Physical Abuse in the Pediatric Patient

Physical Abuse in the Pediatric Patient – EM Reflections October 2021

Authored and Copyedited by Dr. Mandy Peach

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

All cases are imaginary but highlight important learning points.

 

Case:

A young mother presents to the ED with her 8 week old female. She noticed increased irritability and vomiting in the past 2 days. She describes her baby as generally ‘cranky’ but really didn’t notice any significant change until 2 days ago. She has 3 other children at home and describes her house as ‘chaotic’. She has difficulty tracking feeding patterns secondary to poor sleep but thinks her baby is feeding q5-6 hours. She thinks there are the same number of diapers, perhaps lighter. Her baby is formula fed and has always been ‘spitty’ but now she is vomiting non-bilious emesis. The vomiting is not related to feeds. She has been offering bottles more often since the vomiting started. She figured her baby caught something from one of her older children. She presented today as a family member stopped by and was concerned about the baby’s appearance.

On exam you see a pale, drowsy appearing baby. She opens her eyes to loud sound, cries weakly when handled, and withdraws from being touched. Her cap refill is delayed and her extremities feel cool to touch. Mucus membranes appear dry. Weight: 5 kg

Her vital signs: HR 182, RR 56 O2 97% RA. BP was not measured. Gluc 5.2.

GCS can be more challenging to calculate in younger pediatric patients. What is this patients’ Glasgow Coma Scale1?

You calculate the patient’s GCS to be 11 (E-3, V-3, M-5). With the elevated HR and RR you wonder if the decreased LOC is related to dehydration given the hx of vomiting. You quickly move the child to trauma and begin fluid resuscitation.

The learner with you asks if you feel the vomiting episodes are indeed related to a ‘gastro’ from an older child. Without a fever or hx of diarrhea you feel it’s less likely.

What are the causes of vomiting in the infant population?

After 1 month of age2:

  • Infections
  • Metabolic disorders including DM
  • Failure to thrive
  • Cow’s milk intolerance
  • Abuse
  • Intussception
  • Hirschsprungs
  • Gastroenteritis
  • Appendicitis

After an abdominal exam the learner can illicit no tenderness or peritoneal signs. There have been regular stools absent of mucus or blood, making Hirschungs and cow’s milk intolerance less likely. There have been no fevers to suggest infections. You have added a metabolic panel to the work up, but initial glucose at least was normal.

Your differential appears to be shrinking and one concerning diagnosis is moving to the forefront – abuse, something we don’t always consider  with pediatric presentations.

What are some historical factors concerning for child abuse3?

  • Vague explanation or changing information
  • Explanation inconsistent with child’s physical or developmental abilities
  • Different witnesses give different explanations
  • Inadequate supervision resulting in injury
  • Delay in seeking medical care.

Certainly, this mother is not entirely sure of the progression of illness, but you figured it was due to sleep deprivation. Regardless, she presented today because a family member was quite concerned about the child’s drowsy state– something the mother failed to notice. This could potentially be a delay in seeking medical care.

You decide to further dive into the history with the mother.

What are some risk factors for child abuse3?

You determine that the mother is quite young and the biological father isn’t in the picture. She has 3 other children at home and her current boyfriend is the other adult living in the home. She had post-partum depression previously but feels this time around she only has ‘the blues’. She is unemployed and cares for the children, her boyfriend financially supports the family – he has not fathered any of her children. They met during her second trimester and quickly moved in together. She has one aunt who lives locally but otherwise very little support. When asked about her partner she is vague about how he makes a living and his role in the home other than financial support.

While you are getting a further history your resident is doing a more thorough physical exam on the infant.

What are physical exam findings concerning for abuse3?

Remember the 6 B’s

Bruises, Breaks, Bonks, Burns, Bites, Baby blues

 

BRUISES

Bruises– the most common abusive injury. Have a high suspicion if bruising is seen in an infant who is not mobile – over 50% of pre-mobile infants with bruising were victims of abuse.

Bruises in unusual places – follow the TEN-4 FACES Bruising Rule

  • Torso
  • Ears
  • Neck

Any bruise in a child younger than 4 months

  • Frenulum
  • Angle of jaw
  • Cheek
  • Eyelid
  • Subconjunctival Hemorrhage

* Highly suggestive of abuse

Patterned bruises

  • Hand prints or oval marks
  • Loop marks indicating rope, wire or electric cord
  • Linear bruises to buttocks indicating spanking, whipping or paddling
  • Belt marks
  • Linear bruising to the pinna
  • Retinal bleeding * present in 70-80% of children with abusive head injuries
  • Ligature marks
  • Burns

Multiple bruises

  • Compare with the shins as this is a bruise prone area on kids. More bruises than the shins? Concerning.
  • There is a new high-risk bruise screening pathway that may help identify occult injuries in the pediatric population. It involved identifying a concerning bruise in triage, which was any bruising in an infant <6 months or patterned bruising in age 6-48 months  (ears, neck, torso). Overall, in this retrospective validation study high risk bruising pattern was rare, but they did identify occult fracture in 1/3rd of patient with high risk bruising <6 months of age4.

 

BREAKS

There is no pathognomic fracture for abuse, but fractures involve thorough history and physical exam. Fractures in young infants should trigger you into considering abuse.

  • Any fracture in a non ambulatory child
  • Femur fracture in an infant <12-18 months *19x greater odds of being consequence of abuse
  • Humerus fracture in an infant <12-18 months *32x greater odds of being a consequence of abuse
  • Multiple fractures or an unexpected healing fracture
  • Skull fractures
  • Metaphyseal fractures (bucket handle) – indicates violent shaking
  • Rib fractures – especially posterior, these have the highest probability for abuse

 

BONKS

Most skull fractures are accidental, but about 5% are non-accidental. Have a higher suspicion if complex, bilateral, depressed, open, occipital or presents with suture diathesis

BURNS

Accidental burns are usually scald injuries from spilling of hot liquids or touching hot surfaces, so expect injury to palm of hand or burns to anterior body with splash marks.

Concerning burns are usually immersion or contact

  • Immersion will often be stocking or glove distribution from forcing limbs into hot water, or the genital area from submersion in a tub.
  • Contact burns – look for well-demarcated areas like cigarette burns, iron, curling iron, etc.

BITES

Obvious teeth pattern

BABY BLUES

This refers to irritability in the patient, not the care giver. Irritability is a very non specific presentation so a thorough history and physical is vital.

 

The resident meets you outside the room after you finish the history to discuss the physical exam. They confirm the GCS of 11. Pupils appear to be 3mm and sluggish. There is evidence of retinal hemorrhage. They made note of bruising on the anterior chest and shoulder area bilaterally – it appears to be in the shape of fingerprints. Cardiovascular, respiratory, abdominal, and genitourinary exam are unremarkable. Limbs appears to be non-tender and have normal passive range of motion when examined. Other than the bruises mentioned, the skin appears pale and cool to the extremities. Fontanelles were noted to be bulging, instead of the expected sunken appearance one sees with dehydration.

Your suspect non-accidental trauma.

As irritability and vomiting are such common presentations in pediatric patients, is there a tool you can use to objectively determine if non-accidental head trauma should be higher up on your differential?

The Pittsburg Infant Brain Injury Score for Abusive Head Trauma5

This is a validated, clinical prediction rule to help physicians in deciding if an infant is high risk and should undergo a CT head to evaluate for abusive head trauma. The validation study included infants age 30-364 days who were well-appearing, afebrile, with no obvious history of trauma but who presented with a symptom associated with an increased risk of abusive head trauma.

Symptoms included:

  • ALTE/apnea
  • Vomitting without diarrhea (>4 episodes of vomiting in previous 24 hours or ≥3 episodes of vomiting per 24 hours in the past 48 hours)
  • Seizures/seizure like activity
  • Soft tissue swelling of scalp
  • Bruising
  • Other non-specific neurological sx: lethargy, fussy, poor feeding

 

Upon evaluation a 5 point scale was used

  • Abnormality on derm exam (signs of injury as reviewed above in 6 B’s) (2 points)
  • Age ≥ 3 months (1 point)
  • Head circumference > 85th percentile (1 point)
  • Hg < 112 g/L

A score of 2 has a sensitivity of 93.3% and a specificity of 53% for abnormal neuroimaging.

You reevaluate the patient and arrange urgent CT. Does this child require any other screening investigations3?

Screening for other occult injuries depends on age, with more intensive screening done at younger ages when the child cannot vocalize their injuries. As the child gets older investigations are no longer screening, but focused based on presentation.

Your CT confirms a subdural hematoma.

Any intracranial injury can be abusive in etiology but subdural hematomas are the most common.

Epidural hematomas are usually more associated with accidental injury.

What if you were at a rural hospital and wanted to confirm your suspicion of increased ICP in a fussy baby to add to your clinical picture?

PoCUS can evaluate for hydrocephalus, intracerebral hemorrhage or infectious causes of irritability or drowsiness in a pediatric patient with open fontanelles6.

There are only case reports of this being used in the emergency department setting. Subdural hematomas require a view of the superior sagittal sinus which is difficult to achieve. Infectious causes are less likely to seen as well and can have subtle findings.

If you are going to complete the scan, hydrocephalus would be the most useful and easiest scan to complete.

The scan –

Use a linear probe and place directly on the open anterior fontanelle – this allows you to see the brain in the coronal plane and sagittal plane6.

 

Coronal plane with marker towards patient right, sweeping anterior to posterior.

Sagittal plane with marker towards patient’s face and sweeping left to right

 

In a nutshell, findings of hydrocephalus include extra axial fluid and asymmetrical ventricles as seen below6

   

You urgently call neurosurgery for a consult and reevaluate the patient – they are still protecting their airway and have slightly improved vitals post fluid.

You now have to go and speak with the mother.

What are some approaches to having a discussion with the caregiver around concerns for physical abuse3?

Be direct and professional. “As a physician, I worry when I see X, Y and Z and it makes me concerned that someone may have hurt your child.”

Refrain from being accusatory. “It’s not my role to say who hurt your child but it is my obligation to report my concern.”

Encourage the family to focus on the child. “Right now, we need to make sure that your child gets the medical care that he/she needs.”

Call for help. Discuss the case with social work, child protective services, a child abuse consultant (eg. SCAN team), and the primary care physician”

 

How do you approach documentation in a case of pediatric physical abuse3?

This chart will likely be reviewed if/when investigation takes place. Proper, detailed documentation is key.

History

  • Who is providing the history
  • What, when, who
  • Use quotations to document exact statements from child and caregiver
  • Any pain that the child is experiencing
  • Activities that may affect forensic evidence recovery (eg. bathing)
  • Review of systems – changes in behaviour, non-specific symptoms
  • The usual (past medical history, social history, meds, allergies)

Physical Exam

  • Head-to-toe
  • Fully expose the child – this is a trauma patient
  • Describe, draw or even photograph any injuries

Impression

Summary statement

If comfortable, offer an interpretation of the findings in the context of the history”

 

Summary table of approach3

The patient went on to have a surgical evacuation of the hematoma and recovered. Appropriate services were contacted

 

Not every presentation will be this dramatic – up to 25% of patients with physical abuse have a sentinel injury. This is often a trivial minor injury missed by us a sign of abuse7. Bottom line – to catch it, we need to suspect it. Review old charts, do thorough examinations, assess for risk factors and recognize the 6B’s.

 

References & further reading

  1. Teasdale, G. Pediatric Glasgow Coma Scale. Retrieved from https://www.mdcalc.com/pediatric-glasgow-coma-scale-pgcs.
  2. Thomas, A. 2017. CRACKCast E029 – Nausea and Vomiting. CanadiEM. Retrieved from https://canadiem.org/crackcast-e029-nausea-vomiting/
  3. Helman, A, Coombs, C, Holland, A. Pediatric Physical Abuse Recognition and Management. Emergency Medicine Cases. March, 2018. https://emergencymedicinecases.com/pediatric-physical-abuse/. Accessed Nov 16, 2021.
  4. Crumm CE, Brown ECB, Thomas-Smith S, Yu DTY, Metz JB, Feldman KW. Evaluation of an Emergency Department High-risk Bruising Screening Protocol. Pediatrics. 2021 Apr;147(4):e2020002444. doi: 10.1542/peds.2020-002444. Epub 2021 Mar 2. PMID: 33653877; PMCID: PMC8015159.
  5. Berger RP, Fromkin J, Herman B, et al. Validation of the Pittsburgh Infant Brain Injury Score for Abusive Head Trauma. Pediatrics. 2016;138(1):e20153756
  6. Subramanian, S. The Altered Infant – Should we POCUS an open fontanelle? A case of hydrocephalus. The PoCUS Atlas. Accessed Nov 30, 2021. https://www.thepocusatlas.com/new-blog/pedshydrocephalus
  7. Helman, A, Coombs, Holland, A. BCE 67 Child Abuse – Sentinel Injuries. Emergency Medicine Cases. March 2018. https://emergencymedicinecases.com/child-abuse/. Assessed Nov 30, 2021
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Managing alcohol withdrawal

EM Reflections Sept 2021 – Managing alcohol withdrawal

Authored and Copyedited by Dr. Mandy Peach

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

All cases are imaginary but highlight important learning points.

 

Case

A 72 yo male presents to the emergency department with left sided CP after sustaining a fall 3 days ago. He states he hasn’t slept and is having a hard time breathing due to the pain – “ I think I cracked a rib”. On further history surrounding the fall he divulges that he was quite intoxicated at the time of injury and that he does fall quite often when drinking. He drinks 8-10 beers per day, sometimes more, and has done so for many years. He denies any complications of his drinking other than frequent injuries and has never been admitted or attended a rehabilitation facility.

Financially there have been increasing constraints and currently he is unable to obtain alcohol. His last drink was 2 days ago. He states he feels uneasy and slightly nauseous with a mild headache, but he feels it is related to the chest pain.

His PMH is non-contributory – he has no family doctor and has no regular care. He has smoked 1-2ppd for “as long as I can remember”.

His vital signs: 142/76, HR 112, RR 20, O2 93% on RA, T 36.7. He appears diaphoretic, mildly uncomfortable and taking shallow breaths.

Physical exam for signs of trauma reveals no significant injury except for a small area of bruising and tenderness at the L 10th rib with air entry heard bilaterally. As the trauma was 2 days ago, and he is satting 93% on RA on a background of suspected COPD, you feel it is unlikely he has any complication of his fall. Imaging is unlikely to change your management – he needs analgesia.

You instead focus on his alcohol use as you suspect that is what is contributing most to his symptoms.

What are symptoms/signs of alcohol withdrawal? How soon do you anticipate symptoms?1,2

A spectrum – early withdrawal -> seizures -> alcoholic hallucinosis -> delirium tremens (DT).

Symptoms Signs
Abdominal pain Tachycardia
Nausea/vomiting Elevated BP
Headache TremorThe tremor is key to diagnosis. It is an intention tremor – when resting it is not visible. Ask the patient to extend their arms/hands and it becomes apparent. This is a persistent tremor and it does not fatigue
Anxiety Tongue Tremor – more sensitive finding. See video
Hallucinations – clear cognition with hallucinations *High risk deterioration to DT Seizures – occur at 12-48 hours and are typically preceded by tremor

 

 

Tongue tremor1

Symptoms from alcohol withdrawal can start as early as 6-8 hours after the last drink, as the alcohol levels decline.

Symptoms typically peak at 72 hours and are gone by day 5-7.

Delirium Tremens can be anytime from day 3-12 after abstinence.

You examine your patient for signs of withdrawal. From the vitals he is tachycardiac. On exam he appears diaphoretic and he complains of a few symptoms. You ask him to extend his arms and he does have an intention tremor that doesn’t fatigue.

You confirm he is in alcohol withdrawal – this is a clinical diagnosis.

Are there any investigations that should be done for acute alcoholic withdrawal?

It depends on the patient presentation and the level of severity.

Mild cases – lab work/imaging rarely contributory. But there are situations where it is warranted.

  • Severe symptoms with potential DTs – really this could be a patient with acute delirium of any etiology. So screen for :
    • electrolyte abnormalities
    • alcoholic ketoacidosis
    • infection
    • toxidromes
    • thyrotoxicosis
    • neuroleptic malignant syndrome
    • serotonin syndrome
    • hypertensive crisis
    • acute pain
    • ECG – chronic alcohol use leads to hypomagnesemia and electrolyte abnormalities, increasing risk of long QT.
    • CT head – These patients are high risk for falls during both intoxication and withdrawal. Combine this with fragile intracranial bridging veins and potential coagulopathy if underlying liver disease and their risk of ICH goes up substantially.

 

  • Unclear history? Maybe the patient is not in DTs but actually is acutely intoxicated. An alcohol level can be ordered, but keep in mind that patients experiencing withdrawal will have symptoms at varying levels. Chronic users may have withdrawal symptoms at a level that is intoxicating to someone who rarely drinks. Add a urine tox screen if concern for co-ingestants as above.

 

So, if alcohol levels aren’t helpful how do I differentiate between an acute alcoholic intoxication vs severe withdrawal with DTs?1

Giving benzodiazepines to a patient who is acutely intoxicated can lead to decreased LOC.

Before considering treatment look for the withdrawal tremor – if it isn’t present they are likely intoxicated.

 

The CIWA-Ar protocol is one method to monitor withdrawal symptoms and quantify the severity to ensure the patient receives appropriate treatment.

https://insight.qld.edu.au/shop/clinical-institute-withdrawal-assessment-of-alcohol-scale-revised-ciwa-ar-insight-2019

This is a 10 item scale and is done hourly. If a patient scores > 10 they are treated, if  back to back scores are < 10 they can be discharged.

Is there a faster tool that can be used in the ED to quantify alcohol withdrawal?1

SHOT protocol is a 4-item scale. It is done every 1-2 hours. It is not validated, but has been shown to correlate well with CIWA score. It is shorter and easier to administer. Patient can be discharged if back to back scores are 0-1.

You decide to calculate your patient’s SHOT score3.

You calculate the patient’s SHOT score to be 6

  • Sweating: He has beads of sweat on his forehead (2)
  • Hallucinations: He has no hallucinations (0)
  • Orientation: He knows where he is, but gets the month wrong (1)
  • Tremor: he has a moderate intention tremor (3)

Any score over 2 requires medical intervention

Your patient requires intervention.

What medication do you choose to treat alcohol withdrawal?

Longer acting benzodiazepines are preferred as they have a more predictable course and are less likely to result in withdrawal or seizures 1,2,4.

Lorazepam Diazepam
Onset of action Slower Faster
Half-life 8-12 hours 100 hours
Duration of action 12 hours 5 days
Risk withdrawal Higher Lower
Sedation risk Less risk of oversedation

Use if liver dysfunction as less systemic accumulation

Oversedation risk if liver dysfunction, elderly, low albumin, methadone or high dose opiods

Use oral doses if mild withdrawal and the patient can tolerate.

You order oral diazepam for the patient when a trauma team activation is heard overhead – it is a multiple vehicle MVC. Currently the department is critically understaffed, and all available staff are sent to trauma while one nurse manages the acute patients.

A couple of hours have passed and you finally get back to reassess your withdrawal patient. He has since had a CT head that showed the expected atrophy but no hemorrhage. You review his lab values and other than some mild electrolyte abnormalities there are no glaring values or signs of co-ingestants. You hear raised voices in the department and go to assess. Your patient now appears to the hallucinating and is severely agitated. He is not responding to verbal de escalation. A code white is called. The patient is restrained and a glucose is immediately checked to r/o hypoglycemia – it is 5.8. IV access is still intact.

Your patient is likely experiencing DTs and is in severe withdrawal.

What medication do you want to avoid in this agitated patient withdrawing from alcohol1?

Haldol – antipsychotics can prolong QT interval in patients already at risk of long QT. It can also lower seizure threshold.

How do you manage severe alcohol withdrawal 5?

Lots of benzos via IV with the goal of having a calm, cooperative patient.

Start with diazepam 10 mg IV and reassess in 5 minutes, if not suffice then re-dose another 10mg. If still no success than increase the dose increase by 10mg and repeat that pattern, reassessing every 5 mins.

What if the patient doesn’t respond to these treatments?

Once approaching 200mg total – these patients are benzo resistant and will likely require intubation (*keeping in mind you’ve considered other etiologies)5.The same is true for refractory seizures that have not responded to escalating benzodiazepine doses.

Before proceeding to intubation you can consider phenobarbital as adjunct, but there is no evidence that phenobarbital alone is superior to benzos in treating withdrawal. The side effect profile is also higher if using an anticonvulsant instead of a benzodiazepine 2.

If you intubate the patient, consider the following adjuncts6:

Of these – phenobarbital, propofol and dexmedetomidine have been shown to decrease benzodiazepine requirements in severe withdrawal, but none are proven to shorten duration of illness of length of stay in ICU.

If using demedetomidine you must have another adjunct as it does not protect against withdrawal seizures.

The following is a summary1

 

You administer escalating benzodiazepine doses to your patient and eventually he settles. You are charting and preparing to admit the patient when the nurse lets you know the patient is now on 2L of oxygen despite having a normal respiratory rate and end tidal. His GCS is 13 – he opens his eyes to speech, is responding to questions but seems confused still and is moving spontaneously to command.

You go to reassess. You confirm the GCS and don’t feel that it is contributing. You remember the low oxygen saturation on initial vitals you thought was secondary to underlying COPD. You auscultate the lungs and now notice decreased air entry to the L side. In the setting of recent trauma you are concerned your patient had a pneumothorax that worsened.

Would PoCUS have been of benefit in initial assessment of the patient?

It depends on the thoroughness of the scan.

There is evidence that a single view of the anterior chest in the midclavicular line, 3rd intercostal space, is comparable to a 4-zone lung scan for finding a clinically significant pneumothorax in the setting of blunt trauma. In this study clinically significant means those pneumothoraces that required thoracostomy7.

So, using this single view approach smaller pneumothoraces can be missed. But they are less likely to require a chest tube up front.

Could this patient have had a small traumatic pneumothorax that worsened in the setting of his agitation? Could he have had a secondary spontaneous pneumothorax in the setting of COPD?

Without imaging of some sort before hand it is difficult to know with certainty. Keep in mind that CXR has a sensitivity of 20-48% for pneumothorax 6. A thorough PoCUS exam has a higher sensitivity and equivocal specificity for pneumothorax in the setting of blunt trauma6. Gold standard? CT of course.

Regardless, have a low threshold to image elderly people in the setting of trauma.

You place a probe in the 3rd IC space anteriorly and see the following

There is lack of lung slide or comet tails/B lines suspicious for pneumothorax.

What can complicate interpretation of a lung scan for pneumothorax? What is the most specific sign of pneumothorax?

In certain patient populations (ie. critically ill ICU patients, ARDS, pneumonia, fibrosis, pleurodesis, cardiopulmonary arrest) the typical findings of lack of lung sliding and B lines are not reliable.

Absence of lung sliding does not diagnosis pneumothorax (spec 78-91%) in these patients.

Definite sign? Lung point, or the area where the visceral pleural begins to separate from the parietal pleural – it is 100% specific.

You confirm a pneumothorax and place a chest tube without complication. You now CT the patient looking for further injury. The CT confirms multiple L sided rib fractures with a small hemothorax and reinflation of the pneumothorax. There is also stable, but acute, thoracic spine fractures.

The patient is admitted to the ICU for severe alcohol withdrawal in the setting of trauma.

What extra treatments do you consider before handing over to the ICU staff1,2?

Fluids – often these patients are hypovolemic and hypoglycemic. Consider glucose containing fluids.

High dose Thiamine – thiamine deficit patients can develop Wernicke’s encephalopathy. Glucose and thiamine compete for the same co-factor so theoretically giving glucose in a thiamine deficient patient could precipitate Wernicke’s. However, there is no evidence that a single glucose dose will cause this. So, give glucose at the same time or after thiamine, but if critically low glucose don’t wait to administer.

Magnesium – required for thiamine related kinetics and is often low in this population. Check and replace when giving thiamine2.

 

The patient did well and upon discharge he was provided resources and support for seeking treatment. He completed the detox while admitted.

What about patients being discharged from the emergency department with mild alcohol withdrawal? How are they managed 1?

Key is avoiding prescription for benzodiazepine as an outpatient. This has a risk of oversedation, dependence and drug seeking behaviour. Giving diazepam in the ED can prevent seizures due to it’s long half life.

Take home points:

  1. Alcohol withdrawal is a clinical diagnosis – recognize the symptoms and signs.
  2. Persistent intention tremor is a sensitive sign of withdrawal.
  3. Consider other causes in the acutely delirious patient.
  4. These patients are high risk for injury – have a low threshold to image if suspicion of trauma
  5. Quantify the severity for treatment – consider using the SHOT protocol. Diazepam > Lorazepam in the patient with no underlying liver dysfunction.
  6. High, escalating IV benzos for refractory agitation/seizure
  7. Avoid benzodiazepine prescriptions as an outpatient.

 

References and further reading

  1. Helman, A, Borgundvaag, B, Gray, S. Alcohol Withdrawal and Delirium Tremens: Diagnosis and Management.Emergency Medicine Cases. October, 2016. https://emergencymedicinecases.com/alcohol-withdrawal-delirium-tremens/. Accessed [Oct 31, 2021].
  2. Fabian, C. Alcohol: Beyond the “Breakfast Plan”. EM Ottawa. December 2015. https://emottawablog.com/2015/12/alcohol-beyond-the-breakfast-plan/. Accessed [Oct 31, 2021].
  3. Gray S, Borgundvaag B, Sirvastava A, Randall I, Kahan M. Feasibility and reliability of the SHOT: A short scale for measuring pretreatment severity of alcohol withdrawal in the emergency department. Acad Emerg Med. 2010;17(10):1048-54
  4. Hoffman R, Weinhouse G. Management of moderate and severe alcohol withdrawal syndromes. UpToDate. September 2021. https://www.uptodate.com/contents/management-of-moderate-and-severe-alcohol-withdrawalsyndromes?search=alcohol%20withdrawal&sectionRank=1&usage_type=default&anchor=H17&source=machineLearning&selectedTitle=1~150&display_rank=1#H17. Accessed [Oct 31, 2021]
  5. Justin Morgenstern. Management of Delirium Tremens, First10EM, 2016. Available at:

https://doi.org/10.51684/FIRS.1898

  1. Darrel Hughes, “Benzodiazepine-Refractory Alcohol Withdrawal”, REBEL EM blog, April 28, 2016. Available at: https://rebelem.com/benzodiazepine-refractory-alcohol-withdrawal/.
  2. Michael Prats, MD. Comparison of Four Views Versus Single View for Pneumothorax. Ultrasound G.E.L. Podcast Blog. Published on November 7, 2016. Accessed on November 1, 2021. Available at https://www.ultrasoundgel.org/6.
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Euglycemia DKA – don’t miss it!

EM Reflections May 2021 – Euglycemia DKA

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

All cases are imaginary but highlight important learning points.

Authored and Copyedited by: Dr. Mandy Peach

Case

A 65 yo female presents with n/v ongoing for 2 days. She feels fatigued and has not been able to keep down fluids. She denies diarrhea. She has no history of abdominal surgeries. She does describe increasing productive cough that preceded the vomitting. She denies fever, but does complain of shortness of breath.

PMH: DLP, DM, GERD
Medications: Atorvastatin, Empagliflozin, Pantoprazole

Vitals: BP 104/66 HR 110 RR 22 O2 96% RA T 37.8 gluc 7.2

On exam there is obvious dehydration, and she seems fatigued with her eyes closed through most of the exam. She does respond to speech. The abdominal exam is unremarkable for focal tenderness. There are expiratory crackles heard at the R lung base.

You order a portable CXR1 and baseline labs including a VBG and lactate.

You suspect pneumonia with dehydration. You initiate a 1L NaCL bolus and order antibiotics.

You continue seeing other patients when you get a call from the nurse – the VBG is back for the patient.
They appear to have a metabolic acidosis with a pH of 7.10 and an anion gap of 14. The lactate appears surprisingly normal. The patient hasn’t made any urine yet for a sample.

What is the differential for anion gap metabolic acidosis2?

Going through the ‘MUDPILES’ mnemonic and revisiting the history nothing seems to fit. But there is a history of DM.

What red flag should trigger you to consider DKA despite the normal glucose?

The patient is on Empagliflozin. This is a SGLT-2 inhibitor. Patient on these medications are at risk of Euglycemic DKA.

In Euglycemia DKA there is a “relative carbohydrate deficiency state with normalization of serum glucose and concomitant elevation of counter-regulatory stress hormones. This leads to free fatty acid catabolism and ketone production.” 3

In any patient on a “zin” consider euglycemic DKA.

You order a serum ketone as well as β-hydroxybutyrate.

Clinically how do patients present with euglycemic DKA3?

Nausea/vomiting, malaise, shortness of breath – the differential is huge for this presentation. Again, look at the medication list for any diabetic patient. If you see a ‘zin’ – consider euglycemic DKA.

Alternatively if you order a gas and incidentally find anion gap metabolic acidosis in a diabetic patient consider ordering ketones/ β-hydroxybutyrate.

What about if this patient was an alcoholic? How would these complicate the diagnosis4?

Alcoholics can also present quite similarly with alcoholic ketoacidosis – nausea/vomiting, malaise, and similar lab findings. Other than the history one distinguishing characteristic is that alcoholic ketoacidosis tends to have frankly low blood glucose.

Are the triggers for euglycemic DKA any different3?

No, triggers for DKA are the same. Essentially any physiological stress.

A quick way to remember is the 5 I’s

Infection pneumonia, UTI, skin, abdominal
Infarction MI, CVA, bowel infarction
Infant on board pregnancy
Indiscretion dietary nonadherence
Insulin deficient insulin pump failure or non-adherence

Infection and insulin deficient secondary to non-adherence or inappropriate dosing are the most common causes.

I would also consider adding a 6th I – iatrogenic meaning drugs

What drugs commonly trigger DKA3?
– Glucocorticoids
– Diuretics
– Atypical antipyschotics

Are there any patients at risk of euglycemic DKA other than those taking the ‘zins’3?
Yes!

  • Pregnant patients -due to high placental glucose use they can have a relative euglycemia
  • Chronic pancreatitis
  • Bariatric surgery patients – absorption issues

Your patient was straight cathed for a small amount of urine which shows ketones. The beta-hydroxybuterate is also now back and is positive. You confirm euglycemic DKA.

You grab your nearest DKA algorithm to review with the nurses and begin treatment.

Besides ease of use, what are the clinical reasons for using a standardized DKA order set?
Standardized, evidence based DKA order sets have been shown to decrease time to closure of anion gap, reduce length of hospital admission and minimize complications during treatment3.

You get started with the treatment as per the order set. While treatment is commenced you sit down with your medical student and review the goals of DKA3.

Correct fluid deficits – patients in DKA get a osmotic diuresis from hyperglycemia, or dehydration from underlying illness. You want to restore volume before initiating insulin. This improves organ perfusion, renal function and lowers lactate formation.

What fluid to use? Initially NS or RL, but after initial resuscitation consider switching to RL to avoid hyperchloric acidosis associated with large volume resuscitation.

Normal or high corrected sodium? Switch to 0.45% NaCL

1 bag vs 2 bag? Having 2 bags of half NS (one with D10W) both adjusted to maintain maintenance of 250cc/hr and keep euglycemic has been shown to have better outcomes: less hypoglycemia, faster closure of anion gap and less IV insulin required.

Replacement of potassium – patients in DKA have large total body potassium deficits, however due to volume contraction and acidosis the potassium is often read as normal or high.

Starting the insulin infusion will also shift potassium intracellularly. Therefore potassium should be replaced before starting insulin therapy. See the table below for guidance3.

Closure of the anion gap to stop ketone production – the issue with DKA is not necessarily the hyperglycemia, it is the ketoacidosis from low circulating insulin. After fluid resuscitation and potassium replacement, the goal is to treat the excess of serum ketones by providing insulin. This corrects the metabolic acidosis.

Avoiding hypoglycemia secondary to insulin as you correct the acidosis is pertinent. Goal is 12-14mmol/L. Once glucose drops before 14 add D5 infusion to avoid hypoglycemia as you continue the insulin infusion.

Do not stop the insulin infusion if glucose drops! It is needed to correct the ketoacidosis. If it is stopped ketone production will quickly increase again.

Gluc really low? Decrease the insulin infusion by 50%, give an amp of D50 and switch to D10.

Treat underlying precipitant.

 

It’s been a couple of hours. The medicine team is busy with unwell patients on the floor and you are still managing the DKA patient. You have been reassessing gases and the anion gap is not closing.

What could be going on3?
– Inadequate fluid resuscitation
– Inadequate insulin dose
– Malfunction of insulin infusion
– Underlying diagnosis contributing to anion gap hasn’t been addressed.

You reevaluate fluid status and the patient has not made any additional urine other than the small amount attained on straight cath.
You decide to repeat a 500cc bolus to address dehydration as well as increase the insulin infusion.

Could this patient be at risk of cerebral edema3?
Certainly, over-resuscitating too quickly can put patients at risk of cerebral edema. However, our patient has clinical and laboratory signs that they are still fluid deplete.

When replacing fluids consider isotonic fluids ie. D5 RL to decrease the risk.

Avoid lowering serum osmolality too quickly (ie. No more than 3mmol/kg/hr) or decreasing sodium by > 10mmol/L in 24 hours.

The sodium will often increase initially due to glucose moving intracellularly – this is not actually a measure of serum sodium – do not treat.

Admissions are backed up in the ED and you’re still caring for the patient at the end of your shift. You handover to the senior resident working with the incoming staff.

What are your goals for resolution? 3

Glucose < 11.1 AND 2 of:
– Normalization of anion gap
– Venous pH > 7.3
– Serum bicarbonate ≥15 mEq/L

At this point the patient should be mentally alert and able to eat. At this point, switch to their subcutaneous insulin dose at home. Ensure their basal insulin is also administered.

There should be an overlap of 2-4 hours before stopping the insulin infusion – if insulin infusion is abruptly stopped before administering subcutaneous insulin the patient can quickly return to an acidotic state.

What if this is the first presentation of DM and they are not on any treatment at home5?

“In patients with new-onset type 1 diabetes who have presented with DKA, an initial total daily dose (TDD) of 0.5 to 0.8 units/kg units of insulin per day is reasonable, until an optimal dose is established.

Approximately 40 to 50 percent of the TDD should be given as a basal insulin, either as once- or twice-daily U-100 glargine or detemir, or as twice-daily intermediate-acting insulin (NPH).

The long-acting insulin can be given either at bedtime or in the morning; the NPH is usually given as approximately two-thirds of the dose in the morning and one-third at bedtime. The remainder of the TDD is given as short-acting or rapid-acting insulin, divided before meals.”

The resident astutely asks about respiratory status, and if they were to decompensate what would be suggested management3?
Bottom line – avoid intubation DKA patients if possible

  • These patients hyperventilate to try and correct the acidosis, so the ventilator must also match this large volume and RR. This puts them at risk of ventilator injury and ARDS

  • Because they need to compensate with hyperventilation if there is a prolonged period of apnea from complicated intubation the acidosis can significantly worsen, putting them at high risk for circulatory collapse

But if you have to intubate, some pointers:

  • Like any patient, resuscitate first
  • If you paralyze – bag the patient throughout.
  • Consider anti-emetic
  • If the serum bicarb is < 10, considering giving an amp of bicarb
  • Once tubed the vent settings should have a high tidal volume (8cc/kg) and high respiratory rate (24-28)

How about alternative therapies if the patient is tiring, like Bipap?

DKA patients often have gastroparesis so are high risk of aspiration and emesis. Ideally, BiPap should be avoided.
If there are oxygenation issues consider high-flow nasal cannula.

The patient has resolution of their DKA within the ED and is finally admitted for treatment of the underlying cause – community acquired pneumonia.

 

References and further reading

  1. https://radiopaedia.org/cases/right-lower-lobe-consolidation-pneumonia
  2. https://www.picmonic.com/pathways/physician-assistant/courses/standard/pathology-10894/acid-base-disorders-39738/normal-gap-metabolic-acidosis_259
  3. Helman, A. Baimel, M. Sommer, L. Tillmann, B. Episode 146 – DKA Recognition and ED Management. Emergency Medicine Cases. September, 2020. https://emergencymedicinecases.com/dka-recognition-ed-management. Accessed [July 16, 2021
  4. Helman, A. Himmel W. Best Case Ever 58 Euglycemic DKA. Emergency Medicine Cases. June 2017. https://emergencymedicinecases.com/euglycemic-dka/. Assessed July 19, 2021.
  5. Hirsch I, Emmett M. 2020. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. https://www.uptodate.com/contents/diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults-treatment?search=dka&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H23160691
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Elbow Injuries

EM Reflections April 2021 – Elbow Injuries

 

 

Thanks to Dr. Joanna Middleton for leading this month’s discussions.

All cases are imaginary but highlight important learning points.

Authored and copyedited by Dr. Mandy Peach

A 25 yo male presents to the ED with his R arm in a makeshift sling. He’s complaining of elbow pain post fall while trail running in a local park. He describes slipping downhill on some loose terrain and landing with his arm hyperextended behind him as he tried to grab a branch. He is otherwise healthy and takes no medications. His vital signs are within normal limits with the except of a HR of 102, which you attribute to pain. The nurse has placed an IV.

You begin your examination of the R elbow. You see significant swelling of the joint and some superficial abrasions. The joint does not feel warm to the touch. There is no overt bleeding.

Other than palpation for focal tenderness and assessing range of motion, what are some important tips for a focused elbow exam1?

Eliminating gravity when testing flexion/extension so pain is less likely to hinder your exam findings. To do this have the patient point their elbow at you, while the forearm is parallel to the floor and have them flex/extend in this plane2.

Remember to test for supination and pronation – this is also a key part of the elbow exam and assessing both with patient’s arms tucked into their sides can help reveal more subtle injuries. Asking the patient to point their thumbs up can make assessing ROM compared to the ‘normal’ side easier to see.

You examine your patient and they cannot fully extend the elbow, even after pain control. What is the significance of this3?

Your patient needs imaging. The ‘elbow extension test’ can help predict the likelihood of fracture. In both adult and pediatric patients presenting within 72 hours of injury, those who could not fully extend the joint had a 48% chance of fracture, while that percentage decreased to 2% if the patient could fully extend the joint.

How can supination and pronation be helpful in picking up on injury1?

Subtle injuries can be found such as radial head or neck fracture. This ROM brings the radial head out during examination.

An Essex-Lopresti fracture-dislocation is another potential injury: a fracture-dislocation injury involving the radial head (fracture) and DRUJ – distal radioulnar joint (dislocation)4. These are important to identify as they require immobilization with the patient’s limb in supination.

The patient has difficulty with supination and pronation secondary to pain. You are concerned for a radial head injury. On exam he has diffuse tenderness of the joint and you have difficulty identifying landmarks as they are lost – you are concerned about an elbow dislocation as well.

What are potential neurovascular injuries involved with such a significant elbow injury5?

Important neurovascular structures associated with the elbow joint are the brachial artery, radial artery, ulnar artery, median, radial, and ulnar nerve.

The most common injury to the elbow is radial head fractures. The mechanism is usually FOOSH or direct trauma5.

You proceed with a neurovascular exam. Radial and ulnar pulse are palpable, capillary refill is 2 seconds.

What is an easy way to remember the nerve testing for elbow injury1?

You complete your neurovascular exam and send the patient for XR’s. You suspect there will be significant injury.

You quickly review normal elbow anatomy on lateral XR with your learner on shift7.

You point out two important lines in the lateral view of the XR

  1. Anterior humeral line: A vertical running drawn on the anterior surface of humerus. This must run down to intersect middle 1/3rd of CAPITELLUM
  2. Radiocapitellar line : it runs through the central radius and passes the central capitellum on a normal image. Important: this rule applies to EACH image, so not only a purely lateral image

You also point out that that in the AP view the radiocapitellar line should also be drawn and should intersect the central capitellum.

By now your patient’s XR is up for review8.

First you notice the elbow luxation – neither your anterior humeral line or radiocapitellar line intersects the capitellum.
You also can see a radius head fracture.

What other injury should you be concerned about1?

After any proven or suspected radial head injury always look for the second injury. Here you have obvious luxation, but you should also examine the coranoid process and anterior ulna for any subtle irregularity indicating fracture. Coranoid fractures tend to be associated with elbow luxation and often indicate an unstable joint.

On history the mechanism of injury is FOOSH or hyperextension of the elbow.

The mechanism fits and your patient does have both radial head fracture and luxation. You examine the coranoid and notice that the trochlear is not completely smooth. You diagnose a coranoid fracture as well.

What is the significance of these injuries1?

This patient has the ‘terrible triad’ of the elbow.

  • Radial head/neck injury
  • Luxation of the elbow
  • Coranoid fracture

This requires orthopedic consultation immediately – it is an unstable joint. You reexamine neurovascular status again and confirm the limb is still perfused and intact before immobilization. You place the patient in a posterior long arm splint with the forearm in supination and discuss with orthopedics on call.

 

 

You pick up the next chart and there is another elbow pain. It looks like the patient was already sent for XR in triage and is now back and in the orthopedic room. This is a 16 yo female who was participating in an orienteering competition. She tripped while running on a tree root and sustained a FOOSH injury. She describes the grade being on a downward slope and felt her entire weight fall forward onto her wrist. She is otherwise healthy. Her vitals are within normal limits.

You initially examine the patient and see the following, what are the clues that this is a posterior elbow dislocation1,9?

When standing behind the patient you can see the olecranon sitting posteriorly behind the humerus.

You are palpating the elbow for tenderness – in the normal elbow the medial condyle, lateral condyle and olecranon should form a symmetrical triangle. Here they do not – this is suggestive of subluxation/dislocation of the elbow.

You assess neurovascular status and find no abnormalities.

What are the other types of dislocations? Which is most common10?

Posterior is the most common. 50% have associated fractures.

You look at the XR11:

This is a frank posterior dislocation – but, what are clues of subtle subluxations1?

“A smooth, symmetric clear space around the trochlea, similar to assessing the clear space of the ankle mortise.”

What about if your patient described a “popping sensation” during the injury and the XR appears normal1?

Sometimes patients can dislocate and  relocate before presentation to the ED. Although there is no bony injury the mechanism is associated with significant ligamentous injury and should be immobilized.

You prepare for sedation and elbow reduction. You consent the patient and the parent, perform an airway assessment and gather the team.

What are methods to reduce an elbow dislocation?

Before deciding to reduce ensure there are no vascular or neurological deficits and no open fracture/dislocation – this would require immediate orthopedic consultation10.

Your patient is neurovascularly intact and it is a closed dislocation.

Traction-Countertraction1

  1. The patient is seated sitting up
  2. Place the forearm in supination – this allows the trochlea to pass more easily over the coronoid process of the olecranon
  3. Elbow is flexed 30 degrees with an assistant immobilizing it and applying counter traction at the middle or distal end of the humerus
  4. Apply downward traction to the distal forearm

Doesn’t work? Try applying downward pressure at the mid-forearm and the olecranon posteriorly while maintaining in-line traction12

Still no luck1?

While standing at the posterior aspect of the humerus hook the fingers of both hands anterior to the condyles and put both thumbs on the olecranon at the junction with the triceps. Try and push the olecranon up over the trochlear.

Modified Simson12

  1. The patient is in a prone position with the affected arm handing over the side of the bed
  2. Slow downward force is applied on the wrist while the opposite hand attempts to guide the olecranon back into place.
  3. If a second provider is available they can manipulate the olecranon.

 

Which method works best?

I don’t think there is much evidence that one is better than the other! Traction-countertraction is the most commonly described method in the literature.

Working single coverage in a rural area with only one nurse who is doing cardiorespiratory monitoring and administering meds? The Modified Simson can be single provider. If the patient is compliant and not sedated then they can provide counter traction while holding the flexed elbow over the chest12.

 

Another option when you’re flying solo is the Leverage Technique12
1. Gently supinate the patients forearm
2. Interlock your fingers with the patients
3. Place your elbow against the distal potion of the patient’s biceps
4. Slowly draw the patient’s wrist into flexion while using your own elbow as a fulcrum.
5. Use your other hand to apply lateral or medial force as needed

One small study found this technique to be superior to traction-countertraction.

At the end of the day, elbow reductions can be tricky. Having more than one technique in your back pocket can be helpful.

 

You and your learner choose the traction-countertraction method and “clunk” – so satisfying.

How do you immobilize now1?

Immobilize at 90 degress of flexion with a padded backslab.

You arrange for ortho follow up – as this was a simple dislocation with no fracture you ensure the appointment is within 3 weeks as this is the maximal period the joint should be immobilized.

For complicated dislocations associated with fracture – ortho should see within 72 hours as they require ORIF.

The patient has recovered from sedation and is asking what to expect in terms of prognosis for this dislocation1.

In simple dislocations that are reduced and immobilized you advise the patient that they will be unable to extend beyond 30 degrees for 6 weeks, and that it may take up to 3 months before full extension is regained. Given that this is an athletic patient you advise her not to return to weight bearing exercises before 4 months unless directed safe by ortho in follow up.

 

 

You grab one last chart with your learner – surprise! It’s a 50 yo male with an elbow injury. He tripped while doing sprints as part of a work out and fell with arm fully extended in front of him. He is otherwise healthy and his vital signs are within normal limits.

On initial examination there is no obviously deformity. The limb is neurovascularly intact.

You palpate the elbow and there is tenderness over the radial head.

You ask the learner to palpate the radial head, they are unsure where. How do you help guide them1?

You describe the triangle between:
– The lateral aspect of the olecranon
– The lateral condyle (anterior to olecranon)
– Radial head

You also suggest examination in supination and pronation as this can bring out the radial head.

You remember your previous case of the terrible triad and go on to examine the coronoid – there is no concern of injury and the elbow doesn’t grossly appear dislocated.

You order XRs – what are some findings associated with radial head injury1?

  • Disruption of the surface of the radial head
  • Anterior sail sign
  • Posterior fat pad
  • Disruption of the radiocapitellar line

Your patient’s lateral XR13

You see both anterior sail sign and a posterior fat pad, so although no obvious fracture is seen of the radial head you diagnose a radial head fracture.

How long does this patient need to be immobilized for1?

Most fractures are not surgical. They are treated with a sling. Do not immobilize for more than 3 weeks or chronic elbow stiffness can ensue.

What if there was a visible fracture through the radius? How do you know which fractures will require ORIF and more urgent ortho evaluation1?

The 30-3-33 rule

30 degrees angulation
3 mm displacement of the fracture fragment
33% surface area of the radial head involved

References for further reading:

  1. Helman, A. Sayal, A. Dantzer, D. Ten Pitfalls in the Diagnosis and Management of Elbow Injuries. Emergency Medicine Cases. March, 2019. https://emergencymedicinecases.com/elbow-injuries. Accessed [date]
  2. https://www.hep2go.com/exercise_editor.php?exId=36147&userRef=gciaake
  3. Appelboam A, Reuben A D, Benger J R, Beech F, Dutson J, Haig S et al. Elbow extension test to rule out elbow fracture: multicentre, prospective validation and observational study of diagnostic accuracy in adults and children BMJ 2008; 337 :a2428 doi:10.1136/bmj.a2428
  4. https://www.startradiology.com/internships/orthopedics/elbow/x-elbow/index.html
  5. (2) Tintinalli, JE, Stapczynski JS, Ma OJ, Yealy D, Meckler GD, Cline DM. 9th ed. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. New York: McGraw-Hill.
  6. Cornelis, A (2017). Elb-‘ow’! Does my patient with an elbow injury require an x-ray? Resident Clinical Pearl. Emergency Medicine, Saint John. https://sjrhem.ca/rcp-elb-ow-patient-elbow-injury-require-x-ray/
  7. https://www.startradiology.com/internships/orthopedics/elbow/x-elbow/index.html
  8. https://www.orthobullets.com/trauma/1021/terrible-triad-injury-of-elbow
  9. https://litfl.com/elbow-dislocation/
  10. Paris (2016). Elbow Dislocation. Core EM. https://coreem.net/core/elbow-dislocation/
  11. Oppenheim, Osborn (2016). Posterior Elbow Dislocation. Journal of Education & Teaching of Emergency Medicine. DOI: https://doi.org/10.21980/J8X593
  12. Michael Gottlieb, Jessen Schiebout (2018). Elbow Dislocations in the Emergency Department: A Review of Reduction Techniques. The Journal of Emergency Medicine. Volume 54, Issue 6; Pages 849-854. ISSN 0736-4679 https://doi.org/10.1016/j.jemermed.2018.02.011.
  13. https://radiopaedia.org/articles/sail-sign-elbow-1

 

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Code Discussion in the ED

EM Reflections March 2021 – Code Discussion in the ED

Thanks to Dr. Paul Page for leading this month’s discussion.

All cases are imaginary but bring up important learning points.

Authored & Copyedited by Dr. Mandy Peach

 

Case

An 80 yo female is brought in by EMS in respiratory distress. There is a known history of end stage CHF. Collateral from the husband on scene was that his wife has been having increasing shortness of breath for 1 week, increased ankle swelling and was sleeping sitting up in the recliner in the living room. He called EMS today as she could not catch her breath when walking upstairs in the home.

The patient is on CPAP with EMS and has signs of central cyanosis. You direct the RT to switch her to Bipap as she is put on the monitors and a new set of vitals are obtained. You quickly examine the patient and find bilateral pitting edema to the knees and both peripheral and central cyanosis. There are audible crackles throughout both lung fields. You grab your ultrasound probe and find diffuse B-lines bilaterally in the lung fields and a cardiac view demonstrates a severely decreased ejection fraction. The IVC is dilated and not collapsing with respirations. She looks drowsy and is not responding to questions. She is not tolerating Bipap well. Her new vitals are: BP 98/62 HR 112 RR 24 O2 sat 85% on BiPAP T 37.4.

You suspect cardiogenic shock. This patient needs to be intubated. But you stop momentarily – this is an elderly patient with end stage cardiac disease. The prognosis for this patient is likely poor. Is intubation in the best interest of the patient?

This is a scenario we are often placed in as ED physicians. Just because we have the ability to resuscitate a patient doesn’t necessarily mean they will have a positive functional recovery. Here the patient is drowsy and in respiratory distress – she cannot tell us her wishes for care. In many cases, end of life care has not been discussed1 and in this situation the care decisions lie with the family/loved ones or us as physicians.

Current practice is that each patient is a ‘full code’ unless otherwise indicated2. So regardless of age, comorbidities, quality of life – if a deterioration of vital signs is seen every attempt is made to resuscitate this patient regardless of the likelihood of a functional recovery. Unlike the rest of medicine, this care is a ‘one fits all’ approach where initial efforts are carried out regardless of clinical situation. Whether or not this is the right approach is not the focus of discussion. Instead this highlights the importance of advanced care planning and goals of care discussions taking place when a patient is well and normalizing this process.

Back to our patient – they are circling the drain. You ask the medical student working with you to look up the patient chart and see if any previous code discussion has taken place. After a quick review there is no documentation of a code status. Even if there was – would this change your management?

Code discussions are not set in stone. A patient with capacity can change their mind at any time. Loved ones acting as substitute decision makers/power of attorney are also able to make decisions for the patient in the event a patient cannot make decisions for themselves.
Ideally you want to have a discussion with the family to set realistic expectations and together make an informed decision for the patient.

Luckily the husband and patient’s daughter are already in the department. You decide to have a discussion before proceeding with intubation. What are your goals for this discussion3?

  • Choose a quiet location away from the patient
  • Give your clear medical opinion and recommendations rather than options only, this way the family doesn’t feel the decision is completely up to them.
  • Use straight forward language that is easy to understand
  • “Review the risks of progressing to CPR if the patient declines including:
    o Incomplete recovery
    o Prolonged death
    o Uncomfortable investigations and treatments
    o Ventilator dependence”
  • Avoid a power struggle with the family if they choose to go against your recommendations.

What are some barriers we face in the emergency department when discussing and prognosing end of life care with patients or family members3?

We are poor at predicting prognosis, partly because this isn’t within our scope of care in initial resuscitation of patients, but also because there is always uncertainty in medicine – and this should be communicated to the family. As we see elderly or co-morbid patients in the department without a prior code status there may be a feeling that this should be the responsibility of the primary care provider and not the ED doc. Lastly, this is a difficult discussion to have regardless of timing and communicating prognosis may not always go smoothly. We may find ourselves in the same situation as the case above – with a crashing co-morbid patient with no clear goals of care. Unfortunately this is an especially difficult time to have this conversation, but it is a necessary one.

Since this is such a difficult discussion to have, is there any approach that might be helpful3?

Think SILVER

Seeks Information:

  • Elicits information regarding baseline level of function, behaviors, and symptoms that suggest progressive decline
  • Elicits information regarding current diagnosis, prognosis, and treatment plan
  • Elicits information regarding key players in decision making, including family and health care workers
  • Elicits information regarding previous end of life discussions, including advance directives

Life Values:

  • Elicits information regarding the patient’s personality and approach to life
  • Elicits information regarding how the patient views death and dying

Educates/Extends Care:

  • Pr0vides information regarding the patient’s disease process, current condition, and treatment options
  • Explains how end of life decisions will impact further treatment

Responds:

  • Solicits questions from family and offers continued support and availability for further information.”

You have a discussion with the family keeping in mind the above approach. You clearly lay out the poor prognosis and that you would suggest palliating the patient and avoiding any aggressive resuscitation. The daughter is upset and states “So you’re going to do nothing for my mother?”

This is a common misconception – that ‘do not resuscitate’ is the equivalent of doing ‘nothing’. Choosing not to do compressions or intubate a patient is the decision when an arrest or peri-arrest situation arises. However, patients can still receive medical care with goals in mind depending on the clinical situation. For example, using antibiotics in a patient with metastatic cancer who has pneumonia and who is clinically stable. Or in this situation – providing medications and oxygen to ensure a patient is comfortable and without suffering as they near the end of their life.

One approach could be to positively state all the things you will do for her mother, as oppose to what you will not be doing3.

Wording surrounding code status has also moved towards “allowing natural death” instead of “do not resuscitate” – again moving away from the idea that we are not providing a medical service.

You lay out your plan and positively reinforce the care you can provide for the patient. They agree that aggressive care would not be what the patient wanted and they agree to proceed with palliation. The husband asks you how much time she has left, and if they have time to call in family.

What are signs that help predict timing of death3?

Delirium with hypotension and tachycardia: median survival 10 days
Death rattle: medial survival 1 day
Respirations with mandibular movement: median survival 2.5 hours
Cyanosis to extremities: medial survival 1 hour”

Your patient is cyanotic and essentially crashing. You again express that predicting is difficult, but you anticipate she may die soon and you suggest calling in the family.

You discuss interim management of the patient’s symptoms while you await palliative care. As the patient is quite short of breath one of your recommendations is opioids to help. The husband says he does not want opioids given as they will ‘kill her sooner’. How do you respond?

Opiods can help with the sensation of shortness of breath. The doses used for dyspnea are smaller than the doses used for pain.

“Studies have shown that O2 and CO2 levels stay the same despite the decreased respiratory rate associated with opioids. Opioids in the palliative patient are appropriate and ethically permissible as long as the intent is symptoms relief.”3

See the infographic below for symptom management in palliative care patients3. Being familiar with palliative care is pertinent – these patients are ours until consultants take over care, and in current climate often we end up palliating patients.

The husband agrees with your plan. They stay with the wife in the ED and within a short time a bed is available in palliative care. The patient dies comfortably that night. What about if the family wasn’t there? And we had to choose to resuscitate the patient or not?

There is no right answer. Choosing to intubate the patient and have the discussion with family after the fact is one option. Choosing not to intubate the patient and provide conservative management until a discussion can be had is another option. Sometimes these will be patients with end stage disease but the presentation may be a reversible one. Sometimes these will be healthy patients with irreversible presentations.

Regardless, clearly documenting on the chart your rationale and approach can be helpful in laying out your thought process.

These are difficult situations, and at the end of the day you have to be ethically comfortable with your decision. Having open, honest conversations with family/loved ones as outlined above can certainly help us feel at ease with our decisions and help families and patients come to terms with worsening conditions.

 

References and further reading:

Dong, K. CanadiEM Frontline Primer – Advance Care Planning and Goals of Care Review. CanadiEM. 2020. https://canadiem.org/canadiem-frontline-primer-advance-care-planning-and-goals-of-care-review/ (Assessed April 25, 2021)

Kwok, E. From Full Code to No Code. CanadiEM. 2012. https://canadiem.org/from-full-code-to-no-code/. (Assessed April 25, 2021).

Greewal K, Helmin A.Episode 70 End of Life Care in Emergency Medicine. Emergency Medicine Cases. Sept 2015. https://emergencymedicinecases.com/end-of-life-care-in-emergency-medicine/. (Assessed April 25, 2021).

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EM Reflections February 2021 – Bias & Error in the ED

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

It’s your 7th evening shift in a row and the department is in critical overcapacity. You are at the latter end of your shift. You’re answering multiple charge doc calls when a new acute chart is put up to be seen. You pick it up: it’s a 62 yo male with 1 day of LLQ pain radiating to the flank. You start your history: his pain has been worsening over the day and he describes loose stools earlier in the week. He denies fever/chills and any other infectious symptoms on review of systems. He has a history of diverticulitis in the past and thinks it feels similar. He denies any previous admissions or surgical interventions for his diverticulitis in the past.

Vitals: BP 108/78 HR 102 RR 20 O2 98% RA T 36.3

On exam he has mild tenderness throughout, you feel perhaps focal LLQ tenderness, but no peritoneal signs. He looks in mild discomfort but is otherwise well. His U/A is negative.

“I’d just like some antibiotics doc, so I can get back home”.

You order basic lab work which is within normal limits except for a slightly elevated CRP. You diagnose him with uncomplicated diverticulitis and discharge him with oral antibiotics.

Could there be any bias ongoing with this patient1?

Anchoring bias:  “Prematurely settling on a single diagnosis based on a few important features of the initial presentation and failing to adjust as new information become available”.

In this patient he has a history of diverticulitis and it seems similar. We anchor on the previous diagnosis.

Diagnosis momentum: “Similar to anchoring. Once a diagnostic label has been assigned to a patient by another individual, it is very difficult to remove that label and interpret their symptoms with fresh eyes.”

Again, here we have an easy diagnosis previously established. The symptoms sound the same – so it’s easy to again label the patient with diverticulitis.

Confirmation bias: “Once you have formed an opinion, you have a tendency to only notice the evidence that supports you and ignore contrary evidence.”

From the triage note you strongly suspected diverticulitis, so you subconsciously push aside the fact that he has tenderness throughout, and that it radiates to the flank, not just focally in the LLQ.

Premature Closure: “This is the tendency to stop too early in a diagnostic process, accepting a diagnosis before gathering all the necessary information or exploring all the important alternatives.”

Here the patient feels it’s diverticulitis, there was some loose stools earlier in the week so we close the possibility of other diagnosis.

 

You continue your shift – 2 hours later an EMS patches in.

“62 yo male previously discharged from ED today with diverticulitis, found down at home by wife. CPR in progress. Asystole on rhythm checks. Down time 30 min. Intubated on scene. ETA 5 minutes”.

 

You prepare your team to receive the code. As EMS rolls in you recognize the man you discharged earlier in the day. You rack your brain, but don’t remember getting a detailed past medical history other than he had diverticulitis. You are unsure if he had any cardiac risk factors.

You begin the resuscitation and ask the resident working with you to look up the patient’s PMH. They find a recent IM consult – the patient has a history of RA and is on immunosuppressants. He also has a history of HTN, DM and a known AAA last checked 3 years ago. It measured 5cm at that time.

You grab your ultrasound probe and scan the aorta:

You see a large AAA and potentially some free fluid anterior to the aorta.

You scan the RUQ:

 

You see a large amount of free fluid.

You suspect a ruptured AAA. You begin Massive Transfusion Protocol and attempt to resuscitate the patient to ROSC. You give the vascular surgeon on call a heads up. Unfortunately the patient has been down 30 min and your resuscitation is unsuccessful. You call the code.

This would be an unfortunate case: the setting in the department is already chaotic, you are mentally fatigued and bias can take over. As ED docs this is a common situation we find ourselves in often. To err is human, but there are ways we can overcome bias.

 

What are the two types of cognitive approaches we often take2?

Type 1: The Intuitive/Reflexive System: automatic decisions based on pattern recognition. Done quickly and with minimal effort. This is the approach we took with our patient.

Type 2: The Analytical/Problem-Solving System: we step back and critically think about the patient presentation, think about pretest probabilities, other diagnoses and question ourselves more. This is not the fast route.

So, Type 2 must be best then2?

Not really – it’s a blend of the two.  “Experts use their experience and past errors/mistakes to reflect on their knowledge and their biases and develop heuristics (cognitive short-cuts) and cognitive forcing strategies that allow them to use their Type 1 system for rapid decision making in EM rather than having to slow down using their Type 2 system.”

So, we gather knowledge as we see more and more patients, but we also need to use our knowledge wisely.

How do we do this2?

Reflection – learn from your mistakes. Easy in theory but will require some work and time on your part to continue reflecting in a useful manner:

  • Follow up on your cases; try and do so within a few days or on your next shift. Check their inpatient chart. Consider touching base with the patient in some cases.
  • Develop your own cognitive short cuts – ones based on experience and previous analytical problem solving so next time you don’t have to evaluate as critically.
  • Consider dictating your chart, or documenting in the EMR your ED uses – when saying it outloud, or typing it out all at once, it can trigger reflection and may lead you to consider other diagnoses.
  • Before you sign off on a chart and put it in the ‘discharged’ pile look at the evidence one last time – does it have internal congruence? Is there evidence against your diagnosis that may support another?

Try and understand your own personal bias, or any that may exist within your thought process.

When you reflect upon your own personal bias, it can help you develop strategies to prevent it from happening.

 

Do you find yourself anchoring on a diagnosis from the triage note before you even see it patient? Force yourself to truly broaden your differential.

Have you ever found yourself subconsciously pushing some data aside while focusing on results that support your leading diagnosis? Maybe write the pertinent results on your chart so you can’t ignore them.

Bottom line – it takes work and time to reflect upon your practice. We all change our practice based on previous mistakes – this is a type of cognitive forcing strategy. The physician in our case will likely scan each aorta in high risk patients with flank pain from now on. This case has forced them to consider AAA in future cases. He/she has created a cognitive heurisitic to consider AAA in abdo pain presentations.

Emergency Medicine is a team -oriented environment. What other ways can we prevent bias2?

Two minds are better than one . During critical situations our brains often focus on one task and can’t process more outside information. Situational awareness can be lost – having a second doc on board if possible can be exceedingly helpful; If you both have your ‘jobs’ you can cognitively unload some of the information.

Practice, practice, practice – evidence shows that mentally rehearsing critical procedures increases chance of success. See Dr. George Kovac’s approach to taking an airway (start at 3 min mark) for a great example.3

 

Prep your team – have a huddle when the EMS dispatch is received. Review the differential and logistically have medications/equipment you anticipate being needed within arms reach. Assign tasks to each person so everyone knows their job. Call any consultants you suspect will be needed.

Talk to your team – no matter how obvious it may (or may not) seem, confirmatory statements can bring everyone on the same page. “This trauma patient is altered and not protecting their airway, we need to take the airway and urgently get a CT head”. Communication on a patient plan doesn’t need to be only in critical resuscitation situations. We are all involved in patient care. When you see a patient talk to the nursing staff, state your suspected diagnosis, how you plan to investigate and any interventions ongoing in the meantime. Paramedic nearby? Discuss the case with them as well, they have firsthand information from the scene that can be incredibly insightful. Plus, they are as much a part of the team as in hospital staff. They will want an update on the patient as well.

Think ahead – when you communicate your confirmatory statement to your team, it’s also a good time to consider what could go wrong and how to prepare. “This patient likely has a significant intracranial injury and could potentially herniate. We need to monitor for signs of herniation, have mannitol at the bedside and be prepared for urgent neurosurgical intervention”.

Practice, practice, practice some more – with simulation. Acclimatize yourself to stressful situations so you become more desensitized to your body’s physiologic response when faced with a critically ill patient.

Checklists – you can be a pro at resuscitation and stressful situations, but everyone has an off day. Everyone can suffer from fatigue. Take some of the thinking out of the picture – trauma checklists, airway checklists, etc. These can prevent errors by allowing you to follow the list when giving care and can provide a ‘fail-safe’ approach.

When are we more likely to make errors4?

  • Nightshift – especially around 5AM. The EM witching hour.
  • Handover – especially from nightshift
  • The overconfident physician/learner
  • Extremes of age – very young or very old patients
  • High patient volumes with many interruptions
  • The ‘difficult’ or frustrating patient

One study showed an emergency doctor was interrupted on average 30 times during an 180 min work window, while seeing/responsible for on average 12 patients during this time. 5

What can we do to prevent errors4?

  • Rest well before your nights – sleep deprivation is cumulative. It can lead to tolerance of more risk, increased distractability and poor performance at tasks. This is more likely to happen at the latter end of your shift. Ensure you take breaks to eat and hydrate.
  • Formalize handover – consider handover sheets with pertinent information and plan. Similar to SBAR – “Situation, Background, Assessment, Recommendation”
  • If no formal handover sheet, write a clear plan on the chart as well as verbalize it
  • When handing over a patient you are worried about, consider seeing them together with the doc taking over
  • If possible, try and request a ‘no interruption’ time during physician handover unless crucial. We should extend the same courtesy to our nursing staff.

After errors occur how do we learn from them4?

  • Follow up on cases by reading discharge summaries
  • M&M rounds – not to place blame, but for everyone to learn
  • A system in place to make docs aware of bouncebacks or mortality
  • Schedule ED follow up for patients you are concerned about who have poor follow up or no family doctor

Once an error has occurred, how to we disclose to family/loved ones4?

  • “inform the patient and the family of the mishap at the earliest convenient time in the presence of a 3rd party such as a department chief
  • express your concern, lay out the next steps in the course of care and answer any questions
  • notify CMPA
  • consider writing a ‘late note’ in the chart the next day and write a personal note to yourself outlining all the details for your personal file”

 

Errors will happen. Bias will happen. Do your best to reflect upon your practice and take away skills that will help you overcome these barriers.

 

References & further reading

  1. Justin Morgenstern, “Cognitive errors in medicine: The common errors”, First10EM blog, September 15, 2015. Available at: https://first10em.com/cognitive-errors/.
  2. Helman, A, Himmel, W, Hicks, C, Dushenski, D. Decision Making in EM – Cognitive Debiasing, Situational Awareness & Preferred Error. Emergency Medicine Cases. January, 2016. https://emergencymedicinecases.com/decision-making-in-em/. Accessed March 17, 2021.
  3. EMCrit # 253 – the Kovacs Kata to Optimize a Failing Laryngoscopy Attempt. https://www.youtube.com/watch?v=jCgpRd1R7gY&ab_channel=EMCrit
  4. Sinclair, D, Hicks, C, Helman, A. Cognitive Decision Making and Medical Error. February, 2011. https://emergencymedicinecases.com/episode-11-cognitive-decision-making-medical-error/. Accessed March 17, 2021.
  5. Chisholm, Collison, Nelson & Cordell (2000). Emergency department workplace interruptions: are emergency physicians “interrupt-driven” and “multitasking”? Academic Emergency Medicine Nov;7(11):1239-43. doi: 10.1111/j.1553-2712.2000.tb00469.x.

 

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EM Reflections January 2021: TIA Review

 

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

Case

A 69 yo male presents to the ED with dizziness that was ongoing 1 hour. His symptoms began when getting up from the couch and walking to the kitchen. He felt like he was going to ‘pass out’ and ‘couldn’t walk straight’. He also describes having a headache that began around the same time, but says he has headaches from time to time and wasn’t bothered by it. After 1 hour of feeling dizzy and off balance he called EMS. His symptoms resolved en route with EMS in the ambulance.

His vitals in triage are: 128/64, HR 89, RR 16 O2 95% on RA, T 36.3 Glucose 15

The nurse hands you his medication list and ECG

The ECG indicates atrial fibrillation. This is new from his previous ECG. His medications include ramipril, metformin and atorvastatin.

You suspect a transient ischemic attack (TIA), but what other mimics are on the differential1?

 

What are some important causes of TIA to consider? What features make TIA more likely1?

You feel your patient’s abrupt inability to walk straight certainly qualifies as lack of function. The onset was abrupt and symptoms have resolved. Your patient also has new atrial fibrillation, putting them at risk.

What if the patient didn’t have new atrial fibrillation? What other symptoms/features on clinical exam could suggest an alternative cause1?

Think “TIA and”…

TIA and neck pain: cervical artery dissection

TIA and new fever or heart murmur: endocarditis

You complete your physical exam. The patient is neurologically normal including cranial nerves, motor, sensory, reflexes, cerebellar, and gait. There is no new murmur, fever or neck pain. The patient has new a fib of unknown duration that is not anticoagulated. You suspect this is the cause.

Although the patient is normal now, you do wonder if they had objective signs initially with EMS, or with the first nursing assessment. As neuros can change so quickly you review the other documented exams

Of note EMS reports a GCS of 15 and the following description of symptoms:

“off balance, requiring support to walk”

“noticeable trouble speaking with slurred speech”

“patient reports feeling dizzy”.

The symptoms resolved en route. The patient walked unassisted from the ambulance bay to triage.

Nursing notes document a normal neuro exam in triage.

Is there a timeline involved in diagnosis TIA2?

TIA is now defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. The end point, stroke, is biologic (tissue injury) rather than an arbitrary timeline (≥24 hours).

Although the patient is now neurologically normal, this episode is a big red flag for stroke. To determine how urgent a work up is needed you decide to stratify the patient’s risk of stroke. The ABCD2 score likely comes to mind:

 

Is this tool accurate at predicting stroke3?

With the ABCD2 score physicians may misclassify up to 8% of patients as low risk. The sensitivity of the score for high risk patients was found to be only 31.6%3. This score also does not take into account neuroimaging findings – one study found up to 15% of patient’s with high grade carotid stenosis would be missed by using the ABCD2 score. Lastly an Australian study that used the ABCD2 score with ED patients all reported similar rates of strokes at the 30 and 90 day follow up, regardless of stratification using this tool.

Bottom line – ABCD2 is out.

So is there any tool I can use to predict risk of stroke4?

The Canadian TIA Score

This score was initially studied prospectively in over 7500 adult patients diagnosed with TIA in the ED or by a neurologist. The primary outcome was subsequent stroke in 7 days or prompt emergency carotid endarterectomy (CEA) to prevent stroke in less than 7 days. 1.4% of patients had a stroke and 1.0% had CEA in less than 7 days.

The score has recently been validated and is ready for clinical use8.

This score classifies patients as:

LOW risk: -3 to 3 points. Safely discharge following careful ED assessment with elective follow up

MEDIUM risk: 4-8 points. Undergo additional testing in the ED, have antithrombotic therapy optimized, be offered early stroke/neuro follow up

HIGH risk: ≥ 9 points. Fully investigate and manage ideally in consultation with a stroke specialist during the first ED visit.

Your patient is already at medium risk, before imaging is acquired. According to this tool your patient should be investigated with labs and imaging in the ED and offered urgent neuro follow up.

The acute nurse reminds you that it is 2330 and the CT tech leaves at midnight. You need to arrange urgent imaging – but what should you order6?

CT-angiography can be done at timing of non contrast CT and is the standard of care in neurovascular disease. It is well established that there is an association between vascular occlusion or high grade stenotic vessels and stroke recurrency and disability.

Angiography will show high grade stenotic lesions that are amendable to endarterectomy, as well as identify carotid or vertebral artery dissection as an alternative cause.

In high risk patients, CT-A should be the go to. This is based on Canadian Stroke Best Practice Guidelines.

 

Based on the Canadian TIA score my patient is medium risk. Could they still benefit from CT-A?

The Canadian TIA Score is not yet integrated with Stroke Management. According to Best Practice Guidelines high risk features are considered to be:

This patient had transient speech deficit – consider this a high risk feature and get a CT-A in your work up in the department.
You discuss this with your radiologist who agrees a CT-A is warranted.

Luckily a consultant neurologist is also on call and in house dealing with a patient in the neuro ICU. As this patient requires urgent neuro follow up he agrees to see post CT-A.

Your patient has 50% stenosis of the left vertebral artery. There is no sign of infarct or hemorrhage and no space occupying lesion.

The patient is assessed by neuro, while a trauma and STEMI roll into your department. You get back to work.

An hour later the neurologist speaks with you briefly after seeing the patient and agrees this is a TIA. Their plan is to initiate anticoagulation as they suspect a cardio-embolic source as the CT shows no infarct/dissection and the symptoms resolved within an hour. They plan to order an urgent echo and follow up with the patient this week and feel they can be discharged.

What would be a contraindication to starting anti-coagulation for A fib1?

Evidence of completed stroke on CT – these patients are started on anti-coagulation at a later date to prevent bleeding into infarct.

You wonder if the patient should be admitted as they had high risk features in their presenting TIA?

If the patient has a negative CT with no occlusion and no vessels amenable to endarterectomy then they can be discharged and followed-up within 48 hours1.

If there is an occlusion ameanable to endarterectomy, then admission is advisable. Urgent surgery can reduce the risk of stroke over 2 years from 26% to 9% (a 17% absolute risk reduction). If done within 2 weeks the absolute risk reduction is 30%1. This is generally the case for carotid stenosis.
Our patient has vertebral artery stenosis – which usually maximizes medical therapy before considering any surgical options7. If the patient had carotid stenosis, high grade stenosis of over 70% would warrant urgent consultation.

After this consideration you feel more comfortable with the plan and continue the rest of your shift.

You are reviewing the case with a student learner later in the shift and they ask what if the patient didn’t have A fib? What would have been the course of action1?

Investigations 1:
The patient would require holter and echo to assess for potential cardioembolic source from paroxysmal A fib. If admitted these would have beeen done as an inpatient. However, our patient was discharged. More urgent holter and echo is required for patients who:

“1. Patients with known heart disease including rheumatic heart disease, heart failure, severe valvular disease, severe CAD or history of MI.
2. Patients with no obvious cause of their TIA and no classic risk factors to identify an underlying cause of their TIA such as paroxysmal atrial fibrillation, severe valvular disease including endocarditis, PFO etc.”

Management 1:
Early dual antiplatelet therapy (DAPT) initiated within 24-72 hours and continued for 3 weeks decreases risk of stroke by up to 3.5% without increased risk of bleeding.

In the ED: load with ASA 160-325mg PO and Plavix 300mg PO
Discharge: on ASA 81 mg PO daily and Plavix 75mg PO daily x 3 weeks only

After the discussion with the neurologist the patient was discharged and given good advice on symptoms of CVA to return for. He left the ED.

 

1 week passes and you are working an evening shift. There is a stroke patient brought into the trauma bay to be urgently seen – you recognize the same 69 yo male you saw a week earlier with a TIA. On evaluation the patient has symptoms of a posterior circulation stroke. He is slightly dysarthric but can get out some slurred speech. You review his medication list and there is no anti-coagulant. You confirm with the patient he did not start any new medications after leaving the ED a week ago. When asked why he didn’t fill the prescription from the neurologist he communicates that he did not receive one.

What is the risk of stroke following TIA8?
Up to 10% of patients with TIA will have a CVA in 7 days, up to 12% in 90 days.

 

Patients in the ED are our patients, even when evaluated by a consultant and deemed well enough for discharge. In this situation confirming with the consultant who will be providing the prescription as well as confirming the patient has one in hand before leaving the department would have greatly benefited the patient.

 

 

References and further reading:

Helman, A, Himmel, W, Dushenski, D. TIA Update – Risk Stratification, Workup and Dual Antiplatelet Therapy. Emergency Medicine Cases. November, 2018. https://emergencymedicinecases.com/tia-update/. Accessed Feb 9, 2021

Furey & Rost. (2020). Initial evaluation and management of transient ischemic attack and minor ischemic stroke. Uptodate. https://www.uptodate.com/contents/initial-evaluation-and-management-of-transient-ischemic-attack-and-minor-ischemic-stroke?search=tia&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H3011236877. Accessed Feb 9, 2021

Long. Updates on TIA. emDocs. April 2016. http://www.emdocs.net/8538-2/. Accessed Feb 9, 2021

Helman, A. Morgenstern, J. Klaiman, M. Sayal, A. Perry, J, Reid, S. Rezaie, S. EM Quick Hits 18 – Conservative Management Pneumothorax, Microdosing Buprenorphine, Practical Use of CRITOE, Canadian TIA Score, Pediatric Surviving Sepsis Guidelines, Safety of Peripheral Vasopressors. Emergency Medicine Cases. May, 2020. https://emergencymedicinecases.com/em-quick-hits-may-2020/. Accessed Feb 10, 2021.

https://emergencymedicinecases.com/wp-content/uploads/2018/11/Canadian-Stroke-Guidelines-summary-2018-CJEM-1.pdf

American Heart Association (2018). Role of Brain and Vessel Imaging for the Evaluation of Transient Ischemic Attack and Minor Stroke. Stroke. Vol 49 (7) pg 1791-1795

Furie. (2019). Secondary prevention for specific causes of ischemic stroke and transient ischemic attack. Uptodate. https://www.uptodate.com/contents/secondary-prevention-for-specific-causes-of-ischemic-stroke-and-transient-ischemic-attack?sectionName=LARGE%20ARTERY%20DISEASE&search=tia&topicRef=1123&anchor=H2&source=see_link#H3. Accessed Feb 10, 2021

Perry et al. (2021). Prospective validation of Canadian TIA Score and comparison with ABCD2 and ABCD2i for subsequent stroke risk after transient ischaemic attack: multicentre prospective cohort study. BMJ 2021; 372:n49.

 

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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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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. https://sjrhem.ca/pocus-measurements-quick-reference/

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

 

 

 

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EM Reflections October 2020 – Spinal Cord Injury

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


Spinal Cord Injury

  • Recognition of various patterns of spinal cord injury
  • Reviewing EMS record can be helpful for progression of symptoms and baseline exam
  • A normal CT does not rule out spinal cord injury in a patient with neurological deficits
  • Importance of detailed neurological exam and clear communication with consultant
  • Importance of clear documentation of exam – consider using ASIA

Case

A 72 yo female presents complaining of bilateral arm weakness ongoing for 1 day. She has no other symptoms concerning for stroke. She denies any direct trauma to head or neck, but did say she was pushed from behind by a large dog and her neck ‘snapped back’ the day prior. Incidentally she says she also hasn’t urinated in over 8 hours. Her vital signs are within normal limits.


 

You are concerned about a spinal cord injury – what are the various cord syndromes? What in the history predisposes to a particular spinal cord syndrome?

4 Classification of spinal cord syndromes

This woman is elderly, likely with underlying cervical spondylosis, and has a hyperextension injury – predisposing her to a central cord syndrome. This is the most common type of incomplete spinal cord injury. Often these patients are asymptomatic from their spondylosis before the event and the mechanism of injury is usually not severe5.

Central cord syndrome involves both motor and sensory pathways and has a variable presentation. Typically one sees motor weakness in the hands and forearms with sensory preservation. Bladder dysfunction and sexual dysfunction can be seen in severe cases5. A helpful mnemonic is MUD-E6.

 

MUD-E

  • Motor loss > sensory loss
  • UE > LE
  • Distal > proximal
  • Extension type injury

 

You complete a detailed neurological exam and find she does have upper limb weakness distally. A bladder scan confirms urinary retention with 850 cc of urine in her bladder.

You decide to order a CT C -spine to assess for bony injuries. The CT scan is unremarkable.

Does this rule out a spinal cord injury in this patient?

No – normal CT does not rule out SCI in a patient with ongoing neurological deficits. In fact, in elderly patients there is often no bony injury, but the narrowed spinal canal can predispose to buckling of the ligament flava, leading to injury of the spinal cord.

You review EMS notes and nursing documentation – there are subtle differences throughout in how the exam is performed and recorded.

What is one tool that can improve your documentation in terms of accuracy and clarity?

ASIA (American Spinal Injury Association) Classification

You document your findings on ASIA, which allows for clearer communication and documentation with the attending neurosurgeon.


 

References for further reading:

4 Perron & Huff (2010). Chapter 104 Spinal Cord Disorders. Rosen’s Emergency Medicine: Concepts and Clinical Practice. pp 1389-1397. Philadephia, PA

5  Douglas, Nowak et al. (2009). Review article: Central Cord Syndrome. Journal of the American Academy of Orthopedic Surgeons. 17: 756-765

6 A boring guide to spinal cord syndromes. CanadiamEM. https://canadiem.org/a-boring-guide-to-spinal-cord-syndromes/


 

Authored and Edited by Dr. Mandy Peach

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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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