Author Archives: David Lewis

PoCUS in Pericardial Effusion

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Medical Student Clinical Pearl – October 2019

 

Alex Pupek

Faculty of Medicine
Dalhousie University
CC4
Class of 2020

Reviewed and Edited by Dr. David Lewis

 

Case

A 70F with a history of bladder CA, HTN and 4.9cm AAA presented to the Emergency Department (ED) and was Triaged as Level 3 with a chief complaint of generalized weakness. Initial assessment was significant for hypotension and low-grade fever with dysuria elicited on history; she was started on Ceftriaxone with a working diagnosis of urosepsis. Bloodwork and imaging studies were sent to rule out other potential sources of infection.

She had a mild leukocytosis of 12.4, pH of 7.23 and a lactate of 5.0. Point-of-care urinalysis was unremarkable. The chest x-ray revealed an enlarged cardiothoracic ratio of 0.62 compared to 0.46 ten months previously, concerning for a pericardial effusion.

Upon reassessment, the patient appeared unwell with slight mottling to the skin, cool extremities and tenuous blood pressure; point of care ultrasound revealed a large pericardial effusion.  Interventional cardiology was paged; the patient was moved to the trauma area and an emergent pericardiocentesis was performed: 360cc of bloody fluid was removed. The pericardial drain was left in situ.

Post-procedure bloodwork included a troponin of 216 and CK of 204. The patient was admitted to the Cardiac Care Unit and discharged within a week’s time.

 

Pericardial Effusions and The Role of Point-of-Care Ultrasound (POCUS)

The normal pericardial sac contains up to 50 mL of plasma ultrafiltrate [1]. Any disease affecting the pericardium can contribute to the accumulation of fluid beyond 50mL, termed a pericardial effusion. The most commonly identified causes of pericardial effusions include malignancy and infection (Table 1).

 

Table 1 – UpToDate, 2019 – Diagnosis and Treatment of Pericardial Effusions

 

Evaluation of the pericardium with point-of-care ultrasound includes one of four standard views: parasternal long axis, parasternal short axis, subxiphoid and apical (Figure 1). A pericardial effusion appears as an anechoic stripe or accumulation surrounding the heart. Larger effusions may completely surround the heart while smaller fluid collections form only a thin stripe layering out posteriorly with gravity. Seen most commonly post-cardiac surgery, pericardial effusions may be loculated and compress only a portion of the heart. [1,2] (Table 2)

Figure 1[1]

Table 2 [2]

 

Both the pericardial fat pad and pleural effusions can be mistaken for pericardial effusions. The parasternal long-axis view is most helpful to accurately define the effusion with the descending aorta, posterior to the mitral valve and left atrium, serving as a landmark: the posterior pericardial reflection is located anterior to this structure. Fluid anterior to the posterior pericardial wall is pericardial, whereas a pleural effusion will lie posterior. The pericardial fat pad is an isolated dark area with bright speckles, located anteriorly; unlike fluid, it is not gravity dependent. Rather than competing with the cardiac chambers for space within the pericardial sac, the fat pad moves synchronously with the myocardium throughout the cardiac cycle. [1,2] (Figure 2)

Figure 2[1]

A pericardial effusion discovered on POCUS in the ED may be mistaken for tamponade, leading to inappropriate and invasive management in the form of pericardiocentesis.[2]

Patient tolerance of pericardial effusions depends on the rate by which they accumulate. As little as 150-200 mL of rapidly accumulating effusion can cause tamponade whereas much larger amounts of slowly accumulating fluid can be well tolerated. Pericardial effusions formed gradually are accommodated by adaptations in pericardial compliance. A tamponade physiology is reached once the intrapericardial pressure overcomes the pericardial stretch limit.[2] (Figure 3)

Figure 3[2]

The core echocardiographic findings of pericardial tamponade consist of:

  • a pericardial effusion
  • diastolic right ventricular collapse (high specificity)
  • systolic right atrial collapse (earliest sign)
  • a plethoric inferior vena cava with minimal respiratory variation (high sensitivity)
  • exaggerated respiratory cycle changes in mitral and tricuspid valve in-flow velocities as a surrogate for pulsus paradoxus

In the unstable patient with clinical and echocardiographic findings of tamponade, an emergent pericardiocentesis is indicated.[2]

A retrospective cohort study of non-trauma emergency department patients with large pericardial effusions or tamponade, ultimately undergoing pericardiocentesis, found that effusions identified by POCUS in the ED rather than incidentally or by other means saw a decreased time to drainage procedures, (11.3 vs 70.2 hours, p=0.055).[3]

Point of care ultrasound is a valuable tool during the initial evaluation of the undifferentiated hypotensive emergency department patient but should be interpreted judiciously and within clinical context to avoid unnecessary emergency procedures.

Additional Images

From GrepMed



 




echocardiogram-pericardial-tamponade-alternans-effusion


 




References


    

  1. Goodman, A., Perera, P., Mailhot, T., & Mandavia, D. (2012). The role of bedside ultrasound in the diagnosis of pericardial effusion and cardiac tamponade. Journal of emergencies, trauma, and shock, 5(1), 72.
    2. 

  2. Alerhand, S., & Carter, J. M. (2019). What echocardiographic findings suggest a pericardial effusion is causing tamponade?. The American journal of emergency medicine, 37(2), 321-326.
    3. 

  3. Alpert, E. A., Amit, U., Guranda, L., Mahagna, R., Grossman, S. A., & Bentancur, A. (2017). Emergency department point-of-care ultrasonography improves time to pericardiocentesis for clinically significant effusions. Clinical and experimental emergency medicine, 4(3), 128.
    4. 



 

			

		

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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










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. 

  2. Aura consisting of both of the following:

      

    1. Fully reversible motor weakness
      2. 

    2. Fully reversible visual, sensory and/or speech/language symptoms
      3. 

    

    3. 

  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. 

    2. Each individual non-motor aura symptom lasts 5 to 60 minutes, and motor symptoms last <72 hours
      3. 

    3. At least one aura symptom is unilateral
      4. 

    4. The aura is accompanied, or followed within 60 minutes, by headache
      5. 

    

    4. 

  4. Not better accounted for by another ICHD-3 diagnosis, and transient ischemic attack and stroke have been excluded
    5. 



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.  
    2. 






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. 

  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. 

  3. Martin VT, Behbehani MM (2001). Toward a rational understanding of migraine trigger factors. Medical Clinics of North America 85(4):911.
    4. 

  4. Robertson C. Hemiplegic Migraine. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
    5. 

  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. 

  6. Smith J. Acute Treatment of Migraine in Adults. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on December 23rd, 2019.)
    7. 

  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. 

  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.
    9. 




			

		

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EM Reflections – January 2020


				

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Thanks to Dr Paul Page for leading the discussions this month


Edited by Dr David Lewis 


 




Discussion Topics


    

  1. 

    Esophageal Perforation
    

    2. 

  2. 

    Neonatal Status Epilepticus
    

    3. 





Esophageal Perforation – Boerhaave syndrome


A spontaneous perforation of the esophagus that results from a sudden increase in intraesophageal pressure combined with negative intrathoracic pressure (eg, severe straining or vomiting) otherwise known as Effort Rupture.


Difficult diagnosis in first few hours due to nonspecific early symptoms. But, delayed diagnosis results in significant mortality. Diagnosis and surgery within 24 hours carries a 75% survival rate but drops to approximately 50% after a 24-hour delay and approximately 10% after 48 hours.


25 to 45 percent of patients have no clear history of vomiting, and those that do are often confusing with pain sometimes preceding vomiting due to coexisting pathologies e.g gastroenteritis, gastritis, pancreatitis etc.




Clinical manifestations — The clinical features of Boerhaave syndrome depend upon the location of the perforation (cervical, intrathoracic, or intra-abdominal), the degree of leakage, and the time elapsed since the injury occurred. Patients with Boerhaave syndrome often present with excruciating retrosternal chest pain due to an intrathoracic esophageal perforation. Although a history of severe retching and vomiting preceding the onset of pain has classically been associated with Boerhaave syndrome, approximately 25 to 45 percent of patients have no history of vomiting. Patients may have crepitus on palpation of the chest wall due to subcutaneous emphysema. In patients with mediastinal emphysema, mediastinal crackling with each heartbeat may be heard on auscultation especially if the patient is in the left lateral decubitus position (Hamman’s sign). However, these signs require at least an hour to develop after an esophageal perforation and even then are present in only a small proportion of patients. Within hours of the perforation, patients can develop odynophagia, dyspnea, and sepsis and have fever, tachypnea, tachycardia, cyanosis, and hypotension on physical examination. A pleural effusion may also be detected.


Patients with cervical perforations can present with neck pain, dysphagia or dysphonia.  Patients may have tenderness to palpation of the sternocleidomastoid muscle and crepitation due to the presence of cervical subcutaneous emphysema.


Patients with an intra-abdominal perforation often report epigastric pain that may radiate to the shoulder. Patients may also report back pain and an inability to lie supine or present with an acute (surgical) abdomen. As with intrathoracic perforation, sepsis may rapidly develop within hours of presentation.


Laboratory findings — Laboratory evaluation may reveal a leukocytosis. While not part of the diagnostic workup for an esophageal perforation, pleural fluid collected during thoracentesis may contain undigested food, have a pH less than 6, or have an elevated salivary amylase level.


UptoDate


 




Chest X-ray  showing a pneumomediastinum (closed arrows) and silhouette sign over the right heart border (open arrow).


Case Presentation 1


Case Presentation 2


 


Take Home


    

  • The diagnosis of Boerhaave syndrome should be suspected in patients with severe chest, neck, or upper abdominal pain after an episode of severe retching and vomiting or other causes of increased intrathoracic pressure and the presence of subcutaneous emphysema (crepitus) on physical exam.
    • 

  • While thoracic and cervical radiography can be supportive of the diagnosis, the diagnosis is established by contrast esophagram or computed tomography (CT) scan
    • 

  • Delayed diagnosis is associated with high mortality
    • 

  • Radiological signs develop over time, repeat imaging is often useful when considering this diagnosis
    • 





 


Neonatal Status Epilepticus


When an altered few-day-old baby is brought into the ED, other than requesting immediate pediatric support, opening PediStat on you phone and trying to keep calm – consider the causes of altered LOC in pediatrics – Think VITAMINS:


V – Vascular (e.g. arteriovenous malformation, systemic vasculitis)


I – Infection (e.g. meningoencephalitis, overwhelming alternate source of sepsis)


T – Toxins (e.g. environmental, medications, contaminated breast milk)


A – Accident/abuse (e.g. non-accidental trauma, sequelae of previous trauma)


M – Metabolic (e.g. hypoglycemia, DKA, thyroid disorders)


I – Intussusception (e.g. the somnolent variant of intussusception, with lethargy)


N – Neoplasm (e.g. sludge phenomenon, secondary sepsis, hypoglycemia from supply-demand mismatch)


S – Seizure (e.g. seizure and its variable presentation, especially subclinical status epilepticus)


 


Altered Mental Status in Children




 


What elements are highly suggestive of true seizures?


    

  1. Lateralized tongue biting (high specificity)
    2. 

  2. Flickering eyelids, deviation of gaze
    3. 

  3. Dilated pupils with a blank stare
    4. 

  4. Lip smacking
    5. 

  5. Increased heart rate and blood pressure, desaturations in pulse oximetry during event
    6. 



Management of Pediatric Seizures




Newborn Resuscitation




 




Elemental EM: Pediatric Intubation




 

			

		

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Trauma Reflections – December 2019


				

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Thanks to Dr. Andrew Lohoar and Sue Benjamin for leading the discussions this month




 


Major points of interest:


 


A) How are we doing with calling Trauma Codes for qualifying cases?


In the past year, for cases qualifying for trauma team activation, Trauma Codes were called 80% of time.


If a Trauma Code was called, trauma note use increased to 90% and time to disposition to an ICE setting was significantly decreased.


Please review the attached updated SIMPLIFIED activation criteria.


 




B) End of year AWARDS –  the “Crashys”


    

  1. ‘Crashy’ for the Busiest TTL of the Year with 17 cases …
    2. 



P “I don’t see weak and dizzy patients” P


 


    

  1. ‘Crashy’ for the Most Trauma Intubations of the Year with 7 …
    2. 



C “If he’s not move’n, I’m a tube’n” A


 


    

  1. ‘Crashy’ for the Most Trauma Chest Tubes of the Year with 3 …
    2. 



T “Fetch me my scalpel” W


 


        Congratulations to all   (Sorry, there is no monetary gift associated with these awards!)     


 


C) Head injury, combative and on methadone – this should be easy..


Not really. Post-intubation sedation and analgesia can be challenging. Key is to avoid starting medications that could potentially drop blood pressure at very high infusion rates, but we need sedation and analgesia promptly. Under-dosing analgesic is often the reason adequate sedation is a struggle. Bolus, then increase infusion. Repeat.


 


D) End-tidal CO2 is an important vital sign


Especially in intubated patients.


 


E) Pediatric head injury transfer for imaging


Reassessing these patients on arrival, prior to CT, may influence management.


If there has been worsening in clinical condition, neurosurgery can be pre-alerted.


If there has been complete resolution of symptoms, CT scan may be deemed unnecessary.


 


F) “Clearing C-spine” can’t be done remotely..


CT C-spine is not 100% sensitive for ruling out injury. If radiologist reports there is no significant abnormality seen, it is a CLINICIAN”S responsibility to examine the neck before removing c-collar. If there is discrepancy (elevated pain, tenderness or neurologic symptoms/signs) or inability to cooperate with exam, leave the collar in place.


Make it known c-spine has not been cleared.


 


G) Pelvic binders are not used to ‘treat’ the pelvic fracture


They are used to treat any hemodynamic instability caused by the fracture. If a patient is stable or has a pelvic fracture that is not likely causing significant bleeding, the binder can likely be loosened or removed.


A pelvic binder can exacerbate some fractures, such as lateral compression fractures. Orthopedics should be assisting with this decision.


 


H) ‘Shock’ dosing of sedatives


Hypotension is not good for damaged neurons.


Shocked patients should have 1/2 dose of induction agents during RSI.


RSI Drugs




ADULT Rapid Sequence Intubation and Post-Intubation Analgesia and Sedation for Major Trauma Patients – NB Trauma




 

			

		

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Tardive Dyskinesia in an Emergency Setting


				

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Medical Student Clinical Pearl – October 2019




Faith Moore




Faculty of Medicine


Dalhousie University


CC3




Class of 2021


Reviewed and Edited by Dr. David Lewis








Case 


A 48-year-old female was brought to the emergency department by EMS after developing dystonia that morning, a couple hours earlier, following a restless night. The dystonia had begun affecting her arms, torso and buccal region, but eventually moved to also involve her legs. She had a history of recurrent tardive dyskinesia for the past 20 years since taking stelazine and developing tardive dystonia. She was switched to olanzopine after developing dystonia and stayed on it until two months ago. Her citalopram and clozapam dosing had been increased two weeks ago, and she had also started Gingko biloba extract two weeks ago. She had started Nuplazid 3 days ago.


Upon exam she was diaphoretic with no other abnormal findings other than dystonia affecting the entire body.






Tardive Dyskinesia


Pathophysiology


    

  • 

      

    • Tardive dyskinesia is a hyperkinetic movement disorder that is associated with the use of dopamine receptor-blocking medications.1 The exact mechanism is under debate, but the main hypotheses include an exaggerated response by dopamine receptors due to a chronic dopamine blockade, oxidative stress, gamma-aminobutyric acid (GABA) depletion, cholinergic deficiency, altered synaptic plasticity, neurotoxicity and defective neuroadaptive signaling. 2 The most accepted theory of the mechanism is that the chronic dopamine blockade caused by the dopamine receptor-blocking medications results in a hypersensitivity of the receptors, specifically at the basal ganglia. 1
      • 

    • The medications that are known to have the possibility to cause tardive dyskinesia include antipsychotic drugs, anticholinergic agents (ex. Procyclidine), antidepressants, antiemetics (ex. Metoclopramide), anticonvulsants, antihistamines, decongestants (ex. pseudoephedrine and phenylephrine), antimalarials, antiparkinson agents, anxiolytics, biogenic amines, mood stabilizers and stimulants.1
      • 

    

    • 



Who is most at risk?


    

  • 

      

    • The medications that are the most common culprits are first- and second-generation antipsychotics and metoclopramide. The incidence of tardive dyskinesia from chronic first-generation antipsychotic exposure is 5-6% 3, and is 4% for second generation antipsychotics 4. There is no prospective research on chronic metoclopramide use and the risk for tardive dyskinesia at this point and time5, but a study in the UK in 1985 showed 1 case of tardive dyskinesia for every 35 000 prescriptions6.

        

      • Most prominent risk factors

          

        • Old age5
          • 

        • Chronic exposure5
          • 

        • Patients who develop extrapyramidal symptoms while on antipsychotic drugs.7
          • 

        

        • 

      

      • 

    

    • 



Signs and Symptoms


    

  • 

      

    • 

        

      • Repetitive involuntary body movements that may involve the face, tongue, eyes, arms, torso and legs
        • 

      

      • 

    

    • 







Diagnosis


    

  • 

      

    • The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) classifies tardive dyskinesia as “involuntary movements (lasting at least a few weeks) generally of the tongue, lower face and jaw, and extremities (but sometimes involving the pharyngeal, diaphragmatic, or trunk muscles), developing in association with the use of a neuroleptic medication for at least a few months” and that persists for at least one month after the medication is stopped.8
      • 

    

    • 



Differential Diagnosis


    

  • 

      

    • Acute dyskinesia
      • 

    • Akathisia
      • 

    • Parkinsonism and tremor
      • 

    • Perioral tremor
      • 

    • Stereotypies and mannerisms
      • 

    • Spontaneous or idiopathic dyskinesias
      • 

    • Isolated dystonia
      • 

    • Primary movement disorders
      • 

    • Chorea from systemic causes 9
      • 

    

    • 



Key Questions for History and Physical


    

  • 

      

    • Are the movements voluntary?
      • 

    • Is there an accompanied feeling of restlessness?

        

      • If yes, might point towards akathisia.
        • 

      

      • 

    • When did these movements began?
      • 

    • What is the body distribution of the involuntary movements?
      • 

    • Are there any extrapyramidal signs and symptoms?
      • 

    • Are there any associated features?
      • 

    • Have there been any drug changes in the past few months?
      • 

    

    • 





 


Management in the Emergency Department


    

  • 

      

    • First line treatment of tardive dyskinesia generally begins with discontinuation of the offending drug. In the emergency department this should be done after consulting with the treating physician. These patients are often being treated for psychiatric disorder and the treatment of the psychiatric disorder must be balanced with the risk of tardive dyskinesia. It may be appropriate to switch from a first generation antipsychotic medication to a second generation antipsychotic generation medication.
      • 

    • If the symptoms of tardive dyskinesia need to be treated, like in our case with this patient, there are various drugs that can be tried.
      • 

    • Tetrabenazine is considered first line.10

        

      • Suggested doses of 12.5-25 mg starting daily dose with a 25-200 mg/day dose range.10
        • 

      

      • 

    

    • 



    

  • 

      

    • 

    

    • 



    

  • 

      

    • Other treatment options

        

      • Dextromethorphan11

          

        • In a recent case study patients took under 1mg/kg, not exceeding 42 mg/day.11
          • 

        • This was recommended by a local neurologist here at the Saint John Regional Hospital.
          • 

        

        • 

      • Valbenazine 12

          

        • Suggested dose of 40 mg UID, increasing to 80 mg UID after one week.12
          • 

        

        • 

      • Amantadine10

          

        • Suggested dose of 100 mg starting daily dose with a dose range of 100-300 mg/day 10
          • 

        

        • 

      • Benzodiazepines12

          

        • Clonazepam initiated at 0.5 mg and titrated by 0.5 mg increments every 5 days to response up to a maximum dose of 3-4 mg/day. 12
          • 

        

        • 

      • Diphenhydramine suggested dose of 25-50 mg IV13
        • 

      • Botulinum toxin injections12
        • 

      

      • 

    

    • 

  • 

      

    • Commonly used treatments lacking evidence of efficacy

        

      • Benztropine10
        • 

      

      • 

    

    • 









Drug
Starting Dose Recommendations
Dose Range




1st Line




Tetrabenazine
12.5-25 mg UID
25-200 mg UID




Other options




Dextromethorphan
Under 1 mg/kg
Not exceeding 42 mg UID




Valbenazine
40 mg UID
Increase to 80 mg after 1 week




Amantadine
100 mg UID
100-300 mg UID




Clonazepam
0.5 mg
0.5-4.0 mg UID




Diphenhydramine
25 mg IV
25-50 mg IV




Botulinum toxin injection
local injection to treat specific painful dystonia resistant to systemic therapy






 




Case Continued


The patient was given 2mg of Benztropine IV with no effect. Twenty minutes later he was then given 1mg of Ativan SL with no effect. Thirty minutes later the patient was given 150 mg Benadryl IV, and some improvement was then witnessed, the patient was allowed to sleep and was discharged approximately 5 hours after his arrival with no symptoms.




External Resources


Treatment strategies for dystonia


Diagnosis & Treatment of Dystonia




References


    

  1. Cornett EM, Novitch M, Kaye AD, Kata V, Kaye AM. Medication-Induced Tardive Dyskinesia: A Review and Update.Ochsner J. 2017 Summer;17(2):162-174. Review. PubMed PMID: 28638290; PubMed Central PMCID: PMC5472076.
    2. 

  2. Kulkarni SK, Naidu PS. Pathophysiology and drug therapy of tardive dyskinesia: current concepts and future perspectives.Drugs Today (Barc). 2003 Jan;39(1):19-49. Review. PubMed PMID: 12669107.
    3. 

  3. Glazer WM.Review of incidence studies of tardive dyskinesia associated with typical antipsychotics. J Clin Psychiatry. 2000;61 Suppl 4:15-20.  PubMed PMID: 10739326.
    4. 

  4. Correll CU, Schenk EM.Tardive dyskinesia and new antipsychotics. Curr Opin Psychiatry. 2008 Mar;21(2):151-6. doi: 10.1097/YCO.0b013e3282f53132.  PubMed PMID: 18332662.
    5. 

  5. Rao AS, Camilleri M.Review article: metoclopramide and tardive dyskinesia.Aliment Pharmacol Ther. 2010 Jan;31(1):11-9. doi: 10.1111/j.1365-2036.2009.04189.x.  PubMed PMID: 19886950.
    6. 

  6. Bateman DN, Rawlins MD, Simpson JM.Extrapyramidal reactions with metoclopramide. Br Med J (Clin Res Ed). 1985 Oct 5;291(6500):930-2. doi: 10.1136/bmj.291.6500.930. PubMed PMID: 3929968; PubMed Central PMCID: PMC1417247
    7. 

  7. Novick D, Haro JM, Bertsch J, Haddad PM.Incidence of extrapyramidal symptoms and tardive dyskinesia in schizophrenia: thirty-six-month results from the European schizophrenia outpatient health outcomes study. J Clin Psychopharmacol. 2010 Oct;30(5):531-40. doi: 10.1097/JCP.0b013e3181f14098. PubMed PMID: 20814320.
    8. 



    

  1. American Psychiatric Association, Medication-induced movement disorders and other adverse effects of medication, Diagnostic and Statistical Manual of Mental Disorders, fifth edition, American Psychiatric Association, 2013.
    2. 

  2. Tarsy D, Deik A. Tardive dyskinesia: Etiology, risk factors, clinical features, and diagnosis. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on September 9, 2019.)
    3. 



    

  1. DynaMed [Internet]. Ipswich (MA): EBSCO Information Services. 1995 – . Record No.T113751, Tardive Dyskinesia; [updated 2018 Nov 30, cited September 9, 2019]. Available from https://www.dynamed.com/topics/dmp~AN~T113751. Registration and login required.
    2. 



    

  1. Kim J. (2014). Dextromethorphan for Tardive Dyskinesia. International Neuropsychiatric Disease Journal. 2. 136-140. 10.9734/INDJ/2014/7970.
    2. 

  2. Tarsy D, Deik A. Tardive dyskinesia: Prevention, prognosis, and treatment. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on September 9, 2019.)
    3. 



    

  1. Buttaravoli P, Leffler SM. Chapter 1 – dystonic drug reaction. 2012:1-3. doi:https://doi.org/10.1016/B978-0-323-07909-9.00001-5 “.
    2. 


			

		

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Pediatric Hip PoCUS


				

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Pediatric Hip PoCUS


PoCUS Pearl




Dr. Sultan Ali Alrobaian


Dalhousie EM PoCUS Fellowship


Saint John, NB


@AlrobaianSultan


 


Reviewed and Edited by Dr. David Lewis




 


Case:


A 5 year old healthy boy, came to ED with history of limping since waking that morning. He had worsening right hip discomfort. No history of trauma. He had history of cold symptoms for the last 3 days associated with documented low grade fever.


On physical examination, he looked uncomfortable and unwell looking, he had temperature of 38.1 C, HR 130, BP 110/70, RR 20 and O2 saturation of 98% on RA. He was non-weight-bearing with decreased ROM of right hip because of pain.


Pelvis x-ray was unremarkable, he had WBC of 14.4 x 103  and CRP of 40 .


PoCUS of the right hip was performed.






 


Pediatric Hip Ultrasound


Ultrasonography is an excellent modality to evaluate pathologies in both the intra-articular and extra-articular soft tissues including muscles, tendons, and bursae. PoCUS to detect hip effusion can serve as an adjunct to the history and physical examination in case with hip pain.  It is easily accessible, no radiation exposure and low cost.


Technique:


The child should be in supine position. Expose the hip with drapes for patient comfort. If the patient will tolerate it, position the leg in slight abduction and external rotation. A high frequency linear probe is the preferred transducer to scan the relatively superficial pediatric hip, use the curvilinear probe if increased depth is required.


With the patient lying supine, identify the greater trochanter on the symptomatic hip of the patient. Place the linear probe in the sagittal oblique plane parallel to the long axis of the femoral neck (with the indicator toward the patient’s head).


If the femoral neck cannot easily be found, it can be approached using the proximal femur. Place the probe transversely across the upper thigh. Identify the cortex of the proximal femur and then move the probe proximally until the femoral neck appears medially, then slightly rotate the probe and move medially to align in the long axis of the femoral neck.


Assistance is often required from a parent who may be asked to provide reassurance, apply the gel and help with positioning.


Both symptomatic and asymptomatic hips should be examined.


Negative hip ultrasound in a limping child should prompt examination of the knee and ankle joint (for effusion) and the tibia (for toddler’s fracture)


Hip X-ray should be performed to rule out other causes (depending on age – e.g. Perthes, Osteomyelitis, SCFE, Tumour). Limb X-ray should be performed if history of trauma or NAI.


 






Anatomy of the Pediatric Hip:


The ED Physician should readily identify the sonographic landmarks of the pediatric hip. These landmarks include the femoral head, epiphysis and neck, acetabulum, joint capsule and iliopsoas muscle and tendon.




 


A normal joint may have a small anechoic stripe (normal hypoechoic joint cartilage) between cortex and capsule. This will measure less than 2mm and be symmetrical between hips.


 


Ultrasound Findings:


Measure the maximal distance between the anterior surface of the femoral neck and the posterior surface of the iliopsoas muscle. An effusion will result in a larger anechoic stripe (>2mm) that takes on a lenticular shape as the capsule distends. Asymmetry between hips is confirmatory. Synovial thickening may also be visualized.




FH- Femoral Head, S- Synovium, E – Effusion, FN – Femoral Neck


Criteria for a pediatric hip effusion is:


    

  • A capsular-synovial thickness of 5 mm measured at the concavity of the femoral neck, from the anterior surface of the femoral neck to the posterior surface of the iliopsoas muscle
    • 

  • OR a 2-mm difference compared to the asymptomatic contralateral hip
    • 





Right hip effusion, normal left hip, arrow heads – joint capsule, IP – iliopsoas




Interpretation


PoCUS has high sensitivity and specificity for pediatric hip effusion.


    

  • —
    • 

  • Sensitivity of 90%
    • 

  • Specificity of 100%
    • 

  • Positive predictive value of 100%
    • 

  • Negative predictive value of 92%
    • 



 


PoCUS cannot determine the cause of an effusion. It cannot differentiate between transient synovitis and septic arthritis. Diagnosis will be determined by combining history, pre-test probability, examination, inflammatory markers and PoCUS findings. If in doubt, septic arthritis is the primary differential diagnosis until proven otherwise.


Several clinical prediction algorithms have been proposed. This post from pedemmorsels.com outlines these nicely:


 


Septic Arthritis




 


 




 


Back to our case:


Ultrasonography cannot definitively distinguish between septic arthritis and transient synovitis, the ED physician’s concern for septic arthritis should be based on history, clinical suspicion and available laboratory findings.


The patient was diagnosed as case of septic arthritis. The patient received intravenous antibiotics empirically. Pediatric orthopedic consultation was obtained, and ED arthrocentesis was deferred as the patient was immediately taken to the operating room for hip joint aspiration and irrigation, confirming the diagnosis.




 


References





 

			

		

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Palpitations – A Paroxysmal Pearl


				

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Palpitations – A Paroxysmal Pearl


Medical Student Clinical Pearl




Scott Fenwick


Class of 2021




Faculty of Medicine


Dalhousie University






Reviewed and Edited by Dr. David Lewis




Case Presentation:


A 49-year-old female presented with palpitations for the past 2 hours. She had two similar episodes in the last 2 weeks, both of which resolved within 1-2 minutes. She had no other symptoms. She was otherwise healthy, with no past medical history. She was a non-smoke and non-drinker who leads an active lifestyle. She denied weight loss, diarrhea, and heat intolerance.


On physical exam, she was tachycardic at 130bpm with an irregularly irregular pulse. She did not display any tremor or diaphoresis. On auscultation, S1 and S2 were audible, with no murmurs or extra sounds. Respiratory and abdominal exams were unremarkable.




What to ask on History?


Common Symptoms: palpitations, tachycardia, fatigue, weakness, dizziness, light-headedness, reduced exercise capacity, mild dyspnea, and polyuria. It is essential to know when exactly the symptoms started. AF that presents before 48 hours can be safely rhythm controlled without anticoagulation.(1)


Severe/Secondary Symptoms: angina, dyspnea at rest, presyncope and, uncommonly, syncope. Embolic events and heart failure can be severe complications of AF.


Past Medical History: cardiovascular or cerebrovascular disease, diabetes, hypertension, COPD, obstructive sleep apnea, and hyperthyroidism.




What to look for On Examination?


ABCs and vitals: particularly pulse rate and rhythm.


General Assessment: look for signs of thyroid disease, PE, pulmonary disease, alcohol withdrawal, and signs of liver disease from excessive alcohol ingestion.


CVS: precordial scars from prior cardiac surgery, JVP, peripheral edema, and auscultation for murmurs or additional sounds that might suggest valvular AF. There is often an apical-radial pulse deficit where not every apical beat has an associated radial beat due to lack of left ventricular stroke volume.(2)




Case Continued – Testing: 


The patient was put on a cardiac monitor and an ECG was performed, demonstrating atrial fibrillation. There was also a right bundle branch block that was consistent with a previous ECG performed in 2017. Laboratory testing was unremarkable.


Depending on clinical suspicion, initial testing may include CBC, electrolytes, blood glucose, PT/INR, creatinine, BUN, TSH, cardiac enzymes, LFTs, and chest x-ray.2




See Basic ECG interpretation Pearl for a great guide to ECGs


Basic ECG Interpretation






 


Classifying Atrial Fibrillation: 


AF is classically described as an irregularly irregular heartbeat, as can be observed from the variable RR intervals in the ECG above. In AF, there are no distinct P-waves due to the uncoordinated atrial activity. Broadly, AF can be divided into valvular and non-valvular subtypes. Non-valvular AF can be classified into the following categories:(1)


    

  • Paroxysmal – AF terminates spontaneously or with intervention within 7 days of onset.
    • 

  • Persistent – AF fails to terminate within 7 days of onset; often a progressive disease.
    • 

  • Long-Standing Persistent – AF has persisted for greater than 12 months.
    • 

  • Permanent – Joint decision between patient and provider to no longer pursue rhythm control.
    • 



AF commonly progresses from paroxysmal to persistent states. The above classification only refers to primary atrial fibrillation, not AF that is secondary to cardiac surgery, pericarditis, myocardial infarction, valvulopathy, hyperthyroidism, pulmonary embolism, pulmonary disease, or other reversible causes.


For persistent and permanent AF, the CHADS2 score can be used to estimate a patient’s 1-year risk of ischemic stroke without anticoagulation (0 = low risk, 1-2 = moderate risk, 3+ = high risk).(1)




Calculate it here


 


CAEP and CCS now recommend using the CHAD-65 Score to determine anticoagulation requirement.




 




 


Treatment


DC and chemical (e.g. procainamide) cardioversion are two well-described methods of treating uncomplicated AF. The goal of treatment is to return patients to NSR. Some important points about the two methods include:


    

  • DC cardioversion can be administered at an initial energy dose of 100J and increased up to 360J as needed.(2)
    • 

  • Procainamide is often given in doses of 15-18mg/kg, or more simply, 1g over 60 minutes. Average time to cardioversion is about 1 hour.(1)
    • 

  • DC cardioversion requires procedural sedation; whereas, chemical cardioversion does not.
    • 

  • In a recent RCT, combination therapy achieved NSR in 99% of patients; Attempting DC cardioversion first decreased length of hospital stay by 1.2 hours.(3)
    • 

  • Both therapies are generally well-tolerated by patients.
    • 







Case Continued – Treatment: 


The patient was diagnosed with paroxysmal atrial fibrillation. The arrhythmia did not spontaneously resolve in the ED. DC and chemical cardioversion methods were considered and discussed with the patient. Direct Current (DC) cardioversion was performed under procedural sedation with propofol and fentanyl. Shocks of 100J and 200J were unsuccessful in converting the patient into normal sinus rhythm (NSR). A third shock at 300J was ultimately successful. The following ECG was obtained demonstrating NSR. As in the initial ECG, there is a RBBB present.


 




CHADS2 score was 0. Therefore anticoagulation or antithrombotic therapy not indicated.




 


Case Conclusion:


The patient was discharged home within 4 hours of arriving to hospital, anticoagulation was not prescribed. It is likely that she will experience AF again and require anticoagulation later in life.




 


References:


    

  1. January, C. T., Wann, L. S., Alpert, J. S., Calkins, H., Cigarroa, J. E., Cleveland, J. C., et al. (2014). 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: Executive summary. Journal of the American College of Cardiology, 64(21), 2246. doi:10.1016/j.jacc.2014.03.021
    2. 

  2. Wakai, A., & Neill, J.O. (2003). Emergency management of atrial fibrillation. Postgrad Med J, 79(932), 313. doi:10.1136/pmj.79.932.313
    3. 

  3. Scheuermeyer, F. X., Andolfatto, G., Christenson, J., Villa-Roel, C., & Rowe, B. (2019). A multicenter randomized trial to evaluate a chemical-first or electrical-first cardioversion strategy for patients with uncomplicated acute atrial fibrillation. Academic Emergency Medicine, 26(9), 969-981. doi:10.1111/acem.13669
    4. 


			

		

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Color Flow Doppler to Assess Cardiac Valve Competence


				

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Color Flow Doppler to Assess Cardiac Valve Competence


Resident Clinical Pearl (RCP) April 2019




Dr. Scott Foley – CCFP-EM PGY3 Dalhousie University, Halifax NS


Reviewed by Dr. David Lewis


 




 


Background:


When colour Doppler is initiated, the machine uses the principals of the Doppler effect to determine the direction of movement of the tissues off which it is reflecting.


The Doppler effect is the change in frequency of a wave in relation to an observer who is moving relative to a wave source. It was named after the Austrian physicist Christian Doppler who first described the phenomenon in 1842. The classic example is the change in pitch of a siren heard from an ambulance as it moves towards and away from an observer.


These principles are applied to POCUS in the form of colour Doppler where direction of flow is reflected by the colour (Red = moving towards the probe, Blue = moving away from the probe), and the velocity of the flow is reflected by the intensity of the colour (brighter colour = higher velocity).

*Note: the colour does not represent venous versus arterial flow.


 




The use of colour Doppler ultrasound can be useful in the emergency department to determine vascular flow in peripheral vessels as well as through the heart. It is one way to determine cardiac valve competency by focusing on flow through each valve.




 


Obtaining Views:


To optimize valve assessment, proper views of each valve must be obtained. It is best to have the direction of the ultrasound waves be parallel to the direction of flow. External landmarks for the views used are seen below:




    

  • Mitral Valve and Tricuspid Valve: The best view for each of these is the apical 4 chamber view. If unable to obtain this view, the mitral valve can be seen in parasternal long axis as well.
    • 

  • Aortic Valve: The best view is the apical 5 chamber or apical 3 chamber but are challenging to obtain. Instead, the parasternal long axis is frequently used.
    • 

  • Pulmonic Valve: Although not commonly assessed, the parasternal short axis can be used.
    • 

  • Visit 5minutesono.com for video instruction on obtaining views
    • 







Parasternal long axis: MV, AV




Parasternal short axis: PV, TV




Apical 4 chamber: TV, MV




 


Assessing Valvular Competency:


How to examine valvular competency:


    

  1. Get view and locate valve in question
    2. 

  2. Visually examine valve: opening, closing, calcification
    3. 

  3. Use colour Doppler:

      

    1. Place colour box over valve (as targeted as possible (resize select box) to not include other valves)
      2. 

    2. Freeze image and scroll through images frame by frame
      3. 

    3. Examine for pathologic colour jets in systole and diastole
      4. 

    

    4. 

  4. Estimating severity:

      

    1. Grade 1 – jet noticeable just at valve
      2. 

    2. Grade 2 – jet extending out 1/3 of atrium/ventricle
      3. 

    3. Grade 3 – jet extending out 2/3 of atrium/ventricle
      4. 

    4. Grade 4 – jet filling entire atrium/ventricle
      5. 

    

    5. 



See video tutorial below for more






Mitral Regurgitation A4C




Tricuspid Regurgitation A4C




Aortic Stenosis PSLA




Bottom line:


Color flow Doppler on POCUS is a straightforward way to assess for valvular competency in the Emergency Department. A more detailed valvular assessment requires skill, knowledge and experience.


 




Useful Video Tutorials:


Mitral Regurgitation




 


Aortic Stenosis vs Sclerosis






Tricuspid Valve






References:


    

  1. https://www.radiologycafe.com/medical-students/radiology-basics/ultrasound-overview
    2. 

  2. By Patrick J. Lynch and C. Carl Jaffe – http://www.yale.edu/imaging/echo_atlas/views/index.html, CC BY 2.5, https://commons.wikimedia.org/w/index.php?curid=21448310
    3. 

  3. 5minutesono.com
    4. 

  4. ECCU ShoC 2018 powerpoint, Paul Atkinson, David Lewis
    5. 


			

		

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Approach to Resuscitation in Severe Calcium Channel Blocker Poisoning


				

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Medical Student Clinical Pearl




J.L. Dobson




Faculty of Medicine




Memorial University of Newfoundland




M.D. Candidate 2020





Reviewed and Edited by Dr. Luke Taylor and Dr. David Lewis


and Liam Walsh. Pharmacist HHN




 


Introduction:


Calcium channel blockers (CCBs) have multiple clinical uses, including the management of hypertension, angina, and cardiac arrhythmias. [1] While CCBs are no longer the most widely prescribed antihypertensive as they were in the 1990s, their prevalence remains high. [2] This along with the existence of both immediate release and long-acting forms poses a challenge for the Emergency Physician faced with a case of CCB poisoning.


Physiology:


Myocardium in the sinoatrial and atrioventricular nodes uses the slow action potential created by calcium currents to conduct. CCBs act on this tissue by inhibiting this current, thus slowing conduction through the SA and AV nodes. This results in a decreased heart rate, prolonged PR intervals, and lengthened refractory periods through the AV node. Conversely, they also inhibit calcium flow in smooth muscle, resulting in coronary and peripheral artery dilation. This ultimately provides the mechanism for reflex tachycardia, increased AV conduction, and improved myocardial contractility. [3]


Adverse reactions to the physiological effects of CCBs include vasodilatory effects (peripheral edema, headache, palpitations), gastrointestinal effects (nausea, diarrhea, constipation), and negative inotropic effects (hypotension, bradycardia). [4]




 


Case Report:


A 80-year-old male is brought in to Trauma by ambulance with hypotension, bradycardia, and an altered level of consciousness. Report from EMS reveals the patient called about half an hour prior stating that he had taken medications in an attempt to commit suicide. Upon arrival, the pt was alert and oriented, and endorsed taking an unknown quantity of clonazepam and citalopram, and a deficit of up to four grams of Diltiazem was noted from his medications. He denied further substance use. Though initially stable, the patient deteriorated rapidly upon arrival to the emergency department.




In the Emergency Department, initial vitals revealed a BP of 88/68, P of 52 bpm and SPO2 of 93% on RA and a BG of 15. As such nasal prongs were placed and she was immediately given atropine as well as push dose epinephrine. Within ten minutes, there was further decline in mental status of the patient corresponding to a blood pressure of 83/61 and a heart rate persisting in the low 40s bpm. He was successively given further epinephrine, atropine and calcium chloride while toxicology was contacted. Despite recurrent doses of epinephrine and atropine, the patient remained profoundly hypotensive and bradycardic. Insulin (Humulin R) and dextrose were started at 0.5U/kg/hr with a 1U/kg bolus. This infusion was titrated up every thirty minutes with minimal improvement in vitals. At this point, remaining bradycardic at 37bpm, intralipid therapy was deemed necessary and so a bolus of 105mL was given. Having received epinephrine bolus along with a 0.2mcg/kg/hr infusion, maximum dose of atropine, 3g of Calcium chloride, with minimal clinical improvement cardiac pacing was initiated. Once good electrical and mechanical capture were achieved the patient underwent and RSI with ketamine and rocuronium. Once stabilized, he was transferred to ICU for further management. In ICU, the patient had a transvenous pacemaker floated successfully followed by a transitioning off the epinephrine to norepinephrine and vasopressin. Intralipid infusion was started and the insulin and glucose therapy was titrated up to a maximum of 4U/kg/hr. The patient unfortunately did not tolerate whole bowel irrigation. Despite the critical nature of their condition, the patient did slowly improve and pressors were weaned.




 


Discussion:


History & Primary Survey


This patient experienced negative inotropic effects of the extended release calcium channel blocker, resulting in cardiogenic shock. Ingestion of more than 5-10 times the usual dose of CCB results in severe intoxication: this patient was thought to have consumed four grams of Diltiazem, over eleven times the maximum recommended dose. [5] While any CCB can result in hypotension, knowledge of which CCB was taken is useful to set expectations for the patient’s progression: unlike dihydropyridine-type CCBs which would more likely present with reflex tachycardia, non-dihydropyridine CCBs like verapamil and diltiazem result in bradycardia. [6] Another crucial point in the primary survey is that, due to the neuroprotective effects of CCBs, mental status may initially be preserved until cerebral perfusion is severely affected. [5]


Initial Resuscitation


While the patient may initially be able to maintain their airway, mental status and vitals may deteriorate rapidly. [5] It is important to note that like any critical ill patient,  intubation may result in a further drop in heart rate and blood pressure via vagal stimulation. It is crucial to have adequate resuscitation prior to intubation. IV crystalloid fluids , IV atropine (up to three 1mg doses), as well as push dose epinephrine are interventions that can be used quickly at bedside to maintain circulation and heart rate while further investigations and treatments can be organized. [5,8]






Specific Treatments


For a severe CCB poisoning in which hypotension is refractory to IV fluids and atropine, all of the following treatments should be administered simultaneously. If the severity is milder, these treatments should be approached in a stepwise fashion, progressing to the next if the preceding treatment is ineffective. [5]


IV Calcium salt:


As a first line recommendation, a calcium chloride bolus (10-20mL 10%) followed by a continuous infusion (0.5 mEq Ca2+/kg/hr) or the equivalent of calcium gluconate is recommended, though often ineffective. [5] Mortality has been shown to be reduced with its administration, and hypercalcemia occurs only rarely. [7] [8]


IV Insulin with dextrose:


High-dose insulin therapy (1 u/kg bolus and 0.5 u/kg/hr infusion up to 10 u/kg/hr) has been shown to be safe and effective at improving hemodynamics, though response is delayed for 30-60 minutes. [5,7] It should be used with calcium and a vasopressor in the presence of myocardial dysfunction. [8] Blood glucose levels should be monitored every 15-30 minutes for hypoglycemia, and 50mL boluses of dextrose (D50W) given accordingly to maintain levels above 8.25 mM. [5] Hypokalemia is another risk of insulin therapy, therefore electrolytes should be monitored every 30 minutes and 20 mEq of potassium chloride given if needed. [5,7]


IV Vasopressor:


Administration of IV epinephrine has shown improvement in cardiac output. [7,8] In the setting of severe CCB poisoning, doses as high as 150mcg per minute of epinephrine may be needed. It is suggested to start the infusion at 2mcg per minute and titrate up to a systolic blood pressure of 100 mmHg, or a MAP of 65 mmHg. [5] These higher doses may result in a large improvement in patient MAP with minimal change in heart rate.


IV Lipid emulsion therapy:


If the patient is refractory to first-line treatments above, or upon consultation with medical toxicology centre, IV lipid emulsion therapy may be recommended. [8] Most commonly, this is given as a bolus of 1.5 mL/kg of 20% lipid emulsion, repeated up to every three minutes for three total boluses. An infusion of 0.25-0.5 mL/kg/minute may be started. [5] Complications of this treatment are still being studied.




Other considerations:


Studies most often show improvement of hemodynamics and no adverse effects with temporary cardiac pacing for bradycardia refractory to first-line treatments. [7,8] Extracorporeal membrane oxygenation may also be necessary if the patient is near cardiac arrest and remains refractory to previous treatments. [8] Dialysis provides no benefit. [5]


Decontamination:


If the patient is asymptomatic and/or hemodynamically stable, 50g of activated charcoal should be given. In the case of ingestion of extended-release CCBs, whole bowel irrigation should be performed regardless of the presence of symptoms. An asymptomatic patient should be monitored for 6-8 hours for immediate release and 24 hours for extended release forms. [5,8]


Investigations:


ECG may reveal PR interval prolongation due to CCB actions on the SA and AV nodes. Frequent blood glucose measurements are crucial to monitor for the effects of insulin treatment and the need for glucose replacement. Serum electrolytes, notably potassium levels, must be assessed for developed hypokalemia secondary to insulin treatment.








Conclusion:


We present a case and review the physiology of a severe calcium channel blocker poisoning. Key considerations in managing a CCB poisoning include specific dosage and form, initial resuscitation with a low threshold for intubation, fluids, and atropine. Further treatments will be required based on severity, such as intravenous calcium, insulin with dextrose, and lipid emulsion therapy, all of which should be initiated promptly if there is concern for massive over dose and patient declining. Other considerations include the need for further vasopressors and temporary cardiac pacing.


 






FIGURE: Society of Critical Care Medicine key recommendations for management of CCB poisoning. Source: “Experts consensus recommendations for the management of calcium channel blocker poisoning in adults.” Crit Care Med. 2017;45(3):e306-e315. DOI: 10.1097/CCM.0000000000002087




 


References:


[1] Elliott, WJ & Ram,CV. J Clin Hypertens (Greenwich). 2011;13:687–689.


[2] Eisenberg, MJ; Brox, A. & Bestawros, AN. Am J Med. 2004;116(1):35-42.


[3] Singh, BN; Hecht, HS; Nademanee, K. & Chew, CYC. Progress in Cardiovascular Diseases. 1982;15(2):103-132.


[4] Russell, RP. Hypertension. 1988;11(3):II42-44.


[5] Barrueto, F. “Calcium channel blocker poisoning.” UpToDate. 2019.


[6] Hofer, CA; Smith, JL & Tenholder, MF. Am J Med. 1993;95(4):431.


[7] St-Onge, M; Dubé, PA; Gosselin, S; Guimont, C; Godwin, J; Archambault, PM; Chauny, JM; Frenette, AJ; Darveau, M; Le Sage, N; Poitras, J; Provencher, J; Juurlink, DN & Blais, R. Clin Toxicol (Phila). 2014;52(9):926.


[8] St-Onge, M; Anseeuw, K; Cantrell, FL; Gilchrist, IC; Hantson, P; Bailey, B; Lavergne, V; Gosselin, S; Kerns, W; Laliberté, M; Lavonas, EJ; Juurlink, DN; Muscedere, J; Yang, CC; Sinuff, T; Rieder, M & Mégarbane, B. “Experts consensus recommendations for the management of calcium channel blocker poisoning in adults.” Crit Care Med. 2017;45(3):e306-e315.

			

		

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