REBEL Cast

By Salim R. Rezaie, MDMedicine Health & Fitness

REBEL Cast episodes

February 21, 2024REBEL Core Cast 118.0 – IM vs PO NSAIDs
REBEL Core Cast 118.0 – IM vs PO NSAIDs
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Bottom Line Up Top: There is no difference in analgesic efficacy between oral and intramuscular NSAIDs.
Clinical Scenario: A 34-year-old woman presents to the ED with back pain. After your history and physical, you conclude that the patient’s pain is muscular in origin and likely secondary to heavy lifting while moving apartments. You contemplate analgesic options and decide that a NSAID makes sense. Should you give her PO ibuprofen or IM ketorolac?
What Your Gut Says: Give the ketorolac IM. IM ketorolac will provide better pain relief and the patient will be happier with her care since she got an ‘injection’ and, after all, she did come all the way to the hospital.
What The Evidence Says: Unlike with many areas of medicine, there is ample evidence to answer this question and most of that evidence has been around for a couple of decades. Reviewing every study would be tedious and, fortunately, we’ve got a great review article on the topic. One important thing to understand is that the different NSAIDs have widely accepted equianalgesic doses; at the right dose, all NSAIDs (whether it be naproxen, ibuprofen, ketorolac or diclofenac) give equivalent pain relief (Irizarry 2021). This allows us to look at studies with the different NSAIDs and compare them to each other.
A 2007 review of the literature concluded that there was no difference in analgesia between IM ketorolac and PO ibuprofen (Arora 2007). The study included a number of high-quality research studies:
Study
Format
Comparison
Findings
Notes
Wright 1994
Retrospective analysis of prospectively collected data.
PO Ibuprofen 800 mg vs IM ketorolac 60 mg
No difference in analgesic effect.
Ibuprofen superior secondary to cost, ease of administration + lack of pain w/ administration.
Turturo 1995
Double-blind RCT
PO Ibuprofen 800 mg vs IM ketorolac 60 mg
No difference in analgesic effect.
Similar onset of action in mild-moderate pain.
Neighbor 1998
Double-blind RCT
PO Ibuprofen 800 mg vs IM ketorolac 60 mg
No difference in analgesic effect.
Mixter 1998
Double-blind RCT
PO Ibuprofen 800 mg vs IM ketorolac 60 mg
No difference in analgesic effect.
Surgical Patients
Quereshi 2019
Double-blind RCT
IM diclofenac 75 mg vs PO diclofenac 100 mg
Small difference favoring IM in terms of speed to pain relief
Authors conclude PO superior due to time to prepare injection
The data looks fairly clear in terms of analgesic efficacy but, don’t some patients simply prefer to receive a shot? While this dogmatic claim is often made, the data doesn’t appear to support it.
Schwartz and colleagues performed an ingenious trial (Schwartz 2000)
Enrolled 64 ED patients with acute pain.
Treatment arms:
Oral group: Orange drink (800 mg ibuprofen) + placebo “ibuprofen” pill
Injection group: Orange drink (800 mg ibuprofen) + placebo “ketorolac” injection
Essentially, all patients got the same analgesic medication (the orange drink) thinking it was just some juice and an inert study placebo (pill or injection).
No significant difference in analgesia between the two groups.
Bottom Line: Just give the NSAID by mouth. IM NSAIDs may provide slightly faster time to analgesia but, IM dosing comes with the cost of injection, pain , a longer time to prepare the dose and more intensive nursing resources to administer the medication. As long as the patient’s gut works, oral NSAIDs provide similar analgesic effects to IM dosing and should be the preferred route of administration.
Bonus Pearls:
IM injection of ketorolac causes significant pain. If the patient can’t take PO, be kind and pop in an IV.
The ceiling pain relief dose for ketorolac is 15 mg IV (Motov 2017).
Read More
REBEL EM: The Ketorolac Analgesic Ceiling
References
Irizarry E et al. A randomized controlled trial of ibuprofen versus ketorolac versus diclofenac for acute, nonradicular low back pain. Acad Emerg Med 2021; 28(11): 1228-35. PMID: 34133820
Arora S et al. Myth: Parenteral ketorolac provides more effective analgesia than oral ibuprofen. Can J Emerg Med 2007; 9(1): 30-2. PMID: 17391598
Wright JM et al.. NSAID use and efficacy in the emergency department: single doses of oral ibuprofen versus intramuscular ketorolac. Ann Pharmacother 1994;28:309-12. PMID: 8193414
Turturro MA et a. Intramuscular ketorolac versus oral ibuprofen in acute musculoskeletal pain. Ann Emerg Med 1995;26:117-20. PMID: 7618770
Neighbor ML et al. Intramuscular ketorolac vs oral ibuprofen in emergency department patietns with acute pain. Acad Emerg Med; 1998; 5(2): 118-122 .PMID: 9492131
Mixter CG et al. Preemptive pain control in patients having laparoscopic hernia repair: a comparison of ketorolac and ibuprofen. Arch Surg 1998;133:432-7. PMID: 9565125
Qureshi I et al. Intramuscular versus oral diclofenac for acute pain in adults with acute musculoskeletal injuries presenting to the ED setting: a prospective, double-blind, double dummy, randomised controlled trial. 2019; 36: 401-6. PMID: 31217178
Schwartz NA et al. Patient’s perceptions of route of nonsteroidal anti-inflammatory drug administration and its effect on analgesia. Acad Emerg Med 2000; 7: 857-61. PMID: 10958124
Motov S et al. Comparison of intravenous ketorolac at three single-dose regimens for treating acute pain in the emergency department: a randomized controlled trial. Ann Emerg Med 2017; 70(2): 177-84. PMID: 27993418
Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)
The post REBEL Core Cast 118.0 – IM vs PO NSAIDs appeared first on REBEL EM - Emergency Medicine Blog.
5 min
February 07, 2024REBEL Core Cast 117.0 – Infections of Pregnancy
Take Home Points
Infections are a leading cause of maternal mortality worldwide.
Prompt recognition is critical in management.
Most infectious processes will require admission and close observation for improvement or decompensation.
REBEL Core Cast 117.0 – Infections of Pregnancy
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Urinary Tract Infection/Pyelonephritis
Epidemiology:
Occurs in as many as 15% of pregnant women and between 20-40% of pregnant women with asymptomatic bacteriuria will progress to pyelonephritis (Gorgas 2008)
Management:
Uncomplicated UTI
Suggested antibiotics include:
Nitrofurantoin 100mg PO BID x7 days OR
Cephalexin 500mg PO BID x7 days
Pyelonephritis
Hospital admission
Suggested antibiotics include:
Ceftriaxone 1g IV Q24H OR
Aztreonam 2g IV Q8H for beta-lactam allergy
Complications:
Maternal sepsis
Maternal renal injury
Congenital abnormalities of the fetus
Premature rupture of membranes
Low birth weight
Chorioamnionitis
Definition: Also known as intraamniotic infection. Chorioamnionitis is a bacterial infection of fetal amnion and chorion membranes.
Epidemiology:
Occurs in 1 to 10% of all pregnancies (Gorgas 2008)
Incidence increases significantly with preterm labor
Diagnosis:
Chorioamnionitis is defined as maternal fever >38°C and at least two of the following (Apantaku and Mulik 2007):
Maternal tachycardia >100 beats/min for five minutes
Fetal tachycardia >160 beats/min for five minutes
Purulent or foul-smelling amniotic fluid or vaginal discharge
Uterine tenderness
Maternal leukocytosis
Evaluation (Abbrescia 2003):
CBC
Blood cultures
Vaginal fluid for phosphatidylglycerol
Tests for fetal lung maturity
Cervical AND vaginal cultures
Physical Exam
Avoid digital cervical exam
Speculum exam should be done with sterile speculum
Ultrasonography for fetal well being
Management:
Given concern for neonatal sepsis, patients should be admitted for IV antibiotics, supportive cares, and possible early delivery
Most commonly an ascending infection from normal vaginal flora, so antibiotics must be chosen to cover polymicrobial infections
Ex. Ampicillin IV 2g Q6H AND Gentamicin IV 1.5mg/kg Q8H
In PCN allergic patient substitute vancomycin 1 g IV Q12H for ampicillin
Can only be considered cured with delivery of infected products of conception
Complications:
Placental abruption
Premature birth
Neonatal sepsis
Neonatal death
Cerebral palsy
Maternal sepsis
Need for cesarean delivery
Postpartum hemorrhage
Postpartum Endometritis
Definition: Generalized uterine infection
Epidemiology:
Sepsis results in 15% of maternal deaths worldwide (Houry 2014)
More common in surgical than vaginal deliveries
May co-exist with surgical site infection
Diagnosis:
Classic triad includes: fever, lower abdominal pain and uterine tenderness, and foul smelling lochia
Management:
Hospital admission
Cover for polymicrobial infection, including anaerobes
Ex. Clindamycin 900 mg IV Q8H AND Gentamicin 5-7 mg/kg IV Q24H
Septic Abortion
Epidemiology:
The World Health Organization estimates that one in eight pregnancy related deaths worldwide can be directly attributed to unsafe abortion procedures (Gorgas 2008)
Diagnosis:
Clinical presentation includes fever, abdominal pain and uterine tenderness in setting of recent abortion
Presentation can vary from mild infection to septic shock
Evaluation:
Lactate
Cultures of cervix, blood and urine
Coagulation panel to screen for DIC
Abdominal X-ray to evaluate for free air or retained surgical foreign bodies
Pelvic ultrasound to evaluate for retained products of conception or surgical foreign bodies
Management:
Hospital admission may be indicated as infection can progress to septic shock, organ failure, DIC and cardiovascular collapse
Broad-spectrum antibiotics are indicated. Triple antibiotic coverage is recommended. Suggested regimens include:
Ampicillin AND
Gentamicin AND
Clindamycin OR Metronidazole
Update tetanus vaccination
Usually requires dilation and curettage to remove any retained products of conception or foreign bodies.
References:
Abbrescia, K. and B. Sheridan (2003). “Complications of second and third trimester pregnancies.” Emerg Med Clin North Am 21(3): 695-710, vii. PMID: 12962354
Apantaku, O. and V. Mulik (2007). “Maternal intra-partum fever.” J Obstet Gynaecol 27(1): 12-15. PMID: 17365450
Desai, S. and S. Henderson. Labor and Delivery and Their Complications. In: Marx, J et al, ed. Rosen’s Emergency Medicine. 8th ed. Philadelphia, PA: Elsevier Saunders; 2014:2331-2350.
Gorgas, D. L. (2008). “Infections related to pregnancy.” Emerg Med Clin North Am 26(2): 345-366, viii. PMID: 18406978
Houry, D and B. Salhi. Acute Complications of Pregnancy. In: Marx, J et al, ed. Rosen’s Emergency Medicine. 8th ed. Philadelphia, PA: Elsevier Saunders; 2014: 2282-2299.
Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)
The post REBEL Core Cast 117.0 – Infections of Pregnancy appeared first on REBEL EM - Emergency Medicine Blog.
6 min
January 29, 2024REBEL Cast Ep123: Reduced-Dose Systemic Peripheral Alteplase in Massive PE?
Background: Massive pulmonary embolism defined as sustained hypotension (SBP <90mmHg) has a high mortality which is why early recognition and thrombolytic therapy is typically recommended (AHA Class IIA; ESC Class IB) [1]. However, full-dose thrombolytic therapy (Alteplase 100mg (IV) is associated with an increase in bleeding [2]. Because the lungs receive 100% of cardiac output, it has been hypothesized that a lower dose of thrombolytic therapy may still be effective with a better safety profile [3][4].
REBEL Cast Ep123: Reduced-Dose Systemic Peripheral Alteplase in Massive PE?
Click here for Direct Download of the Podcast
Paper: Aykan AC et al. Reduced-Dose Systemic Fibrinolysis in Massive Pulmonary Embolism: A Pilot Study. Clin Exp Emerg Med 2023. PMID: 37188358
Clinical Question: What is the efficacy and safety of low-dose (25mg) prolonged administration (over 6hrs) of alteplase in patients with massive PE?
What They Did:
Single-center, pilot prospective observational cohort trial in Turkey
Thrombolysis
25mg of alteplase without a bolus was administered over 6 hours by peripheral IV infusion
If hemodynamic instability persisted despite first dose of thrombolysis, a second 6hr infusion of 25mg alteplase without bolus was administered (No patients in the study required this)
Did not use concomitant heparin anticoagulation with thrombolysis
Heparin was administered as a 70U/kg bolus followed by a 1000U/h infusion with a target activated PTT between 1.5 and 2.5x the control started immediately after infusion of thrombolysis completed
Patients were all converted to warfarin for discharge
TTE
All patients underwent TTE before thrombolysis, within an hour after thrombolysis, before discharge (5 to 7d) and a month after thrombolysis
PASP estimated from tricuspid valve regurgitant jet velocity
Maximum dimension of RA/LA measured in 4-chamber view
Diameter and collapsibility of IVC noted
Pulmonary HTN defined as PASP >40mmHg
RV enlargement defined as RV/LV ratio >0.9
Tricuspid Annular Plane Systolic Excursion (TAPSE) also recorded
Tissue Doppler Derived Tricuspid Annular Systolic Velocity recorded
Tei-Myocardial Performance Index (MPI/Tei) recorded
CT
All patients underwent 64 slice CTPA for definitive diagnosis of PE at admission
Additional CTPA 24 hours after completion of thrombolysis if eGFR >60mL/min/1.73m2
Criteria for Thrombolytic Success Included:
Doppler documentation of resolution of increased PASP (<40mmHg)
Decreased RV diameter (at least 25% decrease of RV/LV diameter)
Restoration of RV function (TAPSE>16mm)
Systolic Wave Prime (S’) >10.0cm/s
Tissue Doppler Derived RV MPI > 0.55
Clinical improvement of symptoms and restoration of stable hemodynamic status immediately after thrombolysis
Complete success = Clinical improvement of symptoms and restoration of a stable hemodynamic status along with at least 3 other criteria without resultant death and nonfatal major complications
Outcomes:
Primary:
In-hospital mortality
Major complications
Ischemic stroke, ICH, embolism (coronary or peripheral), bleeding requiring transfusion
Pulmonary HTN while in hospital
RV dysfunction while in hospital
Secondary:
6 month mortality
Development of pulmonary hypertension at 6 months
RV dysfunction at 6 months
Inclusion:
Adult patients (≥18 years of age)
Confirmed massive PE
Massive PE Definition
Acute PE with sustained hypotension (SBP <90mmHg for at least 15 minutes or requiring inotropic support, not due to a cause other than PE, such as arrhythmia, hypovolemia, sepsis, or LV dysfunction)
Pulselessness
Persistent profound bradycardia (HR<40BPM with signs or symptoms of shock)
Exclusion:
Prior ICH
Known structural intracranial cerebrovascular disease (i.e. AV malformation)
Known malignant intracranial neoplasm
Ischemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis
Recent surgery encroaching on the spinal canal or brain
Recent significant closed-head or facial trauma with radiographic evidence of bony fracture or brain injury
Results:
37 consecutive patients with massive PE were enrolled
Blood pressure recovered within a few hours after initiation of thrombolysis in all cases
Mortality
Primary Efficacy Outcome: 1 in-hospital death (3.1% in the paper but 2.7% in table 2) on day 6 of hospitalization due to malignant ventricular arrhythmia (Pt had ischemic dilated cardiomyopathy with LVEF of 20% and acute on chronic renal failure)
2 additional deaths within 6 months (Both pts had malignancy)
Not implicitly stated whether these deaths are attributed to PE, however it doesn’t sound like they are based on the patient descriptions
TTE Results from Admission to Post Thrombolysis:
Primary Efficacy Outcome: Mean PASP ≈57mmHg to 34mmHg (p<0.001)
Mean PASP continued to decrease prior to discharge ≈34mmHg to ≈30mmHg (p<0.001)
Mean PASP preserved at 6 month follow up ≈29mmHg
No patients with pulmonary hypertension at 6 months
Primary Efficacy Outcome: Mean TAPSE ≈1.43cm to 2.07cm (p<0.001)
RV/LV Diameter ≈1.37 to ≈0.99 (p<0.001)
Mean MPI/Tei Index≈ 0.47 to ≈0.55 (p<0.001)
Systolic Wave Prime (S’) ≈10 to ≈15
Follow Up CTPA 24hrs After Thrombolysis
Out of 37 patients, 18 (56.3%) underwent repeat CTPA 24hrs after thrombolysis
Out of these 18 pts total lysis of thrombus was observed in 16pts (88.9%) and the remaining 2pts had >75% lysis of thrombus
Complications Post Thrombolysis:
Primary Safety Outcome: No major bleeding or stroke observed
3 patients with minor bleeding
2pts with epistaxis (2 days after thrombolysis)
1pt with gingival bleeding (3 days after thrombolysis)
All bleeding events occurred during heparin infusion and stopped with gentle compression without recurrence
6pts (17.6%) had major bleeding and 2pts (5.68%) had minor bleeding due to warfarin
Strengths:
Consecutive patients enrolled which minimizes selection bias
All patients followed for 6 months (No loss to follow up)
Limitations:
Single center, nonrandomized observational trial
No comparison group receiving standard therapy (i.e. compared to half-dose 50mg or full dose 100mg of alteplase)
Small sample size with few complications makes this an underpowered study to make any firm conclusions about bleeding risks
Lots of missing methodology
Unclear what time period patients were recruited
How strict were authors in consecutive recruitment (? selection bias)
Unclear therapies prior to lytics (i.e. Pressors, heparin, etc)
Who performed echos and unclear degree of consistency (Echo has some subjectivity to it)
Discussion:
PE is a Spectrum of Disease
Massive PE is also a spectrum of disease
This study doesn’t appear to include critically ill massive PE patients who are peri-arrest
Dripping alteplase over 6 hours is most likely not going to be the appropriate therapy in the more severe massive PE patients
Primary Efficacy Outcome
Multiple primary efficacy outcomes were listed in this study, which can be problematic when you get multiple outcomes of varying statistical significance. In this trial all the primary efficacy outcomes were statistically significant, and the authors clearly defined what they meant by complete success in this trial
Complications While in Hospital
No cases of major bleeding or ICH in this study
The 3 patients who had minor bleeding at 48 to 72hrs were most likely due to the heparin infusion and not associated with thrombolysis
The cohort is simply too small with not enough complications for the study to be powered correctly for this outcome
IV Access
These authors gave alteplase through a peripheral IV which we do in stroke patients, but that is typically done over 1hr not over 6hrs
If I was going to do this (25mg alteplase over 6hrs) I would want a central venous catheter to avoid the potential of infiltration or if the patient decompensates further and needs central venous access after the fact there is a higher risk of hematoma/bleeding
Also, I would already have an arterial line in place before starting thrombolysis for continuous hemodynamic monitoring
Heparin Dosing
Heparin was administered as a 70U/kg bolus followed by a 1000U/h infusion with a target activated PTT between 1.5 and 2.5x the control started immediately after infusion of thrombolysis completed
Prior studies have found marked increase in bleeding when lytics and heparin are given together
After thrombolysis I typically don’t bolus heparin and just start the infusion
Also I don’t start the heparin infusion immediately after thrombolysis, I wait for the PTT to be <2x the control before starting
A dose of 0.5 to 4.0mg/hr typically given in EKOS therapy (See Below). This trial gave 25mg over 6hrs (≈4mg/hr)
ULTIMA Trial [5]:
59pts with massive/submassive PE
Used alteplase at a dose of 1mg/hr x5hrs, then 0.5mg/hr x10hrs
Max Dose ≈20mg
No major bleeding
SEATTLE II Trial [6]:
150pts with massive/submassive PE
Used alteplase at a dose of 1mg/hr x24hrs
Max Dose ≈25mg
1 severe/life-threatening hemorrhage (Groin hematoma requiring vasopressor support)
No ICH
OPTALYSE-PE Trial [7]:
101pts with submassive PE
Used alteplase at a dose of 8mg/2hrs (4mg/hr), 8mg/4hrs (2mg/hr), 12mg/6hrs (2mg/hr), and 24mg/6hrs (4mg/hr)
Max Dose 24mg
No major bleeding with 8mg/2hrs, 8mg/4hrs, and 12mg/6hrs
2 major bleeding episodes occurred in the 24mg/6hr group
The max dose any patients got was ≈25mg (Max Dose Range ≈20mg to ≈25mg). Major bleeding seemed to occur in the drips that ran for over 15hrs (3 pts out of 310 [≈1%]); But no cases of major bleeding for drips ≤15hrs
To take this one step further this trial raises the question of whether EKOS even necessary or is it an overly expensive intervention that potentially increases complications without improving outcomes?
Although this was not a randomized clinical trial and there was no comparator arm we do have two trials on submassive PE with half-dose alteplase (50mg) given over 2hours [8] and half-dose alteplase (50mg) given in Massive PE [3]
MOPETT Trial [8]
121pts with submassive PE (Called “moderate PE” in the study)
Randomized to half dose thrombolysis vs anticoagulation alone
For patients weighing ≥50kg a total dose of 50mg given (10mg bolus by IV push followed by 40mg infusion over 2hrs)
For patients weighing <50kg a total dose of 0.5mg/kg given (10mg bolus by IV push followed by the remainder over 2hrs)
Primary endpoints consisted of pulmonary HTN and composite of pulmonary HTN and recurrent PE at 28mos
Pulmonary HTN at 28mos: 16% half dose thrombolysis vs 63% anticoagulation alone
Composite Pulmonary HTN and Recurrent PE at 28mos: 16% half dose thrombolysis vs 63% anticoagulation alone
There were 0 cases of bleeding in either arm
PEAPETT Trial [3]
23 patients with PEA cardiac arrest due to confirmed massive PE
All pts received 50mg of alteplase as an IV push while CPR was ongoing
ROSC occurred in 2 to 15 min after alteplase administration in all but one patient
There was no minor or major bleeding despite chest compressions
What this current trial [9] is really adding to the literature is an even lower dose of thrombolysis (25mg) efficacious?
We already know from the MOPETT trial [8] and PEAPETT trial [3] that half-dose alteplase (50mg) had zero cases of bleeding so this current trial just tells us what we already know. 25mg of alteplase has less risk of bleeding than 50mg of alteplase
Additionally, if 25mg can treat massive PEs [9], this could also be extrapolated to less severe high-risk submassive PEs (Although I would still love to see a head-to-head trial of 25mg vs 50mg)
Author Conclusion: “Results of this pilot study suggest that low-dose prolonged infusion of tPA is an effective and safe therapy in patients with massive PE. This protocol was also effective in decreasing PASP and restoration of RV function.”
Clinical Take Home Point: Low dose (25mg) alteplase given as a prolonged infusion (over 6hrs) is a promising effective and safe therapy in patients with massive PE and provides an alternative to full dose (100mg) and half-dose (50mg) alteplase. Larger RCTs comparing doses of alteplase are warranted to confirm these findings.
References:
Jaff MR et al. Management of Massive and Submassive Pulmonary Embolism, Iliofemoral Deep Vein Thrombosis, and Chronic Thromboembolic Pulmonary Hypertension: A Scientific Statement from the American Heart Association. Circ 2011. PMID: 21422387
Wan S et al. Thrombolysis Compared with Heparin for the Initial Treatment of Pulmonary Embolism: A Meta-Analysis of the Randomized Controlled Trials. Circ 2004. PMID: 15262836
Sharifi M et al. Pulseless Electrical Activity in Pulmonary Embolism Treated with Thrombolysis (from the “PEAPETT” Study). AJEM 2016. PMID: 27422214
Wang C et al. Efficacy and Safety of Low Dose Recombinant Tissue-Type Plasminogen Activator for the Treatment of Acute Pulmonary Thromboemolism: A Randomized, Multicenter Controlled Trial. CHEST 2010. PMID: 19741062
Kucher N et al. Randomized, Controlled Trial of Ultrasound-Assisted Catheter-Directed Thrombolysis for Acute Intermediate-Risk Pulmonary Embolism. Circ 2014. PMID: 24226805
Piazza G et al. A prospective, Single-Arm Multicenter Trial of Ultrasound-Facilitated, Catheter-Directed, Low-Dose Fibrinolysis for Acute Massive and Submassive Pulmonary Embolism: The SEATTLE II Study. JACCC Cardiovasc Interv 2015. PMID: 26315743
Tapson VF et al. A Randomized Trial of the Optimum Duration of Acoustic Pulse Thrombolysis Procedure in Acute Intermediate-Reisk Pulmonary Embolism: The OPTALYSE PE Trial. JACC Cardiovasc Interv 2018. PMID: 30025734
Sharifi M et al. Moderate Pulmonary Embolism Treated with thrombolysis (from the “MOPETT” Trial). Am J Cardiol 2013. PMID: 23102885
Aykan AC et al. Reduced-Dose Systemic Fibrinolysis in Massive Pulmonary Embolism: A Pilot Study. Clin Exp Emerg Med 2023. PMID: 37188358
For More Thoughts on This Topic Checkout:
EMCrit: EMCrit 354 – Reduced-Dose Systemic Peripheral Fibrinolysis in Massive Pulmonary Embolism
Post Peer Reviewed By: Anand Swaminathan, MD (X: @EMSwami)
The post REBEL Cast Ep123: Reduced-Dose Systemic Peripheral Alteplase in Massive PE? appeared first on REBEL EM - Emergency Medicine Blog.
29 min
January 24, 2024REBEL Core Cast 116.0 – Achilles Tendon Rupture
Take Home Points
Achilles tendon rupture is a clinical diagnosis. The Thompson Test should be applied in all suspected cases.
Remember to brace or splint a rupture, even if suspected, in the resting equinus position for optimal healing and prevention of further injury.
Schedule follow up with orthopedics within 1 week for discussion of operative management vs early rehab protocols.
REBEL Core Cast 116.0 – Achilles Tendon Rupture
Click here for Direct Download of the Podcast
Achilles Tendon Rupture Exam (www.lfaclinic.co.uk)
Physical Exam
May have palpable gap or deformity in region of tendon.
Weakness with plantar flexion.
Increased resting ankle dorsiflexion on affected side in prone position with knees bent .
Usually in absence of bony tenderness unless accompanied by other injury
Thompson Test (video)
Place the patient in the prone position, with feet hanging over the end of a stretcher or table. If patient is not able to lay down/there are no stretchers, the patient can kneel on a stool or chair
Squeeze the calf of the normal limb. You will notice the squeeze will cause the ankle to plantarflex appropriately
Squeeze the calf of the limb with the suspected Achilles tendon rupture. You will notice the squeeze will cause no motion if there is a full rupture/tear, and diminished motion if there is a partial tear
Performance Characteristics (Garras 2012)
Sensitivity
Specificity
(+) LR
(-) LR
96-100%
93-100%
13.7
0.04
Imaging
X-Rays
Used to rule out other or concurrent pathology
May show soft tissue swelling and destruction of pre-Achilles fat pad (Kager’s Fat Pad)
Findings are non-specific as tear of tendon unable to be visualized
Ultrasound
Ultrasound is helpful if obvious findings present and to distinguish between partial vs complete tears, however only around 50% sensitive for detecting only partial tears (Kayser 2005)
MRI
Gold-standard imaging modality
Rarely, if ever, necessary in the ED
Used for equivocal physical exam/alternate imaging findings or for assessing the severity of the tear for possible operative management
Findings
A full-thickness tear often shows a tendinous gap filled with edema or blood
Complete rupture shows retraction of tendon ends
ED Management
Provide analgesia
Tendon stabilization in an optimal healing position
Functional bracing/splinting in resting equinus/talipus equinus
AO splint/brace in 20 degrees of plantar flexion for 4-6 weeks (may use tall CAM boot with 20 degrees wedge inserts)
All patients should be non-weightbearing
Any weight-bearing can convert a partial tear to a complete tear
Maintain non-weightbearing status until see orthopedics (within 1 week)
After evaluation by orthopedics, early weight-bearing and early ROM exercises yield better outcomes (can be as early as 2 weeks)
Referral to rehab warranted to improve plantar flexion and decrease risk of re-rupture
ED Ortho consultation: patients with open wounds in the area of trauma, or with concomitant fractures
Operative Management is usually reserved for acute ruptures (approximately <6 weeks) of full thickness with large tendon gaps, failed conservative treatment of partial thickness tears, or high performance athletes
These cases will be determined during follow up with orthopedics and may warrant outpatient MRI to assess severity of tear
Prognosis
For conservative management, there is no significant difference in plantar flexion strength (Willits, 2010)
Some increased risk of re-rupture compared to operative management, although review of evidence shows that this may not be significant if patients used structured, accelerated rehab protocol.
Protocol includes initially non-weightbearing cast with the foot in equinus position as described above, then transitioned to a pneumatic walker with elevated heels (elevation gradually reduced biweekly), and physical therapy to improve gait, strength, and mobility. (Wallace 2011)
If addressed early and appropriately, most patients have good self-reported long-term outcomes regardless of the treatment modality
Links
Orthobullets: Achilles Tendon Rupture
Resources:
Sheth U et al. The epidemiology and trends in management of acute Achilles tendon ruptures in Ontario, Canada: a population-based study of 27,607 patients. Bone Joint J. 2017; 99-B(1): 78-86. PMID: 28053261
Chiodo CP, Wilson MG. Current Concepts Review: Acute Ruptures of the Achilles Tendon. Foot Ankle Int 2006; 27(4): 305-13. PMID: 16624224
Leppilahti J, Orava S. Total Achilles tendon rupture. A review. Sports Med. 1998; 25(2): 79-100. PMID: 9519398
Kayser R et al. Partial rupture of the proximal Achilles tendon: a differential diagnostic problem in ultrasound imaging. Br J Sports Med. 2005; 39(11): 838-42. PMID: 16244194
Margetic P et al. Comparison of ultrasonographic and intraoperative findings in Achilles tendon rupture. Coll Antropol. 2007; 31:279-284. PMID: 17598414
Garras DN et al. MRI is Unnecessary for Diagnosing Acute Achilles Tendon Ruptures: Clinical Diagnostic Criteria. Clin Orthop Relat Res 2012; 470(8): 2268-2273. PMID: 22538958
Willits K et al. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a multicenter randomized trial using accelerated functional rehabilitation .J Bone Joint Surg Am. 2010; 92(17): 2767-75. PMID: 21037028
Wallace RG et al. The non-operative functional management of patients with a rupture of the tendo Achillis leads to low rates of re-rupture. J Bone Joint Surg Br 2011; 93(10):1362-6. PMID: 21969435
Erickson BJ. Is Operative Treatment of Achilles Tendon Ruptures Superior to Nonoperative Treatment? Orthop J Sports Med. 2015; 3(4): PMID: 26665055
Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)
The post REBEL Core Cast 116.0 – Achilles Tendon Rupture appeared first on REBEL EM - Emergency Medicine Blog.
6 min
December 27, 2023REBEL Core Cast 115.0 – Cardiogenic Shock
Take Home Points:
Know clinical (cold extremities, oliguria, confusion, dizziness, narrow pulse pressure) and laboratory markers (metabolic acidosis, elevated creatinine, lactic acidosis) of hypoperfusion.
An elevated lactate is a danger sign and requires explanation.
Norepinephrine is a great first line vasopressor in Cardiogenic shock.
Dobutamine is useful for inotropic support in Cardiogenic shock.
Use POCUS in ED. In addition to echo and VTI for cardiac output, use IVC assessment for central venous pressure/volume status.
REBEL Core Cast 115.0 – Cardiogenic Shock
Click here for Direct Download of the Podcast
Links
Staten Island EM: Only in Staten Podcast
Links: VTI Calculation on Echo: https://www.youtube.com/watch?v=ir5EusiBXhk
Post Created By: Anand Swaminathan MD, MPH
Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie)
The post REBEL Core Cast 115.0 – Cardiogenic Shock appeared first on REBEL EM - Emergency Medicine Blog.
28 min
December 13, 2023REBEL Core Cast 114.0 – Carbon Monoxide Toxicity
Take Home Points:
Carbon monoxide is a colorless, odorless, and tasteless gas that results from incomplete combustion of any carbon containing product. Exposure often occur unintentionally from indoor use of gas powered generators, camp stoves, or faulty home heaters.
The symptoms of mild, acute exposure are non-specific and can be confused with a variety of other disease processes including common viral syndromes.
Testing is done via co-oximetry which determines the amount of carboxyhemoglobin in the blood. Treatment is guided by supplemental oxygen which decreases the half-life of carboxyhemoglobin.
Hyperbaric oxygenation should be considered in patients with severe toxicity (syncope, altered mental status, myocardial ischemia, or neurological abnormalities).
REBEL Core Cast 114.0 – Carbon Monoxide Toxicity
Click here for Direct Download of the Podcast
Definition and Physiology
Carbon monoxide is absorbed via inhalation from the incomplete combustion of any carbon containing substance. Most often, exposures often occur unintentionally from indoor use of gas powered generators, camp stoves, or faulty home heaters.
Toxicity is mediated through multiple mechanisms. Physiologic oxygen carrying capacity is reduced as carbon monoxide binds hemoglobin with a greater affinity than oxygen. Moreover, carbon monoxide shifts the oxygen-hemoglobin dissociation curve to the left which reduces oxygen delivery to tissues. Lastly, carbon monoxide effects cellular oxygen use by impairing oxidative phosphorylation by binding to mitochondrial cytochromes. (Goldbaum 1976)
Clinical Manifestations
Acute, mild toxicity presents non-specifically. Given that most exposures will occur during the winter months, a common misdiagnosis is influenza or the “common cold.” Symptoms include: headache, dizziness, nausea, vomiting, and generalized weakness.
More severe toxicity will present with syncope, altered mental status, neurologic disturbance (ie. ataxia), myocardial ischemia, or cardiac arrest.
Carbon monoxide poisoning may lead to delayed neurologic sequalae – a constellation of dementia, psychosis, parkinsonism, amnestic syndromes, among other neurologic impairments.
Management
Carbon monoxide testing is performed via co-oximetry which determines the amount of carboxyhemoglobin present.
The mainstay of treatment is supplemental oxygenation. The half-life of carboxyhemoglobin drops from 5 hours on room air to 1 hour when breathing 100% oxygen at normal atmospheric pressure (via non-rebreather).
Hyperbaric treatment should be considered for severe toxicity. (Goldfrank’s Toxicology 2019)
Carboxyhemoglobin levels > 25% or >15% in pregnant patients are indications for hyperbarics, independent of signs/symptoms
There is evidence that hyperbaric oxygenation reduces the risk of cognitive sequelae after acute carbon monoxide poisoning. (Weaver 2002)
As always, call your local toxicologist or regional poison control center to help determine the need for hyperbaric therapy.

Take Home Points:
Carbon monoxide is a colorless, odorless, and tasteless gas that results from incomplete combustion of any carbon containing product. Exposure often occur unintentionally from indoor use of gas powered generators, camp stoves, or faulty home heaters.
The symptoms of mild, acute exposure are non-specific and can be confused with a variety of other disease processes including common viral syndromes.
Testing is done via co-oximetry which determines the amount of carboxyhemoglobin in the blood. Treatment is guided by supplemental oxygen which decreases the half-life of carboxyhemoglobin.
Hyperbaric oxygenation should be considered in patients with severe toxicity (syncope, altered mental status, myocardial ischemia, or neurological abnormalities).
References
Goldbaum LR, Orellano T, Dergal E. Mechanism of the toxic action of carbon monoxide. Ann Clin Lab Sci. 1976 Jul-Aug;6(4):372-6. PMID: 962299.
Tomaszewski C. Chapter 122. Carbon Monoxide. In: Nelson LS, Howland MA, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS, , Flomenbaum NE. eds. Goldfrank’s Toxicologic Emergencies, 11e New York, NY: McGraw-Hill; 2019. Accessed November 6, 2023.
Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliott CG, Clemmer TP, Orme JF Jr, Thomas FO, Morris AH. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002 Oct 3;347(14):1057-67. doi: 10.1056/NEJMoa013121. PMID: 12362006.
Post Created By: Sanjay Mohan MD
Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie)
The post REBEL Core Cast 114.0 – Carbon Monoxide Toxicity appeared first on REBEL EM - Emergency Medicine Blog.
12 min
November 29, 2023REBEL Core Cast 113.0 – ACS Therapies and Management
Take Home Points:
All STEMIs should be loaded with dual antiplatelet therapy. Prasugrel (Effient) is avoided as there is an increase in bleeding complications if the patient requires a CABG.
NSTEMI cases can be challenging to manage. Consult Cardiology early and use all available data.
The appropriate medical treatment for ACS patients is as important as PCI.
POCUS is a very valuable tool for ACS patients in the ED.
Clinical presentation trumps all other data. Trust your gut!
REBEL Core Cast 113.0 – ACS Therapies and Management
Click here for Direct Download of the Podcast
Links
Staten Island EM: Only in Staten Podcast
Post Created By: Anand Swaminathan MD, MPH
Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie)
The post REBEL Core Cast 113.0 – ACS Therapies and Management appeared first on REBEL EM - Emergency Medicine Blog.
25 min
November 15, 2023REBEL Core Cast 112.0 – Awareness During Paralysis
Take Home Points:
Dose your RSI meds correctly.
Reach for post-intubation sedation at the same time you are asking for your induction agent and paralytic.
Propofol is a great choice for post-intubation sedation, and if your patient becomes hypotensive do not be afraid of adding on a pressor!
REBEL Core Cast 112.0 – Awareness During Paralysis
Click here for Direct Download of the Podcast
Awareness during paralysis is real. However, data is limited in ED patients. The ED AWARENESS study found a 2.6% rate of prevalence: meaning about three in every one hundred people may experience awareness during paralysis.
We know that rocuronium has a longer half life than its counterpart succinylcholine. However, this is not the problem! The key is starting post-intubation sedation ASAP.
We need to keep this phenomenon in the back of our minds every time we intubate. Here are some things we can do to prevent awareness during paralysis:
Dose your RSI meds correctly.
Reach for post-intubation sedation at the same time you are asking for your induction agent and paralytic.
Propofol is a great choice for post-intubation sedation, and if your patient becomes hypotensive do not be afraid of adding on a pressor!
References
Pappal, Ryan D., et al. “The ED-AWARENESS study: A prospective, observational cohort study of awareness with paralysis in mechanically ventilated patients admitted from the emergency department.” Annals of emergency medicine 77.5 (2021): 532-544.
Links
Staten Island EM: Only in Staten Podcast
Post Created By: Anand Swaminathan MD, MPH
Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie)
The post REBEL Core Cast 112.0 – Awareness During Paralysis appeared first on REBEL EM - Emergency Medicine Blog.
18 min
October 25, 2023REBEL Core Cast 111.0 – Cardiac Testing
Take Home Points:
A CCTA is an anatomic test to determine if a patient has normal coronary arteries, non-obstructive disease, or obstructive disease. The warranty period for a CCTA is anywhere from 3-10 years depending on the characteristics of the plaque.
A nuclear stress test is a functional study that allows for ischemia-driven management. The warranty period of a nuclear stress test is 2 years.
A test is only as good as the data and its interpretation! Trust yourself!
REBEL Core Cast 111.0 – Cardiac Testing
Click here for Direct Download of the Podcast
Links
Staten Island EM: Only in Staten Podcast
Post Created By: Anand Swaminathan MD, MPH
Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie)
The post REBEL Core Cast 111.0 – Cardiac Testing appeared first on REBEL EM - Emergency Medicine Blog.
25 min
October 11, 2023REBEL Core Cast 110.0 – On Shift Learning Pearls
Take Home Points:
Patients with recent onset atrial fibrillation can safely be cardioverted if they are 1) on anticoagulation 2) Low risk based on CHADS-VASC with onset < 48 hours or 3) High risk based on CHADS-VASC with onset < 12 hours.
In anaphylaxis, think, “If A, B or C, give E.” If the patient has compromise to airway, breathing or circulation, they should get immediate epinephrine.
D-dimer can effectively rule out a larger portion of low risk patients if age adjustment or the YEARS criteria are employed.
When reviewing a syncope ECG, scour it for WPW, Brugada, Hypertrophic Cardiomyopathy, Prolonged/Short QTc and ARVC.
REBEL Core Cast 110.0 – On Shift Learning Pearls
Click here for Direct Download of the Podcast
Links
EM: RAP: Atrial Fibrillation Update
REBEL EM: The Pragmatic Combination of YEARS Score and Age-Adjusted D-Dimer
Core EM: Age-Adjusted D-dimer (Using DDU)
REBEL EM: Anaphylactic Shock
REBEL EM: Core Cast 21.0 – ECG in Syncope
Post Created By: Anand Swaminathan MD, MPH
Post Peer Reviewed By: Salim Rezaie MD (Twitter @SRRezaie)
The post REBEL Core Cast 110.0 – On Shift Learning Pearls appeared first on REBEL EM - Emergency Medicine Blog.
12 min