EM Reflections December 2020 – Pelvic Trauma

Big thanks to Dr. Joanna Middleton for leading discussions this month.

All cases are theoretical, but highlight important discussion points.

Authored and Edited by Dr. Mandy Peach

Case

A 46 yo male is transported to the ED via EMS after sustaining multiple injuries in a motorcycle accident. He was helmeted and driving on a community street, he estimates at 70km/hr, when he hit a patch of water and hydroplaned off the road into a ditch. He was not ambulatory on scene and a bystander called EMS. On arrival in the trauma bay his vitals are: BP 100/62 HR 115 Sat 100% on NRB, T 37.2

You begin your primary survey. His airway is patent and he is speaking full sentences. He complains primarily of chest pain with breathing and pain in his hips and legs. His helmet was removed on scene by EMS and is in good condition. He was collared as a precaution. He has obvious bruising over the anterior chest, you suspect from hitting the handlebars, but normal chest rise bilaterally with breathing. He has decreased air entry bilaterally to the bases, PoCUS reveals normal lung slide. You move on to circulation. There is no sign of arterial bleeding. FAST exam shows negative RUQ and LUQ views, however it is indeterminate as the patient was placed in a pelvic binder on scene and you can’t visualize the pelvic views.

Do you remove the pelvic binder to access for pelvic injuries?

No – pelvic ring injuries can result in massive venous hemorrhage. This patient is hypotensive and tachycardic, given the mechanism a pelvic injury is quite likely – therefore removing the binder could stop any tamponade of vessels, leading to move blood loss and an unstable patient.

If a patient is externally hemorrhaging from a source thought to be under the binder than the binder can be transiently removed to control the bleeding1 .

You decide to leave the binder in place and get portable XRs as you work through your trauma survey. XR’s confirm a pelvic ring fracture – you suspect open book that has been ‘closed’ with the binder.

This patient has a pelvic injury, other than hemorrhage what other injuries/complications is this patient at risk of 2,7,8?

Intraabdominal: 16%
Rectal injury – considered open fracture
High risk of infection/sepsis if missed

Urologic injury: <5%
More common in men (10X more likely)
Consider in anterior pelvic fractures

Gynecologic injury (if patient were female): 2-4%
Vaginal injury – considered open fracture

Neurological: 10-15%
Sacral plexus injury
The worsening instability of fracture = higher neurological risk
Cauda equina

Thoracic aortic rupture: 1.4% in pelvic fracture compared to 0.3% in blunt trauma without pelvic fracture

Imagine this patient was dropped off at the door by his friends who lifted him in, instead of being assessed by EMS – what injuries on visual exam would be concerning for pelvic injury3?

Perineal/scrotal bruising or hematomas

Blood at the urinary meatus or vaginal introitus or rectum

Malrotation of the lower limbs

Is a DRE warranted in this patient? In every trauma patient 4?

Rectal exam changes the management in 1.2% of trauma cases.

3 situations where a rectal exam is warranted

Spinal cord injury to access for sacral sparing

Pelvic fracture to determine if fracture is open

Penetrating abdominal trauma to assess for gross blood.

*Consider vaginal exam if consider genital injury as well.

What would be a contraindication to foley insertion?

Concern for genitourinary injury5
– Blood at the urethral meatus
– Penile/scrotal ecchymosis
– Gross hematuria or
– Patient unable to urinate

If possible, insert foley before application of pelvic binder if no contraindications. But in the field foley insertion does not delay the application of a pelvic binder.

If you were concerned about pelvic injury do you want to confirm with XR before placing a binder4?

No – if any concern for pelvic injury bind immediately.
Consider foregoing the pelvic exam and just place the binder on spec if mechanism of injury is concerning for pelvic injury.

If I do examine the pelvis – what is the best approach 4?

Do not place outward pressure or assess for vertical instability
Do not rock the pelvis.
Apply an inward pressure of the iliac wings once to assess for any movement.

Movement felt? Hold that inward pressure and immediately apply a pelvic binder.

How do you place a binder6?
This video reviews both the use of a commercial binder and using a bedsheet if you’re in a ‘bind’.

Remember that the binder goes over the greater trochanters (even though it is called a ‘pelvic’ binder). You can also internally rotate the legs and tape them together at the ankles to decreased anatomic bleed space4

 

Now imagine you are working a peripheral ED and the patient can’t be transported immediately due to mass casualty event at the nearest trauma center. The patient has been stabilized and will likely be in your department for hours.

Other than vitals, monitoring of symptoms and PoCUS assessment, what else should be part of your reassessment for a patient in a pelvic binder?

“Circumferential compression provided by pelvic binders should be released every 12 hours to check skin integrity and provide wound care as required1

The patient had pulmonary contusions and other superficial injuries on exam in additional to an unstable pelvic fracture. He went on to have a successful OR and recovery.

 

References & further reading:

  1. NB Trauma Program (2015). Consensus statement: Pelvic Binders. https://nbtrauma.ca/wp-content/uploads/2018/02/Consensus-Statement-Pelvic-Binders-December-2015.pdf
  2. Thomas (2016). Crackcast Ep 055: Pelvic Trauma. CanadiaEM https://canadiem.org/crackcast-e055-pelvic-trauma/
  3. Nickson (2020). Pelvic Trauma. Life in the fast lane. https://litfl.com/pelvic-trauma/
  4. Helman, A. Bosman, K. Hicks, C. Petrosoniak, A. Trauma – The First and Last 15 Minutes Part 2. Emergency Medicine Cases. January, 2019. https://emergencymedicinecases.com/trauma-first-last-15-minutes-part-2. Accessed Jan 12 2021.
  5. Lipp (2016). Genitourinary Trauma. https://canadiem.org/crackcast-e047-genitourinary-trauma/
  6. How to Apply a Pelvic Binder. CoreEM https://www.youtube.com/watch?v=tWLBZKeWEkg&ab_channel=CoreEM
  7. Fiechtl (2020). Pelvic trauma: Initial evaluation and management. Uptodate. Retrieved Jan 12, 2020.
  8. Li, P., Zhou, D., Fu, B. et al. Management and outcome of pelvic fracture associated with vaginal injuries: a retrospective study of 25 cases. BMC Musculoskelet Disord 20, 466 (2019). https://doi.org/10.1186/s12891-019-2839-y

Pelvic image from: Govaert, Geertje & Siriwardhane, Mehan & Hatzifotis, Michael & Malisano, Lawrence & Schuetz, Michael. (2012). Prevention of pelvic sepsis in major open pelviperineal injury. Injury. 43. 533-6. 10.1016/j.injury.2011.12.002.

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Evidence of Raised Intracranial Pressure on ECG

Evidence of Raised Intracranial Pressure on ECG – A Resident Clinical Pearl

Robert Dunfield, PGY2 FMEM program,  Dalhousie University Saint John

Reviewed & Edited by Dr. Mandy Peach

Case

A 44 year old male presents to your trauma bay with progressive confusion and altered level of consciousness for the past three days. Collateral history reveals possible recent recreational methamphetamine use. No specific abnormal neurological features or findings on history and physical. A full workup is performed and investigations reveal a left frontal intracerebral hematoma with the following CT head (Figure 1) and ECG (Figure 2):

 

1. What clinical (history and physical) features suggest an elevated intracranial pressure? [4, 5]

On history, suspect an elevated intracranial pressure with:

• headaches
• vomiting
• altered mental status (ranging and alternating from drowsiness to coma)
• visual changes (blurred, diplopia, photophobia)
• history of malignancy, trauma

On examination, suspect an elevated intracranial pressure with:

Cushing triad: hypertension, bradycardia and irregular respiration. This is a sign of impending brain herniation
• pupils unequal, unreactive
• disc edema
• optic atrophy
• bulging anterior fontanelle (in infants)
• evidence of trauma

 

2. What features on ECG are in keeping with an elevated intracranial pressure? [1, 2, 6]

Elevations in ICP or brain injuries are commonly associated with the following ECG changes:

• “Cerebral” T waves: widespread giant T wave inversion
• Flat T waves
• ST elevation/depression
• QTc prolongation
• Sinus bradycardia (if seen assess for other features of Cushing triad)
• Increased U wave amplitude
• Osborn (J) waves
• Other dysrhythmias: sinus tachycardia, junctional rhythms, premature ventricular contractions, atrial fibrillation, AV blocks

ECG changes are common with elevated ICP and intracranial hemorrhage. Approximately 56% of patients with intracranial hemorrhage have associated ECG changes.

Most importantly, recognize that these ECG changes can mimic acute coronary syndromes. This is potentially dangerous as a misdiagnosis of STEMI in a patient with an intracranial bleed could lead to unnecessary thrombolytics or PCI. For this reason, keep an elevated ICP in mind when identifying the above ECG changes.

 

3. What is a cerebral T wave? [1, 5]

Cerebral T waves are deep, symmetric, inverted T-waves seen on an ECG in patients with large intracranial bleeds. They are typically widespread

 

4. What other causes, other than elevated ICP, result in inverted T waves and should be kept on your differential? [2]

When analyzing an ECG it is important to recognize other causes of inverted T waves. The differential for inverted T waves includes:

• Myocardial ischemia and infarction
• Bundle branch block
• Ventricular hypertrophy
• Pulmonary embolism
• Hypertrophic cardiomyopathy

 

5. What is the pathophysiological cause for the ECG changes associated with an elevated ICP? [3, 4]

The full pathophysiology of ECG changes related to an elevated ICP is not fully understood.

ECG changes related to an elevation in ICP are thought to be related to neurogenic cardiac injury. This is mostly due to a surge of systemic catecholamines as a result of significant sympathetic activation from the central neuroendocrine axis and activation of the adrenal glands. Additionally, any injury to the hypothalamus or insula can cause dysfunction of the autonomic nervous system and a systemic inflammatory response.

Systemic catecholamine levels can be elevated for as long as 10 days. This prolonged exposure to catecholamines as well as the systemic inflammatory response can result in cardiac injury and dysfunction.

It is also possible for the heart to suffer from “neurogenic stunned myocardium syndrome” (NSM). This is reversible myocyte damage that results in ECG changes, in addition to other cardiac effects, due an excessive release of norepinephrine. The amount of cardiac damage caused by NSM correlates with the degree of brain injury. NSM can develop within four hours of brain injury. Other causes of NSM include pheochromocytoma, near drowning, and severe emotional experiences.

 

6. What are the most common intracranial findings associated with ECG changes related to an increased ICP? [1, 3]

The most common causes of ECG changes related to an elevation in ICP involve massive intracranial hemorrhage, including subarachnoid hemorrhage (49 to 100% of cases)3 and intraparenchymal hemorrhage (57% of cases)1.

Less commonly, ECG changes are associated with massive ischemic stroke causing cerebral edema, traumatic brain injury, or less commonly cerebral metastases.

 

7. How long do ECG changes last with brain injuries related to elevated ICP, and what are the clinical implications for a finding of prolonged ECG changes? [3]

Normally, as brain injuries and elevated ICP resolve, so will ECG changes. Most ECG changes will resolve within three days but have been reported to last up to eight weeks from the etiology of the elevated ICP.

Some reports have shown that prolonged ECG changes are associated with an increased risk for ischemic neurological deficit, poor outcome, and death following a subarachnoid hemorrhage. Specifically, persistent prolonged QTc is associated with poor clinical outcomes and death, whereas recovery of QTc is associated with good clinical outcomes.

 

SUMMARY & KEY POINTS:

• Be aware of Cushing triad on clinical assessment of patients with potential elevation in ICP (sinus bradycardia, hypertension, and abnormal respiratory pattern).

• There are multiple nonspecific ECG changes associated with an elevation in ICP, including: cerebral T waves, ST elevation/depression, sinus bradycardia, increased U wave amplitude, J waves, and other dysrhythmias.

• The exact pathophysiology for the cause of elevated ICP causing ECG changes is complicated and not fully understood. It is thought to mostly be due to excess catecholamine and norepinephrine exposure, along with a dysregulated inflammatory reaction.

• Subarachnoid hemorrhage and intraparenchymal hemorrhage are the most common causes of ECG changes associated with elevated ICP.

• Be aware that ECG changes related to elevated ICP can mimic acute coronary syndrome, so keep intracranial pathologies on your differential when the above ECG changes are found.

 

Of note, the patient described in the clinical scenario was admitted to neurosurgery and observed for nearly two weeks. He recovered without operative management.

 

REFERENCES:

  1. Cadogan M. Raised Intracranial Pressure. Life in the Fast Lane 2020; Last updated: Nov. 3, 2020, Accessed: December 28, 2020. Available from: https://litfl.com/raised-intracranial-pressure-ecg-library/

  2. Gregory T and Smith M. Cardiovascular complications of brain injury, Continuing Education in Anaesthesia Critical Care & Pain. 2012; 12:2, 67–71. Available from: https://doi.org/10.1093/bjaceaccp/mkr058

  3. Levis JT. ECG Diagnosis: Deep T Wave Inversions Associated with Intracranial Hemorrhage. Perm J. 2017; 21:16, 049. doi:10.7812/TPP/16-049

  4. Pinto VL, Tadi P, Adeyinka A. Increased Intracranial Pressure. [Updated 2020 Jul 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482119/

  5. Tannenbaum L. ECG Pointers: Intracranial Hemorrhage. emDocs.net: Electrocardiography. 2018; Last updated: November 14, 2018. Accessed: December 29, 2020. Available from: http://www.emdocs.net/ecg-pointers-intracranial-hemorrhage/

  6. Yogendranathan N, Herath HM, Pahalagamage SP, Kulatunga A. Electrocardiographic changes mimicking acute coronary syndrome in a large intracranial tumour: A diagnostic dilemma. BMC Cardiovasc Disord. 2017;17(1):91. Published 2017 Apr 4. doi:10.1186/s12872-017-0525-2

 

 

 

 

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A case of cholecystitis

Medical Student Clinical Pearl

Alana Jewell

M.D. Candidate, Class of 2022

Memorial University Faculty of Medicine

Reviewed & Edited by Dr. Mandy Peach

All case histories are illustrative and not based on any individual.

 

Case Presentation

A 70-year-old gentleman presented with four days of right upper abdominal pain radiating to the LUQ with nausea + vomiting, anorexia, flatulence, and bloating. Patient has PMHx of Crohn’s disease with a history of small bowel obstruction (SBO) and multiple surgeries. He felt these symptoms were like his SBO but he continued to have normal bowel movements. He had a similar episode a few months ago after eating fast food, but did not seek care for.

You suspect cholecystitis.

 

Differential Diagnosis

Can’t miss diagnoses for atraumatic abdominal pain 4:

ruptured AAA
pancreatitis
cholangitis
mesenteric ischemia
obstruction
perforated viscus
complicated diverticulitis
ruptured ectopic pregnancy

Differential for RUQ pain :

hepatitis
biliary colic
cholecystitis
cholangitis
pancreatitis
pneumonia
pleural effusion
pulmonary embolism

 

There is no single exam finding or laboratory test that has the ability to rule out acute cholecystitis5.

 

A combination of clinical evaluation, laboratory values, and diagnostic imaging are key to differentiate abdominal pain and make a diagnosis.

 

Cholecystitis

Cholecystitis is defined as inflammation of the gallbladder, typically caused by persistent stone obstruction in the cystic duct.

Acute cholecystitis (AC): Stone obstruction leads to bile trapping, increased intraluminal pressure, and an acute inflammatory process, typically presenting with RUQ pain, leukocytosis, and fever1.

Chronic cholecystitis: defined as recurrence of these events and is associated with fibrosis and mucosal atrophy2.

Acalculous cholecystitis: consider in chronically debilitated patients, classically elderly patients in ICU on total parental nutrition after sustained trauma or significant burn injury11.

Ascending (or acute) cholangitis: an important complication of cholecystitis – a serious bacterial infection of the common bile duct. It presents with Charcot’s triad of fever, jaundice, and abdominal pain2.

 

Acute cholecystitis is diagnosed and graded on severity by using the Tokyo Guidelines3.

 

 

 

Gallstones (which cause 95% of acute cholecystitis) are common in Western society, with about 10% of people affected, and 80% of those affected being asymptomatic1,3. The risk of pain or complications is 1-4% per year2.

 

Risk factors for cholesterol gallstones (the most common type) 2:

increased age
female gender
pregnancy
parity
race
high calorie
low fibre diet
low activity
obesity

 

 

 Clinical Presentation and findings

Clinical presentation varies with severity.

On history, a patient may have anorexia, emesis, fever, nausea, and RUQ pain.  On examination, guarding, Murphy’s sign (pain upon deep inspiration while palpating RUQ), rebound tenderness, abdominal rigidity, and RUQ tenderness may be seen2. Patients may describe a history of biliary colic, but with the presenting episode being more severe and longer in duration.

Mild-moderate cases have RUQ pain, fever, leukocytosis, and may have a palpable mass in the RUQ2. The most severe patients may have jaundice and, if have a secondary bacterial infection, could have signs of sepsis.

 

Case Continued

 

Physical Exam

Patient was tender to light palpation over RUQ and epigastric region. No rigidity, rebound tenderness, or guarding was noted.

Bloodwork

  • Elevated WBC with neutrophilic shift
  • C reactive protein > 250
  • Normal lipase, liver enzymes and renal function.

The most common laboratory findings in acute cholecystitis are an increased CRP and leukocytosis2.

 

This patient requires imaging to confirm the suspected diagnosis.

 

Diagnostic Imaging

Ultrasound

Ultrasound is the first-choice modality for imaging of AC. It is easily available in any emergency department, cost-effective, and minimally invasive3. Ultrasound findings can include5,6,9, as seen below 6.

 GB wall thickening > 3.5 mm
pericholecystic fluid
biliary sludge
gallstones
sonographic Murphy sign

 

If an ultrasound is positive, there is no need for further testing.

If negative, a CT should be ordered to exclude other diagnoses2,7.

 

CT findings for AC may include 3,6 as seen below 2:

thickening of GB wall
enlargement of GB
gallstones in GB neck or cystic duct
fluid accumulation around GB
pericholecystic fat stranding

 

Many gallstones are not radiopaque and may be missed on CT7

 

Management

Assessment with Tokyo Guideline diagnostic criteria can be used every 6-12 hours until a diagnosis is clear if initially uncertain, and to check severity until surgical management8.

In the Emergency Department, a patient is best managed with supportive care.

IV fluids,
NPO
Analgesia (NSAIDs are first-line treatment for AC. If ineffective, opioids are second line2. )

 

Secondary infection can result from bile stasis. Empiric antibiotics may be started against E. coli, Klebsiella, and Enterococcus5.

Definitive treatment for AC is cholecystectomy, with the gold standard being done laparoscopically (lap-C)2,7. Having a lap-C within 24-72 hours of symptom onset is recommended to decrease complication rates. If left unoperated for more than 72 hours chronic inflammation may occur, potentially complicating the surgery1. If a patient is ineligible for surgery, percutaneous cholecystostomy (gallbladder drainage) may be performed7.

 

Case Conclusion

Formal ultrasound found a hydropic gallbladder with pericholecystic fluid, thickened wall, and stranding. Cholecystitis was diagnosed. The patient was given analgesia and covered with ceftriaxone and metronidazole10. He went on to have an uncomplicated lap cholecystectomy.

 

References

  1. Indar, Adrian A, and Beckingham, Ian J. “Acute Cholecystitis.” BMJ, vol. 325, no. 7365, 2002, pp. 639–643.
  2. Wilkins, Thad, MD, MBA, et al. “Gallbladder Dysfunction: Cholecystitis, Choledocholithiasis, Cholangitis, and Biliary Dyskinesia.” Primary Care, vol. 44, no. 4, 2017, pp. 575–597.
  3. Yokoe, Masamichi, et al. “Tokyo Guidelines 2018: Diagnostic Criteria and Severity Grading of Acute Cholecystitis (with Videos).” Journal of Hepato-Biliary-Pancreatic Sciences, vol. 25, no. 1, 2018, pp. 41–54.
  4. Anjum, Omar, et al. “Ottawa’s Clerkship Guide to Emergency Medicine.” Department of Emergency Medicine, University of Ottawa, Mar. 2018.
  5. Jain, Ashika, et al. “History, Physical Examination, Laboratory Testing, and Emergency Department Ultrasonography for the Diagnosis of Acute Cholecystitis.” Academic Emergency Medicine, vol. 24, no. 3, 2017, pp. 281–297.
  6. Chawla, Ashish, et al. “Imaging of Acute Cholecystitis and Cholecystitis-Associated Complications in the Emergency Setting.” Singapore Medical Journal, vol. 56, no. 8, 2015, pp. 438–444.
  7. Bagla, Prabhava, et al. “Management of Acute Cholecystitis.” Current Opinion in Infectious Diseases, vol. 29, no. 5, 2016, pp. 508–513.
  8. Mayumi, Toshihiko, et al. “Tokyo Guidelines 2018: Management Bundles for Acute Cholangitis and Cholecystitis.” Journal of Hepato-Biliary-Pancreatic Sciences, vol. 25, no. 1, 2018, pp. 96–100.
  9. Flemming, Lewis & Henneberry (2017). PoCUS – Measurements and Quick Reference http://sjrhem.ca/pocus-measurements-quick-reference/
  10. Bugs & Drugs Medical App
  11. Forsythe (2016). Cholecystitis. First Aid for the Emergency Medicine Boards, Third Edition: Abdominal and Gastrointestinal Emergencies. McGraw-Hill Education. China.

 

 

 

 

 

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Small Bowel Obstruction & PoCUS

Small Bowel Obstruction & PoCUS – Medical Student Pearl

Patrick Rogers, Clinical Clerk (CC3)

Memorial University of Medicine Class of 2021

Reviewed by Dr. Kavish Chandra

Small bowel obstructions (SBO) are a common cause of acute abdominal pain in emergency departments across Canada. Diagnostic imaging plays a key role in the diagnosis and management of SBO as the history, clinical examination and laboratory investigations lack the sensitivity and specificity needed. Furthermore, diagnostic imaging may help differentiate SBO from other causes of abdominal pain (hernias, malignancies, intussusception, etc).

Historically, plain film abdominal radiography (AXR) has been an initial investigation in emergency departments when an SBO is suspected.  However, the current literature suggests that abdominal radiography is a relatively poor test for the diagnosis or exclusion of SBO when compared to other available modalities like US, CT, or MRI. In fact, multiple studies argue for the reduction of abdominal x-rays, especially when patients come in presenting with general abdominal tenderness. 1 Fortunately, there exists a compelling alternative: point of care ultrasound (PoCUS), and is being increasingly used as a first line investigation for SBO. 2

There are several reasons why physicians may start to choose PoCUS over traditional diagnostic modalities:

  • PoCUS avoids the radiation exposure that patients receive from cumulative plain films and abdominal CT’s. 3
  • PoCUS has been shown to reduce time to diagnosis and treatment in comparison to abdominal plain films. 3
  • PoCUS is more sensitive/specific modality when compared to abdominal plain film. 4
  • PoCUS allows for serial examination in the ED. 5
  • PoCUS may be rapidly available to centers with limited access to CT scanner. 6

The current evidence is highly favorable for the diagnostic efficacy of PoCUS in SBO. Here are the findings of peer-reviewed studies on the subject (published between 2013-2020):

  • PoCUS has high diagnostic accuracy and may also decrease time to diagnosis of SBO in comparison to other imaging modalities like CT and plain film.2
  • PoCUS has been found to have superior diagnostic accuracy for SBO in comparison to plain abdominal radiography. 4
  • PoCUS has been shown to be an accurate tool in the diagnosis of SBO with a consistently high sensitivity of 94-100% and specificity of 81-100%. 5
  • Current evidence suggests PoCUS is comparable in sensitivity and specificity to a CT scan when diagnosing SBO. 6
  • Ultrasound was found to be equivalent to CT in terms of diagnostic accuracy with a sensitivity of 92.31% (95% CI, 74.87% to 99.05%) and a specificity of 94.12% (95% CI, 71.31% to 99.85%) in the diagnosis of SBO. 7
  • In a study comparing XR, US, CT, and MRI, the abdominal x-ray was shown to be to be the least accurate imaging modality for the diagnosis of SBO. AXR’s were found to have a positive likelihood ratio of 1.64 (95% CI 1.07 to 2.52). In contrast, CT and MRI were both quite accurate in diagnosing SBO with positive likelihood ratios of 3.6 (95% CI = 2.3 to 5.4) and 6.77 (95% CI = 2.13 to 21.55). The use of ultrasound was found to have a positive likelihood ratio of 9.55 (95% CI = 2.16 to 42.21) and a negative likelihood ratio of 0.04 (95% CI = 0.01 to 0.13) for beside scans. 4

There are two major barriers identified in the literature that may prevent the effective use of PoCUS in the diagnosis of SBO. First, not every emergency physician has been trained on the use of PoCUS. Fortunately, two recent studies show that even minimally trained ED physicians can use it accurately. 8 Secondly, some surgeons have argued that PoCUS does not show the location of the obstruction accurately. This becomes a concern when the care team elects for surgical management of the patient’s SBO. However, recent evidence suggests that PoCUS may lead to quicker time to diagnosis and enteric tube insertion in conservative management. 8

Finally, how can learners use this technology? 5 Here are some specific sonographic findings to look for when evaluating a patient for SBO with US:

 

  • Dilatation of small bowel loops > 25 mm *
  • Altered intestinal peristalsis *
  • Increased thickness of the bowel wall
  • Intraperitoneal fluid accumulation

Figure 1. Dilatation of small bowel loops. Image courtesy Dr. Kavish Chandra

Figure 2. Altered intestinal peristalsis*. Image courtesy Dr. Kavish Chandra

Figure 3. – abnormal peristalsis “to and fro”9

References

  1. Denham G, Smith T, Daphne J, Sharmaine M, Evans T. 2020. Exploring the evidence-practice gap in the use of plain radiography for acute abdominal pain and intestinal obstruction: a systematic review and meta-analysis. International Journal of Evidence Based Healthcare. DOI: 10.1097/XEB.0000000000000218
  2. Guttman J, Stone M, Kimberly H, Rempell J. 2015. Point of care ultrasonography for the diagnosis of small bowel obstruction in the emergency department. CJEM. DOI: 10.2310/8000.2014.141382
  3. Flemming H, Lewis D. 2016. SBO- A New Focus for PoCUS. Saint John Regional Hospital Department of Emergency Medicine
  4. Taylor M, Lalani N. 2013. Adult small bowel obstruction. Academic Emergency Medicine. DOI: 10.1111/acem.12150
  5. Pourman A, Dimbil U, Shokoohi H. 2018. The accuracy of point of care ultrasound in detecting small bowel obstruction in emergency department. Emergency Medicine International. DOI: 10.1155/2018/3684081
  6. Gottlieb M, Peska, G, Pandurangadu A, Nakitende D, Takhar S, Seethala R. 2018. Utilization of ultrasound for the evaluation of small bowel obstruction: A systematic review and meta-analysis. The American Journal of Emergency Medicine. DOI: 10.1016/j.ajem.2017.07.085
  7. Tamburrini S, etal. 2019. Diagnostic accuracy of ultrasound in the diagnosis of small bowel obstruction. Diagnostics. DOI: 10.3390/diagnostics9030088
  8. Carpenter C. 2013. The end of X-Rays for suspected small bowel obstruction? Using evidence-based diagnostics to inform best practices in emergency medicine. Academic Emergency Medicine. https://doi.org/10.1111/acem.12143
  9. The PoCUS Atlas. https://www.thepocusatlas.com/bowel-gi

Copyedited by Dr. Mandy Peach

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EM Reflections Nov 2020 – A Case of Atrial Fibrillation/Flutter

Big thanks to Dr. Paul Page for leading discussions this month.

All cases are theoretical, but highlight important discussion points.

Authored and Edited by Dr. Mandy Peach

Reviewed by Dr. Kavish Chandra

Atrial fibrillation

• Review risk factors and complications
• Features of primary vs secondary arrythmia
• Risk stratifying a patient for stroke
• CHADS-65
• Sedation and cardioversion

Case

A 45 yo male presents to the ED feeling unwell for 2 days. He has a known history of atrial fibrillation but doesn’t consistently take rate control medications. He describes feeling like his heart is racing and he has trouble breathing that ‘comes and goes’. He currently complains of palpitations for 4 consecutive hours. He denies any chest pain or shortness of breath.
His vitals: BP 125/76, HR 134, RR 18, O2 98% RA, T 37.2
His ECG:

He appears to be in atrial flutter.

 

If this patient didn’t have a known history of arrhythmia, what are some risk factors for atrial fibrillation/flutter 1?

 

What are the life threatening complications with atrial fibrillation and their mechanisms?

Stroke – formation of clots in the atria secondary to blood stasis that embolize
Acute Coronary Syndrome – rapid rate decreases coronary blood flow
Pulmonary edema/heart failure – increased pulmonary arterial pressures secondary to increased afterload in atria2

The patient is brought in and attached to cardiorespiratory monitoring. The nurse applies pads and asks if you would like to immediately cardiovert.

 

What are the indications to immediately cardiovert a patient with any tachycardia? Does this patient require cardioversion?

Any sign of clinical instability:
• New severe hypotension (SBP < 90 mmHg) or signs of hypoperfusion
• Chest pain or ST depression > 2mm on ECG
• Acute heart failure2 – shortness of breath, hypoxia, clinical findings on exam

Your patient is experiencing palpitations, has a stable blood pressure and has no shortness of breath. He does not require cardioversion.

 

Is it common for atrial fibrillation to cause instability as the primary arrhythmia? What presentations make secondary arrhythmia more likely?

No – generally there will be a secondary cause for the arrhythmia that should be addressed.

The differential can include:
• ACS
• PE
• Heart failure
• Bleeding
• Sepsis3

Presentations that would make it more likely that this is a secondary cause with an underlying medical condition are:
• Insidious onset onset with no palpitations
• Known atrial fibrillation on previous ECGs and currently on anti-coagulation
• No history of cardioversion
• HR < 150
• Fever, shortness of breath, pain3.

On further history you discover that the patient has presented 2 previous times to the ED and required cardioversion. He has known atrial fibrillation and is on anticoagulation. His previous transthoracic echocardiogram does not indicate a valvular cause You screen him for multiple secondary causes and come up empty. You feel this is a primary arrhythmia.

 

What is one primary arrhythmia that causes instability that should be ruled out and why? What are the ECG features?

Atrial fibrillation/flutter + rapid ventricular pre-excitation (Wolff-Parkinson-White).

In WPW there is an accessory pathway that bypasses the AV node, causing early activation of the ventricles and leading to a tachyarrhythmia. Up to 20% of these patients can also have atrial fibrillation where there are multiple areas of the atria firing at different times as well. It is imperative to recognize this pattern as the use of AV blocking medications will cause more rapid conduction through the accessory pathway – leading to ventricular fibrillation or ventricular tachycardia.4

“Rate > 200 bpm

Irregular rhythm

Wide QRS complexes due to abnormal ventricular depolarization via accessory pathway

QRS Complexes change in shape and morphology

Axis remains stable unlike Polymorphic VT

Atrial Flutter results in the same features as AF in WPW except the rhythm is regular and may be mistaken for VT.”4

 

How do you control this patient’s heartrate?

The patient is stable, you have some time. First consider their risk of stroke.

LOW RISK 3
• onset < 48 hours AND no high risk factors OR
• On anticoagulation ≥ 3 weeks AND
• < 2 risk factors according to CHADS-65

HIGH RISK 3
• No anticoagulation/inadequate (< 3 weeks) AND
• Onset > 48 hours (or unknown) OR
• Onset < 24 hours but ≥ 2 risk factors according to CHADS-65 OR
• Stroke/TIA within 6 months OR
• Valvular heart disease

CHADS-65

You review with your patient and his CHADS-65 is 1 – he has history of hypertension. So based on the fact that he has been anticoagulated long term (and has been med compliant), his time with symptoms is 2 days with clear onset within 4 hours, and he scores < 2 on CHADS-65 you consider him LOW RISK.

LOW RISK

These patients can be treated with rhythm or rate control, however rhythm control is preferable in this population3. Their symptoms resolve immediately, they leave the ED faster and often happier as they don’t have to be admitted to hospital.

You discuss with the patient and decide to do a cardioversion as he is low risk, opting for rhythm control. He is agreeable.

 

What should I use to cardiovert – electricity or pharmacology?

Really either – it’s physician and patient dependent.

The RAF2 trial compared both electricity + pharmacology to electricity + placebo. Both were effective: procainamide followed by electricity had a 97% success rate in converting the patient to sinus rhythm, while the placebo infusion followed by shock was 93% effective. 97% of patients in the trial were discharged from the ED and on follow up 2 weeks later, 95% were still in sinus rhythm5.
Regardless of the method, rhythm control is a good option unless there is a patient preference.

Still not sure what to pick? Whatever worked in the past for the patient.

Our patient has previously had successful electrical cardioversion, so you decide to go with electricity.

You let the team know you will be proceeding with electrical cardioversion so they can prepare the room and patient. RT is on their way and the nurse is asking what drugs to draw up.

 

What are options for sedating a patient for electrical cardioversion? At what dose?

Many options – a systemic review in 2015 looked at studies including IV agents (ie. propofol and etomidate), inhaled agents (ie. Isoflurane) and benzodiazepines (ie. Midazolam) for electrical cardioversion. The primary outcome was adverse events: hypotension, apnea and patient awareness – unfortunately there is little high quality data available to suggest one drug over another6.

In a retrospective chart review from a Canadian ED the most common medications used were fentanyl, propofol, midazolam and ketamine in descending order. Practitioners primarily used combination drugs at that particular facility. The most commonly combined sedatives were propofol and fentanyl followed by midazolam and fentanyl. Adverse outcomes were rare overall. Apneic episodes were similar between these two combinations (both < 1%), as was hypotension (1.3% overall).7 Although a helpful study, this site had very few single agent sedatives, like ketamine, to compare to.

Here is a chart of suggested medications for procedural sedation for painful procedures like cardioversion 8:

 

 

Really it comes down to your comfort with your drug of choice. Even though adverse events seem to be rare, still consider the potential for increased risk of apnea and hypotension when combining sedatives and analgesia. 

You gather your team, give the plan with your drug of choice, consent the patient and complete an appropriate airway assessment. You are ready to begin.

 

Does pad placement matter?

No – anterior-lateral vs anterior-posterior placement is not deemed to be a critical factor in cardioversion for atrial fibrillation/flutter9

You successfully convert the patient to normal sinus rhythm. He is discharged from the department and advised to continue his anticoagulation (a NOAC) as previously prescribed.

 

What if this was a first presentation of atrial fibrillation – would he require anticoagulation for long term stroke prevention?

We go back to our CHADS-65. This patient had a score of 1.

If CHADS-65 positive : anticoagulation

If CHADS-65 negative: no anticoagulation

If CHADS-65 negative with stable CAD, PVD or aortic vascular disease – add ASA 81 mg3

According to the CCS guidelines for Atrial fibrillation anticoagulation is required for ALL patients undergoing cardioversion, regardless of risk factors, for 4 weeks.10 This is not based on strong evidence. Therefore,

 

Anticoagulation and the decision to start should involve shared decision making with the patient.

 

For details on rate control and treatment of high risk patients please see the CAEP Acute Atrial Fibrillation/Flutter Best Practices
Checklist

References and further reading:

  1. Cichon, C (2019). PIRATES illustration on twitter @DocScribbles
  2. Smarandache (2020. The Simple Guide to Management of Non-Valvular Atrial Fibrillation in the ED. CanadiaEM https://canadiem.org/the-simple-guide-to-management-of-non-valvular-atrial-fibrillation-in-the-ed/
  3. Stiell, Scheuermeyer, Vadeboncoeur, Angaran, Eagles, Graham et al. (2018). CAEP Acute Atrial Fibrillation/Flutter Best Practices Checklist. CJEM 20 (3): 334-342
  4. Burns (2020). Pre-excitation syndromes. Life in the fast lane. https://litfl.com/pre-excitation-syndromes-ecg-library/. Accessed Dec 9, 2020.
  5. Helman, A. Swaminathan, A. Juurlink, D. Long, B. Stiell, I. Morgenstern, J. Klaiman, M. Lloyd, T. EM Quick Hits 7 – Status Epilepticus, Codeine Interactions, Anticoagulants in Malignancy, Atrial Fibrillation rate vs rhythm control, Peripheral Vasopressors, Motivational Interviewing. Emergency Medicine Cases. August, 2019. https://emergencymedicinecases.com/em-quick-hits-august-2019/. Accessed Dec 9, 2020].
  6. Lewis, Nicholson, Reed, Kenth, Alderson & Smith (2015). Anaesthetic and sedative agents used for electrical cardioversion (review) Cochrane Database of Systematic Reviews , Issue 3. Art. No.: CD010824
    https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD010824.pub2/epdf/full
  7. Campbell, Magee, Kovacs, Petrie, Tallon, McKinley et al. (2006). Procedural sedation and analgesia in a Canadian adult tertiary care emergency department: a case series. Can J Emerg Med ;8(2):85-93
  8. Scheirer (2018). Procedural Sedation and Analgesia. CanadiaEM https://canadiem.org/crackcast-e195-procedural-sedation-and-analgesia/
  9. Kirkland, Stiell, AlShawabkeh, Campbell, Dickinson & Rowe (2014). The efficacy of pad placement for electrical cardioversion of atrial fibrillation/flutter: a systematic review. Acad Emerg Med Jul;21(7):717-26
  10. Andrade, Verma, Mitchell, Parkash, Leblanc, Atzema & al. (2018) Management of Atrial Fibrillation: Complete CCS Guidelines Listing. Canadian Cardiovascular Society. https://www.ccs.ca/images/Guidelines/Guidelines_POS_Library/2018%20AF%20Update_Supplement_Final.pdf

 

 

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EM Reflections Nov 2020 – Chest pain; expand the differential!

Authored and Edited by Dr. Mandy Peach

 

Big thanks to Dr. Paul Page for leading the discussions in November.

All cases are imaginary, but highlight learning points that have been identified as potential issues during rounds.

Chest pain is a huge topic – this is not a deep dive, but hopefully a helpful review of some useful information for on shift. This post assumes a basic knowledge of bedside ultrasound.

Chest Pain

  • The ‘don’t miss’ diagnoses
  • The ultrasound findings that can be helpful in shortening the differential
  • The evidence for ultrasound in some chest pain diagnoses
  • Select decision rules in chest pain
  • D-dimer and troponin and their uses
  • Ultrasound findings of cholecystitis

Case

48 yo male presents to the ED with 4 hours of substernal CP. He describes the pain as sudden onset and waking him from sleep overnight. He feels sweaty and has had 2 episodes of nausea/vomiting. He denies any fever or diarrhea. He had a similar episode last week that spontaneously resolved after 3-4 hours. He has no history of exertional chest pain. His cardiac risk factors include hypertension and his father died of ‘heart problems’ in his late 60’s.

An ECG is completed:

On exam his vital signs are within normal limits. He appears slightly diaphoretic and uncomfortable. Cardiorespiratory exam is unremarkable.

 

What are the BIG can’t miss diagnoses for chest pain? What bedside tool can be helpful in diagnosing some of these conditions?

Acute Myocardial Infarction (MI)

Pulmonary Embolism (PE)

Tension Pneumothorax

Aortic Dissection

Cardiac Tamponade

Esophageal Rupture

 

The ECG is unremarkable for ischemic change. You order a cardiac work up, including a CXR. While you await these results, you reach for your nearest ultrasound probe. You perform a cardiac and lung scan:

Figure 1 – normal subxiphoid view of the heart

Figure 2: Normal lung slide with visible A lines

You do not see any large pericardial effusion and on an eyeball observation the heart appears to have grossly normal form and function. The lung scan appears unremarkable with no sign of pneumothorax after viewing multiple rib spaces anteriorly and laterally.

 

How accurate is ultrasound at helping you rule in/out some of the major chest pain diagnoses?

Cardiac tamponade – Trained emergency physicians using beside ultrasound are quite effective at identifying significant pericardial effusions with a sensitivity of 96% and specificity of 98%1.

Figure 3: Large pericardial effusion with collapsing of RV

 

Pneumothorax – Lack of lung sliding and comet tails has a specificity of over 90% in ruling in pneumothorax. Time constraints? 1 view has comparable sensitivity to 4 views in picking up a clinically significant pneumothorax2

Figure 4: Absence of lung sliding or comet tails indicating pneumothorax

 

Pulmonary Embolism – Although no one finding is pathognomonic for PE, signs of RV dysfunction in the right clinical context is certainly suggestive of acute PE. Findings of:

  • RV enlargement equal or greater to that of the LV
  • RV systolic dysfunction (RV free wall hypokinesis) or
  • bowing of the RV into LV

have a 99% specificity for PE3.

Figure 5: Enlarged RV with free wall hypokinesis at the apex (McConnell’s sign)

Figure 6: Bowing of RV into LV in parasternal short view “D sign”

For advanced scanners, in patients with abnormal vitals (tachycardiac and hypotensive):

  • normal TAPSE
  • normal RV size
  • absence of RV flattening
  • absence of McConnell’s sign

significantly decreases the post-test probability for PE4

 

Aortic dissection – very specific findings – if you see a dissection flap you found it! If not, it’s still a high risk diagnosis you wouldn’t want to miss. There is evidence that when getting advanced cardiac views, suprasternal notch views and visualizing the abdominal aorta the sensitivity of POCUS is 86%5, however this did not translate into mortality benefit and is likely of more benefit for advanced scanners.

 

With normal vitals and ultrasound findings you feel confident there is no pneumothorax or tamponade. The probability of PE seems quite low given the history. Is there an objective way to risk stratify your patient for PE risk?

 

Apply the PERC rule 6 in the targeted low risk patients like this one where your physician gestalt of likelihood of PE < 15% . In the appropriate population this tool has a sensitivity of 96%;

The probability of him having a PE is < 2%.

 

You revisit the history and physical exam keeping in mind your remaining diagnoses of aortic dissection and esophageal rupture.

Are there any tools I can use to help decide if my patient is high risk for aortic dissection?

This tool is for low-moderate risk patients where dissection is in the differential.  When this rule was applied to a retrospective population only 4% of dissections were missed. When adding a normal CXR the miss rate decreased to 2.7%. Each feature equals 1 point. Essentially the absence of any high risk feature essentially rules out aortic dissection7. If more than 1 high risk feature, proceed to CT-A. If ≤ 1 this tool suggest ordering d-dimer.

Does d-dimer help rule out aortic dissection?

It’s controversial. If your patient is low risk and dissection isn’t high on your differential, a normal d-dimer doesn’t really add any value. If you order anyways and it is positive, it may lead to unnecessary testing. It certainly should not be used in isolation. The above tool combined with d-dimer had a sensitivity of 98.8% in one study, however this has not been externally validated8 – proceed with caution.

Your patient has no high risk features for aortic dissection.

 

Your patient did have episodes of vomiting – could they have a ruptured esophagus (Boerhaave syndrome)?

Mackler’s triad – vomiting, chest pain and subcutaneous emphysema – is present in 14-25% of cases so certainly not reliable. Patients can present with mediastinitis and abnormal vitals.CXR findings include 10:

With a normal CXR and normal vitals this is less likely.

 

So, you’ve considered the major diagnoses for chest pain and cardiac ischemia is left to consider – your first troponin result just become available – it is within normal range.

 

Can you use a single troponin to rule out a cardiac event?

You are now 4 hours from the onset of the event. Over his visit you have ordered a second ECG which is also normal. The troponin is  normal – you feel more reassured.  But your patient does have some risk factors for cardiac disease. You need to decide how at risk your patient is. You use the HEART score 11to help stratify:

Your calculated heart score is 3 which is low risk.

“A single undetectable hs-troponin after 3 hours of symptom onset or a delta 2-hr hs-troponin T <4ng/L plus normal serial ECGs and a HEART score of 0-3 rules out acute MI and lowers 30-day MACE to well below 1%, a threshold below which ancillary testing may cause more harm than benefit12.”

You feel quite confident your patient has no acute life-threatening cause of chest pain. You settle the pain and nausea in the ED and feel his is safe to go home. You suspect gastritis.

3 days later on shift you recognize the same patient – he again is complaining of chest pain, but today he looks much worst. You grab his chart – he is mildly tachycardiac, but otherwise vitals are normal. ECG again looks normal.
Today the patient describes having worsening nausea, fatigue and chest pain. His pain is more persistent and is not relieved with OTC medication at home. When you ask him to point to the pain he points towards his epigastric area – not substernal as he previously complained of.

This visit you complete an abdominal exam and find significant RUQ tenderness.

 

What are some other causes of chest pain, that although not immediately life threatening, should be considered13?

 

You grab your ultrasound probe as you suspect cholecystitis, what are the ultrasound findings?

Thickened gb wall > 3.5mm and fluid surrounding the gallbladder as seen above14.

You confirm cholecystitis and consult surgical service. On formal imaging the radiologist is concerned for potential perforation of the gallbladder.

Bottom line – chest pain has a broad differential! Grab your ultrasound probe and use some evidence based tools to help narrow your differential. Once life threatening causes ruled out consider other causes that can still affect patient morbidity.

 

References and further reading:

  1. Mandavia, Hoffner, Mahaney, Henderson (2001). Bedside echocardiography by emergency physicians. Annals of Emergency Medicine, Vol 38 (4); 377-382
  2. Michael Prats, MD. Comparison of Four Views Versus Single View for Pneumothorax. Ultrasound G.E.L. Podcast Blog. Published on November 07, 2016. Accessed on December 07, 2020. Available at https://www.ultrasoundgel.org/6.
  3. Pulmonary Embolism. The Evidence Atlas, The POCUS Atlas https://www.thepocusatlas.com/ea-echo
  4. Michael Prats. Focused Echo for Pulmonary Embolism in Patients with Abnormal Vital Signs. Ultrasound G.E.L. Podcast Blog. Published on February 17, 2020. Accessed on December 07, 2020. Available at https://www.ultrasoundgel.org/86.https://www.ultrasoundgel.org/posts/KsPSovvURE1CN7eZYELz1w
  5. Michael Prats. Return of the Aortic Dissection – POCUS Accuracy and Time. Ultrasound G.E.L. Podcast Blog. Published on August 31, 2020. Accessed on December 05, 2020. Available at https://www.ultrasoundgel.org/97.
  6. https://www.mdcalc.com/perc-rule-pulmonary-embolism
  7. Ohle, McIsaac, Atkinson (2019). How do I rule out aortic dissection? Just the Facts. CJEM 21(2): 34-36
  8. Nazerian, Mueller, Soeiro, Leidel, Salvadeo, Giachino et al. (2017). Diagnostic Accuracy of the Aortic Dissection Detection Risk Score Plus D-Dimer for Acute Aortic Syndromes: The ADvISED Prospective Multicenter Study. Circulation 137 (3): 250-258
  9. Cadogan, M. Boerhaave syndrome. Life in the Fast Lane. Published on Nov 3, 2020. https://litfl.com/boerhaave-syndrome/
  10. Diaz, G (2018). Boerhaaeve Syndrome. https://www.grepmed.com/images/5441/diagnosis-boerhaave-syndrome-signs
  11. Heart Score https://www.heartscore.nl/
  12. Low Risk Chest Pain and High Sensitivity Troponin – A Paradigm Shift. EM Cases. Published July 30, 2019. https://emergencymedicinecases.com/low-risk-chest-pain-high-sensitivity-troponin/
  13. Chest Pain. CanadiEM. Published June 1, 2020. https://canadiem.org/crackcast-e214-chest-pain/
  14. Flemming, Lewis, Henneberry. PoCUS – Measurements and Quick Reference. SJRHEM. Published 2017. http://sjrhem.ca/pocus-measurements-quick-reference/

All ultrasound gifs from The PoCUS Atlas https://www.thepocusatlas.com/

 

 

 

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“The Mother’s Kiss”

A Tool in Nasal Foreign Body Removal in Pediatric Patients

Melanie Johnston, PGY2 iFMEM Dalhousie University Saint John

Reviewed by Dr. Mandy Peach

 

Introduction:

The highest incidence of nasal foreign bodies is in pediatric patients, ages 2-5.1 The removal of nasal foreign bodies in the emergency department can be challenging.

The most common objects removed are beads, nuts, chalk, eraser heads, pebbles, and other small objects.1,2 While most nasal foreign bodies are benign, some objects can cause severe damage and need to be urgently removed.

The diagnosis of nasal foreign may be obvious as the caregiver may have witnessed the event and present acutely. Others may have delayed presentations of weeks-months after the child develops symptoms of nasal irritation/infection from the retained foreign body. In general, organic foreign bodies (flowers, plants, bugs) tend to be more irritating to the nasal mucosa and cause symptoms much earlier.2

 

Details on history and physical exam findings that should raise suspicion of a potential nasal foreign body in a paediatric patient include:

  • Witnessed insertion of foreign body
  • Unilateral foul-smelling purulent discharge
  • Mucosal erosions/ulceration

  • Unilateral epistaxis

  • Headache focused on the same side as the foreign body
  • Nasal obstruction
  • Mouth breathing2

 

Nasal foreign bodies have the potential to dislodge posteriorly and aspirate.1 Consider aspirated FB if new wheeze/cough/shortness of breath in a child with suspected intranasal FB and be prepared for a precipitous change in the airway. 6 

 

Nasal foreign bodies are most commonly located on the floor of the nasal passage under the inferior turbinate, or superiorly  in front of the middle turbinate.2

Foreign bodies are most frequently located on the right side, due to the right handed dominance of most children.2

Figure 1. Anatomy of the nose.3

 

Examination:

Ensure good lighting to be able to visualize the canal. Place the patient in a sniffing position with caregiver assistance (they may have to firmly hold child for cooperation). Suction should be readily available for nasal discharge and to aid in visualization. Nasal speculum can be used to aid visualization of the canal. Visualization of the foreign body confirms the diagnosis.

 

Figure 2. Marble nasal foreign body in pediatric patient.4

 

ENT referral is warranted if:


– Foreign body suspected, but unable to visualize by anterior rhinoscopy
– Impacted foreign body with marked inflammation (eg button batteries)
– Penetrating foreign body
– Any foreign body that cannot be removed due to poor cooperation, bleeding, or limited instrumentation2

 

Foreign Body Removal Options:

There are a number of techniques for nasal foreign body removal in the Emergency Department: alligator forceps, suction, balloon catheters, cyanoacrylate glue.2 Depending on the patient, these methods can be technically challenging if the patient is uncooperative, and may require the use of procedural sedation. A less invasive alternative for children not willing to cooperate with manipulation in the nasal canal is the Mothers’ Kiss.

 

Mothers’ Kiss Technique:

This technique was first described in the 1960s by a general practitioner in New Jersey and uses positive pressure to mobilize the foreign body from the nasal passage.1 It is effective in approximately 60% of attempts5, and generally most effective for smooth/soft foreign bodies that totally occlude the anterior nasal cavity.2 Even when not successful, it may improve visibility of the foreign body. Theoretical risks include barotrauma to both the tympanic membranes or pneumothorax, but these complications have never been reported.5 The pressure used by the caregiver to attempt expulsion of the foreign body is equivalent to that of a sneeze, approximately 60mmHg.1 The main danger in removing a foreign body from the nose is the risk of aspiration.

Procedure:5
1) Instruct the caregiver to place their mouth over the childs’ open mouth, forming a firm seal (similar to mouth-to-mouth resuscitation).
2) Next, occlude the unaffected nostril with a finger
3) The caregiver should blow until they feel resistance (caused by the closure of the childs’ glottis), then they should deliver a short puff of air into the childs’ mouth
4) The puff of air travels through the nasopharynx, and if successful results in the expulsion of the foreign body
5) If unsuccessful, the procedure can be repeated a number of times

Figure 3: Caregiver performing “Mother’s Kiss”. Shows occlusion of unaffected nare,
with seal formed around childs’ mouth.

 

 

If the caregiver is unable to perform the procedure, the approach can be recreated with a bag-valve-mask as the positive pressure source, ensuring the mask covers only the childs’ mouth.

Figure 4: Positive Pressure Ventilation with Bag-Valve-Mask.6

 

 

For a visual review of these techniques, please refer to the following videos:

“Mother’s Kiss”

 Positive Pressure Ventilation

 

Bottom Line:

Nasal foreign bodies are a common occurrence in the paediatric population. Their removal in the Emergency Department can be challenging as the patient may be fearful and non-cooperative. While there are a number of methods for removal of nasal foreign bodies, the “Mothers’ Kiss” technique provides a relatively non-invasive alternative. It has been shown to be effective in removal of 60% of nasal foreign bodies, and is most effective if foreign bodies are smooth and located in the anterior nasal cavity. If the caregiver is unable to perform the procedure, the approach can be recreated with BVM as the positive pressure source. The risks of this technique are minimal, and even when unsuccessful, can assist in improving the visualization of the nasal foreign body.

 

References:

  1. Cook, S., Burton, M., & Glasziou, P. (2012). Efficacy and safety of the “mother’s kiss” technique: a systematic review of case reports and case series. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne, 184(17), E904–E912. https://doi.org/10.1503/cmaj.111864

  2. Isaacson, G., Ojo, A. (2020). Diagnosis and management of intranasal foreign bodies. Up to Date. Retrieved from https://www.uptodate.com/contents/diagnosis-and-management-of-intranasal-foreign-bodies.

  3. Le, P. (2020). Anatomy, Head and Neck, Nasal Concha. Retrieved from: https://www.statpearls.com/ArticleLibrary/viewarticle/32550

  4. Nose-Foreign Body Nose, Dr Vaishali Sangole. Retrieved Oct 31,2020 from: http://vaishalisangole.com/NOSE_Foreign.html

  5. Glasziou, P., Bennett, J. (2013). Mothers’ kiss for nasal foreign bodies. Australian Family Physician, 42(5): https://www.racgp.org.au/afp/2013/may/mothers-kiss/.

  6. Thoreckzo. (2017). Foreign Bodies in the Head and Neck. Pediatric Emergency Playbook. Retrieved from: https://pemplaybook.org/podcast/foreign-bodies-in-the-head-and-neck/

  7. Pretel, M. Removing object from child’s nose using the kiss technique. Youtube- retrieved from: https://www.youtube.com/watch?v=RR3SxICqdAY.

  8. Dudas, R. Nasal foreign body removal. Youtube- retrieved from: https://www.youtube.com/watch?v=PacvHiJFhNA.

 

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Spontaneous Abortion

Medical Student Clinical Pearl

Miranda Lees, Clinical Clerk II

Dalhousie Medicine New Brunswick, Saint John

Reviewed by Dr. Mandy Peach

Case

A 21yo G3P1A1 female at 6 weeks gestation presented to the Emergency Department with an 8 hour history of vaginal bleeding and abdominal pain. The bleeding is a mixture of bright red and brown blood with no clots, and the abdominal pain is episodic cramping in her suprapubic region.

Her obstetrical history is significant for 2 prior pregnancies, the first of which was carried to term with an uncomplicated vaginal delivery, and the second of which had resulted in a spontaneous abortion at 6 weeks gestation. She is otherwise healthy. The patient noted with both prior pregnancies she had similar vaginal bleeding around 6-8 weeks gestation. She was given RhoGAM due to her Rh- blood type.

On assessment the patient appeared well with all vital signs within normal limits. On physical exam bowel sounds were present, the abdomen was tympanic to percussion, and pain on palpation was present in the patient’s suprapubic region.

 

Differential for life threatening causes of vaginal bleeding in pregnancy

<20 weeks gestation >20 weeks gestation
      ruptured ectopic pregnancy          placental abruption
       retained products of conception          placenta previa
       complication of termination          post partum hemorrhage

Other causes for vaginal bleeding to consider in pregnancy and in non-pregnant patients

Spontaneous abortion
Acute heavy menstrual bleeding
Genitourinary trauma
Uterine arteriovenous malformation
Ruptured ovarian cyst
Ovarian torsion
Pelvic Inflammatory Disease
Fibroids
Polyps
Foreign body
Coagulation disorder
Medication related
Gynecologic malignancy

 

Investigations

A βhCG was ordered to confirm pregnancy and bedside ultrasound was done to look for intrauterine pregnancy.

Transabdominal ultrasound showed the following:

The presence of a gestational sac within the uterus and a fetal heartbeat within the fetal pole confirmed a viable intrauterine pregnancy (IUP). The patient was diagnosed with threatened abortion.

 

Spontaneous Abortion-an overview

Spontaneous abortion is one of the most common complications of pregnancy, occurring in 17-22% of pregnancies2 and is defined as loss of pregnancy prior to 20 weeks gestation, occurring most often in the first trimester3. There are 3 primary causes: chromosomal abnormalities in the fetus, maternal anatomic abnormalities, and trauma.3

Risk factors for spontaneous abortion

age (below 20 and above 35)
moderate to severe bleeding (especially if passage of clots)
prior pregnancy loss
maternal comorbidities (DM, autoimmune conditions, obesity, thyroid disease)
infection (notably parvovirus, CMV and untreated syphilis)
teratogenic medications
maternal radiation exposure
maternal smoking
caffeine
alcohol use

 

Classification4

Missed abortion is characterized by an asymptomatic death of the fetus with a lack of contractions to push out the products of conception.5

Clinical presentation

Spontaneous abortion most commonly presents with vaginal bleeding and cramping, ranging from mild to severe1. However, most women with first-trimester bleeding will not undergo spontaneous abortion1. Bleeding associated with spontaneous abortion often involves passage of clots or fetal tissue, and the cramping can be constant or intermittent, often worse with passage of tissue1.

Diagnosis

Confirmation of spontaneous abortion requires pelvic ultrasound.

In patients with a prior ultrasound showing intrauterine pregnancy, diagnosis of spontaneous abortion can be made if a subsequent ultrasound shows no intrauterine pregnancy or a loss of previously-seen fetal heartbeat1.

In patients with a prior ultrasound showing intrauterine pregnancy with no fetal heartbeat, spontaneous abortion is diagnosed based on the following1:

  • A gestational sac >25mm in diameter containing no yolk sac or embryo
  • An embryo with crown rump length >7mm with no fetal cardiac activity
  • After pelvic ultrasound showing a gestational sac without a yolk sac, absence of embryo with a heartbeat in >2 weeks
  • After pelvic ultrasound showing a gestational sac with a yolk sac, absence of embryo with a heartbeat in >11 days

Case conclusion

The patient was treated with IM RhoGAM, a formal pelvic and transvaginal ultrasound was arranged for the next day, and she was discharged home. The follow-up ultrasound showed a gestational sac present in the uterus, an embryo with crown rump length of 8.1mm and the presence of a fetal heartbeat.

 

References

  1. Borhart D. Approach to the adult with vaginal bleeding in the Emergency Department. In: UptoDate, Hockberger R (Ed), UpToDate, Waltham, MA. (Accessed on October 8, 2020).
  2. Gracia C, Sammel M, Chittams J, Hummel A, Shaunik A, et al. Risk Factors for Spontaneous Abortion in Early Symptomatic First-Trimester Pregnancies. Obstetrics & Gynecology. 2005;106(5):993-999. doi 1097/01.AOG.0000183604.09922.e0.
  3. Prager, Mikes & Dalton. Pregnancy loss (miscarriage): Risk factors, etiology, clinical manisfestations, and diagnostic evaluation. In: UptoDate, Eckler (Ed), UptoDate, Waltham MA. (accessed Nov 28, 2020)
  4. Diaz. 2018. Types of Spontaneous Abortion. In: GrepMed. Image Based Medical Reference. https://www.grepmed.com/images/5425/classification-spontaneous-obstetrics-diagnosis-abortion-obgyn-types (Accessed Nov 28, 2020)
  5. Alves C, Rapp A. Spontaneous Abortion (Miscarriage) [Updated 2020 Jul 20]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK560521/.

 

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CAEP Emergency Physician of the Year – Dr. David Lewis

A huge congratulations goes out to our very own Dr. David Lewis who is one of the recipients of 2020’s CAEP Emergency Physician of the Year – Urban! This is an annual award recognizing excellence in the specialty of emergency medicine and is awarded to a physician who has made outstanding contributions to the field in a number of areas including patient care, community service, healthcare administration and CAEP activities.

Dr. Lewis is an integral part of our emergency department as Assistant Clinical Departmental Head, Ultrasound Program Director, Informatics Lead and as a senior clinician. He has been actively involved with CAEP as a member of the planning committee, ultrasound committee and as Scientific Co-chair. Dr. Lewis continues to contribute to research as an editor with CJEM and as an active contributor to local projects. Last year he co-founded the PoCUS Fellowship program with the intentions of promoting the capabilities of PoCUS, and training fellows who will then carry on this knowledge in administering their own programs. Clinically, he is a seasoned member of the department with a wealth of experience and one committed to excellent patient care.

It comes as no surprise that Dr. Lewis has been awarded this honour – congratulations and SJRHEM is so happy to call you our own!

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EM Reflections October 2020 – Acute Urinary Retention

Big thanks to Dr. Joanna Middleton for leading the discussions in October

All cases are imaginary, but highlight learning points that have been identified as potential issues during rounds.

Edited by Dr. Mandy Peach


 

Acute Urinary Retention (AUR)

  • Categorized as obstructive, infectious/inflammatory, neurological, medication related
  • Physical exam should include a DRE and neurological exam
  • Investigations should include a U/A +/- C&S, creatinine, electrolytes +/- CBC
  • Consider a renal US if any renal impairment
  • PSA – defer at least 2 weeks, as acute urinary retention can cause elevation
  • Consider risk factors for post-obstructive diuresis

Case

A 60 yo male presents to the emergency department with inability to void over 8 hours, despite feeling urgency. He complains of increasing lower abdominal discomfort. He denies any infectious symptoms or new medications. He denies any back pain or recent injury. He does have a history of hesitancy and poor urine stream. He has never had a prostate exam and has no family doctor. His vital signs are within normal limits. He has a significantly distended bladder on physical exam.


Indications to insert a catheter1:

  • Inability to pass urine > 10 hours
  • Abdominal discomfort with bladder distention
  • Signs of acute kidney injury secondary to obstruction
  • Infectious cause of retention
  • Overflow incontinence

You decide to insert a urinary catheter. What else should you consider as part of your physical exam?

Consider the 4 main causes of urinary retention:

In this male patient it is pertinent to do a prostate exam to check for enlargement as well as a thorough neurological exam.

On exam you palpate a large, firm prostate. You are suspicious of prostate cancer – do you do a prostate specific antigen (PSA)?

No – acute urinary retention can transiently elevate PSA measurements up to 2 fold, this can persist for up to 2 weeks2. Defer PSA testing until after this time.

The U/A is negative for infection. The electrolytes are normal but the patient has an acute AKI with an elevated creatinine. Does this patient require renal imaging?

Consider renal imaging in any patient with AUR and abnormal renal function to assess for anatomical cause.

2 hours has passed and you reassess the patient – 1L of urine has drained upon insertion. A minimal amount has been draining since. The post-void residual is now 20 cc.

Is this patient at risk of post-obstructive diuresis?

Risk factors:

  • Abnormal electrolytes or acute creatinine elevation
  • Volume overload
  • Uremic
  • Acutely confused

Although the patient does have an abnormal creatinine, clinically he does not show signs of post-obstructive diuresis which is defined as urinary output > 200 mL for at least 2 hours after urethral catheter insertion, or > 3L in 24hrs AFTER the initial emptying of the bladder. Patients with any risk factors for post-obstructive diuresis should be observed in the ED for 4 hours.

After an appropriate observation period you discharge the patient with an urgent referral to urology given the acute presentation and abnormal prostate exam. You are sending the patient home with an indwelling catheter.

What is the optimum duration of catheter insertion? Does this patient require antibiotics?

Trials are contradictory. Some found increased likelihood of spontaneous voiding after 7 days, while an observational study found improved success if insertion was less than 3 days3.

Expert opinion from urology suggests duration of 7 days to avoid risk of re-catheterization1.

Routine antibiotics are not recommended unless the cause is thought to be infectious. However, if prostatic enlargement is thought to be the cause an alpha-blocker like tamsulosin can be beneficial1

 


 

References for further reading:

1 Ep 143 Priapism and Urinary Retention: Nuances in Management. Emergency Medicine Cases. https://emergencymedicinecases.com/priapism-urinary-retention/

2 Aliasgari, Soleimani, Moghaddam (2005).The effect of acute urinary retention on serum prostate-specific antigen level. Urology journal. Spring 2005;2(2):89-92

3 Acute Urinary Retention. Uptodate. https://www.uptodate.com/contents/acute-urinary-retention?search=post%20obstructive%20diuresis&source=search_result&selectedTitle=1~5&usage_type=default&display_rank=1#H537553020


 

Authored and Edited by Dr. Mandy Peach

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Trauma Reflections – October 2020

Big thanks to Sue Benjamin for her efforts in putting these reviews together!

 

Major points of interest:

 

A) Kudos – Trauma Codes for qualifying cases has improved!

May – September 2020, for cases qualifying for trauma team activation, the rate of calling ‘Trauma Codes’ has improved to 84%. RN trauma note is 93% for the activations.

Many of the missed activations are transfers from peripheral sites

 Please review the attached updated simplified activation criteria – notable changes are:

1/ Removal of minor head injuries without signs or symptoms on anticoagulants under “D”

2/ Addition of pulseless extremity under “C”

 

B) Chest Tubes in trauma – 5 year review

Chest tubes are placed infrequently (~ 1 per month) in our departments.

Review of post procedure x-rays (thanks J ‘Mek1’) showed there was less than optimal tube positioning 60% of the time.

Tube position and function must be critically reviewed post procedure.

Chest tube discussion/demonstration with Dr Russell will take place at next Trauma case review  (January 2021)

C) Oh, that patient is just here for Plastics..

‘Distracting’ injuries are called that for a reason. It is hard to look past deformed limbs, but always perform a head to toe assessment (including FAST) to identify associated injuries to others systems.

Trauma transfers should be re-assessed by ED physician at receiving hospital, to also determine if there are any other concerning injuries that have been missed.

Trauma cases being transferred to consultants, outside of NB trauma line, should be identified by charge MD when taking report.

 

D) “Penetrating neck trauma is en route”

Those words will wake you up in a hurry.

Keys to management are early notification (pre-arrival) of consultants (ENT +/- vascular) and clear airway plans that include a ‘double set’ up for potential need for surgical airway.

 

E) What kind of monster would order a ‘Panscan’ on a child? 

One that can weigh the risks (missed injuries) vs. benefits (minimizing radiation exposure).

Panscans in pediatric patients should never be ordered routinely, but should be considered in cases with high risk for clinically significant multi-system injuries (head, spine, thorax, abdomen).

 

F) Blunt traumatic cardiac arrest

This population has a grave prognosis.

Airway management, continuous chest compressions, rapid fluid/blood resuscitation and consideration for procedural interventions (thoracostomies, pericardiocentesis) are usual steps in care.

Epinephrine has no role unless medical cause for arrest is suspected.

A more in-depth review will be topic of upcoming SJRH ED rounds.

 

G) What did this guy have for supper?

Pizza and beer, and lots of it.

Ducanto catheters – large bore suction catheters – are available on all airway carts in the top drawer. They are much more efficient at decontaminating airways soiled with semi-solid material when compared to Yankauer.

 

H) Updated Trauma checklist:

“SJRH ED Trauma Process Checklist” is in trauma note package in room 19 and is a very useful prompt (see below). K/ T- L spine Traumatic Spine Injury Guidelines also below.

Download (PDF, 98KB)

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A Case of Uveitis

Medical Student Clinical Pearl (RCP) October 2020

Ben McMullin, Clinical Clerk III

Dalhousie Medicine New Brunswick, Saint John

Reviewed by Dr. Mandy Peach

 

Case Presentation

A 40 year old female presented to the Emergency Department with a 5 day history of right sided eye pain. The pain came on insidiously and had gradually been worsening. She had gone to a walk in clinic 3 days prior to presenting to the ED, and was prescribed antibiotics. Her symptoms continued to worsen despite treatment.

In the emergency department, she denied any discharge, and claimed that her eye was not pruritic. She stated that her eye pain was photophobic, but denied any visual disturbances or changes. She did not have fever or chills.

On exam, she did not have any periorbital erythema or conjunctival injection. She did not have any discharge. Normal ocular movements were noted. Her pupils were equal and reactive to light. Her visual acuity was 20/20 in both eyes. Peripheral vision was normal bilaterally. On slit lamp exam, no foreign body or corneal abrasion was identified.

Ophthalmology was consulted emergently, and agreed to assess this patient the same day.

 

Differential Diagnosis

  • Conjunctivitis
  • Acute closed-angle glaucoma
  • Scleritis
  • Keratitis
  • Uveitis
  • Foreign body1

 

Definition

Uveitis refers to inflammation in the uvea, which is the middle portion of the eye. The uvea is made up of the iris and the ciliary body anteriorly, and the choroid posteriorly. Inflammation can be localized anteriorly, posteriorly, or can be generalized.1

Figure 1 : Anatomy of the eye. Rosenbaum, James. “Uveitis: etiology, clinical manifestations, and diagnosis” last modified August 31, 2020

Anterior uveitis can be acute or chronic, and the acute form is the most common form of uveitis. Posterior uveitis, affecting the retina and choroid, and intermediate uveitis, affecting the vitreous body, are less common.2 Uveitis can be classified by location, clinical course or side affected.

Table 1: Classification of uveitis. Muñoz-Fernández S, & Martín-Mola E. (2006). Uveitis. Best Practice & Research Clinical Rheumatology 2006; 20(3), 487-505.

 

Etiology

Approximately 30% of uveitis cases are idiopathic.1 However uveitis can be associated with many rheumatologic conditions such as spondylarthritis, juvenile idiopathic arthritis, psoriatic arthritis, as well as inflammatory bowel disease, multiple sclerosis, and sarcoidosis3. It can also arise from infectious sources such as cytomegalovirus, HSV, varicella zoster virus, lyme disease, syphilis, and tuberculosis, among others. Uveitis can also occur after trauma to the eye.1

 

Clinical Presentation

Anterior and posterior uveitis typically have different presentations.

In anterior inflammation, pain, photophobia, and redness are more commonly seen with a variation in the degree of vision loss (if any). On exam, one can see a ciliary flush where inflammation of the limbus results in redness next to the iris, but not in the periphery of the eye.

Figure 2:  Ciliary flush. https://commons.wikimedia.org/wiki/File:Ciliary-flush.jpg

Photophobia is consensual meaning shining a light in the unaffected eye causes pain in the affected eye due to pupillary constriction.7 On slit lamp examination one may see ‘cells and flare’ when looking at the anterior chamber  in the oblique view – the stereotypical ‘snowflakes in headlights’ appearance.

Figure 3: Cells and flare.http://blog.clinicalmonster.com/2017/08/22/bored-review-anterior-uveitis/cell-flare/

Precipitates or a hypopyon may also be seen.

 

Posterior inflammation is more subtle and can present with non specific vision changes such as flashers/floaters or decreased visual acuity, while pain is less frequently present.1

Visual loss is an important complication of uveitis and can be caused by cataracts, macular edema, epiretinal membrane, and glaucoma.4

 

 

Red Flags for Painful Red Eye

 The following signs and symptoms should prompt urgent referral to ophthalmology:

  • Severe eye pain
  • Vision loss or deficits
  • Loss of pupil reactivity
  • Corneal ulceration
  • Extraocular eye movement stiffness5

 

 

Management

 Uveitis is an ophthalmologic emergency which is vision threatening. Ophthalmological follow up within 24 hours is vital. Without prompt referral to an ophthalmologist for slit lamp examination and treatment, vision loss can be permanent.1

Topical corticosteroids such as prednisolone are often used in the initial management of uveitis. Immunomodulatory agents can also be used6 – both should be used in discussion with an ophthalmologist as inappropriate steroid use could lead to worsening infection or corneal ulceration7.

To help control pain from excessive constriction of the pupil, cycloplegic drops – like Homatropine (1 drop TID of 2‐5% solution) – can be used. Be aware the effects can last a few days.7

A workup for associated conditions is also reasonable, such as chest XR and serologic testing for commonly associated autoimmune and rheumatologic conditions. Screening for associated infections should also be considered.4

 

 

 References

  1. Rosenbaum, James. “Uveitis: etiology, clinical manifestations, and diagnosis” last modified August 31, 2020, https://www.uptodate.com/contents/uveitis-etiology-clinical-manifestations-and-diagnosis?search=uveitis&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H4
  2. Muñoz-Fernández S, & Martín-Mola E. (2006). Uveitis. Best Practice & Research Clinical Rheumatology 2006; 20(3), 487-505.
  3. Brown, H. (2010). Uveitis.Gp, , 34-35. Retrieved from http://ezproxy.library.dal.ca/login?url=https://www-proquest-com.ezproxy.library.dal.ca/docview/744242835?accountid=10406
  4. Dunn, James. Uveitis. Prim Care Clin Office Pract 2015; 42: 305-323.
  5. Dunlop AL, Wells JR. Approach to red eye for primary care practitioners. Prim Care Clin Office Pract 2015; 42: 267-284.
  6. Dupre AA & Wightman JM. (2018). Red and painful eye. In R. M. Walls (Ed.), Rosen’s Emergency Medicine: Concepts and Clinical Practice (9th, pp. 169-183). Philadelphia, PA: Elsevier Inc.
  7. Emergency Medicine Cases (2010). Nontraumatic Eye Emergencies. Retrieved from https://emergencymedicinecases.com/episode-9-nontraumatic-eye-emergencies/

 

Copyedited by Dr. Mandy Peach

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