Polymyalgia Rheumatica

Polymyalgia Rheumatica – A Medical Student Clinical Pearl

Alexis Lamontagne

MD Candidate, Class of 2022

DMNB, Dalhousie University

Case:

A 73 y/o M presents with a 1 week history of proximal muscle aches and stiffness including his hips, shoulders and neck. He describes the stiffness as worse in the morning, recently he has had trouble getting out of bed at all. He finds that the stiffness is relieved and regains function as he begins to move around. He also notes increased stiffness after periods of immobility. It has become progressively worse over the past week which lead to seeking medical help in the emergency department.

There are no other associated symptoms including jaw claudication, headache, weight loss, fevers, chills, night-sweats, vision changes, paresthesias, or preceding cold or illness.

The patient has no significant past medical history. His only regular medication is omeprazole. He does not smoke, consumes 4 alcoholic drinks per day, and uses no other recreational drugs. He lives at home with his wife and they are both retired.

While asking about whether there are any rheumatological conditions that run in the family you learn that his older brother has Polymyalgia Rheumatica (PMR).

 

Polymyalgia Rheumatica:

The clinical syndrome of PMR should be considered in those aged over 50 presenting with pain and stiffness of the neck, shoulders and hips that is typically worst in the early hours of the morning or on waking, and tends to improve over the course of the day. Inflammatory markers (ESR/CRP) are typically elevated and anaemia may be present due to inflammation. Symptoms of PMR should resolve rapidly with low-dose glucocorticoids.

Differential:

Although weight loss, fever and synovitis/tenosynovitis have all been described in PMR, they should raise suspicion of :

  • malignancy,
  • deep-seated or disseminated infection (such as endocarditis or osteomyelitis),
  • inflammatory arthritides such as rheumatoid arthritis (RA), spondyloarthropathy, or crystal arthropathy.

 

Investigations:

Bloodwork reveals a normal CBC and an elevated CRP at 108.

 

Treatment:

Prednisone is initiated at 15mg PO daily. If the initial dose of 15mg does not demonstrate clinical improvement in one week, this can be increased to 20mg or a maximum dose of 25mg.

Once symptoms are controlled for 2 to 4 weeks the dose of prednisone can be tapered. Prednisone can be reduced by 2.5mg every 2 to 4 weeks until 10 mg daily is reached. The dose can then be further tapered by 1 mg per month until cessation or symptoms flare. There is no consensus regarding an optimal tapering regime.

Should a flare occur during the taper, a CRP should be measured and prednisone increased to the lowest dose that relieves symptoms. If a patient relapses several times during the taper, dose reductions can be lengthened to six to eight weeks. If a relapse occurs after the cessation of glucocorticoid use, a CRP should be obtained and prednisone can be initiated at the original dose which managed symptoms.

CRP should be measured again 2 months after the initiation of glucocorticoid therapy and 3 to 6 months thereafter during the course of treatment. Monitoring for symptoms of PMR and Giant Cell Arteritis (GCA) should also take place throughout treatment.

 

Pathophysiology:

The cause of polymyalgia rheumatica (PMR) is unknown.

The strongest risk factor for PMR is increasing age. It is unheard of in those under 50 years old and incidence increases with each decade, peaking around 75 years. Proposed mechanisms include ageing of the immune system (immunosenescence), ageing of the tissues, and ageing of neurohumoral regulatory systems. Based on the clustering of cases in space and time, it has been proposed that PMR may be triggered by infection. This could lead to persistent inflammation on a background of chronic low-grade inflammation secondary to decline in adaptive immunity and a compensatory increase in innate immune mechanisms. (Mackie 2013)

 

Relationship to Giant Cell Arteritis:

There is a well-known association between PMR and giant cell arteritis (GCA). Many patients with GCA also have polymyalgic symptoms and some patients with PMR subsequently develop GCA (Mackie 2010). There is some discussion as to whether PMR and GCA are separate disease entities or two conditions on a single pathophysiological spectrum. For the practising clinician it is important to realise that PMR and GCA are treated with different doses of glucocorticoids and that treatment of GCA is a medical emergency, whereas the immediate priority with PMR is to exclude other conditions before starting treatment. All patients with PMR should be assessed for signs and symptoms of GCA at diagnosis and screened for underlying GCA at follow-up visits. These symptoms include constitutional symptoms, headache, jaw claudication, ocular involvement, large vessel involvement, and anemia.

 

Conclusion:

With a prescription for prednisone, a follow up was arranged with the patient’s family doctor in one week. The patient was advised that the family doctor would taper his prednisone, monitor CRP, and screen for symptoms of PMR and GCA. Additionally, monitoring for the adverse effects of glucocorticoids, including osteoporosis, glucose intolerance, and hypertension would take place.

 

References:

Mackie SL. Polymyalgia rheumatica: pathogenesis and management. Clin Med (Lond). 2013;13(4):398-400.

Mackie SL. Et al. Can the prognosis of polymyalgia rheumatica be predicted at disease onset? Results from a 5-year prospective study. Rheumatology (Oxford). 2010 Apr; 49(4):716-22.

 

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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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It’s Not Over Till It’s Over – ECMO Resuscitation in the ED

It’s Not Over Till It’s Over – ECMO Resuscitation in the ED: A Medical Student Clinical Pearl

Ryan Buyting

Med III, Class of 2022

Dalhousie Medicine New Brunswick (DMNB)

Reviewed by Dr. Luke Taylor

Copyedited by Dr. Mandy Peach

Extracorporeal Membrane Oxygenation (ECMO), also sometimes referred to as extracorporeal life support (ECLS), employs components from traditional cardiopulmonary bypass machines to augment a patient’s heart and/or lung capacity for a prolonged duration of days to weeks. Importantly, ECMO is not a treatment but a bridge to native heart/lung recovery or durable organ replacement. 1

 

ECMO has been a hot topic of discussion over the past year based on its role in supporting patients with severe COVID-19 infections. The Extracorporeal Life Support Organization (ELSO), the World Health Organization and the Surviving Sepsis Campaign (SSC) Guidelines recommend considering ECMO, in specialized centers, for patients with COVID-19 who develop severe acute respiratory distress syndrome (ARDS). 2 Many of these cases made use of veno-venous ECMO, which exclusively provides pulmonary bypass for severe respiratory failure.

 

This article will focus on veno-arterial ECMO (which provides both cardiac and pulmonary bypass) and seeks to provide readers with an overview of the following:

  • What is an Extracorporeal Cardiopulmonary Resuscitation (ECPR) code?
  • Which patients should be considered for acute ECMO initiation?
  • What care will patients need in the ED post-circuit initiation?
  • What is the evidence for the use of ECPR?

 

 

Calling an ECPR Code and Patient Selection

An ECPR code essentially mobilizes the cannulation team to initiate an ECMO circuit in a previously high-functioning patient. The goal is to restore end-organ perfusion, buying time to investigate the underlying causative pathology, with hopes of improving long-term survival and neurological outcomes. Emergency physicians should consider calling an ECPR code for severe cardiac and/or pulmonary failure deemed refractory to conventional therapies. 3 Patients in cardiac arrest are potential candidates for ECPR if they meet the following:

  • reversible cause of arrest
  • witnessed arrest with bystander CPR
  • total chest compression time < 60 minutes
  • no known preexisting terminal illnesses

 

Review the reversible causes of cardiac arrest or see the image below outlining the “Hs and Ts” mnemonic.

Figure 1: The Hs and Ts / Reversible Causes of Cardiac Arrest 4

The timing at which an ECPR code should be initiated is (at present) left to physician discretion, but often depends on the availability of the cannulation team. ECMO as an option for a given patient should be anticipated and considered early amid a code to allow the team and equipment to be assembled. Most often the procedure is performed by a cardiac surgeon, however there is growing interest and involvement from vascular, general, and trauma surgeons. 5

 

The initiation of ECMO is divided into 3 stages:

(1) vascular access,

(2) insertion of ECMO cannulas and connection to the circuit once the patient is determined to be an ECMO candidate,

(3) pump initiation.

 

In emergent situations, unilateral peripheral cannulation is the preferred and most expedient method. 6 This approach also allows for the continuation of high-quality CPR while access is obtained. Either through surgical exposure or under ultrasound guidance, a venous drainage cannula is placed in the femoral vein. Blood is returned from the machine through a similarly placed cannula in the adjacent femoral artery. Several alternative circuits are possible in extenuating circumstances depending upon patient injuries or characteristics. 1

Figure 2: Veno-arterial peripheral ECMO via unilateral femoral-arterial and femoral-venous cannulation. 7

 

Post-Circuit Initiation Critical Care

After the circuit has been initiated, the lines should be closely examined; the venous drainage blood should be dark red and the arterial return blood should be bright red. Given the proximity of the vessels and the fact that these procedures are often done with ongoing CPR, this confirmation of placement is crucial.

 

Next, it is important to reassess the patient’s rhythm; if the patient is in VFIB, defibrillation should be repeated after a few minutes on circuit as it is important to have an ejecting left ventricle on ECMO to prevent distention. 8

 

At this point, the team should obtain a right radial arterial line (for accurate measurement of the MAP) and an ABG (to assess for adequate oxygenation and the need for setting adjustments). Vasopressors and/or inotropes should be initiated as required to meet a target MAP of 60-80mmHg. If LV distention (as assessed based on arterial line pulsatility >10mmHg or POCUS) is not improved with these medications on board, an LV vent (such as an Impella or intra-aortic balloon pump) may be needed. 8

 

Important next steps in the process include the initiation of therapeutic hypothermia, planning for the placement of a distal perfusion catheter to prevent leg ischemia, and, based on the etiology of the arrest, any other appropriate treatment (such as transfer to the cardiac catheterization laboratory for acute coronary syndrome).

 

Current Evidence for ECPR

No randomized trials concerning the use of ECPR have been published to date. Sonneville and Schmidt recently summarized the four most robust observational studies comparing the use of ECPR versus conventional CPR in patients with out-of-hospital cardiac arrest. 9 They describe a large study that reported similar low survival rates between 525 patients managed with ECPR and 12,666 patients with conventional CPR, with no significant effect of ECPR on outcomes after adjusting for confounders. 10 However, more recently, after instituting very strict patient selection criteria, Bartos et al. reported a relative risk reduction of 29% for death or poor neurological outcome (95% CI, 18%–41%) for patients receiving between 20 and 59 minutes of CPR and 19% (95% CI, 10%–27%) for patients receiving more than 60 minutes of CPR. 11 This group has since published the University of Minnesota ECPR Protocol here. 12

 

Until results from randomized trials become available, it is likely that difficult continuation decisions will need to be made on a case-by-case basis at physician discretion. Protocols requiring objective data input such as specific time periods, lactate level and oxygenation status upon arrival, may help ease this burden in the meantime, if only marginally.

 

References

  1. Badulak JH, Shinar Z. Extracorporeal Membrane Oxygenation in the Emergency Department. Emerg Med Clin North Am. 2020;38(4):945-959. doi:10.1016/j.emc.2020.06.015
  2. Ramanathan K, Shekar K, Ling RR, et al. Extracorporeal membrane oxygenation for COVID-19: a systematic review and meta-analysis. Crit Care. 2021;25(1):211. doi:10.1186/s13054-021-03634-1
  3. Extracorporeal Life Support Organization (ELSO). Guidelines. Accessed August 29, 2021. https://www.elso.org/Portals/0/ELSO%20Guidelines%20General%20All%20ECLS%20Version%201_4.pdf
  4. @lightssirensaction. Hs and Ts. Accessed August 28, 2021. https://www.instagram.com/p/CA4MMdVBy8V/
  5. McCallister D, Pilon L, Forrester J, et al. Clinical and Administrative Steps to the ECMO Program Development. IntechOpen; 2019. doi:10.5772/intechopen.84838
  6. Stoecklein H, Slack S, Tonna JE, Youngquist ST. ECMO & ECPR. JEMS. Published December 2, 2017. Accessed August 28, 2021. https://www.jems.com/patient-care/ecmo-ecpr/
  7. Lawler PR, Silver DA, Scirica BM, Couper GS, Weinhouse GL, Camp PC. Extracorporeal Membrane Oxygenation in Adults With Cardiogenic Shock. Circulation. 2015;131(7):676-680. doi:10.1161/CIRCULATIONAHA.114.006647
  8. Cevasco M, Takayama H, Ando M, Garan AR, Naka Y, Takeda K. Left ventricular distension and venting strategies for patients on venoarterial extracorporeal membrane oxygenation. J Thorac Dis. 2019;11(4):1676-1683. doi:10.21037/jtd.2019.03.29
  9. Sonneville R, Schmidt M. Extracorporeal Cardiopulmonary Resuscitation for Adults With Refractory Out-of-Hospital Cardiac Arrest. Circulation. 2020;141(11):887-890. doi:10.1161/CIRCULATIONAHA.119.044969
  10. Bougouin W, Dumas F, Lamhaut L, et al. Extracorporeal cardiopulmonary resuscitation in out-of-hospital cardiac arrest: a registry study. Eur Heart J. 2020;41(21):1961-1971. doi:10.1093/eurheartj/ehz753
  11. Bartos JA, Grunau B, Carlson C, et al. Improved Survival With Extracorporeal Cardiopulmonary Resuscitation Despite Progressive Metabolic Derangement Associated With Prolonged Resuscitation. Circulation. 2020;141(11):877-886. doi:10.1161/CIRCULATIONAHA.119.042173
  12. Yannopoulos D, Bartos JA, Martin C, et al. Minnesota Resuscitation Consortium’s Advanced Perfusion and Reperfusion Cardiac Life Support Strategy for Out‐of‐Hospital Refractory Ventricular Fibrillation. J Am Heart Assoc. 5(6):e003732. doi:10.1161/JAHA.116.003732
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Just the Facts: Sympathectomy for Frostbite

Just the Facts: Sympathectomy for Frostbite – A Resident Clinical Pearl

Robert J. Dunfield

PGY-3 – Integrated Family Medicine/Emergency Medicine Program

Reviewed by: Dr. Devon Webster

Copyedited by: Dr. Mandy Peach

Case:

You’re working in a rural emergency department when a 76 year old man is brought in by ambulance after being found laying in a snowbank on the side of the road, next to his parked car. The temperature outside is -20°C and it’s snowing quite heavily. As far as you can gather, the man has a history of cognitive impairment and lives alone.

You perform an appropriate initial resuscitative workup. His core temperature is warmed to 36.5°C and he is stabilized, but complains of ongoing left hand pain. You note that the man’s left hand has the following features: it is cold, throbbing, his phalanges are covered in blisters, surrounded by edema. You suspect frostbite.

Figure 1: Frostbite. [Peer-Reviewed, Web Publication] Herndon, A. Amick, A. (2021, Mar 15). Health Risks Imposed by the Beach. [NUEM Blog. Expert Commentary by Lank, P]. Retrieved from http://www.nuemblog.com/blog/health-risks-imposed-by-the-beach.

  1. What features on clinical examination distinguish first, second, third, and fourth degree frostbite? [1, 2]

In the emergency department setting, distinguishing between degrees of frostbite is not accurate and not clinically useful. Similar to burns, it is more useful in the acute setting to classify frostbite as superficial or deep to help determine prognosis. Tissue involvement can change through rewarming and progress with time. All frostbite injuries are treated with a similar approach, no matter the degree of involvement.

Classically, however, frostbite injuries have been categorized as first, second, third, or fourth degree. The following table outlines the characteristics for each of these classifications.

Clinical features indicating favourable prognosis:
* Intact sensation to pinprick
* normal skin color
* large blisters with clear fluid

Clinical features indicating poor prognosis:
* Non-blanching cyanosis
* Dark fluid-filled blisters
* Hard, non-deforming skin.

2. What treatment options are available for rewarming a peripheral frostbite injury? [1, 3, 4, 5, 6]

The treatment for frostbite requires a careful approach that starts immediately during the pre-hospital stage. These patients should:

1) be removed from the cold environment,
2) have any cold and wet clothing removed,
3) begin rewarming of affected area in circulating warm water bath (37 to 39*C)

*Avoid rewarming with dry heat, vigorous rubbing, or fire.

Once these patients have arrived to your emergency department, initial resuscitation of the whole patient should be the primary focus of treatment. Follow your ABC’s and ensure their core temperature is stabilized prior to focusing on the frostbitten limb.

 

In terms of rewarming, the traditional approach has implicated the following interventions:

1) Analgesia: thawing can be extremely painful. Administer anti-inflammatories and/or short acting opioids as needed.

2) Warm and wet immersion: immerse the frostbitten limb in circulating water/saline warmed to 37 to 39°C.

3) Fluid resuscitation: as needed, particularly if there is concern for cold diuresis in the setting of hypothermia.

4) Movement: encourage gentle movement of the affected limb as tolerated, but ensure no rubbing/friction is applied to the frostbitten area.

5) Topical aloe vera q6h: this treatment has shown to be effective in fighting the arachidonic acid cascade that promotes inflammation and prostaglandin formation, thereby reducing tissue damage in frostbite. Can be considered when available.

6) Tetanus toxoid

7) Careful wound care: this is an important aspect of ongoing management. Prior approaches to frostbite discuss the possibility of debridement of blisters and soft tissue, but this does not need to occur in the acute setting. Incision and drainage of white, cloudy blisters remains controversial.

8) Affected limb elevation

 

3. What management options exist for post-rewarming pulse deficits in frostbite? [1, 5, 6, 7]

If a hand continues to demonstrate ongoing evidence of ischemia or rewarming therapy fails to achieve reperfusion, the following management strategies are suggested:

1) If not already done, emergently consult local frostbite management expertise, such as plastic or vascular surgery.

2) Consider vascular imaging of the affected area.

3) Intravenous or intraarterial thrombolytic (Tpa 0.15 mg/kg bolus then 0.15 mg/kg over 6 hours). After Tpa is administered, start IV unfractionated heparin (2 mg/kg/min) for 24 to 72 hours. This reduces the risk of digital amputation.

4) Iloprost* IV (where available) 2 mg/kg/min, 6 hours per day for 5 days.
*Iloprost is not currently available commercially in Canada, but many Canadian physicians working in northern regions of the country are currently advocating for its increased availability. Iloprost is an arterial vasodilator, often used in pulmonary arterial hypertension.

 

4. What role does local anaesthetic play in rewarming a frostbitten hand? [8, 9]

Studies have assessed the role of regional anesthesia to create a chemical sympathectomy for patients with frostbite. Hand surgeries performed under local anaesthetic have shown to reduce sympathetic innervation of the hand, resulting in hyperemia (increased blood flow) while simultaneously providing pain control. Hyperemia is likely a result of the sympathetic blockade that results in increased blood flow and vasodilatation peripherally. This peripheral nerve block focuses on the ulnar and median nerves.

One study looked at 39 patients undergoing carpal tunnel release. It showed that a volar nerve block resulted in 74% of patients having a temperature increase of >1°C in their distal fingers following distal forearm anaesthetic block.

Concerns about finger vasoconstriction as a result of epinephrine use in anaesthetic injected at the wrist, theoretically worsening ischemia and necrosis risk in the fingers, are currently unfounded. Local anaesthetic without epinephrine comparatively will have a shorter duration of hyperemia and analgesia.

In general, there is limited research available around the use of local anaesthetic in frostbite.
No clear guidelines outlining indications and contraindications to local anaesthetic sympathectomy in the treatment of frostbite presently exist. Currently, its use as an adjunct to other routine management of acute frostbite is recommended.

5. How is a local anaesthetic sympathectomy performed in the hand? [8]

1) Materials needed:

-Aseptic cleaning wipe/solution
-10 mL syringe
-1% lidocaine with epinephrine
-18G needle (to draw up local anaesthetic)
-27G needle (to inject local anaesthetic)
-Sterile marking pen

2) Identify your landmarks: injection of the local anaesthetic should be performed between the palmaris longus and flexor carpi ulnaris tendons, just proximal to the wrist crease. Mark the area.

3) Clean the area with an antiseptic solution.

4) Inject 10 mL of 1% lidocaine to the area landmarked, subfascially. There is no need to fan the needle during this injection.

5) Continue to monitor the temperature of the involved fingers. It is possible the area near the wrist infiltrated by the local anaesthetic will blanche, but the hand and fingers distal to this area should become warmer and hyperemic.

 

  1. How long do the effects of local anaesthetic sympathectomy last? [8]

It is estimated that hyperemia will last for approximately 2 hours. Numbness may last up to 6 hours.

https://handsurgery.org/multimedia/files/preCourse/Frostbite%20treatment%20with%20blocks.pdf

 

SUMMARY AND KEY POINTS:

-Classifying frostbite in an acute setting is notoriously unreliable due to the ability of the insult to progress over time. Your approach to frostbitten patients should be consistent despite their initial tissue involvement.

-Initial management of the frostbite patient should focus on resuscitation and core rewarming.

-Removing the patient’s exposure to hypothermia and cause of frostbite, pain control, warm and wet rewarming, tetanus vaccination, topical aloe vera, wound care, considering thrombolysis, and consulting experts in frostbite management are core tenants of frostbite care.

-Consider local anaesthetic sympathectomy using distal volar wrist nerve block as an adjunctive therapy in patients with hand frostbite.

-Iloprost is currently unavailable commercially in Canada but advocacy is ongoing to increase its availability for treatment of frostbite, especially in northern areas of the country.

 

REFERENCES:

 

  1. Tintinalli, J.E., Ma, O.J., Yealy, D.M., Meckler, G. D., Stapczynski, J.S., Cline, D., Thomas, D.M. (2016). Tintinalli’s emergency medicine: A comprehensive study guide(Ninth edition.). New York: McGraw-Hill Education. Chapter 208: Cold Injuries.
  2. Comp, L. Brrr! ED Presentation, Evaluation, and Management of Cold Related Injuries. net: Practice Updates. 2018; Last updated: May 21, 2018. Accessed: June 01, 2021. Available from: http://www.emdocs.net/brrr-ed-presentation-evaluation-and-management-of-cold-related-injuries/
  3. Thomas, A. CRACKCast E139 – Frostbite. org. 2017; Last updated: December 28, 2017. Accessed: June 01, 2021. Available from: https://canadiem.org/crackcast-e139-frostbite/
  4. Handford, C., Buxton, P., Russell, K., Imray, C. E., McIntosh, S. E., Freer, L., Cochran, A., & Imray, C. H. 2014. Frostbite: a practical approach to hospital management. Extreme physiology & medicine3, 7. https://doi.org/10.1186/2046-7648-3-7
  5. Basit, H., Wallen, T.J., Dudley, C. 2021. Frostbite. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nih.gov/books/NBK536914/
  6. Poole, A., and Gauthier, J. 2016. Treatment of severe frostbite with iloprost in northern Canada. CMAJ, 188 (17-18): 1255-1258. https://doi.org/10.1503/cmaj.151252
  7. Yun, T. 2021. ‘It’s a promising result’: Made-in-Yukon treatment reducing amputations in most severe frostbite cases. CTV News: Health News. Last updated: March 3, 2021. Accessed: June 01, 2021. Available from: https://www.ctvnews.ca/health/it-s-a-promising-result-made-in-yukon-treatment-reducing-amputations-in-most-severe-frostbite-cases-1.5331820
  8. Chandran GJ, Chung B, Lalonde J, Lalonde DH. The hyperthermic effect of a distal volar forearm nerve block: a possible treatment of acute digital frostbite injuries? Plast Reconstr Surg. 2010 Sep;126(3):946-950. doi: 10.1097/PRS.0b013e3181e60400.
  9. Rakower SR, Shahgoli S, Wong SL. Doppler ultrasound and digital plethysmography to determine the need for sympathetic blockade after frostbite. J Trauma. 1978 Oct;18(10):713-8. doi: 10.1097/00005373-197810000-00006.
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Advanced cardiac echo – a review of E-point septal separation

Dr. Kyle Traboulsee, PoCUS Fellow

Reviewed by Dr. David Lewis

Copyedited by Dr. Mandy Peach

Background:

Often hypotensive, or acutely dyspneic patients, present to the emergency department in significant distress, and emergency physicians must work quickly to evaluate, stabilize, and treat these patients. In the past, determining whether there was a cardiac etiology to these presentations often relied solely on history, physical exam, and varies biochemical markers. Point-of-care ultrasound has increasingly been adopted as a tool to assess cardiac function, and specifically left ventricular ejection fraction (LVEF). Different methods can be used to estimate LVEF (such as “eyeballing”, and the Simpson method), but they can have large inter-reader variability, and require significant cardiac PoCUS experience. E-point septal separation is a measurement of how close the anterior mitral valve leaflet comes towards the interventricular septum and has been shown to be a quick and easy method for estimating LVEF. (1)(2)

 

Anatomy/pathophysiology

               Blood flow is determined by pressure gradients, where blood will travel from areas of high pressure to low pressure. Such a pressure gradient exists between the left atrium and left ventricle. During diastole, the left ventricle relaxes, and the intraventricular pressure decreases until the pressure falls below that of the left intra-atrial pressure. When the left atrial pressure exceeds the left ventricular pressure, the mitral valve opens, and blood passively flows from the high(er) pressure atrium to the lower pressure ventricle. This occurs early in diastole, and the flow of blood from atrium to ventricle is further assisted by an atrial contraction (termed atrial kick) later in diastole. In a healthy individual the atrial-ventricular (A-V) gradient is sufficient to open the mitral valves and bring the anterior mitral leaflet in proximity (or contact) with the intraventricular septum. (1)(2)(3)

In the case of reduced LVEF, the diastolic pressure inside the left ventricle increases due to a decreased ability to eject blood during systole. This can occur due to several reasons, but often result in left ventricular dilation to compensate and preserve LVEF. As LVEF decreases, the ventricular diastolic pressure increases, and the atrial-ventricular (A-V) gradient decreases, leading to a decreased flow rate from atrium to ventricle during diastole, and thus a decreased mitral valve opening. That, paired with LV dilation, leads to an increased (measurable) distance between the anterior mitral valve leaflet and the intraventricular septum during diastole, which can be used as a surrogate marker for left ventricular function. (1)(2)(3).

 

PoCUS Technique

The E-point septal separation measurements will be made using a parasternal long axis (PLAX) view

Obtaining PLAX view

Steps:

  • Place probe at the left parasternal border, just caudal to manubrium (second intercostal space), perpendicular to the chest. Ensure the probe indicator is placed towards to the patient’s right shoulder.
  • Slowly slide the probe down each successive intercostal space, as well as medially (not exceeding patient midline), and laterally, until the highest quality images are obtained (this will likely be around 3-5th intercostal space, left parasternal border, but may differ from patient to patient)
  • Once the best view has been located from step 2, slowly rotate the probe to elongate the left ventricle as much as possible. The probe may need to be rocked (heeled) to center the image.

The optimal PSL image includes the left ventricle (LV) in continuity with the aortic outflow tract. The right ventricle will be near field, the left atrium far field, and the mitral valve, aortic valve, and LV cavity are in between (in the middle of the field).  The apex of the left ventricle will be screen left. (4)(5).

Parasternal long axis view- probe orientation (6)              Parasternal long axis view-anatomy (7)

Parasternal long axis view: normal (own image)

EPSS measurements

EPSS measurements are commonly obtained using M-mode.

  • Once a parasternal long axis view (PLAX) is obtained, turn on M-mode, and place the cursor over the apical tip of the anterior mitral valve leaflet.
  • The M-mode will demonstrate movement of the anterior mitral leaflet, with respect to the intraventricular septum. The image should show 2 peaks per heart cycle, under a hyperechoic line. The first, larger peak (E), represents the initial opening of the mitral valve from passive blood flow in early diastole caused by the A-V gradient. The second, usually smaller peak (A), represents the atrial kick, occurring later in diastole. This M mode image is commonly referred to as a “cloudy sky over two hills”
  • Measure the distance from the top of the E wave to the intraventricular septum. (1)(5)

A normal EPSS measurement with M-mode (8)

PSL: normal EPSS, M-mode (own image)

An abnormal EPSS measurement with M-mode (8)

EPSS measurements can alternatively be measured in B mode

  • Once a parasternal long axis view (PLAX) is obtained, ensure anterior mitral valve leaflet and septum are well visualized over 3-5 cardiac cycles
  • Freeze the image and cycle through the previous 3-5 cardiac cycles, stopping on the image where the anterior mitral valve leaflet lies closest to the intraventricular septum.
  • Measure the distance between the tip of the anterior mitral valve leaflet and the intraventricular septum.

PSL-Poor mitral valve opening (own image)

PSL view- abnormal EPSS measurement in B mode (9)

 

Interpretation

An EPSS < 7mm is considered normal

An EPSS >7 mm has been suggested as 87% sensitive and 75% specific for an EF <50% (10)

Another study suggested that an EPSS >7 mm was 100% sensitive and 51.6% specific for an EF<30% (11).

One MRI study came up with the following formula to calculate EF (4):

EF=75.5 – (2.5 x EPSS in mm)

 

Pitfalls

               Although a quick and relatively simple surrogate measurement for LVEF, there are some patient populations and situations in which EPSS may give in inaccurate estimate of cardiac function. Patients with mitral stenosis may have poor valve opening, leading to a high EPSS, in the context of an otherwise normally functioning left ventricle. Patients with aortic regurgitation may also have poor anterior mitral valve leaflet motion, and thus have a falsely high EPSS. For these reasons, it would be reasonable to apply color doppler across the mitral and aortic valves to assess for signs of regurgitant jets, as well as close assessment of the valves for signs of calcification. Off-axis measurement, regional wall motion abnormalities, and left ventricular hypertrophy may also result in false interpretations concerning LVEF (1)(3)(4).

 

Bottom line

               E-point septal separation is a relatively easy and reproducible technique that can be used to generate a quick estimation of left ventricular function and can help point towards a cardiac etiology in the undifferentiated patient.  It is important to keep in mind factors (as discussed) that may lead to false EPSS interpretations, and EPSS results should not preclude a more global cardiac assessment.

 

References:

  • Boon, S. C., Lopez Matta, J. E., Elzo Kraemer, C. V., Tuinman, P. R., & van Westerloo, D. J. (2020). POCUS series: E-point septal separation, a quick assessment of reduced left ventricular ejection fraction in a POCUS setting. Netherlands Journal of Critical Care, 28(3), 139–141.
  • Cisewski , D., & Alerhand, S. (2018, December). Fellow corner: E-point septal separation in the patient with congestive heart failure. ACEP // Home Page. Retrieved October 18, 2021, from https://www.acep.org/how-we-serve/sections/emergency-ultrasound/news/dece/fellow-corner-e-point-septal-separation-in-the-patient-with-congestive-heart-failure/.
  • Miller, T., Salerno, A., & Slagle, D. (2021, May 25). Advanced Critical Care Ultrasound: E-Point Septal Separation to Estimate Left Ventricular Ejection Fraction. EM resident . Retrieved October 2021, from https://www.emra.org/emresident/article/epss/.
  • Atkinson, P., Bowra, J., Harris, T., Jarman, B., & Lewis, D. (2019). Point-of-care ultrasound for Emergency Medicine and Resuscitation. Oxford University Press.
  • Socransky, S., & Wiss, R. (2016). Essentials of point-of-care ultrasound: The ede book. The EDE 2 Course, Inc.
  • SonoSpot, & SonoSpot. (2012, September 17). Sonotip&Trick: “I can’t get a good parasternal long view.” really? well, try this… Retrieved October 18, 2021, from https://sonospot.wordpress.com/2012/08/07/sonotiptrick-i-cant-get-a-good-parasternal-long-view-really-well-try-this/.
  • Roma, Ak, Sparks, M., Kelly, C., (@NephroP), A. K., Dowd, R., Crosson, D. A., Deepali, D., Singh, N., Andreea, Aya, S.A., A., Panchal, L. M. R., & Murthy, J. (2019, June 7). Introduction to focused cardiac ultrasound: The parasternal long axis view. Renal Fellow Network. Retrieved October 18, 2021, from https://www.renalfellow.org/2019/06/07/introduction-to-focused-cardiac-ultrasound-the-parasternal-long-axis-view/.
  • Miller, T., Salerno, A., & Slagle, D. (2021, May 25). Advanced Critical Care Ultrasound: E-Point Septal Separation to Estimate Left Ventricular Ejection Fraction. EM resident . Retrieved October 2021, from https://www.emra.org/emresident/article/epss/.
  • Satılmış Siliv, N., Yamanoglu, A., Pınar, P., Celebi Yamanoglu, N. G., Torlak, F., & Parlak, I. (2018). Estimation of cardiac systolic function based on mitral valve movements: An accurate bedside tool for emergency physicians in DYSPNEIC patients. Journal of Ultrasound in Medicine, 38(4), 1027–1038. https://doi.org/10.1002/jum.14791
  • Ahmadpour H, Shah AA, Allen JW, et al. Mitral E point septal separation: a reliable index of left ventricular performance in coronary artery disease. Am Heart J. 1983;106(1 Pt 1):21-8
  • McKaigney, C. J., Krantz, M. J., La Rocque, C. L., Hurst, N. D., Buchanan, M. S., & Kendall, J. L. (2014). E-point septal separation: A bedside tool for emergency physician assessment of left ventricular ejection fraction. The American Journal of Emergency Medicine, 32(6), 493–497. https://doi.org/10.1016/j.ajem.2014.01.045
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