Whose Line is it Anyway? – PoCUS in a Patient with Dyspnea

Medical Student Clinical Pearl – March 2020

Nguyet (Na) Nguyen

MD Class of 2021
Memorial University of Newfoundland

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual


 

Case Report

ID: 60 y/o M with dyspnea presenting to the ED late evening

HPI: Patient complained of increasing SOB starting the morning on day of presentation, with a worsening 3 days of non-productive cough. No chest pain or other cardiac features. No complaint suggestive of URTI or GI illness. Patient was given Atrovent and Ventolin en route by EMS, and was allegedly moving more air into his lungs after this intervention. Patient reports no ankle swelling, paroxysmal nocturnal dyspnea, but reports using 2 pillows to elevate himself when sleeping. Patient reports no fever, unexplained weight loss or fatigue.

Past medical history includes chronic back pain, DM, atrial fibrillation, peripheral DM-related ulcers, chronic kidney disease, BPH, colon cancer with hepatic metastases. Past surgical history significant for 5x CABG, liver and colon resection.

His medications are amitriptyline 10mg PO qhs, acetaminophen 650mg PO BID, dutasteride 0.5mg PO daily, ferrous sulfate 300mg PO daily, furosemide 40mg PO BID, metformin 500mg BID, pantoprazole 40mg PO BID, pregabalin 150mg PO BID, primidone 125mg PO daily, rosuvastatin 40mg PO qhs, rivaroxaban 15mg PO daily.

He has a distant 10 pack-years smoking history, drinks alcohol occasionally, and does not use recreational drugs. The patient lives with his wife in their own home.

Physical exam: Patient was markedly pale, non-diaphoretic, in tripod position with increased work of breathing. His temperature was 36.9, regular pulse rate at 105, respiratory rate 22, oxygen saturation 90% on room air and a nebulizer mask through which he was receiving aerosolized Atrovent and Ventolin. His BP was 125/78mmHg.

Cardiovascular exam revealed distant S1S2 in a chest with no visible deformity. His JVD was at the level of the sternal angle, there was no pedal edema bilateral. Capillary refill was 3 seconds bilateral at the thumbs. Percussion revealed no focal dullness, however on auscultation, basal crackles were heard more prominently in the right lung base, though also present on the left. There were also wheezes noted in the upper lobes heard in the anterior chest. Abdomen was soft, non-distended, non-tender. Neurological exam unremarkable.

Investigations: ECG showed sinus tachycardia with a LBBB, bloods drawn for routine labs, VBG, lactate, CXR ordered.

Differential diagnosis: AECOPD vs congestive heart failure.

PoCUS (Arrival Time + 10 mins): B-lines were observed in both lungs when a curvilinear probe was placed over different areas of the anterior chest. A small pleural effusion was also noted at the bottom of the right lung. B-lines represent increased fluid in an area of the lung, and given different clinical contexts maye represent pulmonary edema, pneumonia, or pulmonary contusion. In this case the most likely explanation for bilateral diffuse B-Lines is CHF and Pulmonary Edema. 

Working Diagnosis (Arrival Time + 10 mins): CHF and Pulmonary Edema

Management (Arrival Time + 15 mins): Pending transfer fo CXR and results of investigations the patient was treated with intravenous diuretics. He passed 500mls of urine and his symptoms improved considerably.

 

Investigations Results (Arrival Time + 45 mins): leukocytes 6.4, hemoglobin 83, platelet 165, sodium 140, potassium 5/0, chloride 101, creatinine 120, urea 11.7, glucose 17.0. Venous blood gas showed pH 7.31, pCO2 555, HCO3- 28 and lactate 2.7.

CXR (Arrival Time + 45 mins):

CXR was similar to above, this image is from: https://radiopaedia.org/cases/acute-pulmonary-oedema-6

 

Final impression: Congestive heart failure


What are B Lines?

These are the ultrasound equivalent of Kerley-B lines often reported on chest X-ray, which indicate edema in the lungs. For an exam to be positive (i.e indicative of pathology), one needs to see a minimum of 3 B-lines per view. B-lines look like flashlight beams traveling undisrupted down the entire ultrasound screen, as seen in the images above obtained during the exam.

These need to be distinguished from other artifacts such as ‘A-lines’ and ‘comet tails’. A-lines are seen in normal lungs. These are ‘repetitive reverberation’ artifacts of the normal pleura in motion. (Figure 1)(1)

‘Comet tails’- reported first by Lichenstein et al. in 1998 (although he was describing B-Lines in this paper) (Figure 2) (1), are ‘short, hypoechoic artifacts’ that only descend vertically partially down the screen. These are normal lung artifacts. This paper explains “a common misunderstanding in lung ultrasound” nomenclature that stems from Lichtenstein’s original paper.

Download pdf

 

From: https://www.mdedge.com/emergencymedicine/article/96697/imaging/emergency- ultrasound-lung-assessment

 


More on Comet Tails Artifact in this post from LitFL:

Comet tail artefact

 


 

Protocols

There are multiple protocols that guide the ultrasound technique (4) , some of which are:

  • Lichenstein et al (1998): longitudinal scans of anterior and lateral chest walls of patients in semi- recumbent position. Positive test defined as bilateral multiple B-lines diffuse anterolateral or lateral. The protocol had reported sensitivity (true positive) of 100%, and specificity (true negative) 92% for cardiogenic pulmonary edema. Blue Protocol (2015)
  • Liteplo et al (2008): anterior and lateral chest walls with patient supine: each chest divided into 4 zones (anterior, lateral, upper and lower). Positive test: pathologic pattern found in >1 zone on each side, with both sides involved.
  • Volpicelli et al. (2008): longitudinal scans of supine patients with chest divided into 11 areas (3 anterior R, 3 lateral R, 2 anterior L, 3 lateral L) to obtain score 0-11. Scores strongly correlated with radiologic and BNP (lab marker of CHF) at presentation.

 

 


 

What is the Evidence?

Al Deeb et al. conducted a systematic review and analysis of prospective cohort and prospective case-control studies in the ED, IDU, inpatient wards and prehospital settings (n = 1075). This was published in Acad Emerg Med (2014), which reported a sensitivity of 94.1% for using B-lines to diagnosis acute cardiogenic pulmonary edema (ACPE), and a specificity of 92.4% for patients with a moderate- high pretest probability for ACPE.

The SIMEU Multicenter study reported in 2015 reported a significantly higher accuracy (97% sensitivity and 97.4% specificity) with an approach incorporating lung ultrasound (LUS) in differentiating acute decompensated heart failure (ADHF) and non-cardiac causes of acute dyspnea, compared to approaches using the initial clinical workup (past medical history, history of presenting illness, physical examination, ECG, ABG), chest X-ray alone and natriuretic peptides.

Martindale et al. reported in 2016 (Academic Emergency Medicine) high positive likelihood ratio of pulmonary edema observed on lung ultrasound and low negative likelihood ratio of B-line pattern on lung US in affirming the presence of acute heart failure, after a systematic review and analysis of 57 prospective and cross-sectional studies (n = 1,918).

A useful Systematic Review “Emergency department ultrasound for the detection of B-lines in the early diagnosis of acute decompensated heart failure: a systematic review and meta-analysis ” from McGivery et al from SJRHEM (7), was published in 2018.


 

Learning Point

For a patient presenting to the ER with dyspnea, using PoCUS to observe 3 or more B-lines in two bilateral lung zones +/- pleural effusion can rapidly guide an accurate diagnosis of acute congestive heart failure.


 

References

  1. Taylor, T., Meer, J., Beck, S. Emerg Med. (2015) https://www.mdedge.com/emergencymedicine/article/96697/imaging/emergency- ultrasound-lung-assessment Last accessed Feb 29, 2020
  2. Lee, FCY, Jenssen, C., Dietrich, CF Med Ultrason (2018); 20(3): 379-384
  3. Ang SH. & Andrus P Curr Cardiol Rev. 2012 May; 8(2): 123-136https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3406272/
  4. Al. Deeb M., Barbic S., Featherstone R., Dankoff J., Barbic D. Acad Emerg Med 2014 Aug; 21(8): 843-52 https://www.ncbi.nlm.nih.gov/pubmed/25176151
  5. Pivetta E et al. Chest. 2015 Jul; 148(1): 202-210 https://www.ncbi.nlm.nih.gov/m/pubmed/25654562/
  6. Martindale JL, Wakai A, Collins SP, Levy PD, Diercks D, Hiestand BC, Fermann GJ, deSouza I, Sinert R, Acad Emerg Med. 2016 Mar; 23(3): 223-242 https://www.ncbi.nlm.nih.gov/pubmed/26910112
  7. McGivery K, Atkinson P, Lewis D, et al. Emergency department ultrasound for the detection of B-lines in the early diagnosis of acute decompensated heart failure: a systematic review and meta-analysis. CJEM. 2018;20(3):343‐352. doi:10.1017/cem.2018.27

 

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Acute Kidney Injury

Medical Student Clinical Pearl – January 2020

Carine Nzirorera

 

Faculty of Medicine
Dalhousie University
CC3
Class of 2021

Carine Nzirorera- ResearchGate

 

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual


 

Acute kidney injury (AKI) is defined as an abrupt decrease in kidney function and is classified based on changes in serum creatinine level, reduction of urine output, and need for renal replacement therapy [1]. The Kidney Disease: Improving Global Outcomes (KDIGO) is the most preferred definition and staging system. According to KDIGO guidelines AKI is define as an 1) increase in serum creatinine by ≥0.3 mg/dL (≥26.5 µmol/L) within 48 hours, or 2) an increase in serum creatinine ≥ 1.5 fold from baseline within 7 days, or 3) urine output <0.5 mL/kg/hour for 6 hours [2].

KDIGO staging criteria [2]

Stage 1 an increase of serum creatinine level of 1.5 to 1.9 times baseline, OR increase in serum creatinine by ≥0.3mg/dL (≥26.5 µmol/L) OR a urine output less than 0.5 mL/kg/hour for 6 to 12 hours.

Stage 2 an increase of serum creatinine level of 2 to 2.9 times baseline OR a urine output less than 0.5 mL/kg/hour for more than 12 hours.

Stage 3 an increase of serum creatinine level of greater than 3 times baseline OR increase in serum creatinine to ≥4.0 mg/dL (≥353.6 µmol/L), OR a urine output less than 0.3 mL/kg/hour for ≥24 hours OR anuria output ≥12 hours OR initiation of renal replacement therapy such as dialysis.


 

Case Presentation

69y male with a history of kidney stones had experienced 1 week of hematuria, 1 month of bilateral flank pain and unintentional 20 lbs weight loss over 2 months. Patient was scheduled for a CT scan of his urinary tract and was urgently sent to emergency department after his creatinine levels were found to be severely elevated (2300 µmol/L).

Patient had a 20 year history of kidney stones and previous abdominal CT scans showed small stones in both kidneys =/< 2mm. Patient was afebrile, had no dysuria or increased frequency but complained of difficulty initiating urination and noticed a reduction of the stream even when his bladder felt full. Patient noted no vomiting, diarrhea or decrease in fluid and food intake. Patient had a positive family history of bladder cancer and was a smoker for 30+ years.


 

Etiology

Causes of acute kidney injury are organized based on located of the insult (Table 1) [1]. Causes related to decrease in renal perfusion are classified as prerenal injury. Decrease renal perfusion is seen in sepsis due to decreased arterial pressure from systemic vasodilation; intravascular volume depletion from vomiting, diarrhea or overuse of diuretics can also reduce circulation to the kidneys [1]. Lastly drugs like nonsteroidal anti-inflammatory drugs (NSAIDs) and angiotensin-converting enzyme (ACE) inhibitor can lower intraglomerular pressure causing reduced glomerular filtration rate. NSAIDs and calcineurin inhibitors constrict afferent (or preglomerular) arterioles while ACE inhibitors and angiotensin receptor blockers dilate efferent (or postglomerular) arterioles [3].

Direct renal damage to glomeruli, tubules, interstitium or vasculature are classified as Renal injury. Nephritides can be caused by infection (viral, bacterial, and fungal), medication (antibiotics, antivirals, protein pump inhibitors) toxins (ethylene glycol, aminoglycoside, rhabdomyolysis) or are secondary to conditions like hypertension, prolonged hypotension, lupus, diabetes mellitus and vasculitis.

Impaired drainage of urine distal to the kidneys due to obstruction of the urinary tract is classified as Postrenal cause of acute kidney injury.  Common causes of obstruction are kidney stones, injury, prostate, cervical or bladder cancer.

Previously 70% of community acquired cases of acute kidney injury are classified as prerenal causes [4], a more recent study found 55% of community acquired acute kidney injury were renal disease, 35% pre-renal disease and 10% were postrenal [5].

 


 

Clinical Presentation, History and Physical Exam

Clinical presentation of acute kidney injury varies with severity and varies with prerenal, renal and postrenal causes (Table 2). Patients with mild to moderate acute kidney injury are usually asymptomatic and identifiable by laboratory testing. Severe cases would present with vomiting, confusion, fatigue, anorexia, nausea, weight gain or edema [6]. Decline in mental status, asterixis or neurologic symptoms can be indicative of uremic encephalopathy, anemia or bleeding caused by uremic platelet dysfunction [1].

History and physical exam should determine cause of the kidney injury. Screening questions should be used to determine renal perfusion, any potential source of renal injury and any symptoms suggestive of obstructive uropathy (Table 2). Decreased renal perfusion can be assumed from a history of gastrointestinal illness, poor oral intake, use of diuretics, NSAIDs or ACE inhibitors [1,7]. Past medical history of diabetes mellitus, cardiac or liver disease can also indicate reduced renal perfusion [1,7]. Source of renal injury can be screen by assessing current medication for recent antibiotics, antiviral and protein pump inhibitors use, inquiring about past medical history of systemic illnesses such as lupus, viral, bacterial, or fungal infection or symptoms of infection such as rash, arthralgias, fatigue, and hematuria [1,7]. Postrenal cause can be determined from a history of gross hematuria, difficulty urinating, urgency or hesitancy to urinate or a history of kidney stones or bladder, prostate or cervical cancer [1,7].

 


 

Case continued

Blood work

  • CBC: elevated leukocytes (13.5) decreased erythrocytes (3.32), decreased hemoglobin (97), decreased Hematocrit (0.304) normal MCV
  • INR (1.2) APTT (44.3)
  • Liver function test were normal
  • Creatinine (2300)
  • Venous blood gas: decreased pH (7.17), decreased bicarbonate (13), pCO2 (36) and lactate (1.9 )
  • Electrolytes: elevated potassium (7.9), decreased sodium (131), decreased chloride (93), elevated glucose (10.7)

Figure 1. ECG of patient showing Sinus Rhythm and peaked T waves in V2, V3, and V4, an early manifestation of hyperkalemia. Other manifestations (not demonstrated here) include prolonged PR segment, loss of P wave, bizarre QRS complexes and sine wave.

 

PoCUS Imaging

Figure 2. Ultrasound imaging showing moderate hydronephrosis, areas of anechoic fluid indicated by red arrows.

CT Imaging

Figure 3. A) Pelvic CT showing bladder with diffuse wall thickening with a posterior globular neoplasm. B) Pelvic CT showing bladder with calculi within the neoplasm. C) Abdominal CT showing moderate bilateral hydronephrosis.

 

Diagnosis

It was determined that the cause of the acute kidney injury was diffuse thickening of the bladder wall causing obstruction of the ureterovesical junctions (Figure 3A and B). This resulted in bilateral moderate hydronephrosis (Figure 2 and 3C). Additionally, previous CBC reports showed the patient had chronic anemia likely from an underlying chronic kidney disease. This affected EPO production and resulted in decreased erythrocytes production from bone marrow.  With reduce erythrocytes, hemoglobin and hematocrit levels were also decreased. The acute kidney injury resulted in elevated creatinine level, leading to hyperkalemia and metabolic acidosis.

Management

Patient was admitted and fluid resuscitated. To correct his hyperkalemia patient was given 5 to 10 units of regular insulin and dextrose 50% intravenously to shift potassium out of circulation and into the cells. Calcium gluconate (10 mL of 10% solution infused over 5 mins) was given to reduce risk of arrhythmias.

To treat his bilateral hydronephrosis patient was sent to interventional radiology for placement of percutaneous nephrostomy tube. Follow up surgery will be needed to clear the ureters and biopsy of the bladder will be needed to determine treatment for the growth.  Depending on the remaining kidney function after treatment of the acute kidney injury the patient may require dialysis.


 

References

  1. Rahman, Mahboob, Fariha Shad, and Michael C. Smith. “Acute kidney injury: a guide to diagnosis and management.” American family physician 86.7 (2012): 631-639.
  2. KDIGO Clinical Practice Guideline for Acute Kidney Injury, Kidney Int Suppl. 2012;2(Suppl 1):8
  3. Erdbruegger Uta, Okausa Mark. “Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in adults”. Uptodate (2019)
  4. Kaufman J, Dhakal M, Patel B, Hamburger R. Community-acquired acute renal failure. American Journal of Kidney Disease 2 (1991): 191–198.
  5. Obialo CI, Okonofua EC, Tayade AS, Riley LJ. Epidemiology of de novo acute renal failure in hospitalized African Americans: Comparing community‐acquired vs hospital‐acquired disease. Archives of Internal Medicine 160.9 (2000): 1309– 13.
  6. Meyer TW, Hostetter TH. Uremia. New England Journal of Medicine 357.13 (2007): 1316–1325.
  7. Mesropian, Paul Der, et al. “Community‐acquired acute kidney injury: A challenge and opportunity for primary care in kidney health.” Nephrology 21.9 (2016): 729-735.

 

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PoCUS in Pericardial Effusion

Medical Student Clinical Pearl – October 2019

 

Alex Pupek

Faculty of Medicine
Dalhousie University
CC4
Class of 2020

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual


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. 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. 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.

 

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Hemiplegic Migraine

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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Tardive Dyskinesia in an Emergency Setting

Medical Student Clinical Pearl – October 2019

Faith Moore

Faculty of Medicine
Dalhousie University
CC3
Class of 2021

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual



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. 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. 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. 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. 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. 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. 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.
  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. 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.)
  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.
  1. Kim J. (2014). Dextromethorphan for Tardive Dyskinesia. International Neuropsychiatric Disease Journal. 2. 136-140. 10.9734/INDJ/2014/7970.
  2. Tarsy D, Deik A. Tardive dyskinesia: Prevention, prognosis, and treatment. In: UpToDate, Eichler A (Ed), UpToDate, Waltham, MA. (Accessed on September 9, 2019.)
  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 “.
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Palpitations – A Paroxysmal Pearl

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. 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. 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
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Approach to Resuscitation in Severe Calcium Channel Blocker Poisoning

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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A focus on PoCUS – A reflection on the value of a PoCUS elective as a medical student

Medical Student PoCUS Elective Reflection

Nick Sajko

Class 2019 Dalhousie Medicine

@saj_ko

 

Nick Sajko, reflects on his experience after completing the SJRHEM PoCUS Elective. Nick is now a PGY1 in Emergency Medicine at the University of Alberta.


 

When my fourth and final year of medical school came around, I was at a crossroads: What did I want to do for the rest of my life? As many will attest, this question influences the choices you make in your clerkship years, especially in deciding on fourth year electives. I was ironically unfortunate in the fact that I had a broad range of interests in a system that does not always benefit those in my situation. I chose electives in Emergency Medicine, Internal Medicine, and Family Medicine – all of them providing valuable learning opportunities and a chance to hone my skills as a junior clinician. However, these “classic” or “bread and butter” electives paled in comparison to the experiences I obtained through my Point of Care Ultrasound (PoCUS) elective at SJRH – a unique elective opportunity relevant to any medical trainee.

 

It is my hope that this reflection piece will provide insight into those deciding on their elective choices and convince some of you to choose a few electives that are off the beat and path and unique. In particular, an elective in the field of PoCUS – a tool that is more useful than some may consider.

 


 

What does a PoCUS elective at SJRH entail? What can I expect?

 

My elective consisted of regularly scheduled shifts within the Emergency Department, paired with senior staff who have specialized training in PoCUS. During these shifts, I would see patients as if I was conducting a bread and butter Emergency Medicine elective, however, cases would be chosen based on the potential for ultrasound practice. This allowed me to gain a remarkable appreciation for the breadth of PoCUS applications within the primary care setting, while also allowing me to gain extremely valuable hands on time with ultrasound in a supervised setting.

 

In addition to the above, I was provided with numerous resources so as to allow for self-directed learning. One of the most valuable resources provided was the opportunity to use the SJRH EM state-of-the-art PoCUS simulator – an invaluable tool for any level of PoCUS experience. Closer to the end of this elective experience, I was offered opportunities to write PoCUS focused case-reports, as well as undergo PoCUS competency exams to solidify my skills within this setting.

The skills I learned in this elective carried forward with me into my various other electives, and provided me with a unique skill-set as a junior learner. Whether it was doing point of care ECHO in my cardiology elective, FAST scans during trauma-codes in my other Emergency Medicine electives, or assessing volume status in complex general internal medicine patients, my competency in these PoCUS applications definitely impressed both residents and staff alike during my fourth year!

 


Why is PoCUS relevant to me as a medical student wanting to specialize in: (insert hyper-specific / niche specialty here)

One question many people may have at this point is, “why would I do this if I wasn’t interested in Emergency Medicine?”. PoCUS is a constantly evolving field, with new and innovative applications being seen in clinical practice constantly. With this, PoCUS can play a huge role in many different specialties: Internal Medicine physicians use PoCUS to provide support to presumed diagnoses and perform certain procedures (such as placing central lines), while surgeons can utilize PoCUS in the examination of traumas, as well as to support diagnoses in the pre- and post-operative patient. PoCUS is steadily becoming a sought after skill in most of the medical and surgical specialties, where proficiency in its use and interpretation can set you apart from other trainees, and more importantly, add to the competency of your patient care!

The value of having this elective through the Emergency Department allows for students to test their skills in the undifferentiated patient – something that will provide learners with enhanced deduction and reasoning skills, no matter what specialty they are interested in. It also allows learners to have access to a huge pool of patients, with a wide breadth of medical problems, thus optimizing this unique elective’s value.

 


 

Is choosing a “unique”, “niche”, or “extra-focused” elective, such as PoCUS, detrimental to my CaRMS application?

Fourth year electives and CaRMS amalgamate into a cruel and unusual game – while most medical school staff and administrators will tell you that your fourth year electives are to be used to “try new things”, this is often not the reality. With the competitiveness of specialties on a constant upward trend, more and more learners choose to conduct the majority of their electives in the single specialty they are interested in. This is great for those who are certain about the field they want to practice in, but creates a predicament for those of us who want to explore a number of options before making a decision.

As I mentioned above, I was in the latter group – with interests spanning 3 different specialties, including some very competitive ones. I chose to go against the grain, so to speak, and opted to conduct a variety of electives in different specialties – including some niche electives in things such as PoCUS. Not only were these opportunities fantastic from a learning point of view, I would argue that they allowed me to stand out amongst a sea of similar applicants and provided me with a unique skill set – something that I think most programs will find enticing! But most importantly, they were fun, exciting, and allowed me to experience my fourth year of medical school the way its advertised.

For those that know their specialty of choice, I would provide the same advice – use this year to experience new things and create a unique learning identity that will set you apart from the rest.

 


 

After all the worry and panic with my elective choices, feeling like I wasn’t committed enough to one specific specialty, I ended up matching to my first-choice field and location. I think this is in large part due to the fact that I was well-rounded in my experiences and had taken the chance to explore unique learning opportunities through this fantastic elective at SJRH. The staff, the environment, and the resources that come with the PoCUS elective at SJRH EM are second to none – I am confident in saying that this elective was the most beneficial and enjoyable component to my fourth year training. Hopefully my thoughts and reflections on this experience will allow some of you to follow a similar path.

 

Nicholas Sajko, B.Sc, MD

Emergency Medicine PGY1

University of Alberta

 


 

Click here for more information on the SJRHEM PoCUS Electives and Fellowships

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SJRHEM @Halifax CAEP 2019

Congratulations to all our researchers presenting at CAEP Halifax 2019. This year we have had a total of 12 research abstracts accepted for either oral or poster presentations, 5 invited presentations, 3 panel discussions, 5 track chairs, and 1 national award! We are also involved in many administrative, academic and research committee meetings across the conference.


2019 CAEP Abstracts Links for Department of Emergency Medicine, Saint John Regional Hospital, Saint John, New Brunswick

Previous SJRHEM @ CAEP


Does point-of-care ultrasonography improve diagnostic accuracy in emergency department patients with undifferentiated hypotension? An international randomized controlled trial from the SHoC-ED investigators

P. Atkinson, M. Peach, S. Hunter, A. Kanji, L. Taylor, D. Lewis, J. Milne, L. Diegelmann, H. Lamprecht, M. Stander, D. Lussier, C. Pham, R. Henneberry, M. Howlett, J. Mekwan, B. Ramrattan, J. Middleton, D. van Hoving, L. Richardson, G. Stoica, J. French

https://doi.org/10.1017/cem.2019.65


Does point-of-care ultrasonography change actual care delivered by shock subcategory in emergency department patients with undifferentiated hypotension? An international randomized controlled trial from the SHoC-ED investigators

P. Atkinson, S. Hunter, M. Peach, L. Taylor, A. Kanji, D. Lewis, J. Milne, L. Diegelmann, H. Lamprecht, M. Stander, D. Lussier, C. Pham, R. Henneberry, M. Howlett, J. Mekwan, B. Ramrattan, J. Middleton, D. Van Hoving, L. Richardson, G. Stoica, J. French

https://doi.org/10.1017/cem.2019.111


Diagnostic accuracy of point of care ultrasound in undifferentiated hypotension presenting to the emergency department: a systematic review

L. Richardson, O. Loubani, P. Atkinson

https://doi.org/10.1017/cem.2019.140

[pdf-embedder url=”http://sjrhem.ca/wp-content/uploads/2019/05/CAEP-2019-Systematic-Review-Poster-Trial-2-PA.pdf” title=”CAEP 2019 Systematic Review Poster Trial 2 PA”]


Does specialist referral influence emergency department return rate for patients with renal colic? A retrospective cohort study

A. Kanji, P. Atkinson, P. Massaro, R. Pawsey, T. Whelan

https://doi.org/10.1017/cem.2019.260

[pdf-embedder url=”http://sjrhem.ca/wp-content/uploads/2019/05/Does-Disposition-Influence-ED-Return-in-Renal-Colic-AK-PA.pdf” title=”Does Disposition Influence ED Return in Renal Colic- AK PA”]


Introduction of an ECPR protocol to paramedics in Atlantic Canada; a pilot knowledge translation project

C. Rouse, J. Mekwan, P. Atkinson, J. Fraser, J. Gould, D. Rollo, J. Middleton, T. Pishe, M. Howlett, J. Legare, S. Chanyi, M. Tutschka, A. Hassan, S. Lutchmedial

https://doi.org/10.1017/cem.2019.302

[pdf-embedder url=”http://sjrhem.ca/wp-content/uploads/2019/05/COLIN-caep-2019-pdf.pdf” title=”COLIN caep 2019 pdf”]


The Devil may not be in the detail – training first-responders to administer publicly available epinephrine – microskills checklists have low inter-observer reliability

R. Dunfield, J. Riley, C. Vaillancourt, J. Fraser, J. Woodland, J. French, P. Atkinson

https://doi.org/10.1017/cem.2019.228

[pdf-embedder url=”http://sjrhem.ca/wp-content/uploads/2019/05/CAEP-2019_POSTER_Final_RJD_RIM-PA.pdf” title=”CAEP 2019_POSTER_Final_RJD_RIM PA”]


How to get your departmental web content to work for you: one department’s experience with free open access medical education

K. Chandra, D. Lewis, P. Atkinson

https://doi.org/10.1017/cem.2019.209

[pdf-embedder url=”http://sjrhem.ca/wp-content/uploads/2019/05/KC-FOAMed_CAEP19-002.pdf” title=”KC FOAMed_CAEP19 (002)”]


Management of first trimester bleeding in the emergency department

R. Amiro, R. Clouston, J. French, P. Atkinson

https://doi.org/10.1017/cem.2019.197

[pdf-embedder url=”http://sjrhem.ca/wp-content/uploads/2019/05/Poster-Presentation-Renee-Amiro-CAEP-PA.pdf” title=”Poster Presentation Renee Amiro CAEP PA”]


Obtaining consensus on optimal management and follow-up of patients presenting to the emergency department with early pregnancy complications – a modified Delphi study

A. Cornelis, R. Clouston, P. Atkinson

https://doi.org/10.1017/cem.2019.215

[pdf-embedder url=”http://sjrhem.ca/wp-content/uploads/2019/05/Allyson-C-early-preg-caep-2019-PA.pdf” title=”Allyson C early preg caep 2019 PA”]


Emergency department staff perceived need and preferred methods for communication skills training

M. Howlett, M. Mostofa, J. Talbot, J. Fraser, P. Atkinson

https://doi.org/10.1017/cem.2019.256

[pdf-embedder url=”http://sjrhem.ca/wp-content/uploads/2019/05/Howlett-caep-2019-jf.pdf” title=”Howlett caep 2019 jf”]


Designing team success – an engineering approach to capture team procedural steps to develop microskills for interprofessional skills education

R. Hanlon, J. French, P. Atkinson, J. Fraser, S. Benjamin, J. Poon

https://doi.org/10.1017/cem.2019.253

[pdf-embedder url=”http://sjrhem.ca/wp-content/uploads/2019/05/Hanlon-Prototyping-caep-2019-new-PA.pdf” title=”Hanlon Prototyping caep 2019 – new PA”]

[pdf-embedder url=”http://sjrhem.ca/wp-content/uploads/2019/05/Hanlon-Mico-skills-caep-2019-new-PA.pdf” title=”Hanlon Mico-skills caep 2019 – new PA”]



[pdf-embedder url=”http://sjrhem.ca/wp-content/uploads/2019/05/CAEP-19-Emergency-Medicine-Poster-Final.pdf” title=”CAEP 19 Emergency Medicine Poster Final”]

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PoCUS – Dilated Aortic Root

Medical Student Clinical Pearl

James Kiberd

Class 2019 Dalhousie Medicine

Reviewed and Edited by Dr. David Lewis


Case:

A 66 year-old female presented to the Emergency Department with shortness of breath and back pain. She had a known dilated aortic root, which was being followed with repeat CT scans. Given the nature of her presenting complaint, a PoCUS was performed to assess her aorta.

 

 

 

Long Axis Parasternal View:

PoCUS for Cardiac imaging has been studied in the acute care setting; focusing on the assessment for pericardial effusion, chamber size, global cardiac function, and volume status, and cardiac arrest.1

In the setting of acute aortic dissection, further evaluation is often recommended depending on the practitioner’s skill level.2 There have been case reports where ultrasound has been used to assess both Type A and Type B aortic dissections.3–5

In order to assess the aortic root, have the patient in a supine position. Either the phased array or the curvilinear probe can be used depending on examiner’s preference. The probe should be positioned with the marker towards the patient’s right shoulder on the anterior chest to the left of the patient’s lower left sternal border. By tilting the transducer between the left shoulder and right hip, long axis views are obtained at different levels with the goal of identifying four main structures; the aorta, the left atrium, and the right and left ventricles. The parasternal long axis view of our patient is shown in Figure 1, where her aortic root measured 3.83cm.

 

Figure 1: Parasternal Long Axis View of Heart: Patient’s root diameter was found to be 3.83cm.

More generally, this view can be used to assess left ventricular contractility and the presence of pericardial effusion, which were not present in this patient. She went on to have a confirmatory CT scan where her aortic root was found to be unchanged from her last scan and was 3.8 cm in diameter as assessed by PoCUS.

In Summary:

Although not rigorously studied to assess aortic root dilatation at the bedside, we present a case where PoCUS was reliable in the assessment of the aortic root. There have been other cases of aortic dissection identified by ultrasound in the emergency department setting, however confirmatory studies (either CT scan or formal echocardiography) are still recommended.


References:

  1. Labovitz AJ, Noble VE, Bierig M, et al. Focused cardiac ultrasound in the emergent setting: A consensus statement of the American society of Echocardiography and American College of Emergency Physicians. J Am Soc Echocardiogr. 2010;23(12):1225-1230. doi:10.1016/j.echo.2010.10.005.
  2. Andrus P, Dean A. Focused cardiac ultrasound. Glob Heart. 2013;8(4):299-303. doi:10.1016/j.gheart.2013.12.003.
  3. Perkins AM, Liteplo A, Noble VE. Ultrasound Diagnosis of Type A Aortic Dissection. J Emerg Med. 2010;38(4):490-493. doi:10.1016/j.jemermed.2008.05.013.
  4. Bernett J, Strony R. Diagnosing acute aortic dissection with aneurysmal degeneration with point of care ultrasound. Am J Emerg Med. 2017;35(9):1384.e3-1384.e4. doi:10.1016/j.ajem.2017.05.052.
  5. Kaban J, Raio C. Emergency department diagnosis of aortic dissection by bedside transabdominal ultrasound. Acad Emerg Med. 2009;16(8):809-810. doi:10.1111/j.1553-2712.2009.00448.x.
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PoCUS – Pleural Effusion

Medical Student Clinical Pearl

James Kiberd

Class 2019 Dalhousie Medicine

Reviewed and Edited by Dr. David Lewis


Case: 

A 90 year-old male presented with worsening shortness of breath on exertion, crackles bilaterally at the bases on auscultation with known history of congestive heart failure. Bedside ultrasound was performed to assess for pleural effusion

Lung Views:

In order to perform ultrasound of the lungs, there are four views that are obtained (see Figure 1). Place the patient supine. The high frequency linear array transducer is often used, but either the phased array or curvilinear transducers can be used. The first views are taken at both right and left mid-clavicular lines of the anterior chest. With the marker of the transducer pointed toward the patient’s head, a minimum of 3-4 rib spaces should be identified. The next views are of the posterior-lateral chest. The patient can be supine or in the sitting position. It is these views where a pleural effusion can be identified.

Figure 1: Chest views with ultrasound. ‘A’ are anterior chest view positions and ‘B’ are posterolateral view positions

Pleural Effusion

Pleural effusion is assessed by ultrasound placing the transducer in the midaxillary line with the marker oriented toward the patient’s head. On the patient’s right side the diaphragm, the liver, and the vertebral line can be seen. On the left, the diaphragm, spleen, and vertebral line should be in view. In a patient without pleural effusion, one should not be able to visualize the lung as it is mostly air and scatters the sound produced by the transducer. However, in the presence of pleural effusion, the area above the diaphragm is filled with fluid and therefore will appear anechoic. In addition, the vertebral line will be present past the diaphragm as the fluid allows the sound waves to propagate and not scatter. This is known as the ‘spine sign’ (also known as the ‘V-line’). Finally, one is often able to see the atelectatic lung float and move with respirations in the fluid, this is known as the ‘sinusoid sign.’ These are the three criteria outlined by consensus statements in the identification of pleural effusions.1 Occasionally, the area above the diaphragm may look like spleen or liver, but this is known as ‘mirror image’ artifact and is normal.2 Figure 2 shows both the right and left views of our patient.

Figure 2: Pleural effusion showing anechoic pleural fluid, atelectatic lung, and ‘spine sign

Accuracy with Ultrasound

Ultrasound is more accurate than either chest x-ray or physical exam in the identification of small pleural effusions.3 For a chest x-ray to identify fluid there usually needs to be more than 200cc present.2 A meta-analysis found that ultrasound had a mean sensitivity of 93% (95%CI: 89-96%) and specificity of 96% (95%CI: 95-98%).4

 

Our patient went on to have a chest x-ray where he was found to have bilateral pleural effusions (see Figure 3).

Figure 3: Bilateral pleural effusions seen on chest radiography in our patient.

In Summary

Three criteria are used to identify pleural effusion on ultrasound; anechoic fluid above the diaphragm, the ability to visualize the spine above the diaphragm (‘spine sign’), and atelectatic lung moving with respirations (‘sinusoid sign’). Lung ultrasound for the detection of pleural effusion is more reliable to identify small effusions in comparison to both radiography and physical exam.


References:

  1. Volpicelli G, Elbarbary M, Blaivas M, et al. International evidence-based recommendations for point-of-care lung ultrasound. Intensive Care Med. 2012;38(4):577-591. doi:10.1007/s00134-012-2513-4.
  2. Liu RB, Donroe JH, McNamara RL, Forman HP, Moore CL. The practice and implications of finding fluid during point-of-care ultrasonography: A review. JAMA Intern Med. 2017;177(12):1818-1825. doi:10.1001/jamainternmed.2017.5048.
  3. Wong CL, Holroyd-leduc J, Straus SE. CLINICIAN ’ S CORNER Does This Patient Have a Pleural Effusion ? PATIENT SCENARIO. Jama. 2010;301(3):309-317. doi:10.1001/jama.2008.937.
  4. Grimberg AI, Carlos Shigueoka DI, Nagib Atallah III Á, et al. Diagnostic accuracy of sonography for pleural effusion: systematic review Acurácia diagnóstica da ultrassonografia nos derrames pleurais: revisão sistemática
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