not taking any medications and had no history of smoking or substance use.

On physical exam, the patient appeared well with all vital signs within normal limits. Cranial nerve exam was unremarkable apart from ongoing photophobia in her left eye. There was normal motor, strength, sensation, tone and reflexes bilaterally. There was no evidence of gait disturbance or dysdiadochokinesia.

Migraine Overview

Migraines typically present as severe episodic headaches often accompanied by photophobia, phonophobia and/or nausea, however presence of an aura can yield a variety of presentations. Migraines are currently thought to be neurologic in origin, although the exact pathophysiology remains unknown (2). Migraines were previously thought to be due to vascular changes, with vasodilation causing headache and vasoconstriction causing aura, however this theory is no longer viable (2).

Migraines affect 17% of women and 6% of men, with an overall prevalence of 12% (2). Migraines typically flow through four phases (2):

  1. Prodrome: Change in affect or vegetative symptoms 24-48hrs prior to onset of headache.
  2. Aura: Focal neurologic symptoms, including visual, sensory, language or motor disturbance.
  3. Headache: Often unilateral but can be bilateral, typically throbbing or pulsatile in quality, frequently accompanied by photophobia, phonophobia, nausea or vomiting.
  4. Postdrome: Sudden movement may trigger transient pain in location of the resolved headache.

While many types of migraines exist, 75% of migraines do not have an aura (2). Some patients also experience aura without headache. Factors thought to be involved in precipitation of migraine include stress, menstruation, fasting, weather, nitrates, wine and visual triggers (2, 3).  

Hemiplegic Migraine

  1. At least two attacks fulfilling criteria B and C
  2. Aura consisting of both of the following:
    1. Fully reversible motor weakness
    2. Fully reversible visual, sensory and/or speech/language symptoms
  3. At least two of the following four characteristics:
    1. At least one aura symptom spreads gradually over ≥5 minutes, and/or two or more symptoms occur in succession
    2. Each individual non-motor aura symptom lasts 5 to 60 minutes, and motor symptoms last <72 hours
    3. At least one aura symptom is unilateral
    4. The aura is accompanied, or followed within 60 minutes, by headache
  4. Not better accounted for by another ICHD-3 diagnosis, and transient ischemic attack and stroke have been excluded

Familial hemiplegic migraine requires one first or second degree relative to meet the above criteria for hemiplegic migraine. Sporadic hemiplegic migraine encompasses those who do not meet familial criteria. (4, 5).

  1.  

Treatment

Treatment of acute migraine in the emergency department follows similar principles to abortive management in an outpatient setting (6):

Abortive Agents

  • Triptans
    • Sumatriptan 6mg SC
  • Antiemetics / Dopamine Receptor Blockers
    • Metoclopramide 10mg IV, Prochlorperazine 10mg IV or Chlorpromazine 0.1mg/kg IV up to 25mg IV)
    • Diphenhydramine: given with parenteral antiemetics to prevent akathisia or dystonia. 12.5-25mg IV (q1h up to two doses)
  • Dihydroergotamine 1mg IV + Metoclopramide 10mg IV can be given if Metoclopramide monotherapy is ineffective.

  • Dexamethasone 10-25mg IV (or IM): Recommended in conjunction with the above treatments to lower risk of early headache recurrence.

In general, hemiplegic migraines can be treated the same as typical migraine with aura (4). Triptans and ergotamine are currently contraindicated due to their effect on vasoconstriction and theoretical risk of ischemic events, although this recommendation may change with evolving theory of migraine pathophysiology (4, 7).

Opioids are not recommended as first-line therapy and should not be routinely used in the acute management of migraine (6, 8).  

Case Continued – Treatment

The following medications were given in the emergency department:

  1. 10mg Metoclopramide IV
  2. 1mg Benztropine IV (for prevention of dystonia)
  3. 10mg Dexamethasone IV

Case Conclusion

The patient’s headache resolved with IV medications. She was advised to take it easy and consider scaling back on her shifts at work – a significant source of her stress. The patient was very pleased with her treatment and was discharged home.

Sources

  1. Donnelly K (2011). Homonymous Hemianopsia. In: Kreutzer J.S., DeLuca J., Caplan B. (eds) Encyclopedia of Clinical Neuropsychology. Springer, New York, NY. DOI: https://doi.org/10.1007/978-0-387-79948-3_739
  2. Cutrer F. Pathophysiology, clinical manifestations, and diagnosis of migraine in adults. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
  3. Martin VT, Behbehani MM (2001). Toward a rational understanding of migraine trigger factors. Medical Clinics of North America 85(4):911.
  4. Robertson C. Hemiplegic Migraine. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
  5. Headache Classification Committee of the International Headache Society (IHS) (2013). The International Classification of Headache Disorders, 3rd edition (beta version). Cephalalgia 33(9):629-808. DOI: 10.1177/0333102413485658
  6. Smith J. Acute Treatment of Migraine in Adults. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
  7. Russell MB, Ducros A (2011). Sporadic and familial hemiplegic migraine: pathophysiological mechanisms, clinical characteristics, diagnosis, and management. Lancet Neurology 10(5):457-70. DOI: 10.1016/S1474-4422(11)70048-5
  8. Friedman BW, West J, Vinson DR, Minen MT, Restivo A, Gallagher EJ (2015). Current management of migraine in US emergency departments: an analysis of the National Hospital Ambulatory Medical Care Survey. Cephalalgia 35(4):301.
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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 – October 2019

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Thanks to Dr Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis 

Discussion Topics

  1. Subarachnoid Hemorrhage

    • Misdiagnosis of SAH is not infrequent and usually results from common errors
      • Failure to appreciate the spectrum of clinical presentations associated with SAH
      • Failure to obtain a head CT or to understand its limitations in the diagnosis of SAH

  2. Spontaneous Bacterial Peritonitis

    • Like peritonitis but different…
    • Early iv albumin in selected case reduces mortality

Subarachnoid Hemorrhage

Headache is one of the most common reasons for presentation to the emergency department (ED), seen in up to 2% of patients. Most are benign, but it is imperative to understand and discern the life-threatening causes of headache when they present. Headache caused by a subarachnoid hemorrhage (SAH) from a ruptured aneurysm is one of the most deadly, with a median case-fatality of 27–44%. Fortunately, it is also rare, comprising only 1% of all headaches presenting to the ED

Approach to the Diagnosis and Management of Subarachnoid Hemorrhage

 

Missed Diagnosis

Missed Diagnosis of Subarachnoid Hemorrhage in the Emergency Department

Over 3 years there were 1603 patients hospitalized with a diagnosis of nontraumatic SAH; 1507 (94.0%) of these were admitted through the ED. Of the 176 EDs in the province, 147 (83.5%) admitted at least 1 patient with SAH, ranging from 1 to 49 per ED. Of these, 38 (25.9%) were in small hospitals, 93 (63.3%) in community hospitals, and 16 (10.9%) in teaching hospitals. With the exception of age, triage level, and hospital type, persons with missed SAH did not differ from those initially diagnosed with SAH.

A total of 150 (10.0%; 95% CI, 8.5 to 11.6) patients had an ED visit in the 14 days preceding their SAH admission. SAH was missed on a prior ED visit in 81 (5.4%; 95% CI, 4.3 to 6.6) cases.

The majority of missed cases were diagnosed with “migraine” or “headache” at the prior related visit

 

Spontaneous Bacterial Peritonitis

…spontaneous bacterial peritonitish…

similar but more subtle

The signs and symptoms of SBP are subtle compared with those seen in patients with bacterial peritonitis in the absence of ascites – By separating the visceral from the parietal peritoneal surfaces, ascites prevents the development of a rigid abdomen

 

Fever = >37.8

Who to test?

In addition, patients with ascites admitted to the hospital for other reasons should also undergo paracentesis to look for evidence of SBP. A low clinical suspicion for SBP does not obviate the need for testing

E.coli ~50%

 

Intravenous Albumin?

It is estimated that 12-25% of patients with ascites in the ED will have spontaneous bacterial peritonitis (SBP) but the classic triad of fever, abdominal pain, and worsening ascites is often absent (Borzio 2001)(Runyon 1988). With a mortality rate approaching 40%, rapid diagnosis and evidence-based treatment is critical in the management of patients presenting with SBP (Salerno 2013).

The 2012 AASLD Guidelines, based largely on the trial by Sort, et al., recommend that patients with ascitic fluid PMN counts greater than or equal to 250 cells/mm3 and clinical suspicion of SBP, who also have a serum creatinine >1 mg/dL, blood urea nitrogen >30 mg/dL, or total bilirubin >4 mg/dL should receive IV albumin (1.5 g/kg) within 6 hours of detection and 1.0 g/kg on day 3. (Class IIa, Level B)

Should You Give Albumin in Spontaneous Bacterial Peritonitis (SBP)?

 

 

Further Reading

Spontaneous Bacterial Peritonitis

 

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EM Reflections – June 2019 – Part 2

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Thanks to Dr. Joanna Middleton for leading the discussions this month

Edited by Dr David Lewis 

Discussion Topics

  1. When is a pregnancy not a pregnancy? (see part 1)
  2. Caustic Ingestions (see part 1)
  3. Transient Ischemic Attack – ED Questions

 

Transient Ischemic Attack – ED Questions

 

Transient Ischemic Attack (TIA): A brief episode of neurological dysfunction caused by focal brain, spinal cord or retinal ischemia, with clinical symptoms and without imaging evidence of acute infarction. Transient ischemic attack and minor stroke are the mildest form of acute ischemic stroke in a continuum that cannot be differentiated by symptom duration alone, but the former typically resolves within one hour.

https://www.strokebestpractices.ca/

 

Dual Anti-Platelet Therapy (DAPT)?

Patients who present within 48 hours of a suspected transient ischemic attack are at the highest risk for recurrent stroke

Uptodate – DAPT for high-risk TIA, defined as an ABCD2 score of ≥4

For CVA – ASA only unless already on ASA, then DAPT.  For minor CVA/TIA – DAPT

Hold Birth Control?

 

Admission?

Of all ischemic strokes during the 30 days after a first TIA, 42 percent occurred within the first 24 hours.

 

Stroke Assessment Pocket Cards

Saskatchewan TIA Referral Pathway

Saskatchewan TIA Patient Information Leaflet

 

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It’s all in your head, literally! – Seizures versus Psychogenic Non-epileptic Seizures

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It’s all in your head, literally! – Seizures versus Psychogenic Non-epileptic Seizures

Resident Clinical Pearl (RCP) May 2019

Allyson Cornelis – PGY2 FMEM Dalhousie University, Saint John NB

Copyedited by Renee Amiro

Reviewed by Dr. David Lewis

 

 

 

Background

When patients present with seizure like activity it can be difficult to distinguish true seizure/epilepsy from psychogenic non- epileptic seizures (PNES; also known as pseudoseizures). This task is made more difficult by the fact that 10-30% of patients with PNES can have true epilepsy as well4. The risks associated with diagnosing a psychogenic non-epileptic seizure as true seizure are mainly associated with administration of anti-epileptic drugs during both acute episodes and chronically, with the potential for associated side effects3-4,6. The most severe of these include sedation and even intubation if large enough doses are administered during an acute seizure episode. Additionally, there is added cost to both the patient and the healthcare system for continued use of medications and hospital admissions/investigations.

The underlying mechanism for PNES is believed to be psychiatric in origin, often attributed to conversion disorders, and patients are often not aware of their seizure like behaviours.

 

Risk factors for PNES include:

  1. childhood trauma
  2. PTSD
  3. depression
  4. anxiety
  5. personality disorders
  6. female gender

The challenge remains distinguishing between true seizures and PNES. There are various historical features and seizure characteristics that can assist in differentiating the two, though no one feature is confirmatory for seizure.

 

Distinguishing between PNES and true seizure3-8

Sign/symptom Seizure PNES
Eyes *open Closed, resist forced opening by examiner

 

*Fluttering
Seizure onset *abrupt Gradual
Awareness during seizure Not aware * awareness during episode
Influence of the presence of others Does not change seizure *May intensify or alleviate

 

activity may only occur/be triggered by the presence of others
Seizure activity Generalized tonic clonic

 

Synchronous

 

Stereotyped (first stiff and in extension, then develops synchronous clonic activity)

 May be asynchronous, asymmetrical, waxing and waning

Thrashing/violent

Pelvic thrusting
Post ictal *Confusion May recall events during their apparent unresponsive event
head One sided Side to side head turning during event
**incontinence common occasional
***Tongue biting Common, may be severe, usually on SIDE of tongue Occasional, rare to be severe, may be on tip of tongue or the lip
Post ictal corneal reflex impaired normal
Post ictal babinksi upgoing downgoing
Hand drop test negative Positive (patient moves hand away from face)
Response to sternal rub/nail bed pressure Usually nonresponsive May stop seizing, withdraw from stimuli
****Vital signs Desaturation more likely

Ictal apnea

Ictal bradycardia

  

 

 

*represents elements found to be most useful in distinguishing PNES and ES8

** incontinence has little utility in distinguishing between PNES and true seizure5

*** lateral tongue biting was 100% specific for true seizure vs 38% sensitivity and 75% specificity for any type of tongue bite5

****prospective trial7

 

Lab Values

No lab value has proven consistently useful for confirming seizure versus PNES.

A note on Prolactin:

The American Academy of Neurology released guidelines in 2005 recommending the use of prolactin following a seizure event2.

  1. Best when drawn 10-20 minutes after the event and can be used to differentiate between PNES and true seizure
  2. If >6 hours later prolactin should be at baseline levels
  3. Cannot be used to differentiate seizure from syncope
  4. Not applicable in status epilepticus or repetitive seizures

 

Bottom Line: 

  1. Challenging to differentiate between PES and true seizure and some patients can have both!
  2. No definitive distinguishing measure but eye opening, abrupt seizure onset, and confused post-ictal state can help point toward true seizure.
  3. A normal prolactin is more helpful in ruling out seizure while an elevation is non-specific and cannot be used to confirm seizure.

 

References

  1. Abubakr A, Wambacq I. Diagnostic value of serum prolactin levels in PNES in the epilepsy monitoring unit. Neurol Clin Pract. 2016 Apr; 6(2): 116–119.
  2. Graham L. AAN releases guidelines for the use of serum prolactin assays in diagnosing epileptic seizures. Am Fam Physician. 2006. Apr; 73(7): 1284.
  3. Huff JS, Murr N. Seizure, Pseudoseizures. [Updated 2018 Oct 27]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2018 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK441871/
  4. Mellers JDC. The approach to patients with “non-epileptic seizures.” Postgrad Med J. 2005 Aug;81(958):498-504.
  5. Nowacki T, Jirsch JD. Evaluation of the first seizure patient: Key points in the history and physical examination. 2017 Jul;49:54-63. doi: 10.1016/j.seizure.2016.12.002. Epub 2016 Dec 8.
  6. Panayiotopoulos CP. The Epilepsies: Seizures, Syndromes and Management. Oxfordshire (UK): Bladon Medical Publishing; 2005. Chapter 1, Clinical Aspects of the Diagnosis of Epileptic Seizures and Epileptic Syndromes. Available from: https://www.ncbi.nlm.nih.gov/books/NBK2609/
  7. Pavlova M, Abdennadher M, Singh K, Katz E, Llewellyn N, Zarowsly M, et al. Advantages of respiratory monitoring during video- EEG evaluation to differentiate epileptic seizures from other events. Epilepsy Behav. 2014 Mar; 32: 142–144.
  8. Syed Tu, LaFrance WC Jr, Kahriman ES, Hasan SN, Rajasekaran V, Gulati D, et al. Can semiology predict psychogenic nonepileptic seizures? A prospective Ann Neurol.2011 Jun;69(6):997-1004
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EM Reflections – October 2017

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Thanks to Dr Joanna Middleton for leading the discussion this month

Edited by Dr David Lewis

Top tips from this month’s rounds:

  1. Imaging reports can underestimate the clinical impact of an incidental finding

  2. Neuro ICU in the Emergency Department?

 

Imaging reports can underestimate the clinical impact of an incidental finding

Not all benign conditions have a benign outcome. A CT report will occasionally underestimate the clinical impact of an incidental finding. Its always worth reviewing the images yourself.

For example – a report might read – “No acute bleed or infarct, incidental finding of frontal bone fibrous dysplasia” –  may sound innocuous and unrelated to the patient’s headache, until you review the scans yourself:

 

Fibrous dysplasia is a benign condition which can present with new craniofacial asymmetry. Whilst the condition itself may be benign, the location and speed of growth can result in symptoms, especially headache and even cranial nerve compression.

Clinical Guidelines for managing craniofacial fibrous dysplasia

 

Neuro ICU in the Emergency Department?

 

Management of Intracranial Hemorrhage in the Emergency Department can be complex. The diagnosis is usually straightforward with CT (providing it has been considered as a possibility – subarachnoid hemorrhage can present with syncope alone) and the broad category of bleed determined by the history, patient age, CT appearance, etc.

ED Management will depend on the category of bleed (Primary ICH, Subdural, Epidural, Traumatic SAH, Spontaneous SAH).

From ALIEM.com, click here for the full article

 

Initial management of intracranial hemorrhage can be simplified / summarized as follows:

Airway – ET Intubation if GCS < 9

Breathing – Ventilate if GCS < 9 (SaO2 >94%, ETCO2 35-45 mmHg)

Circulation

  1. Stop the bleeding
    1. Neurosurgery (see here for indications)
    2. Reverse anticoagulation
    3. ?Tranexamic acid
  2. Maintain an adequate cerebral perfusion pressure (CPP) to ensure adequate tissue oxygenation
    1. CPP = Mean Arterial Pressure (MAP) – Intracranial Pressure (ICP)
      1. Seems simple enough? – ensure the patient’s blood pressure is high enough to overcome the ICP
    2. However, the optimal CPP following acute brain injury is not known (general consensus suggest 50-70 mmHg)
      1. In the normal brain CPP is maintained by autoregualtion
      2. Autoregulation is less effective after brain injury
      3. If the CPP is too low brain hypoxia occurs
      4. If the CPP is too high there may be a risk of hematoma expansion
    3. However, it’s not easy to measure the ICP
      1. Methods of non-invasive ICP estimation:
        1. Level of consciousness
        2. Papilledema
        3. CT appearances
        4. Transcranial doppler
        5. Sonographic Optic Nerve Sheath Diameter
        6. Lots of others
        7. None of these are perfect
      2. Invasive ICP measurement
        1. External Ventricular Drain – Neurosurgical procedure
        2. Setting up the EVD and measuring ICP requires experienced nursing staff (see below)
    4. Even measuring the MAP is not without its own problems in the ED
      1. MAP = (Systolic BP + 2(Diastolic BP))/3
      2. However non invasive measurement of MAP (based on SBP and DBP peripheral sphygmomanometry) is not accurate.
      3. An accurate measurement of MAP requires invasive monitoring via an arterial line.
    5. Assuming that we are able to accurately measure ICP and MAP, there is then the question of how to adjust these values reliably via therapeutic interventions.
      1. ICP Management (Normal = 0-15, Goal < 20)
        1. Patient position, head up
        2. Sedation and paralysis, if patient aggitated
        3. Mannitol – potential risk of acute kidney failure in prolonged use
        4. Hyperventilation – will also reduce cerebral blood flow – so PaCO2 no lower than 35 mmHg
        5. CSF Drainage : 
        6. Hypothermia
      2. MAP Management
        1. IV Fluid (crystalloid vs colloid?)
        2. Diuretics / Antihypertensives vs Inotropes
        3. A very detailed guide to blood pressure management in stroke can be viewed here: BP-Stroke

I suspect that most emergency physicians/nurses are wondering whether this level of care falls within their remit. In most hospitals the answer will be NO, these cases are stabilised and managed in an Intensive Care Unit. However, there are occasions when this level of care is required prior to transfer to another unit/hospital, in which case it is likely that the care will be directed by the local neurosurgeon / neurointensivist and the receiving specialists.

EVD Drainage System and ICP Monitoring

 

Suggest ICP Protocol from Vancouver General ICU

Download (PDF, 110KB)

 

 

CME QUIZ

 

ED Reflections - CME Quiz - Oct 2017

ED Reflections – CME Quiz – Oct 2017

 

 

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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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HINTS exam in Acute Vestibular Syndrome

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The eyes are the window to the brain: HINTS exam in acute vestibular syndrome

Resident Clinical Pearl

Jacqueline MacKay, PGY2 iFMEM, Dalhousie University, Saint John, New Brunswick

Reviewed by: Dr Joanna Middleton and Dr David Lewis

 

Acute vestibular syndrome (AVS) is the rapid onset of vertigo, nausea/vomiting, and gait unsteadiness combined with head-motion intolerance and nystagmus that lasts days-weeks. Often these dizzy patients have a benign, self-limiting cause for their symptoms, however it is estimated that up to 25% of AVS presentations to emergency departments are due to posterior circulation infarcts.

 

CT scan has low sensitivity for identifying acute infarct, especially in the posterior fossa. MRI is not always available, and will often have false-negative results in acute posterior circulation strokes. Are bedside predictors able to identify central causes of acute vestibular syndrome?

 

The HINTS exam is a bedside test that carefully assesses eye movements. HINTS stands for Head Impulse-Nystagmus-Test of Skew.

Untitled

Head Impulse: test of vestibulo-ocular reflex function. A normal Head Impulse test (HIT) strongly indicates a central localization for the AVS. An abnormal HIT usually indicates a peripheral lesion.

Untitled1

Nystagmus: bilateral nystagmus which changes direction on eccentric gaze or primarily vertical nystagmus is predictive of central pathology.

Untitled2

Skew Deviation: a vertical ocular misalignment that is assessed by alternate cover testing

Watch the video! A short and excellent description of the exam with good examples of normal and abnormal:

https://vimeo.com/133033089 (Courtesy of EMCrit)

 

Interpretation

A benign HINTS exam is defined as abnormal HIT + direction-fixed horizontal nystagmus + absent skew.

A dangerous HINTS exam is defined as any one of:

  • Normal/untestable HIT
  • or direction-changing horizontal nystagmus present/untestable
  • or skew deviation present/untestable

(Untestable refers to those patients with obvious oculomotor pathology or lethargy in whom the tests were unable to be completed).

 

The acronym INFARCT can be used to remember what constitutes a dangerous HINTS exam:

Impulse Normal

Fast-phase Alternating

Refixation on Cover Test.

 

A dangerous HINTS result was found to be 100% sensitive and 96% specific for the presence of a central lesion when applied to patients with acute vestibular syndrome (continuous vertigo and nystagmus) with at least one stroke risk factor. In fact, the HINTS exam is more accurate than MRI to diagnose stroke in patients with AVS in the first 48 hours!

 

Bottom Line:

In the acutely dizzy patient with at least one stroke risk factor, remember the HINTS to an INFARCT

 

References:

  1. Kattah, J. C., Talkad, A. V., Wang, D. Z., Hsieh, Y. H., & Newman-Toker, D. E. (2009). HINTS to diagnose stroke in the acute vestibular syndrome three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke, 40(11), 3504-3510. DOI: 10.1161/STROKEAHA.109.551234
  2. EMCrit http://emcrit.org/misc/posterior-stroke-video/ – original source of the videos is http://novel.utah.edu/Newman-Toker/collection.php

Update:

GRACE 3 (March 2023) –Guidelines for reasonable and appropriate care in the emergency department 3 (GRACE-3): Acute dizziness and vertigo in the emergency department.

Excellent GRACE 3 Summary from Skeptics – SGME:

SGEM#403: Unos, Dos, Tres – Vertigo: The GRACE-3 Guidelines

 

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