An 82 yo male presents to the ED via EMS with 1 day of abdominal pain that started in the late evening. He describes feeling well all day, eating a healthy size dinner and then having sudden onset abdominal pain and distension just before bedtime. He can’t describe or localize the pain but states it is a ‘hard pain’ and has been associated with 2 episodes of nausea/vomiting. He doesn’t think he has had a fever. He is unsure of his last bowel movement and complains of frequent constipation. When asked about urinary changes he describes what sounds like a long-standing history of issues with urinary hesitance. He is unsure if there has been any acute change. He thinks there is no history of abdominal surgeries but “he’s been around a long time”. He is a lifelong non smoker.
PMH: DLP, HTN
Meds: Atorvastatin, Ramipril
Vitals: BP 110/60 HR 102 RR 18 O2 97% RA T – 36.5
On exam he appears in mild discomfort, with his eyes closed. His abdomen is mildly distended. He has generalized tenderness throughout the abdomen, no guarding or peritonitis. The testicles and inguinal region appear normal.
What are some barriers to assessing abdominal pain, or any presentation, in the geriatric patient?1,2
History may be difficult to intrepret, sometimes with vague symptoms
History may be difficult to obtain due to physical deficits like hearing loss
Vitals are not reliable – most patients are on beta blockers so their heart rate may not be elevated, and ‘normal’ blood pressure may actually be hypotensive for a geriatric patient who will often run much higher at baseline.
Blunted immune response – they may not illicit the typical fever or elevated WBC that we often count on to lead us to infectious/septic processes.
Decreased abdominal wall muscles lead to less guarding or rebound on exam – * peritoneal signs are often absent
Shrinkage of omentum leads to decreased containment of intraabdominal process
Higher rate of perforation and ischemic gut due to chronic issues like atheroscleoris and low flow states
He doesn’t look to be terribly unwell, you plan to treat his pain and nausea and order some labs.
What would be the drug of choice for abdominal pain in the elderly2?
Hydromorphone as it is not renally excreted.
You are ordering your labs – CBC, Cr, electrolytes, LFT’s, bilirubin, lipase and a urinanalysis.
Should you order a VBG and lactate in this man with ‘normal’ vitals and a non-specific abdominal exam2?
If the patient is presenting with pain out of proportion (ie. Ischemia symptoms) these tests are a must. But consider in any patient with risk factors for cardiovascular disease or atrial fibrillation. Our patient has a history of dyslipidemia and hypertension – you order the additional tests and ECG.
Elderly patients have vague abdominal pain all the time – what percentage are actually surgical?
Up to 60% of cases are surgical.
The associated mortality rate of those requiring abdominal surgery is upwards of 7x greater than younger patients with similar presentations.
What are the main causes of surgical abdominal pain the elderly1,2?
Cholecystitis – consider when working up a septic patient with no obvious source
Appendicitis
Bowel Obstruction – femoral hernia is a commonly missed cause
Hernia
Your patient had already been sent for an abdominal series after they were triaged. Certainly with the history of abdominal pain with n/v obstruction is high on the differential, even in a native abdomen.
What are useful findings on abdominal series3,4?
You are looking for the following:
Pneumoperitoneum (but really, you should be getting a CT if this is a concern)
Air fluid levels seen in obstruction
Certainly, in a busy department XR is quick, cheap and has minimal radiation. In patients with repeated SBO an XR may be suffice. Findings for SBO on XR include:
Dilated bowel with air fluid levels
Proximal bowel is dilated, but distal bowel is not
Gasless abdomen – where there is a large amount of fluid within the bowel loops, which may underestimate the level of obstruction. There may be a ‘string of pearls’ sign in upright films where small amount of air is seen between valvulae conniventes.
The sensitivity, specificity, and accuracy are 79-83%, 67-83%, and 64-82%, respectively3 – not enough to rely on when the mortality rate is so high in this population. A normal abdominal series does not rule out any serious pathology.
Certainly CT would be the gold standard – it would give the site, severity and etiology of obstruction. Complications such as necrosis, ischemia and perforation would be identified as well as other causes for abdominal pain on your differential. In elderly patients in particular, it has been shown to be more high yield for clinical decision making2.
But a CT takes time in an overcapacity and understaffed ED. While you wait for it to be completed you grab for your ultrasound probe – specifically you are looking for signs of SBO as that is top of your differential.
What is the accuracy of PoCUS for SBO5?
Sensitivity 88%, specificity 96%
What is an approach to a SBO scan with PoCUS?
Using your curvilinear probe ‘Mow the lawn’ starting in the RLQ and cover the entire abdomen using graded compression. Take your time6.
What are the findings5,7?
Dilated bowel loops >2.5cm
Thickened bowel wall >3mm
‘To and fro’ peristalsis
Tanga sign – triangular shaped areas of free fluid between bowel loops. Concerning for high grade obstruction
You do confirm all signs of SBO, including tanga sign which is concerning.
By now your patient is over in the scanner when you get some lab results back – although the WBC is at the upper end of normal the lactate is significantly elevated.
While the patient is in CT waiting for a porter to come back you get a call from the radiologist confirming closed loop bowel obstruction with signs of ischemia and necrosis.
Bottom line – have a low threshold to order CT in geriatric abdominal pain. They are high risk patients, with high mortality rates.
Melady, D, Lee, J, Helman, A. Geriatric Emergency Medicine. Emergency Medicine Cases. July, 2013. https://emergencymedicinecases.com/episode-34-geriatric-emergency-medicine/. Accessed July 19, 2022
Bordeianou, L & Yeh, D. (2021) Etiologies, clinical manifestations, and diagnosis of mechanical small bowel obstruction in adults. Uptodate. Accessed July 2019 from https://www.uptodate.com/contents/etiologies-clinical-manifestations-and-diagnosis-of-mechanical-small-bowel-obstruction-in-adults?search=bowel%20obstruction%20adult&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H2918585369
Jones, J., Ramsey, MD, A. Small bowel obstruction. Reference article, Radiopaedia.org. (accessed on 19 Jul 2022) https://doi.org/10.53347/rID-6158
Atkinson P, Bowra J, Lewis D. (2019). Point of Care Ultrasound for Emergency Medicine and Resuscitation.
Thanks to Dr. Joanna Middleton for leading the discussion
All cases are imaginary but highlight important learning points
Case
An elderly male is brought to the ED by EMS after being found wandering the streets downtown. A local resident was concerned and called 911. He looks disheveled and is dressed in light clothing despite the cold weather. He has no identification. He is agitated but not aggressive. He is speaking short sentences, with recognizable words, but is nonsensical. He can give no identifying information.
His vitals are 90/62 HR 132 RR 22 O2 93% RA T – 40.1°C. Gluc 12
On exam he has no obvious neurological deficits but will not follow command for strength or coordination testing. He walked unaided into the department. His pupils are 3mm and reactive bilaterally. He will not follow your finger for oculomotor testing. He does have some dried blood on his right ear – there appears to be a scalp laceration superior to the ear. There are no other signs of head injury. His neck appears to be supple as you draw his attention to things in the room. Cardiac, abdominal and skin exam are non-contributory. You hear expiratory crackles to the right lung base.
Patients with an altered level of consciousness, especially in the geriatric population, are becoming increasingly more common. What is an easy mnemonic to remember the differential1?
You order a broad scope of investigations including a tox screen, TSH, LFT’s and coags, VBG, blood and urine cultures and CXR.
Is a CT head always a requirement6?
No, CT brain scan should not be used routinely but should be considered in patients with the following indications:
New focal neurological signs
Reduced level of consciousness not adequately explained by another cause
History of recent falls
Head injury
Anticoagulation therapy.
While that is pending, what is your approach to management?
From an airway perspective they are talking, they are maintaining their oxygen saturations. There is borderline hypotensive and tachycardia with a fever.
Initially you decide to cover for sepsis, potentially a respiratory source given your findings on exam. You obtain bilateral IV access, start fluids and antibiotics post cultures. Tylenol is given for fever. You apply oxygen as saturations are low 90’s.
Although infectious causes are common there are a vast number of presentations to consider with a febrile, altered patient2.
Heat stroke
CNS causes other than infectious: ICH, Stroke, Status Epilepticus
Thyroid storm
Lithium toxicity
Salicylate toxicity
Anticholinergic toxicity
Alcohol and Benzo Withdrawal
Malignant Hyperthermia
Neuroleptic Malignant Syndrome
Serotonin Syndrome
Chances are this is sepsis so you initiate your therapy and cognitively unload yourself.
Portable CXR is done showing potentially a slight haziness in the right lower lobe. No pulmonary edema. It’s not a slam dunk infiltrate, but common things being common you still suspect sepsis.
The VBG comes back first – its normal. WBC is also back and it is upper end of normal – unexpected given how febrile this patient was. Now you’re starting to question your diagnosis – you go back to your differential for a febrile, altered patient. You decide to add lithium level to your work up as well LFT’s and extended lytes. Heat stroke is unlikely given the cool weather ongoing this week. Otherwise, you can consider CT head for CNS causes but the remainder will require some sort of collateral history.
While you are mulling this over there is a call from the lab – they are giving a verbal for a critically low TSH level and critically high T4 levels.
You are worried this patient is in thyroid storm.
What are signs/symptoms of thyroid storm3,5?
High fever
Altered mentation: ranges from agitation and delirium to stupor and coma
Cardiovascular instability: tachycardia (often exceeding 140 bpm), hypotension and potentially arrythmia and cardiovascular collapse
Does the degree of hyperthyroidism matter? Ie. The severity of the lab disturbance3?
No, the levels of TSH and and T4/T3 are typically similar to those seen in uncomplicated thyrotoxicosis.
Are there any other lab derangements that would help point in the direction of thyroid storm3?
mild hyperglycemia due to catecholamine-induced inhabitation of insulin release and increased breakdown of glucose stores
mild hypercalcemia due to hemoconcentration and increased bone resorption.
abnormal liver function tests as thyroid hormones are metabolized in the liver
leukocytosis or leukopenia
Given that lab values can be similar to thyrotoxicosis are there any criteria to diagnose thyroid storm vs impeding thyroid storm?
No validated criteria exist, however there are scoring systems in circulation similar to this one3.
A value > 45 confirms thyroid storm, a value between 25-45 is concerning for impeding thyroid storm.
You score your patient at 65, assuming that the pneumonia is the precipitating factor. You feel confident thyroid storm is the diagnosis.
Where you wrong to initiate treatment for sepsis5?
Typically for thyroid storm the patient has a history of hyperthyroidism but is tipped into instability with a precipitating factor. Given your clinical findings and CXR this patient potentially has pneumonia that precipitated his presentation. However, if infection doesn’t seem to be the most likely trigger it is not necessary to cover with antibiotics. Consider others causes.
Other than infection what are other risk factors for thyroid storm3,5?
Recent surgery
Trauma
Iodine load ie. Initiating amiodarone treatment
Pregnancy/toxemia of pregnancy
PE
Acute MI
DKA
Hyperemesis
CVA
Your patient is becoming increasingly agitated – what is the management plan5?
Benzos are the drug of choice to manage agitation in this patient. Other supportive therapies include fluids, cooling and monitoring and treating electrolyte/glucose disturbance as needed. However now that the diagnosis is confirmed, treating the cause of the agitation can now be initiated.
What is the treatment for thyroid storm? And the order given?
You reassess your patient after the tylenol, fluid bolus, benzos and antibiotics.
BP 102/62 HR 120, RR20 O2 98% on 1L NC, 39.9°C
You commence cooling and begin beta-blockade with propranolol. You continue fluids and plan to treat with methimazole as currently the patient is not in cardiovascular collapse. You treat with potassium iodide 1 hour later. ICU are now there to do a consult and admit.
Take home points –
Consider a broad differential with any altered patient, remember AEIOU
A febrile, altered patient isn’t always sepsis! See this great algorithm for differential as well as treatment
Untreated thyroid storm has a high mortality – add TSH to your investigations and remember the order of treatment matters to prevent worsening thyrotoxicosis.
Helman, A. Long, B. Khatib, N. Strayer, R. Hensley, J. Foohey, S. Petrosoniak, A. EM Quick Hits 36 – Surviving Sepsis, Angle Closure Glaucoma, Bougies, Frostbite, Hot/Altered Patient, Central Cord Syndrome. Emergency Medicine Cases. March 2022. https://emergencymedicinecases.com/em-quick-hits-march-2022/. Accessed [June 21, 2022].
Ross, D (2021). Thyroid Storm. UptoDate. Accessed June 21 2022 from https://www.uptodate.com/contents/thyroid-storm?search=thyroid%20storm&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H57436952
Altered Mental Status – Delirium. Chang A, Marsden J. 2020. Point of Care Emergency Summary, BC Emergency Medicine Network.Assessed July 6, 2022 from https://www.bcemergencynetwork.ca/clinical_resource/altered-mental-status-delirium/
Big thanks to Dr. Paul Paul for leading discussion.
All cases are imaginary but highlight important learning points
Case
A 72 yo male presents with acute onset L sided scrotal pain radiating to the groin ongoing 3 hours. In triage he denied any associated trauma. He has no history of scrotal issues. He has vomited once from the pain. He took a leftover morphine tablet he had post knee surgery and that helped temporarily. He denies any fever or diarrhea. He was well prior to the onset of pain.
PMH: OA with R TKA, DLP
Vitals: BP: 157/92 HR 102 RR 20 O2 98% RA T – 36.7
The department is in critical overcapacity, with admitted patients being boarded in hallways. While the nurse is triaging she is interrupted three times with questions from both staff and patients asking when they are to be seen. A testicular exam is not completed at that time.
What is the differential for acute scrotal pain in an adult1?
Epididymitis/epididymo-orchitis
Fournier’s gangrene
Trauma
Inguinal hernia
Mumps orchitis
Testicular cancer
Henoch-Schönlein purpura
Acute idiopathic scrotal edema
Post-vasectomy pain
Referred pain
Testicular torsion
This patient had no history of trauma, and was otherwise well. He was afebrile and had suspected elevated BP and HR secondary to pain. Tylenol and advil are administered.
2 hours have passed, the patient continues to have ongoing pain and presents back to triage as he has started vomiting again. Repeat vitals are unchanged.
When finally assessed by a physician there is extensive L sided scrotal edema and redness. It is exquisitely tender. The testicle appears to be lying abnormally. You are concerned for torsion.
Other than a swollen, red testicle what are other signs/symptoms of torsion2?
Acute onset of unilateral testicular pain: the presentation can actually vary; Some present with gradually increasing pain, others fluctuating pain if the testicle is intermittently undergoing torsion and detorsion and some have minimal pain. The patient may describe the pain as radiating to the abdomen, groin or flank.
20% of patients with torsion complain of lower abdominal pain.
Affected testicle lying high and horizontal: seeing this certainly increases the odds of the patient having torsion, but depending on timing of presentation and swelling it may be difficult to determine the position of the testicle.
Absent cremasteric reflex: With an intact cremasteric reflex lightly stroking the inner thigh will cause the ipsilateral testicle to retract/elevate3. In torsion, the twisting of the spermatic cord interrupts this reflex. However, the sensitivity of this sign is only 60%
Presence of a normal cremasteric reflex does not rule out torsion
Swelling is a sensitive, but not specific sign. It can be found in a number of conditions as listed in the differential above.
Nausea/vomiting may be associated, if present there is increased likelihood of torsion (OR 8.87)4 but it is a non-specific sign seen in many presentations. It’s importance is when it is seen in conjunction with the other signs of torsion.
What is Prehn’s sign and what is its utility in assessing for torsion2?
In epididymitis, elevation of the affected testicle can result in relief of scrotal pain. This is Prehn’s sign. If the pain is worsened with this maneuver it is thought to be associated with torsion. This technique is not reliable in differentiating epididymitis from torsion. One study found the majority of patients with torsion, over 90%, had a positive Prehn’s sign.
Combining all these findings into the TWIST score for pediatric patients under the age of 18 years can help guide management in cases where it is unclear5.
High risk with 7 points – PPV 100% for torsion
<5 points – NPV 96%
To avoid missing irreversible ischemia, use this took as a rule in score only – if a score of 7 consult urology directly to consider surgical intervention without doppler ultrasound2.
This patient is in his 70’s, why would we even consider torsion1?
Torsion typically happens in neonates and postpubertal males, but it can occur in adult males. One retrospective chart review found that 39% of hospitalized males with torsion were age 21 and over. Although rare, it can happen in older adults.
In any male with abdominal pain, regardless of age, consider testicular torsion
This male has pain ongoing for hours, what are the odds the testicle is salvageable2?
Previous thought was that 6 hours was the window and that after that the testes is beyond salvage. However, there are longer survival percentages greater than 6-8 hours depending on the history (ie. Intermittent torsion) leading to a range in timelines for irreversible ischemia. Therefore, regardless of duration of pain, the case should be treated as a surgical emergency.
So, you urgently call urology for consult. They expect to be in house within 20 minutes. They are requesting a formal ultrasound in the meantime. It’s now after midnight so the ultrasound tech has to be called in. Time is ticking, so you grab your ultrasound probe.
What is the evidence for point-of-care ultrasound in testicular torsion?
Sensitivity 88-100%
Specificity 90%2
One chart review of pediatric patients presenting with symptoms suspicious of torsion found point of care scrotal ultrasound performed by pediatric EM physicians was 100% sensitive and 99.1% specific6.
What are the findings concerning for testicular torsion on ultrasound?
Many – it depends on the timing.
From a blood flow perspective
Initially as the spermatic cord twists the venous system is most susceptible to obstruction. So if very early, there may be normal appearance of blood flow.
As time goes on venous flow may look to still be present, but looks less compared to unaffected testicle.
Before, or after, venous flow completely obstructs, arterial flow can show signs of impending obstruction as well with a high resistance pattern on doppler.
Finally, there will be no flow present in the testicle and it may shows signs of necrosis.
Obtaining doppler to confirm both venous and arterial flow is imperative when assessing for torsion
Other signs on ultrasound
Enlarged, edematous testicle
Surrounding fluid within the scrotum
Loss of homogenous appearance with hypoechoic areas of infarct
Whirlpool sign showing the twisted spermatic cord
Review some images:
Normal appearance testicle7 with flow
Absence of flow (note the affected testicle is also quite edematous)
Normal venous appearance7 – a low flow pattern that stays consistent
Normal arterial appearance7 – notice the peak and gradual trough associated with systole and diastole
High resistance pattern8 concerning for impeding arterial obstruction
Whirlpool sign9 – notice the yellow coloration of doppler in this image. This is power doppler – it is more sensitive than color doppler for picking up on low flow states10. It is not indicative of direction of flow, just intensity of flow ie. Brighter = more flow.
You see absence of flow on the affected testicle of your patient.
The urologist is in house and you review the images on PoCUS – the patient is brought to the OR.
What if you were rural and transport would be hours? Should you attempt to detort the testicle manually?
The open book maneuver where you ‘open’ or turn the testicle outward to attempt to detort11 is only recommended if there is an anticipated delay of hours to the OR.
The reason? Poor success rate, up to a 1/3 of patients will actually be torting in the opposite direction2.
Bottom line:
Suspect testicular torsion in any male, of any age, with abdominal pain.
Many classic findings are not reliable to rule out torsion
Use bedside ultrasound to assess for color doppler flow, consider using power doppler to detect low states. Findings vary but classically – no flow in the testicle is seen with torsion.
Ischemic time is variable, and longer than initially thought, treat every presentation as a surgical emergency regardless of timing of presentation.
High suspicion? Don’t wait for formal imaging – call urology.
Interested in PoCUS for other scrotal presentations? Review this awesome post by Dr. Rawan AlRashed, PoCUS fellow
Helman, A. Krakowsky, Y. Wolpert, N. Testicular Torsion: A Diagnostic Pathway. Emergency Medicine Cases. July, 2020. https://emergencymedicinecases.com/testicular-torsion. Accessed [June 13, 2022]
Tali Beni-Israel, Michael Goldman, Shmual Bar Chaim, Eran Kozer. Clinical predictors for testicular torsion as seen in the pediatric ED. The American Journal of Emergency Medicine, Volume 28, Issue 7,2010. Pages 786-789,ISSN 0735 6757,https://doi.org/10.1016/j.ajem.2009.03.025. (https://www.sciencedirect.com/science/article/pii/S0735675709001569)
Barbosa JA, Tiseo BC, Barayan GA, et al. Development and initial validation of a scoring system to diagnose testicular torsion in children. J Urol. 2013;189(5):1859-1864.
Friedman N, Pancer Z, Savic E, Tseng F, Lee MS, Mclean L et al. 2019. Accuracy of point-of-care ultrasound by pediatric emergency physicians for testicular torsion. Journal of Pediatric Urology. VOLUME 15, ISSUE 6, P608.E1-608.E6, DECEMBER 01, 2019DOI:https://doi.org/10.1016/j.jpurol.2019.07.003
Personal ultrasound images from a case of suspected testicular torsion. Deidentified.
Modified from: Cronan KM, Zderic SA. Manual detorsion of the testes. In: Textbook of Pediatric Emergency Procedures, 2nd ed, King C, Henretig FM (Eds), Lippincott Williams & Wilkins, Philadelphia 2008. Assessed June 14, 2022 https://www.uptodate.com/contents/image?imageKey=EM%2F112358
Big thanks to Joanna Middleton for leading this month’s discussion
All cases are imaginary but highlight important learning points.
Case
A 70 yo female presents via EMS with potential syncope accompanied by nausea/vomiting. She describes feeling weak for 2 days and hasn’t eaten or drank much. She got up to go to the washroom and her ‘legs gave out’. She felt diaphoretic after and vomited. She denies any other GI symptoms, abdominal pain or fever. She denies any recent chest pain, shortness of breath, headache or neurological symptoms. You confirm she has had no med changes recently.
Her PMH includes: DM, HTN, DLP, GERD, cholecystectomy.
Her medications include: metformin, ramipril, atorvastatin and pantoprazole.
Her vitals are: BP 108/72 HR 58 RR 20 O2 96% on RA T 37.4 glucose 8.2
On exam, she appears pale and slightly clammy but overall perfusion is normal. Her cardiac and respiratory exam is unremarkable. Her abdomen is soft and non tender. Her neuro exam is grossly normal with no obvious deficits or focal weakness. Aorta scan on PoCUS is determinant and negative, the cardiac views are suboptimal, and IVC appears minimally collapsible.
As per usual, the department is in overcapacity and there are a number of critically ill patients. You begin a small fluid bolus, treat the patient’s nausea and order labs.
What is the differential for this vague presentation in a geriatric patient?
HUGE.
Weakness in the elderly can associated with a number of diagnoses1:
Focal weakness – ICH, CVA, SAH, tumor, SCI
Acute Non focal weakness -delirium, metabolic, infectious, cardiac
This patient sounds like she may have had a vagal episode – she could be dehydrated, her anti-hypertensives may now be too high, she may have underlying infection…
Since you don’t see any glaring red flags you await lab work up and continue to see other patients.
An hour has passed and you review her labs: her CBC, CRP, VBG, electrolytes and extended electrolytes are normal. Renal function looks down from previous. You reassess but despite some fluids and Zofran your patient still feels nauseous and lightheaded. Her feeling of generalized weakness has not improved. She now appears drowsy, but responds to voice, and her extremities are now cooler than before. Her BP is lower at 98/68 and HR 56. Other vitals are otherwise unchanged.
Something doesn’t fit.
The ECG tech hands you the ECG that was ordered at triage for ‘syncope’ but was delayed in getting done due to the back log.
Gulp. An inferior STEMI
What do you see2?
ST elevation in the inferior leads (II, III, aVF)
ST elevation in V1, V2 and V3 – V1 is the only lead that looks directly at the RV.
Reciprocal ST depression in lateral leads (I, aVL and V6)
*ST depression in aVL is a sensitive marker for inferior infarct – it truly is the only lead that is reciprocal to the inferior wall. 91% of ‘subtle’ inferior ST elevations that don’t quite meet STEMI, but have ST depression in aVL, have occlusion on PCI4.*
What changes suggest RV involvement2? Where is the culprit lesion?
ST elevation in V1 – ST elevation in this lead should always make you think of RV involvement, especially if it exceeds STE in V2
If STE is isoelectric, look for ST depression in V2
ST elevation in lead III > lead II (lead III is more rightward facing)
The majority of RV infarcts(80%) occur secondary to occlusion of the proximal RCA before the marginal branches break off to supply the RV and give the expected ECG findings above. A small percentage (18%) are left sided dominant, with the circumflex artery supplying the RV4. Those with chronically occluded RCAs may also develop collateral left sided circulation.
If left sided circulation is occluded leading to RV infarct expect changes in the lateral part of the inferior wall
ST elevation in lateral leads: I and V5-6.
STE lead II = lead III
Absence of reciprocal ST depression in lead I.
“One quarter to one third of inferior STEMIs are associated with RV infarction, and nearly 90% of RV infarctions occur with coexistant inferior MI2.”
So – if you have an inferior MI – look for the RV infarct. You order right sided leads
Sure enough – there is elevation in V4.
Are there any signs/symptoms that could have tipped off this patient was having an RV MI3?
Bradycardia in the absence of any beta blockers, especially with hypotension, is a red flag. Patient’s presenting with RV MI can have AV node dysfunction from ischemia – or vagal excess – resulting in bradycardia, AV block or hypotension with clear lungs. They can exhibit more vagal symptoms like nausea, vomiting, diaphoresis, and pallor.
You urgently reassess and begin going through contraindications for thrombolysis. As you are questioning the patient she says she doesn’t feel well and is now experiencing chest pain– her HR has dropped to 45, it appears to be sinus. Her BP is now 80/56.
How do we treat her symptoms?
Certainly, you can treat the pain, but improving her perfusion will improve her symptoms.
Avoidingnitroglycerin is a bit of a no brainer when the BP is this low, but on initial presentation when her SBP was above 100, one still has to avoid nitroglycerin – these patients are preload dependent. How sensitive depends on the extent of the infarct of the RV. Large infarcts lead to dyskinesis of the free wall, poor filling and poor cardiac output despite intact systolic function3. Optimize the preload as much as possible with judicious fluids – considering reassessing the lungs first with PoCUS for signs of pulmonary edema.
Maintaining her heartrate – stroke volume of the RV is relatively fixed, so in addition to improving filling with fluids, the heartrate has to be maintained to ensure cardiac output3. Depending on the rhythm (ie. Normal sinus vs AV block) atropine may not be beneficial. Consider early pacing if atrophine is not beneficial or there is complete heart block.
Improving her blood pressure with vasopressor agents if fluid alone isn’t suffice. Typically start with an alpha-agonist agent (norepinephrine). There is evident that norepinephrine improves survival benefit in patients with LV related cardiogenic shock, but no studies support RV infarct related shock3.
The ultimate way to improve her symptoms is reperfusion.
You have initiated pressors, another small fluid bolus and atropine as the rhythm is normal sinus. You are preparing pacing pads as you finish questioning on contraindications for thrombolysis – she has none. Anti-platelets and anti-coagulants are being prepared.
Should you thrombolyse this patient?
We know reperfusion is what she needs, but should that be with lysis or PCI?
In an ideal world PCI is first line for everyone, but realistically we work peripherally in smaller areas or STEMIs present after cath lab hours. We also don’t really know the onset of this event since the patient has such vague symptoms – presumably it started yesterday.
You need to decide if the patient is truly in cardiogenic shock – for those in shock the first line treatment is PCI/CABG. Early revascularization has been shown to have a mortality benefit 6 months out from the event.5
What defines cardiogenic shock6?
Reduced contractility resulting in a SBP < 90mmHg, or the need for vasopressors to support BP AND evidence of end organ dysfunction.
Keep in mind patient’s with a lower BP that is above 90mmHg may still be in occult shock if there are signs of end organ dysfunction – have a high suspicion.
Signs of end organ dysfunction:
Skin assessment
Cool, mottled, prolonged cap refill
Mental status
Ranges from drowsy, ALOC , comatose
Urine output
Oliguria often
PoCUS findings
Advanced measurements if within your scope of practice:
Your patient’s skin assessment and mental status are altered on your last assessment and she is requiring vasopressor support. This patient is in cardiogenic shock secondary to an acute inferior STEMI involving the RV.
As decreased cardiac contractility is the cornerstone of cardiogenic shock you repeat cardiac views with the patient positioned in the left lateral decubitus. You get this parasternal long view:
How can you assess cardiac function7?
If you are unable to accurately assess all these, eyeball the size and ‘squeeze’ of the LV – are all the walls thickening uniformly?
An easy way to roughly gauge ejection fraction is to look at the mitral valve – if the anterior leaflet touches off the wall of the LV when it opens the EF is likely normal. If not you can measure the E point septal separation (EPSS) in M mode. EPSS >7mm is 100% sensitive for a severely depressed EF < 30%8.
On PoCUS, heart failure caused by acute ischemia will typically show a large RV and small LV secondary to low filling pressures, which is best seen on the apical 4 chamber view9.
You determine the EF to be decreased.
You urgently call interventional cardiology to discuss and arrange cath lab. Currently the cardiologist just started a case and isn’t immediately available but will take the patient to the cath lab as soon as they are finished.
What are the other priorities of care in a patient with cardiogenic shock6?
First is determining the cause to optimize the overall management -here we suspect acute coronary syndrome and this patient needs reperfusion, but in other patient’s without obvious ACS consider:
Mechanical issues like valvular problems, free wall rupture or endocarditis
Myocarditis
Progressive non-ischemic heart failure
Next optimize oxygenation, usually this is done with NIPPV but caution in patient’s with RV failure – too much positive pressure can increase RV afterload. The patient’s recent O2 sat was above 90% – you apply oxygen via nasal cannula and reassess again – there are still clear lungs on auscultation and no B lines on PoCUS.
Optimize fluid status – in RV infarct judicious fluid can help increase preload. However, ideally at time of presentation complete a through fluid assessment for hypervolemia, euvolemia or hypovolemia. PoCUS can be helpful here – consider the following measurements6
Up front, as we didn’t suspect cardiac cause, we treated for hypovolemia in the setting of nausea/vomiting and poor intake. She has received fluid to improve pre-load and still appears to have clear lungs.
Improving blood pressure with vasopressors as discussed above6 – she is on vasopressors and has received atropine. We are targeting a MAP of 65-80. Norepinephrine is the first line agent – it has been shown to have a lower risk of refractory hypotension compared with epinephrine.
Improving cardiac contractility – can start dobutamine. This is a beta-1 and beta-2 agonist so it has inotropic effects, but it also vasodilates. Therefore – begin norepinephrine before starting dobutamine to avoid worsening hypotension. When comparing dobutamine to other inotropes like milrinone there was no difference in clinical outcome for cardiogenic shock, however dobutamine is shorter acting and may therefore be easier to titrate.
Reassess clinically for improvement in skin perfusion, urine output and mental status.
You reassess your patient – mental status is improving, there has been a temporary improvement in BP and HR. A foley is inserted. She is being prepped for PCI.
If she were to continue to worsen despite your efforts while you await PCI what would be the next management step6?
This patient has a clear cause for their shock. You can consider mechanical support to bridge the patient to the intervention, in this case – PCI. Discuss with cardiology and CV surgery early if you suspect you will require mechanical support. These supports can include intra-aortic balloon pumps (IABP), percutaneous ventricular assist devices (PVAD – Impella, Tandem Heart), and veno-arterial extracorporeal membrane oxygenation (VA-ECMO).
The patient goes on to the cath lab but arrests on the table. Despite these interventions ROSC isn’t achieved.
RV involvement is associated with increased risk of cardiogenic shock and death with a mortality of 50% within the first 48 hours8.
To review:
RV infarcts can present with hypotension with clear lungs, bradycardia, nausea/vomitting, pallor and diaphoresis. Have a low threshold to order an ECG.
Suspect RV involvement in any inferior MI – get right sided leads. Have a closer look at avL – ST depression in this lead is strongly associated with occlusion MI.
Cardiogenic shock is SBP < 90mmHg with signs of end organ dysfunction. You can still have ‘shock’ with a BP higher than this. Again, high suspicion.
Keys points of managing cardiogenic shock
Determine cause and if reversible
Improve fluid status
Improve cardiac contractility
Improve blood pressure
Improve oxygenation
Consider mechanical support, like ECMO, as a bridge to interventions. Discuss cases with cardiology and CV surgery early
Hochman JS, Sleeper LA, Webb JG, Sanborn TA, White HD, Talley JD, Buller CE, Jacobs AK, Slater JN, Col J, McKinlay SM, LeJemtel TH. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med. 1999 Aug 26;341(9):625-34. PMID
Atkinson P, Peach M, Lewis D. Just the Facts: The Five F’s of Focused Echocardiography in Shock. CJEM. 2020 Sep;22(5):655-657. doi: 10.1017/cem.2020.440. PMID: 32787986.
Big thanks to Dr. Paul Page for leading this month’s discussions
All cases are imaginary but highlight important learning points.
Case
You are working a day shift at a tertiary hospital that sees both adult and pediatric patients. You receive dispatch for a 2 year-old female with potential sepsis. Parents report high fevers for 4 days and poor intake. EMS report a somnolent child, febrile and tachycardic. ETA of 5 minutes.
On arrival the child appears mottled and drowsy, paramedics have placed a non-rebreather and are supporting the airway. You rapidly complete an assessment while the patient is being placed on cardiorespiratory monitoring and nurses attempt access. The patient responds to voice with whimpers. A paramedic is performing a jaw thrust while another bags. Breathing is shallow and rapid. She is mottled with cool extremities and delayed capillary refill.
Vitals: BP 60 SBP, HR 160 sinus tachycardia, T 39.7 RR 50 O2 88% on 100% NRB.
Gulp. You ask the nurse to page the pediatrician on call as you are worried about this patient.
Pediatric vitals are interpreted by weight or age, but you don’t need a table to see that these vitals are abnormal and this kid is altered. Frankly, this patient is pre-arrest if intervention doesn’t take place soon.
Not so sick kid? Here’s a reminder of expected vitals per age1.
Pediatric patients tend to compensate and compensate – until finally they don’t. Are there earlier signs of sepsis to be on alert for when assessing a patient1?
tachycardia out of proportion to fever – fever can give an expected increase in HR by 10 bpm,
tachypnea – RR tends to increase by 5 breaths/min for every 1 deg over 38°C.
poor perfusion – this can range from poor cap refill to altered level of consciousness.
When it’s later stages – it’s obvious. But sepsis doesn’t always have all these signs – a high suspicion is needed to recognize sepsis before it gets to critical stages.
What is the most concerning vital sign of our patient1?
Hypotension – this is a late sign of sepsis and if untreated the patient will arrest.
You suspect this child has septic shock given the brief history and temperature. Currently, their airway is being well managed by paramedics who have added NC under the mask and with continued jaw thrust they have improved oxygen saturation – but this is temporary.
You want to initiate management for sepsis and potentially need to intubate this child.
But before any of that can occur you need IV access.
Nurses have attempted twice and failed – it’s been 2 minutes. What next?
Do not hesitate to move to intraosseous (IO). This child may imminently arrest. Fluid resuscitation and administration of antibiotics are vital. If you can’t obtain IV access in 60 secs – obtain IO1
Preferred sites in pediatric patients (altered from EMdocs.net)2
Worried about hurting the child? Flush lidocaine through the IO – evidence suggests pain is more from infusions and medications through the IO than the insertion itself.1
Have more time with a relatively stable patient? Consider using PoCUS to help obtain peripheral lines
You obtain IO access and immediately request fluids. You want them to run in as fast as possible, but the child is too small for a level 1 infuser. What’s your approach?
First, choose the fluid type. Normal saline or Ringer’s lactate is fine to start. 20cc/kg is the typically starting bolus over the first 5 minutes of resuscitation. This can be repeated twice more up to 60cc/kg in the first hour. For this patient, and any patient under 2, load a 30-60cc syringe with crystalloid and manually bolus.
Signs of fluid overload?
Hepatomegaly and crackles auscultated in the lungs
A better sign – pulmonary edema seen on PoCUS3.
Normal vs B lines
IO assess has been obtained in both tibia, a nurse is pushing fluid manually while another asked you what antibiotics you want drawn up.
What are the broad-spectrum antibiotics suggested by age1?
You go back to reassess the patient’s airway. They are now satting 92% on 100% NRB + 5L NC. There is still some spontaneous whimpering. You estimate the GCS to be 9: E- 3 V- 2 M -4. This patient’s respiratory status is worsening and they have a low GCS. You feel they need intubation. Repeat vitals are obtained after first bolus.
BP 64 SBP, HR 158 sinus tach, T 39.8, RR 48 O2 as above.
Do you immediately intubate?
This patient is in profound shock, their catecholamine surge is deplete and any induction agents, even ketamine, would likely still worsen their hypotension and potentially precipitate arrest. If successfully intubated there is then the complication of increasing intrathoracic pressure – thus reducing blood flow back to the heart and decreasing cardiac output1.
The principle of resuscitate before you intubate is especially true in this situation.
You order repeat bolus of fluid to be manually given while antibiotics are being infused in the other IO. A nurse has now achieved peripheral IV access.
You prepare drugs and airway equipment for RSI – you plan to intubate once fluid boluses are complete if vitals have improved.
What drugs will you use? What drugs would you avoid5,6,7,8,9?
Avoiding worsening hypotension is key – ketamine is the drug of choice for sedation in children as it is considered hemodynamically neutral, but again expect drop in BP when the body is in shock. Ketamine also preserves airway reflexes and ventilatory drive.
Conversely propofol creates vasodilation and suppresses the myocardium – causing hypotension. It also can cause respiratory depression and apnea.
There is some evidence that etomidate is associated with less adverse events in septic patients, specifically hypotension. In one observational study in an adult population, ketamine was shown to be complicated by post-intubation hypotension more frequently when compared to etomidate.
In the pediatrics population etomidate for intubation in the ED setting has also been shown to be associated with minimal change in blood pressure – but this was a small, retrospective study. Currently etomidate is not recommended in patients < age 10 and more evidence is needed. One could also consider the potential for adrenal suppression post etomidate (etomidate inhibits functioning of an enzyme required to make cortisol, aldosterone and corticosterone). There are various studies – some in pediatric patients showing decreased plasma cortisol levels at 24 hours post etomidate. A similar effect was seen in other critically ill adult patients. The CORTICUS trial indicated a higher 28 day mortality in patients who received a single dose etomidate vs those that did not, regardless of being given exogeneous steroid.
For paralytics succinylcholine should be used cautiously in pediatric patients – it can precipitate hyperkalemia, bradycardia and even arrest. Rocuronium does have fewer side effects and contraindications, but it’s duration of action lasts approximately 50 mins – compared to approximately 6-10 minutes with succinylcholine. So strongly consider your choice – if you feel this is a ‘can’t intubate, can’t ventilate’ situation rocuronium is a dangerous choice.
You decide to go with ketamine and rocuronium and the drugs are being drawn up – what doses will you use?
In an adult population a safe choice in the shocked patient is to half the sedative and double the paralytic. The reason being even with ketamine you can get myocardial suppression and potential apnea.
For the paralytics use higher dose as the onset of action will be slower – double the dose.
For pediatric patients there is no evidence in the literature to support this practice, currently practice is to choose agents that have the least effect on hemodynamics – typically ketamine and rocuronium.
The RT is asking what size tube and airway equipment you would like.
Quick answer – Broslow tape. In this unstable patient this is the easiest way to get what you need without having to do any mental math. You request a cuffed tube – decreases the need for ET tube changes4.
While airway equipment is being set up you move now to prepare the patient. How do you position this 2 year old5,10?
Children have larger heads that naturally lies in flexion when supine. To align the mouth, larynx and trachea often the position has to be changed. You can roll up a towel to help with placement. As a rule of thumb:
Keeping a patient supine can also worsen hypoxemia as children have increased chest wall compliance and therefore increased work at baseline to maintain tidal volume. This can eventually lead to intrapulmonary shunting.
So although this patient doesn’t require additional positioning with a towel based on age we would still put the head of the bed up.
Someone asks if they can remove the additional oxygen mask or nasal cannula in preparation for intubation so it’s out of your way. Your response5?
No – pre-oxygenation is vital in the intubation of any patient, especially a child as they desaturate so quickly. In this 2 year old patient we expect a time of less than 4 minutes to desaturate to 90%. Children have much less surface area or ventilation channels as the alveoli continue to develop until the age of 8. In this patient with potential underlying respiratory illness there could be areas of atelectasis, worsening lung ventilation.
What other airway considerations are going through your head for a pediatric patient10?
Remember CHILD
For a great overall review see this infographic5
You are about to reassess the airway and obtain new vitals when the patient’s breathing changes to agonal and her whimpering has ceased. There is cardiac activity on the monitor, it be appears to be tachycardia with a widened QRS. Someone yells – check a pulse!
Do you need a pulse to initiate CPR in this patient?4
No – given the frequency of bradycardia and hypovolemia, pulse checks are not reliable. If apnea and unresponsive, initiate CPR.
At what rate should CPR be initiated in this patient4?
Use the encircling hands technique for infant CPR – it is shown to give better hemodynamics. Push hard (>1/3 AP diameter of chest) and fast (100-120 bpm), minimizing interruptions and allowing full recoil of the chest between compressions.
As this is an in-hospital cardiac arrest an LMA is immediately inserted to prevent interruption in compressions and to provide oxygenation.
Aim for 20-30 breaths/minute when an advanced airway is in place.
Out of hospital cardiac arrest4? Resuscitation with bag valve mask results in the same resuscitation outcomes as advanced airways -don’t underestimate the value of a good seal and a 2 person technique.
CPR is ongoing, an LMA has been inserted. The initial rhythm did not appear to be shockable. This is a PEA arrest.
What is your priority?
Determining the cause and in the meantime administering epinephrine – early administration within 5 minutes of non-shockable rhythms increases survival4.
You review your H’s and T’s.
You are pushing fluids for hypovolemia, the patient maintained oxygenation throughout with 2 sources of oxygen and had a normal oxygen saturation before arrest, the patient could be acidotic – but you are drawn to hypoglycemia. You rack your brain but can’t remember the glucose. You verbalize to the room, but no one knows if a glucose was done.
You quickly obtain one – 0.5.
You must correct glucose rapidly:
5cc/kg D10W IV push followed by an infusion of D10NS at 5cc/kg/hr (max at 250cc/hr)11
After the correction of glucose and additional round of CPR you get ROSC.
Obtaining a glucose is VITAL in any pediatric patient – something you know but failed to recognize as you had an unstable patient in front of you.
ABC + DEFG = ABC and DON’T EVER FORGET GLUCOSE1
What other metabolic abnormality must you consider1?
Hypocalcemia is commonly seen in critically ill pediatric patients, even without clinical signs like seizure or arrythmia it is recommended to treat.
Calcium gluconate 10% 0.5-1 cc/kg slowly over 5 minutes (max of 20 cc)
You reassess the vitals and the patient is still hypotensive and tachycardic despite 3 boluses and fluid circulating throughout the arrest. The oxygen saturation is 100%. The RT is still bagging via LMA. Clinically they appear cool and mottled with pulses weaker distally.
The patient is in cold shock. What is the vasopressor of choice11?
You initiate epinephrine at 0.05 mcg/kg/min IV and titrate up by 0.02 mcg/kg/min.
You assess cardiac function and lung fields via bedside ultrasound – the heart is hyperdynamic, lung fields are clear. You continue another bolus.
The patient’s GCS post arrest is back to 9. They are being easily bagged. You plan to wait until vitals have stabilized to switch out the tube.
At this point a pediatric attending arrives and you give an update.Immediately the staff begins verbalizing orders to the room for pressors, fluids and antibiotics. They begin questioning RT and direct them to intubate. The staff look to you for direction.
What do you do at this point?
This can be an uncomfortable situation to be in – this patient is still your patient; they are still unstable at this point and you have been guiding resuscitation. You have developed a sense of trust with your team and more than one leader can often lead to confusion.
You ask the attending to step out and together you review the management up to that point. This was a complex case with a lot of intervention. You discuss each medication given and the outcome. You make your suggestions on pressor support and fluid and reinforce what has been given. Together you are on the same page and go back in to reassess with the team.
It’s important to respectfully gain additional input from consultants and work together to ensure optimum care, but still realize that you are running the room. In other cases you may be at a loss for what to do and need guidance for what to do next – but again, once a plan is decided with your consultant it’s important that you verbalize to the room and give clear instruction to your team.
Overwhelmed and need to pass off? No problem – once you have help verbalize to the room that the consultant will now be leading resuscitation and stay nearby to assist and learn.
Lastly, what other medication should you consider if the patient’s hemodynamics or clinical picture do not improve1?
Steroid – up to 25% of pediatric patients with septic shock have adrenal insufficiency. This may be from the infectious process itself, from previous steroid use or from primary adrenal insufficiency.
You administer hydrocortisone 2mg/kg IV.
What markers of a successful resuscitation will you look for1?
Capillary refill < two seconds
Normal blood pressure
Normal pulses with no differential betweencentral and peripheral pulses
Warm extremities
Urine output > 1 ml/kg/hr
Normal mental status
Normal lactate
The patient gets admitted to the ICU for Pneumococcal sepsis and after a prolonged admission does well.
Pediatric patients are scary – use the resources you have, verbalize your thought process to the room and ask for help. Continuously reassess
ABC + DEFG = ABC and DON’T EVER FORGET GLUCOSE1
References and further reading:
EM Cases Digest – Vol 2. Pediatric Emergencies. Chapter 2: Sepsis and septic shock. Helmon, A. Lloyd, T. 2016. Toronto, ON.
Highlights of the 2020 American Heart Association Guidelines for CPR and ECC
Tolmie, A 2021. PEM Pearls01: Pediatric Airway Differences. CanadiEM. Retrieved Jan 20, 2022 from https://canadiem.org/pem-pearls-01-pediatric-airway-differences/
Mohr NM, Pape SG, Runde D, Kaji AH, Walls RM, Brown CA 3rd. Etomidate Use Is Associated With Less Hypotension Than Ketamine for Emergency Department Sepsis Intubations: A NEAR Cohort Study. Acad Emerg Med. 2020 Nov;27(11):1140-1149. doi: 10.1111/acem.14070. Epub 2020 Jul 20. PMID: 32602974; PMCID: PMC8711033.
Guldner G, Schultz J, Sexton P, Fortner C, Richmond M. Etomidate for rapid-sequence intubation in young children: hemodynamic effects and adverse events. Acad Emerg Med. 2003 Feb;10(2):134-9. doi: 10.1111/j.1553-2712.2003.tb00030.x. PMID: 12574010.
Sprung CL, Annane D, Keh D, Moreno R, Singer M, Freivogel K, Weiss YG, Benbenishty J, Kalenka A, Forst H, Laterre PF, Reinhart K, Cuthbertson BH, Payen D, Briegel J; CORTICUS Study Group. Hydrocortisone therapy for patients with septic shock. N Engl J Med. 2008 Jan 10;358(2):111-24. doi: 10.1056/NEJMoa071366. PMID: 18184957.
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
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.
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.
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.
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
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
Tremor – The 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.
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:
Alcohol withdrawal is a clinical diagnosis – recognize the symptoms and signs.
Persistent intention tremor is a sensitive sign of withdrawal.
Consider other causes in the acutely delirious patient.
These patients are high risk for injury – have a low threshold to image if suspicion of trauma
Quantify the severity for treatment – consider using the SHOT protocol. Diazepam > Lorazepam in the patient with no underlying liver dysfunction.
High, escalating IV benzos for refractory agitation/seizure
Avoid benzodiazepine prescriptions as an outpatient.
References and further reading
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].
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
Justin Morgenstern. Management of Delirium Tremens, First10EM, 2016. Available at:
https://doi.org/10.51684/FIRS.1898
Darrel Hughes, “Benzodiazepine-Refractory Alcohol Withdrawal”, REBEL EM blog, April 28, 2016. Available at: https://rebelem.com/benzodiazepine-refractory-alcohol-withdrawal/.
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.
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.
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
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.
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
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
Anterior humeral line: A vertical running drawn on the anterior surface of humerus. This must run down to intersect middle 1/3rd of CAPITELLUM
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
The patient is seated sitting up
Place the forearm in supination – this allows the trochlea to pass more easily over the coronoid process of the olecranon
Elbow is flexed 30 degrees with an assistant immobilizing it and applying counter traction at the middle or distal end of the humerus
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
The patient is in a prone position with the affected arm handing over the side of the bed
Slow downward force is applied on the wrist while the opposite hand attempts to guide the olecranon back into place.
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:
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]
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
(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.
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/
Paris (2016). Elbow Dislocation. Core EM. https://coreem.net/core/elbow-dislocation/
Oppenheim, Osborn (2016). Posterior Elbow Dislocation. Journal of Education & Teaching of Emergency Medicine. DOI: https://doi.org/10.21980/J8X593
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.
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).
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
Justin Morgenstern, “Cognitive errors in medicine: The common errors”, First10EM blog, September 15, 2015. Available at: https://first10em.com/cognitive-errors/.
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.
EMCrit # 253 – the Kovacs Kata to Optimize a Failing Laryngoscopy Attempt. https://www.youtube.com/watch?v=jCgpRd1R7gY&ab_channel=EMCrit
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.
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.
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.
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
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.
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
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.
