Welcome back to Small Talk.  Every first Wednesday of the month we will release high yield PEM content written by PEM talent from around the country.  We hope you enjoy these reviews. Comments, questions, accolades or concerns: feel free to reach out to Joe Ravera, MD (pemgemspod@gmail.com).

Author: Joe Ravera MD (@pemuvm1, Director of Pediatric Emergency Medicine, Assistant Professor of Surgery, Division of Emergency Medicine, University of Vermont Medical Center) // Reviewed by: Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Background

I have (somewhat) joking called pediatric urinary tract infections- “the last thing left in pediatric emergency medicine”.  As we are all aware, fever in a common chief complaint in the emergency department and in well appearing children, the overwhelming etiology of a fever is a virus¹. However, it is our due diligence to consider the possibility of a bacterial etiology that would require antibiotic treatment.  Many bacterial sources can be evaluated clinically (e.g. a skin or soft tissues infection) and do not require diagnostic testing other than a through exam. Additionally, the advent of vaccines (particularly Pneumococcal and Hemophilus vaccinations) has made the rate of bacteremia and meningitis extremely very low and as such well appearing children outside the neonatal do not routinely require invasive testing (e.g. blood and spinal fluid). ¹ However, despite our advances in reducing pretest probability of invasive bacterial disease urinary tract infections remain a common entity seen in everyday clinical practice that both requires treatment and have complications if missed.

Whom to Test and How to Test

The decision of whom to test is probably the most difficult decision involved in pediatric UTI. If a child appears ill or has known abnormal renal/GU anatomy, they will likely need testing. In otherwise healthy, older children, life is usually made easier by two pediatric milestones.  Children become verbal and potty trained around the same age (typically somewhere between 2 and 3). Once a child is verbal and potty trained the decision to test becomes easy as we can relay on more symptoms (such as dysuria) and obtaining a urine is less invasive if we are able to obtain a clean catch.

However, before these milestones, the first challenge is the paucity of identifiable urinary symptoms like dysuria or frequency.  Children in this group typically have fever and abdominal symptoms such as vomiting; but it should be noted that fever alone can be a presentation of UTI.  On the flip side we don’t want to test every child with a fever as the vast majority will not have a UTI.

There are clinical calculators (e.g. https://uticalc.pitt.edu/)² that can predict a pretest probability and guide management. In my practice, I approach this question in two steps:  First what is the chance the patient has a UTI? Second, what are the consequences of missing a UTI at this ED visit?

To answer the first question there are several published risk factors that increase the likelihood of a UTI include^2,3,4:

• Prior UTI
• Female sex
• Younger age
• Uncircumcised male under 1 year
• Fever >39 degrees
• Fever >48 hours
• Associated vomiting
• No clear viral source

The second question is not as well studied but intuitive risk factors for a worse outcome with a missed UTI include:

• Younger age
• Concomitant medical disease
• Inability to access to primary care/return to the ED

Using a combination of the pretest probability and the outcome in conjunction with a conversation with the parents can help guide management on whether to test.

How to Test and How to Interpret the Results

While the decision of whom to test is complicated the recommendation for how to test is straight forward: a catheter or suprapubic aspiration (SPA) is the preferred method. However, SPAs are not routinely performer and different hospitals may have different comfort levels at performing catheterizations in younger children^3,4.   There has been some data and obtaining clean catches in young children by utilizing suprapubic and back message, the so called “Quick Wee” method. ⁵ If nursing staff is comfortable with this technique, it can be a reasonable alternative to catheterization.   Another tip can be to utilize a point of care ultrasound (or bladder scan) pre-catheterization to confirm there is urine in the bladder prior to performing the invasive procedure.  As a last resort you can use a urine bag but in this authors experience this often delays care and if the bag is positive the child, then needs a definitive urine sample with catheterization.

While the definitive test is a positive culture in the presence of symptoms, we often only have preliminary urinalysis in the emergency department.  Urine dipstick is also frequently used to rapidly screen for infection.  There is mixed data on younger children however, as with a UA, a dipstick at its extremes (i.e. 4+ leukocytes and positive nitrites or negative/negative) is clinically useful.⁶  The same calculator that estimates pretest probability will also estimate the chance a positive culture based on dipstick results (https://uticalc.pitt.edu/).²

Disposition and Anti-Microbial Therapy

There are no hard and fast criteria for whom to admit versus discharge with a suspected UTI.  Suggested admission criteria are obvious and include^3,4:

• Age <2 months (infants discussed below)
• Clinical urosepsis (eg, toxic appearance, hypotension, poor capillary refill)
• Patients who are immune compromised or concomitant severe medical disease
• Vomiting or inability to tolerate oral medication
• Lack of adequate outpatient follow-up (eg, no telephone, live far from hospital, etc.)

For patients with a concerning dipstick or urinalysis, antimicrobial therapy is the mainstay of treatment. E. coli is the causative agent in 80-90 percent of cases as such initial therapy with a cephalosporin is recommended^3,4,7.  For admitted patients’ receiving parenteral antibiotics initial therapy with Ceftriaxone 50 mg/kg is recommended.  For outpatients a 2^nd or 3^rdgeneration cephalosporin is preferred, possible options include^3,4,7:

-Cefixime 8 mg/kg once daily

-Cefdinir 14 mg/kg by mouth once daily

In more well appearing children the first-generation cephalexin 50 mg/kg divided BID may also be an appropriate choice.

Duration of therapy is also variable and somewhat symptom depended.  For simple cystitis without fever in older children 3-5 days may be appropriate.  For younger children, particularly with fever a longer duration (7-14 days) is recommended.^3,4,7

Follow Up and After Care

Patients discharged should have follow up with there pediatrician.  In older children with vulvas education about proper hygiene is critical to prevention of recurrent infections. In older children with penises a UTI would be unusual (particularly if circumcised) and requires closer follow up with the pediatrician.

In younger children the question of an undiagnosed renal anomaly (such as reflux) is often considered.  It is important to let families know that these children may require an outpatient renal ultrasound.⁷ Ultrasound in the setting of acute infection can be difficult to interpret for reflux and as such should only be ordered if there is a clinical suspicion acute infectious complication such as an abscess.⁷

Special Populations: Children with Complex Medical Disease and Neonates

Children with complex medical disease and specifically complex renal or GU abnormalities require special attention.  Often these children require more testing and consultation with sub specialists, and in the case of a UTI are at higher risk for atypical infections and there should be a very low threshold to manage these patients as inpatients.

In neonates a urine is obtained as part of the standard fever work up.  For further reading about the latest infant fever guidelines, you can refer to a previous piece on EM docs (http://www.emdocs.net/small-talk-hot-off-the-presses-the-latest-aap-guidelines-for-the-febrile-neonate/).  However since that article was written there has been a subsequent publication addressing the clinical question: what is the chance a neonate with a UTI has disseminated an infection to the CNS, so called “uromeningitis”? The upshot is that in absence of elevated inflammatory markers (ANC and Procalcitonin) the risk is extremely small, and the LP may be omitted.⁸

Pearls, Pitfalls and Take-Home Points

• Urine testing in preverbal non toilet trained kids is based on the pre-test probability of disease and the risk of a delayed diagnosis.
• There is no hard and fast rule for admission when a patient has a UTI, it is based on a myriad of clinical factors.
• Imagining in the ED should be reserved for patients with a suspected infectious complication (e.g. renal abscess).
• Neonates with a positive UA have an extremely low risk of meningitis if they have negative inflammatory markers.

References

1. Cioffredi LA, Jhaveri R. Evaluation and Management of Febrile Children: A Review. JAMA Pediatr. 2016 Aug 1;170(8):794-800.
2. Shaikh N, Hoberman A, Hum SW, Alberty A, Muniz G, Kurs-Lasky M, Landsittel D, Shope T. Development and Validation of a Calculator for Estimating the Probability of Urinary Tract Infection in Young Febrile Children. JAMA Pediatr. 2018 Jun 1;172(6):550-556.
3. SUBCOMMITTEE ON URINARY TRACT INFECTION. Reaffirmation of AAP Clinical Practice Guideline: The Diagnosis and Management of the Initial Urinary Tract Infection in Febrile Infants and Young Children 2-24 Months of Age. Pediatrics. 2016 Dec;138(6):e20163026
4. Kaufman J, Temple-Smith M, Sanci L. Urinary tract infections in children: an overview of diagnosis and management. BMJ Paediatr Open. 2019 Sep 24;3(1)
5. Kaufman J, Fitzpatrick P, Tosif S, Hopper SM, Donath SM, Bryant PA, Babl FE. Faster clean catch urine collection (Quick-Wee method) from infants: randomised controlled trial. BMJ. 2017 Apr 7;357:j1341.
6. Glissmeyer EW, Korgenski EK, Wilkes J, Schunk JE, Sheng X, Blaschke AJ, Byington CL. Dipstick screening for urinary tract infection in febrile infants. Pediatrics. 2014 May;133(5):e1121-7.
7. Mattoo TK, Shaikh N, Nelson CP. Contemporary Management of Urinary Tract Infection in Children. Pediatrics. 2021 Feb;147(2):e2020012138.
8. Mahajan P, VanBuren JM, Tzimenatos L et. al. Pediatric Emergency Care Applied Research Network (PECARN). Serious Bacterial Infections in Young Febrile Infants With Positive Urinalysis Results. Pediatrics. 2022 Oct 1;150(4):e2021055633.

The post Pediatric Small Talk – Urine Trouble: An Approach to Pediatric UTIs appeared first on emDOCs.net - Emergency Medicine Education.

Today on the emDOCs cast with Brit Long, MD (@long_brit), we cover ovarian torsion and several myths.

Episode 67: Ovarian Torsion

Background:

• Ovarian torsion occurs when the ovary completely or partial rotates on the ligamentous supports, resulting in ovarian necrosis and infertility if missed.
• Ovarian torsion is the 5^th most common acute gynecologic disease, but it’s still rare: incidence is 5.9/1000,000 annually.
• Most patients have a cyst or mass > 5 cm.
• The classic presentation is sudden onset lower abdominal pain, associated with nausea and vomiting.
• Ovarian torsion can be a difficult diagnosis, and what we learn or classically consider can lead to misdiagnosis.

1. Myth: Ovarian torsion only occurs in women of reproductive age

• The most common patient population affected is reproductive age women (most common age is 30 years). 80% of these patients have an adnexal mass or cyst.
• 15% of cases occur during infancy or childhood. While it is more common in postmenarchal patients, in can occur in premenarchal patients or infants. Over half of pediatric patients have normal ovaries.
• Postmenopausal women can experience torsion. One study found 25% of torsion cases occurred in this age group. Another found 14/58 of torsion cases occurred after menopause. Nearly all patients in this age group have a known mass or enlarged ovary.
• Clinical Bottom Line: Ovarian torsion affects women of all ages.

2. Myth: All patients with ovarian torsion present with acute, severe pain and vomiting.

• Pain occurs due to occlusion of the vascular pedicle and ischemia. Classically its abrupt and radiates to the flank or groin, but only half present with abrupt severe pain.
• Some form of pain is present in 90%. Can present insidiously/gradually/intermittent, especially in those with polycystic ovarian syndrome or ovarian cysts.
• There may be mild to severe pelvic or abdominal pain, abdominal bloating, nausea, or vomiting. Pain can be constant or intermittent because the ovary torses and detorses.
• Fever may also be present (up to 20%).
• Don’t rely on nausea and vomiting. These are absent in 30% of patients.
• Clinical Bottom Line: The classic presentation of ovarian torsion is not always present. Patients may have gradual onset pain, intermittent pain, or very mild pain. Nausea and vomiting may not be present.

3. Myth: A normal physical exam, including pelvic exam, can rule out torsion.

• Up to a third of patients have no abdominal or pelvic tenderness on exam.
• Bimanual exam is unreliable. Patients may or may not have cervical motion tenderness, uterine tenderness, adnexal mass/tenderness.
• EM physician inter-examiner reliability for detection of pelvic masses is less than 25% and less than 32% for adnexal tenderness on bimanual examination. OBGYN exam not much better. Sensitivity for detecting adnexal mass > 5 cm is 15-36%.
• Exam is even less reliable in patients over 200 lbs and in older patients (> 55 years).
• Absence of a mass does not rule out torsion. Torsion can occur in those with a normal-sized ovary (one study found 15% of torsion cases had a normal sized ovary, which is even higher in pediatric patients).
• Clinical Bottom Line: Do not rely on a normal pelvic or bimanual examination to rule out torsion.

4. Myth: Normal arterial flow on Doppler ultrasound rules out ovarian torsion.

• Transvaginal ultrasound (TVUS) with gray-scale imaging and Doppler flow is usually our go-to imaging modality to evaluate for torsion.
• High specificity but poor sensitivity, ranging from 35-85%.
• Most common finding is an enlarged ovary, often a mass. Other signs include an ovary displaced to the midline. The string of pearls sign (enlarged ovary is lined around the periphery by follicles) suggests torsion.
• Grayscale may demonstrate a hypoechoic appearance of the ovary due to edema. Color doppler may reveal decreased or absent intraovarian venous flow, which may be followed by absent arterial flow later in the disease.
• However, the ovaries have dual blood supply (ovarian and uterine ovaries). Torsion initially occurs with lymphatic and venous outflow obstruction. Arterial inflow is not compromised until later in the disease course.
• Arterial flow is completely normal in over 25% of patients with surgery-confirmed torsion, and over half of patients will have detectable arterial flow.
• Combining findings can improve the sensitivity and specificity; can’t focusing on only vascular flow. Evaluate for free fluid within the pelvis, ovarian enlargement and edema, and vascular flow (improves sensitivity).
• The whirlpool sign is strongly suggestive of torsion (circular collection of blood vessels within an enlarged ovary or mass).
• Clinical Bottom Line: Normal arterial flow on Doppler US cannot rule out torsion. Consider using a combination of ultrasound findings.

5. Myth: A completely normal computed tomography (CT) scan of the pelvis requires an ultrasound to rule out torsion.

• CT can assist in evaluating for torsion.
• CT findings with high specificity for ovarian torsion: twisted vascular pedicle, thickened fallopian tube with target/beak-like appearance, absent or reduced ovarian enhancement with contrast, and enlarged ovary with afollicular ovarian stroma and peripherally displaced follicles. Can rule in diagnosis.
• Common findings but not specific: enlarged ovary, an adnexal mass, adnexal mass mural thickening, free pelvic fluid, fat stranding surrounding the ovary, uterine deviation towards the torsed ovary, and ovarian displacement towards the uterus.  If one of these is present, speak with OBGYN and obtain TVUS.
• If these findings are not present and there is normal ovarian size, no pelvic fluid, and no cyst or mass, sensitivity nears 100% for excluding torsion using CT.
• Clinical Bottom Line: A normal abdominal/pelvic CT significantly decreases the likelihood of torsion. Certain findings on CT are highly suggestive of torsion.

6. Myth: Pregnant patients with lower abdominal pain should have ectopic pregnancy and miscarriage ruled out. Once this is done, the evaluation is complete.

• Pregnancy increases the risk for torsion (progesterone increases the formation of ovarian cysts), and pregnant patients account for anywhere between 10% and 25% of torsion cases.
• Most cases during pregnancy occur in the first 17 weeks (81%), and 73% of these patients have undergone fertility therapy. Fertility treatments can result in ovarian hyperstimulation, further increasing the risk of ovarian cyst formation.
• Prior pelvic surgeries and tubal ligation increase the risk of torsion.
• Signs and symptoms of torsion are similar between pregnant and nonpregnant women.
• Clinical Bottom Line: Pregnant women can experience ovarian torsion, with increased risk if they are undergoing fertility treatment or have had prior torsion.

7. Myth: Surgery is useless if the patient has had symptoms for more than just a few hours.

• Torsion is time sensitive, but the exact timing of ovarian necrosis is unclear.
• Studies suggest ovarian viability ranges from several hours up to days (one study found 168 hours).
• Outcomes are worse with prolonged ischemia, so the earlier the ovary is detorsed, the higher likelihood of viability.
• Clinical Bottom Line: Patients may have symptoms for several days and still have viable ovaries after surgery. If you’re suspicious of torsion based on your history and exam, speak with your OB/GYN before obtaining imaging.  If you do not have an OB/GYN available, consult the general surgeon on call.

Summary:

• Key risk factors for ovarian torsion include the presence of an ovarian mass or cyst and prior pelvic surgery.
• Ovarian torsion most commonly affects reproductive-aged women. A significant number occur in premenarchal females, pregnant women, and postmenopausal women.
• Up to 90% of women have some form of abdominal pain, but this is not always sudden in onset and severe. Pain may be gradual and episodic. Up to 70% experience nausea and vomiting.
• Up to one-third of patients with torsion have no abdominal or pelvic tenderness.
• US is considered the primary imaging modality and has high specificity, but a normal US cannot rule out torsion.
• CT with IV contrast may show reduced or absent ovarian enhancement with contrast, peripherally displaced follicles, enlarged ovary with a follicular ovarian stroma, and a thickened fallopian tube with target/beak-like appearance.
• Consult OBGYN; there is no clear time to necrosis in ovarian torsion.

References:

• Robertson JJ, Long B, Koyfman A. Myths in the Evaluation and Management of Ovarian Torsion. J Emerg Med. 2017 Apr;52(4):449-456. doi: 10.1016/j.jemermed.2016.11.012. Epub 2016 Dec 14. PMID: 27988260.
• Bridwell RE, Koyfman A, Long B. High risk and low prevalence diseases: Ovarian torsion. Am J Emerg Med. 2022 Jun;56:145-150. doi: 10.1016/j.ajem.2022.03.046. Epub 2022 Mar 31. PMID: 35397355.

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Authors: Olivia Victoriano, MD (PGY 2, UHS SoCal MEC Emergency Medicine Residency, Temecula, Ca); Jacob Avila, MD, RDMA (Core Faculty, UHS SoCal MEC Emergency Medicine Residency, Temecula, Ca) // Reviewed by: Stephen Alerhand MD (@SAlerhand); Brit Long, MD (@long_brit)

Case

An 86-year-old female with a history of osteoporosis and mild cognitive impairment presents to the emergency department for right hip pain after a fall from her bed at home. She has not been able to move her right hip since that time or put any weight on her right lower extremity. When she arrives at the ED, you notice that her right hip is held in an abducted and flexed position. Her right leg is rotated outward and appears shorter than the left leg. She has an ecchymotic area of the lateral aspect on the right thigh.  X-ray imaging of the hip is ordered and shows a right-sided intertrochanteric fracture. The patient is clearly uncomfortable and shouting any time she is moved. Her current systolic blood pressure is hovering in the low 100’s and EMS reports that they administered 25 micrograms of fentanyl IV and she subsequently required 2L O2 nasal cannula to keep her oxygen saturation in the 90’s. On arrival to the ED, she immediately requests pain medicine.

What are some issues with parenteral opiates in the ED?

• Opiate use can cause delirium in the elderly, especially in those with baseline impaired cognition
• Opioids decrease respiratory drive (via the mu-opioid receptors in the CNS) which may cause hypoxia
• In addition to decrease in respiratory drive, opioids can cause other undesirable side effects such as oversedation
• Tolerance to opioids in chronic opioid users cause them to be less effective in the acute setting
• Opiate addiction is an ongoing public health crisis that necessitates utilization of alternative therapies for pain

Approach to Hip Fractures in the Elderly

Acute pain is the most common reason for visiting the emergency department. There is an association with treatment of pain and opiate use disorder which accounts for 5.8 million additional years lived with disability. Alternatives to opiates for the acute management of pain, such as local administration of topical anesthetic, can reduce opiate dependence and side effects. Additionally, local anesthetics in the treatment of pain decreases the incidence of systemic side effects, including effects on the central nervous system. Here we will outline treatment options for an acute hip fracture using local anesthetic administration.

Innervation of the proximal femur

The proximal femur has a relatively complex innervation, with contributions from the femoral nerve (FN), the obturator nerve (ON) and the sciatic nerves (SN).

While anesthetizing any of these nerves will be beneficial with regards to pain management, the goal should be to attempt to block the largest quantity of nerves. The hip blocks will block the ON and FN to variable degrees.

This guide will cover the infrainguinal fascia iliaca block, the suprainguinal fascia iliaca block and the pericapsular nerve group (PENG)

Fascia Iliaca Compartment Nerve Block

Indications: Hip and knee analgesia, anterior thigh analgesia (i.e. femur fractures, pubic ramus fractures, acetabular fractures and hip dislocations)

Contraindications: Anticoagulation (not including NSAIDs or aspirin), overlying cellulitis at site of needle insertion, or fractures at risk for compartment syndrome on the same extremity (i.e. tibial plateau fractures)

Advantages of this block: relatively far from critical vascular structures like the femoral artery (FA) and femoral nerve. In addition, the analgesic effect has been shown to be superior to parenteral opioids in alleviating pain with movement of the hip. This may aid in post-operative rehabilitation.

Distribution: FN ± lateral femoral cutaneous nerve and the ON.

Anesthetic distribution of fascia iliaca block. (NYSORA.com)

Equipment:

• Linear Ultrasound transducer (6-14 MHz) with sterile sleeve and sterile gel
• Two 20 mL syringes, or 60mL syringe
• 80-mm to 100-mm, 22-gauge nerve block needle
• Extension tubing to connect to syringe and nerve block needle (as shown below)
• 10mL syringe with 25 gauge needle for local wheal
• 30-40mL of dilute (0.25% of bupivacaine) long-acting anesthetic, making sure to not go over the maximum number of local anesthetic for the specific patient.
• 5mL of 1% lidocaine (for “skin wheal”)
• Sterile gloves
• Chlorhexadine
• Ideally, a secondary operator to help with administration of anesthetic

Syringe with nerve block needle set up (AliEM.com)

LANDMARKS, POSITIONING, AND TECHNIQUE

Infra-Inguinal Fascia Iliaca Nerve Block Approach

Patient will need to be lying in a supine position with the bed flattened. Ideally, you will position yourself and your equipment on the side of the affected extremity and the ultrasound machine on the contralateral side of the fracture to maintain appropriate line-of-sign between your needle/transducer and the ultrasound screen. Transducer will be placed on the inguinal crease in a transverse position. The FA will be identified as a pulsatile and the most medial neurovascular structure, bordered laterally by the femoral vein (FV).  Lateral to the FV, a triangular structure will be seen, which represents the FN and a small bundle of adipose cells.  Just superficial to the FN, a hyperechoic (white) line will be seen that represents the fascia iliaca.

(FV = Femoral vein, FA = Femoral artery, FN = Femoral nerve, IM = Iliacus muscle, FI = Fascia iliaca)

Another visualization of landmarks for cognitive priming of infra-inguinal nerve block.

FA, femoral artery; FV, femoral vein; FN, femoral nerve; GnFN, genitofemoral nerve; LFcN, lateral femoral cutaneous nerve. (From Compendium of Regional Anesthesia)

The target for injection will the area just lateral to the FN, deep to the fascia iliaca and superficial to the iliacus muscle. Once you find the appropriate location for injection using ultrasound guidance, you will prep the patient in a sterile manner:

• Prepare your anesthetic mixture of bupivacaine in a 30 or 40 mL syringe.
• Clean the inguinal region with copious chlorhexidine and place sterile drape over the region of interest.
• Inject lidocaine as a skin wheal in the region where the injection will take place
• Don sterile glove and place the sterile ultrasound cover on the transducer.
• Attach the nerve block needle tubing to the syringe that an assistant is holding.
• Place the sterile ultrasound transducer over the area of interest once again, while holding the probe in your non-dominant hand and the needle in your dominant hand
• The needle should be placed in-line with the long-axis of the transducer.  The angle of insertion should be around 45-60 degrees. As the needle advances into the patient, it should be visualized in the long axis with the ultrasound transducer. Care should be taken to always keep perfect visualization of the needle.

• The goal is for the needle tip to be JUST underneath the fascia iliaca (you usually will feel a pop, or change in resistance)
• Once you visualize the appropriate position of the needle tip, have the secondary operator introduce a small aliquot (~1mL) of the anesthetic to ensure you are in the correct position.
  • If your positioning is correct, you will see hydrodissection, or clear separation between the fascia iliaca and the iliacus muscle
  • Make the necessary adjustments if you are too inferior (in the iliacus muscle) or superior (above the level of the fascia)
  • Always use negative pressure before inserting anesthetic to confirm you are not in a vascular structure
• Once in the appropriate position, instill the remainder of the 30-40mL of your anesthetic into the space (a volume of at least 30mL is generally necessary to accomplish appropriate “spread” within fascia iliaca)
  • You want to see that the anesthetic is moving medially (toward the femoral nerve) and laterally (toward the sartorius muscle) in the same fascial plane.

 (Example of an intra-inguinal fascia ilaca block. FV = Femoral vein, FA = Femoral artery, FN = Femoral nerve, LA = Local anesthetic, FI = Fascia iliaca)

For a video on the technique of performing a fascia iliaca block, check out this link.

Other types of nerve blocks are also available for providing analgesia for a proximal femur fracture.  These include the suprainguinal fascia iliaca block and the PENG block

Suprainguinal Fascia Iliaca Nerve Block Approach

The suprainguinal approach may result in more proximal spread of the anesthetic and successful analgesia. A disadvantage of this approach is that it requires visualization of the internal oblique muscle, which may be smaller and more difficult to locate in the elderly population.  In this approach, the position of the patient and equipment remains the same. You will even use the same initial approach to locate the iliacus muscle. At this point, you will begin to move the probe superiorly until you are above the inguinal canal and the ASIS. You will then rotate the probe marker 90 degrees so that it is pointing toward the umbilicus. You will see the sartorius and internal oblique form a “bowtie” with the iliacus in the middle and inferiorly.

Use the same approach as above, but your goal now will be the middle of the bowtie, under the fascia iliaca and above the iliacus muscle. with the exception of the ultrasound probe, which will be positioned in a parasagittal orientation, as illustrated above.

Cognitive priming for supra-inguinal fascia iliaca nerve block. (From Compendium of Regional Anesthesia)

PENG: Pericapsular Nerve Group block

The final technique we will talk about is the PENG block.  This block is likely superior with regards to the other two blocks described, due to it’s more reliable penetration of the obturator nerve, its more motor-sparing effect and the fact that it may be beneficial in acetabular fractures, which are fractures that the fascia iliaca blocks don’t reliable anesthetize. The downside is that it can be more technically challenging to perform due to the depth at which the anesthetic needs to be distributed.

LANDMARKS, POSITIONING, AND TECHNIQUE

The patient, operator and probe placement will be similar to the previously described blocks. However, instead of the traditional linear transducer, a curvilinear transducer should be placed in a transverse orientation at the proximal thigh (probe marker to patient’s right). The transducer should then rotated 45 degrees such that it is parallel to the inguinal crease.

Operator must first identify the femoral artery and femoral head.

The transducer can then slide slowly in a cephalad direction until the ilium, anterior inferior iliac spine (AIIS) and iliopubic eminence (IPE). You will see the psoas tendon overlying the ilium. The target for administration of anesthetic will be the subfascial plane immediately overlying the ilium, deep to the psoas tendon.

After the identification of the appropriate landmarks, patient can be prepped in a sterile manner. This process will be similar as in the fascia iliaca blocks. The overall technique is similar, except for the fact that a longer nerve block needle (often 3 inches) will need to be used in order to reach the region of the pelvis deep to the psoas tendon.

• Using an in-plane technique in a lateral-to-medial direction, insert the nerve block needle until you visualize the needle tip deep to the psoas tendon until you contact the ilium
• Have the second operator insert 2cc of saline to confirm placement
  • You should visualize the lifting of the psoas tendon off of the pelvic floor with local anesthetic administration.
  • Make necessary adjustments if the liftin of the psoas tendon is not visualized.
  • Remember to always use negative pressure to ensure your needle tip is not in the intravascular space
• Once you confirm placement, insert 30-40mL of the long acting anesthetic into the plane.

Additional reminders for nerve blocks

‘The target for the local anesthetic should not be the nerves themselves, but rather the fascial planes in which the nerve lie.

Adequate analgesia may take 30 minutes to 1 hour.

Always ensure that you have adequate positioning and view of landmarks before starting the procedure. Set the table before you eat!

Consistent needle visualization and landmark visualization throughout these dynamically-guided procedures is important to preventing accidental intramuscular injection (which can in turn cause femoral nerve blockade and reduction of motor function).

There are many anesthetics to choose from, but the best anesthetics to use in the case of an acute hip injury are long-acting. Always ensure that you correct for the patient’s weight when choosing an anesthetic and determining volume.

Local amide-based anesthetic agents and their pharmacokinetic effects, adapted from Goldfrank’s Toxicologic Emergencies^{​ (ACEP.org)}

Case Resolution

Patient is reevaluated in the emergency department 40 minutes after the nerve block was performed. You have consulted orthopedic surgery, who is planning for operative repair. She is now having significant resolution of her pain and pending her operation.

Further Resources:

^{https://www.acep.org/emultrasound/newsroom/apr2021/pericapsular-nerve-group-peng-block-for-patients-with-hip-or-pelvis-fractures-in-the-ed/#:~:text=The%20pericapsular%20nerve%20group%20(PENG,accessory%20obturator%20nerve%20(AON).} 

^{https://www.nejm.org/doi/full/10.1056/NEJMra1807061#:~:text=Well%2Dknown%20drugs%20such%20as,analgesic%20regimens%20for%20postoperative%20pain.}

^{https://www.aliem.com/fascia-iliaca-nerve-block/}

^{https://www.nysora.com/topics/regional-anesthesia-for-specific-surgical-procedures/lower-extremity-regional-anesthesia-for-specific-surgical-procedures/ultrasound-guided-fascia-iliaca-block/}

^{www.coreultrasound.com}

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Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

Answer: Bartholin’s Abscess

Background:

• Bartholin’s glands^[1]
  • Pea-sized glands located bilaterally at the 4 o’clock and 8 o’clock positions of the posterior introitus
  • Provide lubrication to the vagina by secreting mucus via ducts into the introitus
  • If normal, usually cannot be felt by simple palpation

Epidemiology:

• 2% of women have a lifetime incidence of a Bartholin’s cyst or abscess^[3]
• Much more common in reproductive-age women

Pathogenesis:

• When a Bartholin’s duct is obstructed, mucoid secretions cannot be released^[3,4]
• Secretions build up inside the duct and eventually form a Bartholin’s cyst^[4]
• If the cyst becomes infected, it develops into a Bartholin’s abscess
  • However, an abscess does not always need a cyst to precede it
• Initially thought to be caused solely by STI organisms, but that is no longer the case^[3]

History:

• Important points to consider^[4,5]

• • How long have symptoms been occurring?
  • What is the extent of the patient’s pain? Is it occurring with simple movements such as walking or intercourse?
  • History of prior Bartholin’s cyst or abscess?
  • Obtain a thorough sexual history to differentiate various genital lesions

Physical Exam:^[3,5]

• Perform both an external and internal exam to determine extent of patient’s symptoms
• Important points to consider during your exam:

• • Are there multiple lesions?
  • Is the lesion painful?
  • Are there any overlying skin changes?
  • Are there systemic symptoms?
  • If there is vaginal discharge or cervical motion tenderness, an STI etiology may be more likely

Clinical Presentation:^[5]

• Usually painful, unilateral, and located at the 4 o’clock or 8 o’clock position
  • A Bartholin’s cyst, while located in the same position, is usually not painful
• Fluctuant mass with possible induration/erythema on overlying skin
• May already be draining purulent fluid

Differential Diagnosis:

• Soft Lesion: Bartholin’s cyst, Bartholin’s abscess, Skene’s duct cyst, Epidermal inclusion cyst^[3,5]
• Firm Lesion: Leiomyoma, Lipoma, Squamous cell carcinoma^[3,5]

Management:

• Rarely resolves on its own. If a patient has pain, intervention will likely be needed^[6]
• Treatment begins with an incision and drainage. Afterwards, a Word catheter or Jacobi ring must be used
• I&D: This step will be like any other I&D
• Anesthetize the area with lidocaine
• Using a #11 blade, make a vertical incision posterior to the labia minora. This location will prevent notable scarring
• Break up loculations with a hemostat to allow proper drainage
• Send off a culture after collecting purulent fluid on a culture swab
• However, a Bartholin’s abscess I&D is not a definitive treatment^[7]
  • ~13% of patients will have recurrent abscess
  • This is due to premature closure of the tract which prevents further drainage
• To allow continued drainage and thereby prevent recurrence, a Word catheter or Jacobi ring should be placed
  • Word catheter: Short, rubber catheter with a balloon tip^[8]

• Word catheter provides a tract for continued drainage of the abscess^[10]
  • Pus does not flow out through the catheter itself. It drains from the space between the mucosa and rubber catheter
• Steps to place a Word catheter^[11,12]
  • Once the incision is made and fluid is drained, place the catheter through the opening
  • After the catheter is placed, inflate the balloon with saline. This will prevent it from being dislodged when the patient goes home
  • The Word catheter stays in place for 2-4 weeks until it is removed
  • For removal: Balloon is deflated, and the catheter is simply pulled from the abscess cavity

• To place a Jacobi ring:^[13]
  • Inject lidocaine
  • Make an initial stab into the mucosa
  • Break up loculations with a hemostat
  • Create a tract with the hemostat and make another stab incision into the other end of the tract
  • Take tubing from a butterfly catheter (cut off the needle end) and pass it through the tract you created
  • Tie the two ends of the tubing, but be sure not to tie too tightly

• Antibiotics^[11]
  • Should only be given if a patient has a recurrent Bartholin’s abscess or if there is overlying cellulitis
  • Should cover Gram-positive organisms, including MRSA
  • Choices include Bactrim 800mg/160mg BID x7 days or Doxycycline 100mg BID x7 days
  • Consider IV antibiotics for immunocompromised patients or those with poorly controlled diabetes
• For further care at home, the patient should do Sitz baths and refrain from intercourse^[8]
• Patient should follow up with an OB/GYN after discharge due to risk of recurrence

Take Home Points:

• If a patient presents with a painful fluctuant mass near the introitus and you suspect a Bartholin’s abscess, intervention is almost always needed
• A simple I&D is usually not a definitive treatment for a Bartholin’s abscess
• A Word catheter or Jacobi ring can prevent recurrence of a Bartholin’s abscess
• Antibiotics are needed for recurrent abscesses, overlying cellulitis, or an immunocompromised patient

Further Reading:

The post EM@3AM: Bartholin’s Abscess appeared first on emDOCs.net - Emergency Medicine Education.

Welcome back to the “52 in 52” series. This collection of posts features recently published must-know articles. Post #21 looks at targeted temperature management after cardiac arrest with non-shockable rhythm, or the Hyperion trial.

Author: Brannon Inman (Chief Resident, Emergency Medicine Physician, San Antonio, TX) // Reviewed by: Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

• Positive study
• There is limited external generalizability due to one country being included and the practice patterns of the aforementioned country (stopping sedation in the intervention group in patients with suspected brain death during the trial period).
• There was a slightly longer time to randomization in the hypothermia group. If therapeutic cooling works, it probably is time sensitive. This could skew the data toward the null.
• Quite a few patients in the normothermia group actually had a fever. It’s not explicitly stated in the text whether these patients were included in the analysis or not. This may have biased the data/outcomes.
• The failure to maintain normothermia in the control group questions the intensity of nursing and support staff care provided in the control group vs. the intervention group (therapeutic cooling is known to become labor intensive, with more nursing care etc.). Hyperthermia is what we try to avoid post arrest.
• There are a lot of differences between the two groups:
  • Longer duration of therapeutic cool in the intervention group (up to 64 hours) vs the control (48 hours)
  • The intervention group sedated to a RASS of -5, vs RASS of 0 in the control
  • Longer time to randomization in the intervention group

My Take:

• This is extremely fragile data supporting the use of therapeutic cooling patients with non-shockable rhythms with coma following ROSC.
• In light of other data suggesting no benefit, these fragile data have not meaningfully convinced me of the benefit of therapeutic cooling. This study has limited applications due to the reasons mentioned above, and issues with randomization.

References:

1. Bagci Z, Arslan A, Neselioglu S. Pediatric Carbon Monoxide Poisoning: Effects of Hyperbaric Oxygen Therapy on Thiol/Disulfide Balance. Pediatr Emerg Care. 2022;38(3):104-107. Doi: 10.1097/PEC.0000000000002619

The post 52 in 52 – #21: The Hyperion Trial appeared first on emDOCs.net - Emergency Medicine Education.

Authors: Dominic Nicacio, MD (EM Resident Physician, Carolinas Medical Center, Charlotte, NC); Ann-Jeannette Geib, MD (EM Attending Physician, Medical Toxicologist, Carolinas Medical Center, Charlotte, NC) // Reviewed by: James Dazhe Cao, MD (@JamesCaoMD, Associate Professor of EM, Medical Toxicology, UT Southwestern Medical Center, Dallas, TX); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case One:

A 3-year-old male presents to the pediatric emergency department (ED) via EMS, actively seizing. Blood glucose is 87, and vitals are stable. Physical exam shows equal and reactive pupils bilaterally, no gaze deviation, dry skin, no rashes, and no palpable abdominal masses. Two rounds of IV lorazepam at 1.5 mg do not stop the seizures.  The patient becomes hypoxic and end-tidal CO₂ begins to fall. He is subsequently intubated and started on propofol but continues to have subtle seizure activity. The patient’s mother arrives and tells you that she thinks her child got into her purse which contains some of her daily medications. She cannot remember all the names of them but tells you she’s being treated for latent tuberculosis. She hands over a nearly empty bottle of isoniazid (INH), filled two days ago.

Question:

• What is the treatment for INH toxicity?

Answer:

• Pyridoxine

Mechanism of Action:

• In the liver, pyridoxine is converted to pyridoxal-5-phosphate (PLP). PLP is a cofactor for glutamic acid decarboxylase (GAD) that converts glutamic acid to γ-aminobutyric acid (GABA), which is the major inhibitory neurotransmitter in the central nervous system (CNS)
• PLP complexes with INH to form isonicotinic hydrazide that is excreted in the urine.
• INH metabolism leads to formation of hydrazones that inhibit pyridoxine phosphokinase which converts pyridoxine to active form PLP
• Depletion of pyridoxine and inhibition of pyridoxine phosphokinase cause a reduction in GABA concentrations in synapses, resulting in CNS excitability and ultimately seizures¹
• A gram-equivalent dose of pyridoxine has been associated with cessation of seizures and improvement in coma scores and pH in INH- poisoned patients²

Pyridoxine Dosing:

• Known INH dose: 1 g IV per gram of INH ingested
• Unknown INH dose: 70 mg/kg IV in children or 5 g IV adults
• Repeat dosing: Can repeat above dosing one time if seizures continue to be refractory
• Infusion rate: 0.5 g/min until seizures stop
• If your ED has insufficient pyridoxine vials, you can give the remaining dose as oral formulation via nasogastric tube³

Asymptomatic Overdose:

• If a patient presents within 2 hours of ingestion of a potentially toxic dose, some textbooks recommend prophylactic pyridoxine at the same dosing¹

Case Two:

You are working in a community ED during a warm June summer day when a 37-year-old female with unknown past medical history comes in via EMS after seizing at home; blood glucose 94 mg/dL en route. EMS states she was found seizing on the floor beside the kitchen table, with a hot bowl of mushroom soup on the table. The mushrooms looked wrinkled and “brain shaped.” The daughter reports her mother attended a mushroom gathering community event earlier today and was collecting morels.

Question:

• What toxicity should you be concerned about, and what is the treatment?

Answer:

• Gyromitrin toxicity from Gyromitra mushroom of the false morel family; treatment is pyridoxine

Mechanism:

• Gyromitrin is metabolized to hydrazines that inhibit the enzyme converting pyridoxine to PLP, ultimately resulting in decreased GABA synthesis^4,5

Dosing:

• Same as in INH toxicity, 5 g IV over 10 minutes, or 70 mg/kg in children

Case Three:

Four industrial workers arrive to your ED following a blast incident at an aerospace engineering facility. There was a blast and exposure to fumes. Two patients have minor burn injuries. They are all deemed stable after decontamination and initial ED assessment. During their stay three of the workers had seizures that responded poorly to benzodiazepines. You ascertain that they were working with rocket fuels just prior to the blast.

Question:

• What toxicity is likely implicated, and what is the treatment?

Answer:

• Likely hydrazine-containing jet fuels, which is treated with pyridoxine when it causes seizures and altered mental status
• Hydrazines are also found in esculenta mushrooms⁴

Mechanism of Action:

• Hydrazines inhibit pyridoxine phosphokinase, the enzyme that converts pyridoxine to PLP, which results in decreased GABA synthesis⁶

Dosing:

• There are limited data regarding optimal dosing, but pyridoxine is likely safe in doses used for INH and Gyromitra toxicity⁷

Other Occasional Uses of Pyridoxine:

Indications and dosing are based on extremely limited clinical data⁸

Ethylene Glycol Toxicity:

• Decreases oxalic acid production responsible for renal tubular necrosis & hypocalcemia by shunting metabolism of organic acid metabolites down a less toxic pathway⁷
• Pyridoxine treatment dose is 100 mg IV daily⁷

Hyperemesis Gravidarum:

• Pyridoxine is used in pregnancy with doses of up to 25 mg PO TID for nausea and vomiting
• Pyridoxine is FDA category A for use in pregnancy⁹

Wilson’s Disease:

• Pyridoxine is often added to medication regimens in patients with Wilson’s disease as penicillamine induced neurological deterioration is thought to be related to pyridoxine deficiency^10,11

Theophylline Toxicity-associated Seizures:

• Limited evidence shows that theophylline decreases PLP levels, theoretically decreasing GABA synthesis, causing seizures
• There is mixed evidence in animal models showing some efficacy in decreasing seizures and death, in groups receiving pyridoxine¹²

References:

1. Hernon C, and Lai JT. “Antituberculous Medications” in Nelson LS et al, eds. Goldfrank’s Toxicologic Emergencies, 11 ed. McGraw-Hill Education, 2019.
2. Wason S, Lacouture PG, Lovejoy FH Jr. Single high-dose pyridoxine treatment for isoniazid overdose. JAMA. 1981 Sep 4;246(10):1102-4. PMID: 7265398.
3. Dilrukshi MDSA, Ratnayake CAP, Gnanathasan CA. Oral pyridoxine can substitute for intravenous pyridoxine in managing patients with severe poisoning with isoniazid and rifampicin fixed dose combination tablets: a case report. BMC Res Notes. 2017 Aug 8;10(1):370. doi: 10.1186/s13104-017-2678-6. PMID: 28789699; PMCID: PMC5549285.
4. Goldfrank LR. Mushrooms. In: Nelson LS, Howland M, Lewin NA, Smith SW, Goldfrank LR, Hoffman RS. eds. Goldfrank’s Toxicologic Emergencies, 11e. McGraw Hill; 2019. Accessed January 18, 2022.
5. White J, Weinstein SA, De Haro L, Bédry R, Schaper A, Rumack BH, Zilker T. Mushroom poisoning: A proposed new clinical classification. Toxicon. 2019 Jan;157:53-65. doi: 10.1016/j.toxicon.2018.11.007. Epub 2018 Nov 12. PMID: 30439442.
6. Dhennin C, Vesin L, Feauveaux J. Burns and the toxic effects of a derivative of hydrazine. Burns Incl Therm Inj. 1988 Apr;14(2):130-4. doi: 10.1016/0305-4179(88)90218-5.
7. Howland M (2019). Pyridoxine. Nelson L.S., & Howland M, & Lewin N.A., & Smith S.W., & Goldfrank L.R., & Hoffman R.S.(Eds.), Goldfrank’s Toxicologic Emergencies, 11e. McGraw Hill.
8. Lheureux P, Penaloza A, Gris M. Pyridoxine in clinical toxicology: a review. Eur J Emerg Med. 2005 Apr;12(2):78-85. doi: 10.1097/00063110-200504000-00007. PMID: 15756083.
9. Nuangchamnong N, Niebyl J. Doxylamine succinate-pyridoxine hydrochloride (Diclegis) for the management of nausea and vomiting in pregnancy: an overview. Int J Womens Health. 2014 Apr 12;6:401-9. doi: 10.2147/IJWH.S46653. PMID: 24748822; PMCID: PMC3990370.
10. Roberts, E.A. and Schilsky, M.L. (2008), Diagnosis and treatment of Wilson disease: An update. Hepatology, 47: 2089-2111. https://doi.org/10.1002/hep.22261
11. Dong QY, Wu ZY. Advance in the pathogenesis and treatment of Wilson disease. Transl Neurodegener. 2012 Nov 27;1(1):23. doi: 10.1186/2047-9158-1-23. PMID: 23210912; PMCID: PMC3526418.
12. Glenn GM, Krober MS, Kelly P, McCarty J, Weir M. Pyridoxine as therapy in theophylline-induced seizures. Vet Hum Toxicol. 1995 Aug;37(4):342-5. PMID: 8540225.

The post ToxCard: Pyridoxine Uses in Clinical Toxicology appeared first on emDOCs.net - Emergency Medicine Education.

Author: Philip Jarrett, MD, MBA (Emergency Medicine, University of Texas Southwestern Medical Center) // Reviewed by: Alex Koyfman, MD (@EMHighAK) and Brit Long, MD (@long_brit)

We pride ourselves as expert resuscitationists. We train to optimize every facet of cardiac arrest management from chest compression fraction and medication selection to team dynamics and debriefs. Hospital resources are expended at a hurried pace as plastic packaging collects on the floors and empty glass vials aggregate. We contemplate reversible causes as the clock ticks down to oblivion. Bedside ultrasound shows a dilated right ventricle. Thrombolytics are drawn up and pushed. Maybe it’s a pulmonary embolism (PE)…

PE is the cause of approximately 3-5% of cardiac arrests.^1-3 This diagnosis plagues our minds as one of the most considered differential diagnoses in emergency medicine. With the broad availability of oral Xa inhibitors (and XIa agents on the way⁴), treatment is decreasingly invasive for most patients. More nuanced discussions remain on the topic of risk stratification and disposition, but even among cases of impending cardiovascular collapse, thrombolysis has become a mainstay of treatment with mounting evidence to support its benefit.^5,6 If all else fails, many institutions are finding success with thrombectomy, catheter-directed thrombolysis, and even ECMO!⁷ Our toolbox is rounding out for PE where historical practice drew from far fewer available interventions, but, what if the patient lacks a pulse? This article will review the most noteworthy evidence in the emergency medicine literature to decipher whether, and when, thrombolysis may be appropriate to treat cardiac arrest if PE is a suspected cause.

The PEAPETT Study (2016)

This case series evaluated whether a population of patients with confirmed PE in pulseless electrical activity (PEA) would benefit from half-dose alteplase (tPA).⁸ Patients were retrospectively enrolled after a diagnosis of PE was made. These patients were followed prospectively to measure the effect of thrombolysis when cardiac arrest occurred. Of the 23 patients who suffered cardiac arrest, 17 occurred in the emergency department while two were in the intensive care unit, one was in a floor bed and three were in the radiology department. After administration of half-dose tPA, return of spontaneous circulation (ROSC) was achieved in 22 of the 23 studied patients. Furthermore, 87% of patients survived to 22 +/- 3 months of follow-up.

All-comers with in-hospital cardiac arrest (IHCA) in the United States (US) prior to the initial COVID surge suffered a mortality of 24.2%.⁹ Compared against this broader population, the PEAPETT outcomes boast a number-needed-to-treat (NNT) of 1.6 for survival to 22 months (Figure 1). It is not an entirely fair assessment to derive a NNT across unrelated studies, but could tPA be the wonder drug for patients who suffer a PEA arrest?

Not so fast! In this cohort without controls, the time to administration of thrombolytics was 6.5 +/- 2.1 minutes. Evidenced by at least one study and the anecdotal experience of my own institutions, most cardiac arrests begin in the pre-hospital setting.¹⁰And when the US national average arrival time for emergency medical services is 7.0 minutes in urban settings and 14.5 minutes in rural settings, the chance of receiving thrombolysis as quickly as patients in this case series falls flat.¹¹ Thrombolysis may work under ideal conditions among admitted patients with a known diagnosis, but ideal conditions are few and far between in the realm of emergency medicine.

The TROICA Trial (2008)

A double-blinded, multicenter, randomized controlled trial published in the New England Journal of Medicine evaluated a broader population of patients who suffered witnessed out-of-hospital cardiac arrest (OHCA).² Böttiger, et al successfully enrolled 1,050 patients and assigned 1:1 treatment of either placebo or Tenecteplase (tNK). Pre-hospital intensive care paramedics administered treatment on-scene prior to hospital transport. The trial was terminated early due to futility.

For the primary endpoint, the tNK cohort achieved a 30-day survival of 14.7% compared to 17.0% in the placebo group (Figure 2). For the secondary endpoint of ROSC at any point, tNK offered no benefit over placebo (55.0% vs. 54.6%, respectively; P = 0.96). Clearly, there is no benefit to administration of thrombolytics among all-comers, and with the astronomical price of thrombolytics in the U.S., the cost-benefit analysis to stock this medication in every ambulance for pre-hospital care may never add up.¹² So, was the PEAPETT trial a fluke?

The Javaudin Study (2019)

A retrospective, observational, multi-center study published in CHEST asked whether a subgroup of OHCA patients who had subsequent confirmation of PE stood to benefit from pre-hospital administration of thrombolytics.¹³ These patients coded in the pre-hospital setting, received thrombolysis, and then had a confirmatory study or autopsy showing PE.

Among 328 patients with a final diagnosis of PE, 246 were evaluated in the study. The 82 excluded patients were removed either because ROSC was achieved prior to arrival of the mobile intensive care unit (MICU) that coordinated study enrollment and drug administration, or because the ROSC status was initially unknown by the MICU upon arrival. Of the 246 included patients, 58 received thrombolysis.

As shown in Figure 3, 30-day survival in the thrombolysis group was significantly higher than the placebo group (16% vs. 6%; P = 0.05). However, good neurologic outcome among survivors in each group did not differ (Adjusted Relative Risk, 1.97; 95% CI, 0.70 – 5.56). This study appropriately tempers the conclusions of the PEAPETT trial for emergency physicians, wherein the NNT for 30-day survival among OHCA patients with confirmed PE settles at 10. But, we don’t practice emergency medicine with the retrospectoscope in hand. Nearly always, the patient in front of us is undifferentiated. How can we decipher which coding patients have a PE?

Predictors of PE in Cardiac Arrest (2016)

A publication in Circulation evaluated the well-described Sudden Death Expertise Center registry from Paris to shed light on patient factors that may predict PE-related cardiac arrest.³ Among the 2,926 patients who were admitted alive to a hospital, 82 had a confirmed diagnosis of PE. Factors predictive of PE included patients with initial non-shockable rhythms, female gender, and those with prior thromboembolism (Figure 4).

The combination of initial non-shockable rhythm and prior thromboembolism yielded a positive predictive value of 31% (95% CI, 19% – 42%) and a negative predictive value of 98% (95% CI, 97% – 98%). Now, there’s a population worthy of trialing thrombolysis! Granted, this study would benefit from external validation with much larger sample sizes. But no one ever said cardiac arrest research is easy.

Interestingly, exclusion of patients with right ventricular failure on echocardiogram found consistent results. This is troublesome. Bedside ultrasound has become the emergency physician’s third hand, manifesting within the 2020 Advanced Cardiac Life Support guidelines as a Class 2b Recommendation for standard patient evaluation during cardiac arrest.^6,14 Although it may be used to evaluate for cardiac tamponade, tension pneumothorax, and right heart strain, more recent evidence has shown that it probably should not be used to aid in the decision to terminate resuscitation.¹⁵ So, what role does an evaluation of right heart strain play in the prediction of PE-related cardiac arrest?

Right Heart Strain in Cardiac Arrest

A prospective observational study published in Resuscitation in 2019 evaluated 33 OHCA patients presenting either with ongoing cardiopulmonary resuscitation (CPR) or ROSC.¹⁶ A 4-view transesophageal echocardiogram was obtained in all patients. Of note, 12% of cases thought to be in asystole were found to have fine ventricular fibrillation, prompting defibrillation. More importantly for the PE discussion, right ventricular dilation (RVD) was observed in 57% of intra-arrest cases. Though ultrasound evidence of RVD may be a poor physician’s guide to PE among living patients in one systematic review and meta-analysis (sensitivity: 53%, 95% CI: 45-61%; specificity: 83%, 95% CI: 74-90%)¹⁷, RVD was a typical finding during cardiac arrest in this population.

A separate Resuscitation article published in 2021 also evaluated right ventricular strain (RVS) via electrocardiogram (ECG).¹⁸ This retrospective cross-sectional study reviewed continuous ECG tracings on admitted patients who subsequently suffered IHCA. RVS was defined by the authors as, “progressive RV depolarization delay in lead V1 with at least one supporting finding of RV ischemia or right axis deviation.” In this study, 47% of patients developed evidence of RVS immediately prior to loss of pulses. The positive predictive value and negative predictive value of RVS for the diagnosis of a respiratory cause of cardiac arrest was 81% (95% CI, 64-95%) and 58% (95% CI, 36-81%), respectively. Among patients who underwent evaluation of PE either by autopsy or computed tomography angiogram of the chest, only 6/23 (26.1%) were confirmed. The right ventricle may not be as predictive of PE during cardiac arrest as we would hope.

Summary

PE is a challenging diagnosis to make during ongoing CPR. There is understandable temptation to consider thrombolysis for patients in cardiac arrest to address all reversible causes. However, the limited evidence on this topic fails to demonstrate benefit among the undifferentiated cardiac arrest patient. Consider early administration of thrombolysis for patients with a combination of predictive factors that support an increased likelihood of PE-related cardiac arrest. On the other hand, resist the urge to use signs of right heart strain as a sole indicator of this pathology. Of note, this article defers the discussion on duration of CPR after administration of thrombolytics due to the wide range of recommendations from various resuscitation authorities. Recommendations span 30 – 90 minutes after drug administration based on limited evidence.^6,19

Pearls and Pitfalls

• Thrombolysis for the patient with undifferentiated cardiac arrest is unlikely to provide mortality benefit and is associated with tremendous financial cost.^2,12
• Among patients with confirmed PE who code, thrombolysis should be considered and should be given as early as possible.^8,13 The NNT may be as low at 10 in this rare cohort.
• Factors with predictive value for PE-related cardiac arrest that, in combination, should support thrombolysis include (in order of decreasing odds ratio): initial non-shockable rhythm, prior thromboembolism, absence of cardiac history, and female gender.³
• Right heart strain, in isolation, should not be used to select for thrombolysis candidates, given its high incidence among all-comers in cardiac arrest.^16,18

References

1. Henriksson CE, Frithiofsson J, Bruchfeld S, Bendz E, Bruzelius M, Djärv T. In-hospital cardiac arrest due to pulmonary embolism – Treatment and outcomes in a Swedish cohort study. Resusc Plus. 2021 Nov 1;8:100178. doi: 10.1016/j.resplu.2021.100178. PMID: 34766067; PMCID: PMC8571515.
2. Böttiger BW, Arntz H-R, Chamberlain DA, et al. Thrombolysis during resuscitation for out-of-hospital cardiac arrest. N Engl J Med. 2008;359(25): 2651-2662.
3. Bougouin W, Marijon E, Planquette B, Karam N, Dumas F, Celermajer DS, Jost D, Lamhaut L, Beganton F, Cariou A, Meyer G, Jouven X; Sudden Death Expertise Center. Factors Associated With Pulmonary Embolism-Related Sudden Cardiac Arrest. Circulation. 2016 Dec 20;134(25):2125-2127. doi: 10.1161/CIRCULATIONAHA.116.024746. PMID: 27994026.
4. Quan ML, Pinto DJP, Smallheer JM, Ewing WR, Rossi KA, Luettgen JM, Seiffert DA, Wexler RR. Factor XIa Inhibitors as New Anticoagulants. J Med Chem. 2018 Sep 13;61(17):7425-7447. doi: 10.1021/acs.jmedchem.8b00173. Epub 2018 May 18. PMID: 29775297.
5. Lott C, Truhlář A, Alfonzo A, Barelli A, González-Salvado V, Hinkelbein J, Nolan JP, Paal P, Perkins GD, Thies KC, Yeung J, Zideman DA, Soar J; ERC Special Circumstances Writing Group Collaborators. European Resuscitation Council Guidelines 2021: Cardiac arrest in special circumstances. Resuscitation. 2021 Apr;161:152-219. doi: 10.1016/j.resuscitation.2021.02.011. Epub 2021 Mar 24. Erratum in: Resuscitation. 2021 Oct;167:91-92. PMID: 33773826.
6. Panchal AR, Bartos JA, Cabañas JG, Donnino MW, Drennan IR, Hirsch KG, Kudenchuk PJ, Kurz MC, Lavonas EJ, Morley PT, O’Neil BJ, Peberdy MA, Rittenberger JC, Rodriguez AJ, Sawyer KN, Berg KM; Adult Basic and Advanced Life Support Writing Group. Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2020 Oct 20;142(16_suppl_2):S366-S468. doi: 10.1161/CIR.0000000000000916. Epub 2020 Oct 21. PMID: 33081529.
7. Yusuff HO, Zochios V, Vuylsteke A. Extracorporeal membrane oxygenation in acute massive pulmonary embolism: a systematic review. Perfusion. 2015 Nov;30(8):611-6. doi: 10.1177/0267659115583377. Epub 2015 Apr 24. PMID: 25910837.
8. Sharifi M, Berger J, Beeston P, Bay C, Vajo Z, Javadpoor S; “PEAPETT” investigators. Pulseless electrical activity in pulmonary embolism treated with thrombolysis (from the “PEAPETT” study). Am J Emerg Med. 2016 Oct;34(10):1963-1967. doi: 10.1016/j.ajem.2016.06.094. Epub 2016 Jun 30. PMID: 27422214.
9. Chan PS, Spertus JA, Kennedy K, Nallamothu BK, Starks MA, Girotra S. In-Hospital Cardiac Arrest Survival in the United States During and After the Initial Novel Coronavirus Disease 2019 Pandemic Surge. Circ Cardiovasc Qual Outcomes. 2022 Feb;15(2):e008420. doi: 10.1161/CIRCOUTCOMES.121.008420. Epub 2022 Jan 31. PMID: 35098727; PMCID: PMC8852282.
10. Høybye M, Stankovic N, Holmberg M, Christensen HC, Granfeldt A, Andersen LW. In-Hospital vs. Out-of-Hospital Cardiac Arrest: Patient Characteristics and Survival. Resuscitation. 2021 Jan;158:157-165. doi: 10.1016/j.resuscitation.2020.11.016. Epub 2020 Nov 19. PMID: 33221361.
11. Mell HK, Mumma SN, Hiestand B, Carr BG, Holland T, Stopyra J. Emergency Medical Services Response Times in Rural, Suburban, and Urban Areas. JAMA Surg.2017;152(10):983–984. doi:10.1001/jamasurg.2017.2230
12. Julie Washington cleveland.com. ‘do something about this:’ one drug treatment cost $45,500; why prescription drug prices are so high and vary so much. Cleveland. https://www.cleveland.com/business/2021/11/one-drug-treatment-cost-45500-heres-why-prescription-prices-are-so-high-and-vary-so-much.html. Published December 1, 2021. Accessed November 17, 2022.
13. Javaudin F, Lascarrou JB, Le Bastard Q, Bourry Q, Latour C, De Carvalho H, Le Conte P, Escutnaire J, Hubert H, Montassier E, Leclère B; Research Group of the French National Out-of-Hospital Cardiac Arrest Registry (GR-RéAC). Thrombolysis During Resuscitation for Out-of-Hospital Cardiac Arrest Caused by Pulmonary Embolism Increases 30-Day Survival: Findings From the French National Cardiac Arrest Registry. Chest. 2019 Dec;156(6):1167-1175. doi: 10.1016/j.chest.2019.07.015. Epub 2019 Aug 2. PMID: 31381884.
14. Paul JA, Panzer OPF. Point-of-care Ultrasound in Cardiac Arrest. Anesthesiology. 2021 Sep 1;135(3):508-519. doi: 10.1097/ALN.0000000000003811. PMID: 33979442.
15. Reynolds JC, Del Rios M. Point-of-care cardiac ultrasound during cardiac arrest: a reliable tool for termination of resuscitation? Curr Opin Crit Care. 2020 Dec;26(6):603-611. doi: 10.1097/MCC.0000000000000766. PMID: 33002970.
16. Teran F, Dean AJ, Centeno C, Panebianco NL, Zeidan AJ, Chan W, Abella BS. Evaluation of out-of-hospital cardiac arrest using transesophageal echocardiography in the emergency department. Resuscitation. 2019 Apr;137:140-147. doi: 10.1016/j.resuscitation.2019.02.013. Epub 2019 Feb 16. PMID: 30779977.
17. Fields JM, Davis J, Girson L, Au A, Potts J, Morgan CJ, Vetter I, Riesenberg LA. Transthoracic Echocardiography for Diagnosing Pulmonary Embolism: A Systematic Review and Meta-Analysis. J Am Soc Echocardiogr. 2017 Jul;30(7):714-723.e4. doi: 10.1016/j.echo.2017.03.004. Epub 2017 May 9. PMID: 28495379.
18. Do D.H., Yang J.J., Kuo A. Electrocardiographic right ventricular strain precedes hypoxic pulseless electrical activity cardiac arrests: looking beyond pulmonary embolism. 2020;151:127–134.
19. Soar J, Böttiger BW, Carli P, Couper K, Deakin CD, Djärv T, Lott C, Olasveengen T, Paal P, Pellis T, Perkins GD, Sandroni C, Nolan JP. European Resuscitation Council Guidelines 2021: Adult advanced life support. Resuscitation. 2021 Apr;161:115-151. doi: 10.1016/j.resuscitation.2021.02.010. Epub 2021 Mar 24. Erratum in: Resuscitation. 2021 Oct;167:105-106. PMID: 33773825.

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Authors: Matt Kostura, MD (Staff Physician, Emergency Services Institute of the Cleveland Clinic Foundation, Assistant Professor of Emergency Medicine, and Assistant Program Director CWRU/Metrohealth Medical Center/Cleveland Clinic Emergency Medicine Residency Program), Courtney Smalley, MD (Staff Physician, Emergency Services Institute of the Cleveland Clinic Foundation, Associate Professor of Emergency Medicine, and Assistant Program Director CWRU/Metrohealth Medical Center/Cleveland Clinic Emergency Medicine Residency Program) // Reviewed by: Marina Boushra, MD (Staff Physician, Emergency Services Institute of the Cleveland Clinic Foundation); Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Case 1:

A 58-year-old male with a history of CAD, HTN, and a 40-pack-year smoking history presents to the emergency department (ED) for shortness of breath (SOB).  His SOB has been progressive for one week but has acutely worsened over the last day.  The patient has associated chest tightness, wheezing, and worsening of chronic leg swelling.  He was treated two months ago for bronchitis. HE tried using some nebulized albuterol at home but his symptoms persisted, prompting the ED visit.  The patient is vaccinated against COVID and he was infected with COVID one year ago.

Vital signs on arrival to the ED are HR 120 bpm, BP 76/42 mm Hg, RR 30 per minute, O2 87% on room air, T 37.0 C (98.6F).   On exam, he has moderate respiratory distress with diminished breath sounds bilaterally and bilateral pitting edema to the lower extremities.  ECG is negative for STEMI and a stat portable CXR is negative for pneumonia, pneumothorax, or pulmonary edema.  While the differential diagnosis in this patient is broad, careful consideration in the next steps of resuscitation and management in order to “do no harm” is necessary.

Case 2:

A 47-year-old female with a history of pulmonary arterial hypertension (PAH) presents with a medication problem.  She woke up this evening with an alarm from her treprostinil pump.  She states that her continuous infusion of the medication stopped working about 2 hours prior to arrival and she is concerned that the central line is not working.  She tried flushing her PICC line but it does not flush or draw back.  She denies any symptoms currently but presents to the emergency department at 3 am because her pulmonologist told her that she can “get sick” if she does not take her medication.

Treprostinil is not a typical medication that is stocked in the ED pyxis and may not be available in small hospitals or community settings. Furthermore, the PICC team is not available in the middle of the night to troubleshoot her central line.

Clinical Relevance

Both of the above cases demonstrate patients with a history and presentation that is concerning for an acute right heart failure (RHF) exacerbation.  Early recognition of RHF and its underlying cause is a key component to the successful management of these patients in the ED.  The presentation of RHF may be complex, and the treatment and resuscitation of a patient with acute RHF differ from some of the other diagnoses that mimic this disease process.  This focused post will highlight the pearls and pitfalls of the ED management of RHF patients.  A more detailed review from which this post was based can be found here.⁸³

What is Right Heart Failure?

Right heart failure is defined as impaired right ventricular (RV) contractility due to myocardial dysfunction, elevated pressures, or volume overload.^1,83  RHF can result from many underlying conditions, some of which are listed in Table 1 below. ^8,83

The true prevalence of RHF is challenging to estimate as it depends on how RHF is defined.  Current literature suggests that RHF is observed in 3-9% of all acute heart failure admissions.^4-7 While RHF is rare compared to left heart failure (LHF), the presence of RHF contributes to patient morbidity and mortality.  Overall mortality from RHF is estimated to be between 6% to 14%.^4,5,83

RV Physiology

Understanding the basic physiology of the RV can aid the clinician in understanding and treating a patient with acute RHF.   About 75% of RV contraction occurs via longitudinal contraction, a bellows-like inward movement mechanism of the RV free wall that pulls the tricuspid annulus towards the cardiac apex.^14,15,83   In patients with normal physiology, the RV pushes against a highly compliant, low-resistance pulmonary vascular system, and therefore generating RV output requires only about one-fifth the amount of energy needed to generate LV output.¹⁶  Table 2 compares the physiology of the RV to the LV.

Table 2. Left and Right Ventricle Physiology. RV= right ventricle, LV = left ventricle, EF = ejection fraction, PVR = pulmonary vascular resistance, SVR = systemic vascular resistance ⁸³

RV systolic function is highly sensitive to changes in RV afterload.¹⁷  An acute RHF exacerbation often occurs due to an abrupt increase in RV afterload or a decrease in myocardial function, rather than an acute change in volume status or preload.^1,17 In an acute RHF exacerbation, the RV initially compensates by stretching, but this abrupt change in preload can worsen RV hemodynamics, causing patient decompensation.^1,25-27

Figure 1 outlines the cyclic physiology of a right heart failure exacerbation, noting examples of underlying causes of RHF and entry points into the cycle.⁸³  One key to understanding this cycle is that RV overdistention can lead to bulging of the interventricular septum into the LV and ultimately systemic hypotension (known as ventricular interdependence).^17,18  RV overdistention can be due to a maladaptive physiologic response to an acute increase in RV afterload or pulmonary vascular resistance (PVR), or it can be due to gradual volume overload in a patient with chronic RHF.^17,18  Systemic hypotension in a patient with RHF leads to worsening right coronary artery (RCA) perfusion of the RV, promoting more RV ischemia, and continuing the cycle of decompensation.^27,28

Figure 1. Cyclic physiology of right heart failure.  Ovals represent examples of underlying causes leading to right heart failure.  PVR = pulmonary vascular resistance, RV = right ventricle, RHF = Right heart failure, PE = Pulmonary Embolism, STEMI = ST-elevation myocardial infarction, RCA = right coronary artery⁸³

Pulmonary Hypertension

One of the common pathologic causes of chronic RHF is increased RV strain over time due to pulmonary hypertension (PH).^20,29,83   PH has been classically defined as mean pulmonary artery pressure greater than 25 mm Hg as measured by right heart catheterization.^30,83  While the gold standard of RV dynamic measurements is cardiac magnetic resonance imaging (MRI), an RV pressure greater than 35 mmHg on echocardiogram strongly suggests PH.^31,32

PH is caused by a number of etiologies, which are divided into five World Health Organization (WHO) sub-categories.^30,33

• Group 1: Pulmonary Arterial Hypertension – Rare, causes include underlying genetic conditions, infectious diseases such as HIV or schistosomiasis, toxins, or idiopathic
• Group 2: Chronic Left Heart Disease – Most common cause of PH
• Group 3: Chronic Lung Conditions – Second most common cause of PH
• Group 4: Sequela of Thromboemboli
• Group 5: Multifactorial or unknown mechanisms

RHF is the leading cause of death in patients with PAH.^20,34  A patient with PH can be “tipped” into the cycle of acute RHF by a number of underlying mechanisms.

 ED Presentation and Evaluation

The most common complaint in patients with PH is dyspnea.^35,83  Depending on the severity of RHF, the patient may also present with chest pain, fatigue, peripheral edema, or lightheadedness.^35.83  Syncope and pre-syncope in a patient with PH or RHF are concerning and warrant further evaluation for dysrhythmia, valvular pathology, and elevated RV pressures.^25,83

The following labs and imaging studies can aid the clinician in the initial workup of a patient with RHF.  If the patient has underlying PH or chronic RHF, trending labs may be useful.⁴⁰

• CBC
• CMP
• Cardiac markers including troponin and brain natriuretic peptide (BNP)
• Chest X-ray (CXR)
• ECG
• Echocardiogram

There are no specific findings on ECG to diagnose RHF or PH. Common ECG findings in patients with PH include the following:^{41,42, 83}

• Right axis deviation
• Right bundle branch block
• Normal sinus rhythm
• ST depression or T wave inversions in V1 and the inferior leads

Imaging studies such as CXR may aid in the diagnosis of RHF.  CXR findings in a patient with chronic RHF include the following and are demonstrated in Figure 2:^45,46

• RV enlargement
• Globular cardiac silhouette with loss of the retrocardiac space
• Enlarged right atrium with rightward displacement of the cardiac silhouette beyond the spine

Figure 2. CXR in a patient with chronic right heart failure due to pulmonary arterial hypertension.

POCUS in RHF

Point of care cardiac ultrasound (POCUS) is a valuable tool in a patient with suspected RHF, not only to look for signs of acute RHF but also to identify other causes of the patient’s symptoms that may mimic RHF. POCUS assessments particular to RHF include an assessment of the following:⁴⁸

• RV free-wall thickness
• Inferior vena cava (IVC) size and respirophasic variability
• RV to LV ratio
• Tricuspid annular plane of systolic exertion (TAPSE)
• Interventricular wall flattening

A normal RV wall is less than 5mm and is ideally measured in the subxiphoid view such as demonstrated in Figure 3.⁴⁹  A thickened free wall indicates chronic RV failure which can be due to a number of underlying causes.⁴⁹

Figure 3. Thickened RV free-wall measured in a subxiphoid view in a patient with chronic RHF.⁸³

An IVC diameter greater than 2.1 cm and less than 50% collapse with patient sniff suggests high right atrial pressures.⁴⁹  In acute RHF, this may indicate excess volume or an acute change in RV afterload, but interpretation should be clinically correlated with the patient’s history and physical examination.^44,83  IVC measurements are more difficult to interpret clinically in a patient with chronic PH.⁸³  Video 1 demonstrates a dilated IVC with minimal respiratory variation in a patient who is volume overloaded.⁸³

Video 1. POCUS with dilated IVC and minimal respirophasic variation.⁸³

Video 1- Dilated IVC

The overall RV size and the ratio of the RV to the LV can be measured in an apical 4-chamber cardiac view at the base of the heart in end-diastole.  A normal RV to LV ratio is 0.6:1.0 .^48,52  An RV to LV ratio of 1:1 or an RV basal diameter greater than 41 mm is concerning for RV dilation.^48,49  Video 2 demonstrates a dilated RV in a patient with chronic RHF.⁸³

Video 2. Dilated RV on apical 4 chamber view in a patient with chronic RHF.⁸³

Video 2 – A4ch

TAPSE measurement gives an assessment of RV systolic function due to the bellows-like motion of the RV contraction.^48,49  TAPSE is measured by placing the M mode cursor over the lateral portion of the tricuspid annulus in an apical 4-chamber view.⁴⁹  Normal measurement from peak to valley of the tricuspid motion in M-mode is greater than 17 mm.^49,53   Figure 5 demonstrates a normal TAPSE measurement.   Limitations of TAPSE measurement include decreased accuracy in patients with regional differences in RV function, inability to distinguish between acute and chronic RHF, and the numerical value can be affected by the angle of the M-mode cursor over the tricuspid annulus.^49,50

Figure 4. The blue lines in the M-mode image demonstrate a normal TAPSE measurement, which in this case was 23 mm.⁸³

Finally, the parasternal short-axis view can be used to assess for interventricular flattening or RV bulging.  Interventricular flattening is also known as the “D-sign”, as the LV takes on a D shape, rather than the circular shape in normal physiology.⁴⁹  In extreme build-up of RV volume or pressure, septal dyskinesia may be present, in which the RV bulges into the LV, thus compromising the patient’s hemodynamics.⁴⁹  Video 3 shows a patient with acute on chronic RHF with volume overload and interventricular flattening on the parasternal short axis view.⁸³

Video 3. Parasternal short axis view in a patient with acute on chronic RHF who is volume overloaded. Note the “D” shape to the RV and LV.⁸³

Video 3 – PSAX

ED Management of RHF

RHF can present acutely with signs of cardiogenic shock or more insidiously.^20,25,83  One of the tenets of management of an acute RHF exacerbation is to find, treat, and reverse the underlying cause.  The underlying causes of an RHF exacerbation can include the following:

• STEMI
• Massive Pulmonary Embolism
• Arrhythmia
• Medication non-compliance in a patient with chronic RHF
• Sepsis
• GI bleeding
• Acute respiratory illness / COPD exacerbation

While searching for the underlying cause of RHF, it is important to manage the patient’s “ABCs” (airway, breathing, and circulation).  Placing a hypoxic RHF patient on supplemental oxygen is helpful for resuscitation.⁷⁵  More advanced airway adjuncts such as high flow nasal cannula (HFNC) or non-invasive positive pressure ventilation (NIPPV) may be needed to improve oxygenation. If possible, one should avoid intubating a patient with RHF, as positive pressure ventilation.⁷⁵  Patients with acute dysrhythmia such as atrial fibrillation benefit from rapid electrical cardioversion, as loss of atrial kick can further impair RV cardiac output.^24,55,83 If the ECG is concerning for an acute RV myocardial infarction, emergent coronary reperfusion is indicated, however nitrates or diuretics should be avoided, as the decrease in preload can result in patient decompensation.⁴⁴

Optimizing hemodynamics such as preload, afterload, and contractility is important in RHF in order to prevent further decompensation.^20,32

Preload

While a failing RV is preload dependent, hypotension does not necessarily mean the patient is hypovolemic, and an accurate assessment of volume status is necessary.^20,44  Patient history, physical exam, and POCUS findings should be synthesized to help a clinician decide if the patient needs fluids, diuresis, or nothing (indicating the patient is euvolemic).⁴⁴  If the patient appears intravascularly depleted, small boluses of isotonic fluids (250 ml boluses) and frequent patient reassessment are recommended to avois the risk of causing RV overdistention, i.^32,44

Afterload

The afterload of the RV is dependent on the pulmonary vascular resistance (PVR).¹⁷  Areas of the lung that are hypoxic and acidotic will lead to pulmonary vasoconstriction, increasing PVR, and thus increasing RV afterload.  So optimizing oxygenation such as with HFNC or improving respiratory acidosis with nebulized beta-agonists can improve RV afterload.^32,55  However, intubation increases intrathoracic pressure which decreases RV preload and worsens RV hemodynamics.^55,75  Thus intubation should be avoided if possible.^55,75  NIPPV may be an acceptable alternative in some patients with persistent hypoxia but even NIPPV can also affect preload so this should be carefully monitored.^20,55,75

Though evidence in RHF is limited, other medications that have the potential to reduce RV afterload are listed below.

• Inhaled nitric oxide – causes pulmonary vasodilation which can improve V/Q mismatch ⁶⁰
• Diuretics – hypervolemia increases afterload ⁵⁹
• IV pulmonary artery vasodilators (IV epoprostenol or IV treprostinil)
  • These infusions are reserved for patients with chronic PAH (Group 1 PH) and are not well studied in the acute RHF setting.⁶³
  • Withdrawal from IV pulmonary artery vasodilators can precipitate a pulmonary hypertension crisis and acute RHF, so if a chronic infusion stops, restart medication administration as soon as possible via a peripheral or central IV line.^25,65
• Inhaled epoprostenol – may not benefit all patients, but could be considered for acute RHF in consultation with an intensivist or pulmonology.⁷⁷

Contractility

Either dobutamine or milrinone can be used in a patient with acute RHF to increase contractility and lower PVR.^67,68  The lowest effective dose is recommended to decrease the risk of dysrhythmias or systemic hypotension, which can occur with either of these medications.⁷²

If systemic hypotension occurs due to any cause in a patient with RHF, one should quickly start IV vasopressors.³²  If the patient’s systolic blood pressure drops below RV pressures, right heart hemodynamics can quickly worsen and the patient may decompensate.^20,27-28  IV vasopressors to consider in an RHF patient with hypotension are listed below.

• Norepinephrine – First line ⁷²
• Vasopressin – Second line ⁷³
• Phenylephrine- NOT recommended as it worsens PVR ⁷⁴

Crashing Patient

In an ideal situation, one should recognize RHF early and treat the patient in a stepwise fashion as described here and summarized in Figure 6.⁸³  However some patients may present critically ill and require emergent intubation.  If intubation is required, it is recommended to be performed by the most experienced provider with a vasopressor infusion running during intubation or quickly available at the bedside.⁷⁸  The risk of intubation and mechanical ventilation is that the increase in intrathoracic pressure worsens preload and RV hemodynamics putting the patient at risk for cardiac arrest.^55,75  Therefore, if the patient is mechanically ventilated the following settings are recommended in order to limit the effects of positive pressure ventilation on the right heart.

• Low Tidal Volume ⁷⁸
• Low PEEP ⁷⁸
• Keep Plateau pressure < 30 mmHg ²⁵
• Avoid hypoxia and hypercapnia (leads to increased PVR) ^78,81

Keeping all of these goals in balance while preventing the patient from decompensating can be challenging, so consider early consultation with a pulmonary intensivist.

While the literature on extracorporeal membrane oxygenation (ECMO) in acute RHF is limited, it can be considered as a bridge while reversible causes are treated (such as a thrombectomy for a PE),or as a bridge to RV assist device implantation.⁸²  Mechanical RV assist devices (RVADs) are under study, but use is currently limited to end-stage disease or as a bridge to transplantation in patients with PH.^20,83

Most patients presenting with acute RHF will require admission to the ICU, depending on the severity of the disease and its underlying cause.

Figure 6. Summary of key management points in a patient presenting with acute RHF.⁸³

Case Resolutions

Case 1:  COPD exacerbation or PE are highest on the differential diagnosis at this point.  Nebulized beta-agonists are started and the patient is placed on HFNC with improvement in his oxygenation to 92%.  POCUS assessment is notable for a thin RV free wall, positive “D sign” on parasternal long axis view, a dilated IVC, and a TAPSE of 12 mm.  On chart review, the prior echocardiogram was notable for a normal LV ejection fraction, but moderately elevated RV systolic pressures.  There is concern for an acute PE, but given the patient’s current hypotension and POCUS findings, there is also a concern for acute RHF.  An IV infusion of norepinephrine is started to improve the patient’s BP to 90s/60s.  Dobutamine is also started to augment RV contractility prior to the patient going to the CT scanner.  CT angiogram of the chest is notable for acute PEs in the left and right pulmonary arteries.  A PE resuscitation team is consulted to decide on IV thrombolytics vs a thrombectomy and the patient is admitted to the medical ICU in critical but improved condition.

Case 2: Recalling the short half-life of treprostinil of 2-4 hours, it is important to mobilize the ED resuscitation team quickly to establish a good functioning peripheral IV.  Rather than waiting on the central pharmacy for a medication that the hospital may not carry, consider working with the patient to attach the treprostinil pump to the peripheral IV and begin the infusion.  The pump appears to be functioning well and the medication is successfully restarted.  It is imperative to ensure that she has an adequate supply of treprostinil with her for the next day.  The patient is then admitted to the hospital overnight so that the PICC team can replace her central line in the morning.

Pitfalls and Pearls

• Keep RHF on the differential diagnosis in patients with underlying pathology that affects the right heart and lungs.
• Treat the underlying cause of an acute RHF exacerbation while optimizing preload, afterload, and contractility.
• POCUS, along with patient history and physical exam, is key to assessing patient volume status.
• Dobutamine or milrinone can improve the contractility of the RV. Phenylephrine should be avoided when possible due to increase in PVR.
• Avoid systemic hypotension and be quick to use norepinephrine and/or vasopressin if the patient decompensates.
• Avoid intubation when possible, utilizing HFNC or NIPPV first, as mechanical ventilation worsens RV hemodynamics.

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Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 17-year-old male with history of asthma presents to the ED with a chief complaint of sore throat for the past 3 days, associated with decreased oral intake. He denies sick contacts. Vital signs include Temp 100.6F, BP 124/78, HR 92, RR 16, 96% on RA. On exam the patient has swollen, erythematous tonsils with grayish exudate, as well as enlarged, tender anterior and posterior cervical chain lymph nodes.

What is the most likely diagnosis?

Answer: Infectious mononucleosis ^[1-14]

Etiology

• Epstein-Barr Virus (EBV) is responsible for the vast majority (90%) of Infectious mononucleosis (IM) cases
  • EBV spreads through contact, typically via salivary secretions
  • Toy and utensil sharing in young children and kissing in adolescents are thought to be primary modes of transmission
  • Oral shedding persists for a median duration of 6 months after illness onset ^[1]
• Infectious mononucleosis is a syndrome marked by pharyngitis, cervical lymphadenopathy, and fever. Not all people who contract EBV will have the full syndrome or be symptomatic.
• Roughly 10% of individuals with IM will not have EBV as the causative agent ^[2]
  • Other viruses that may cause IM include CMV, HIV, Adenovirus, Hepatitis A, Toxoplasma, and Rubella

Epidemiology

• Estimated 90-95% of people worldwide become seropositive for EBV in their lifetime ^[3]
• Clinical prevalence of Infectious Mononucleosis (IM) peaks between 15 and 24 years of age ^[4]
  • The disease does not display seasonality ^[5]
  • A prospective study of primary EBV infection in college freshmen demonstrated 89% with symptomatic infection: 77% with full IM syndrome and 12% with atypical symptoms ^[1]
  • While primary EBV infection is common in young children, it is most often clinically asymptomatic, with <10% developing symptoms
• Differences in children and young adults regarding symptomatic infection are not fully understood, the size of viral inoculum at time of infection is considered a possible factor

Pathophysiology

• Initial spread via salivary secretions
• Once the virus has infected B cells in lymphoid areas in the oropharyngeal epithelium, it disseminates to the bloodstream ^[7]
  • EBV-infected B cells then disseminate infection throughout the lymphoreticular system, causing enlargement of lymphoid tissues
• Primary EBV infection of B lymphocytes induces an immunologic response in the form of circulating antibodies directed against the viral antigens and other unrelated antigens, including those found on sheep and horse red cells (heterophile antibodies) ^[8]
• This immunologic response is likely responsible for the clinical manifestations of IM

Clinical Features

• The most common signs and symptoms of IM include fever, pharyngitis, lymphadenopathy, and fatigue
• Physical exam may show pharyngeal inflammation, tonsillar exudates that are white, grey/green, or even necrotic appearing, and palatal petechiae
  • Palatal petechiae has 95% specificity for IM in patients with sore throat ^[9]
• Splenomegaly seen in 7-53% of patients with IM ^[9]
  • Splenic rupture is a rare but potentially fatal complication of IM
  • Estimated prevalence of 1-2 ruptures per thousand cases of IM ^[10]
  • Rupture most common in men who are <30 years old, with 84% occurring within 4 weeks of symptom onset^[11]
  • Systematic review demonstrated average time of rupture to be 14 days after symptom onset ^[11]
  • Rupture is spontaneous in 50% of cases
• Clinical variants of IM exist, including a “typhoidal form” which involves fever and lymphadenopathy without pharyngitis
  • These cases may be heterophile antibody negative
  • Possible causes of heterophile antibody negative IM include CMV, acute HIV, and toxoplasmosis
• The most important viral infection to differentiate from IM is acute HIV infection, as earlier diagnosis of HIV can make a significant difference in the outcomes for patients
  • abrupt onset of symptoms, including diarrhea or pharyngeal edema without associated tonsillar exudate or hypertrophy are features that help to distinguish acute HIV from EBV mononucleosis ^[12]
  • mucocutaneous ulcerations also help distinguish acute HIV from EBV mononucleosis.

Evaluation

Physical Examination

• Begin with evaluation of airway, breathing and circulation
• Evaluate face and exposed skin for presence of morbilliform rash
• Examine for cervical, axillary, and inguinal lymphadenopathy
  • Presence of posterior cervical, axillary, or inguinal adenopathy increase likelihood of IM diagnosis ^[9]
• Examine pharynx for tonsillar hypertrophy or exudates, inspect palate for presence of petechiae
• Examine abdomen for presence of splenomegaly or abdominal pain to palpation

Labs

• Labs that may assist with evaluation for IM include:
  • Elevated WBC, which may reveal increased lymphocyte count or presence of atypical lymphocytes
    • The presence of greater than 10% atypical lymphocytes significantly increases the likelihood of mononucleosis, especially when accompanied by lymphocytosis ^[9]
  • A self-limited rise in LFTs is seen in the majority of patients with IM
    • When coupled with pharyngitis abnormal LFTs strongly suggest IM
    • Routine testing for LFT elevation is not indicated, and there is not a need to trend LFTs in immunocompetent patients with IM ^[13]

DDX

• Cytomegalovirus infection, Toxoplasmosis, Strep pharyngitis, Neisseria gonorrhoeae, adenovirus infection, human immunodeficiency virus infection, acute leukemia ^[3]

Diagnosis

• Diagnosis can be suspected based on clinical exam findings listed above
• Heterophile antibody test or EBV specific antibody testing should be done to confirm diagnosis
  • Heterophile antibody testing may be falsely negative early in clinical course, as high as 25% falsely negative during first week of symptoms
  • Repeat testing or EBV-specific antibodies should be pursued when strong clinical suspicion exists
  • Diagnostic testing especially important in pregnant patients as CMV, HIV, and toxoplasma can have significant adverse effects ^[3]
• Confirming the diagnosis of EBV IM is helpful in that patients can be informed of rare complications of IM such as splenic rupture and airway obstruction. It can also help explain a prolonged course of fatigue.

Treatment

• Supportive care is the mainstay of primary EBV Infectious mononucleosis
  • NSAIDs (ibuprofen 400 mg PO q4-6h prn) or Acetaminophen (325mg PO q4-6h prn) for fever, pharyngitis, malaise
  • Adequate hydration and nutrition
• Use of corticosteroids are not typically recommended in IM except for certain indications, such as impending airway closure, or other severe/rare conditions such as aplastic anemia or fulminant liver failure
• Antivirals such as acyclovir have not been shown to have clinical benefit and should not be routinely used ^[14]
• Given the risk of splenic rupture, all patients should be advised to avoid contact sports or other similar activities for 4 weeks after symptom onset
  • Consider ultrasound of the spleen prior to return to play

Disposition

• Patients are typically safe for discharge home with outpatient follow up and return precautions

Summary and Pearls

• If a patient presents with mononucleosis-like syndrome but has abrupt onset of symptoms, diarrhea, or mucocutaneous lesions, consider HIV work up
• Axillary, inguinal, or posterior cervical adenopathy, palatal petechiae, and splenomegaly greatly increase likelihood of mononucleosis in the correct clinical setting
• Splenic rupture is a rare but potentially fatal effect of IM. The greatest risk is in males under the age of 30, within 4 weeks of symptom onset. Avoid contact sports for 4 weeks and give return precautions for any new-onset abdominal pain
• False-negative rate of heterophile antibody testing can be as high as 25% in first week of symptoms, consider repeat test or EBV specific antibody testing, especially for pregnant patients

Further Reading:

https://wikem.org/wiki/Infectious_mononucleosis

emDOCs.net – Emergency Medicine Education Splenic Infarction in Mononucleosis: Pearls and Pitfalls – emDOCs.net – Emergency Medicine Education

emDOCs.net – Emergency Medicine Education Strep Throat Mimics: Pearls & Pitfalls – emDOCs.net – Emergency Medicine Education

References:

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Welcome back to the “52 in 52” series. This collection of posts features recently published must-know articles. Our twentieth post looks at hyperbaric oxygen in CO toxicity.

Author: Christiaan van Nispen, MD (Emergency Medicine Physician Resident, San Antonio, TX) and Brannon Inman (Chief Resident, Emergency Medicine Physician, San Antonio, TX) // Reviewed by: Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

• Hyperbaric therapy significantly decreased the levels of plasma native thiols and total thiol levels, and normobaric oxygen therapy did not cause significant changes. Study authors conclude that hyperbaric therapy should therefore be titrated to minimal duration necessary to not excessively drive down antioxidant such as plasma native and total thiol levels.
• This study deals in exclusively non-patient centered outcomes – levels of antioxidants – with no mention of actual outcomes, other than mentioning all patients in all groups survived; it is unclear whether this change in plasma native and total thiol levels is clinically important.
• It appears that patients only received normobaric therapy if their carboxyhemoglobin level was less than 15% and not associated with cardiac or neurological compromise, so it is impossible to state if one is superior or even non-inferior to the other group. This study was not randomized; patients who were sick or had high Co-Hb levels went to hyperbaric therapy.
• Patients were excluded unless they were otherwise in perfect health, i.e., they could not have any chronic disease or use any medications at baseline, which is not realistic to normal patients.
• Overall, other reasons for being excluded were opaque (the flowchart of the study lists 22 patients as “exclusion,” then additional 7 as “other exclusion criteria”.
• Based on these data it does not appear that TDH is significantly impacted by hyperbaric therapy, though this may be impacted by the observational nature of the study, sample size, and practice patterns (sick CO poisoned patients go to the dive chamber).

My Take:

Though published in the journal Pediatric Emergency Care and related to an important emergency complaint of carbon monoxide poisoning, it remains unclear to what degree this would impact emergency department management. Respectfully, the study authors’ conclusion that hyperbaric therapy should be used for just the right amount of time to ensure clinical improvement/resolution is somewhat obvious without any of these data, just as any particular therapy for any illness should only be administered for the right amount of time to ensure resolution of that illness.

References:

1. Bagci Z, Arslan A, Neselioglu S. Pediatric Carbon Monoxide Poisoning: Effects of Hyperbaric Oxygen Therapy on Thiol/Disulfide Balance. Pediatr Emerg Care. 2022;38(3):104-107. Doi: 10.1097/PEC.0000000000002619

The post 52 in 52 – #20: Pediatric Carbon Monoxide Poisoning: Effects of Hyperbaric Oxygen Therapy on Thiol/Disulfide Balance appeared first on emDOCs.net - Emergency Medicine Education.

Today on the emDOCs cast with Brit Long, MD (@long_brit), we discuss necrotizing soft tissue infection pearls and pitfalls with Jess Pelletier, MD.

Jess is an emergency medicine physician and Education Fellow at Washington University School of Medicine. This second part looks at imaging and management of NSTI. For background, presentation, and laboratory evaluation, please see Part I.

Episode 66: NSTI Pearls and Pitfalls Part II

Pearl #5: Imaging has variable sensitivity for NSTI and can delay definitive operative management.

Pitfall: Relying on imaging to secure a diagnosis.

• NSTI is a clinical diagnosis; don’t wait for imaging to treat and speak with surgical specialist
• Plain radiographs may show gas, but sensitivity is 25-49%
• CT sensitivity is 80-88.5%, and specificity is 93.3-98%
• MRI has a sensitivity of 90-100% for NSTI when looking specifically at fascial thickening with T2 weighting
  • MRI is limited in availability and requires a significant amount of time, usually making it impractical

Pearl #6: POCUS may support the diagnosis of NSTI but is insufficient to exclude the condition.

Pitfall: Not utilizing POCUS in NSTI evaluation.

• POCUS can expedite the diagnosis
• “STAFF” mnemonic –  subcutaneous thickening, air and fascial fluid
• Fluid accumulation is likely the most reliable POCUS finding for NSTI, with a sensitivity of 42.3%-88.2% and a specificity of 93.3%; look for over 2 mm of fascial fluid

Pearl #7: Ensure the patient is hemodynamically optimized and has received antibiotics before transfer to the surgical suite.

Pitfall: Withholding antibiotic therapy if the diagnosis of NSTI is not entirely clear.

• ED management focuses on surgery consultation, aggressive fluid resuscitation, early broad-spectrum antibiotics, and initiation of vasopressors if fluid resuscitation does not maintain adequate perfusion
•  Delays to the surgical suite may lead to worsened spread of the underlying infection and subsequent increase in risk for amputation, hospital length of stay, and mortality
• Adjunctive therapies include hyperbaric oxygen and intravenous immunoglobulin (IVIG), but they remain controversial
  •  There are not currently evidence-based guidelines to endorse the use of either of the adjuvant therapies, and they should be considered on a case-by-case basis when and if available

Pearl #8: A definitive diagnosis can be made at bedside with a scalpel in some patients.

Pitfall: Failing to explore all avenues to help the patient with a NSTI achieve early surgical consultation and source control.

• The pathophysiology of NSTI involves tissue death at the microvascular level with rapid spread along fascial planes
• Clinicians can perform bedside incision after local anesthesia to assess for ‘dishwater’ fluid or the ability to use one’s finger to ‘probe’ the necrotic tissue without impedance usually encountered with intact fascia
  • Make a small incision (i.e. enough to insert a gloved finger) at the location of suspected NSTI (i.e. area is anesthetic, has dusky coloration, hemorrhagic bullae, or other signs of NSTI)
  • Confirmed diagnosis with ‘dishwater’ appearing fluid or if finger can be used to explore the wound freely in all directions with minimal resistance
• While this may not be needed if general surgery is readily, this technique can confirm the diagnosis and expedite transfer for definitive surgical management in institutions where surgical consultation is not possible

Pearl #9: Source control in NSTI is the most significant factor in reducing mortality.

Pitfall: Failure to appreciate the importance of early and aggressive source control.

• In all NSTI subtypes, inflammation of local tissues leads to microvascular thrombosis, preventing host immune cells from responding to the infection and leading to decreased tissue oxygen and necrosis
• Once this microvascular thrombotic process has progressed and local tissue perfusion is poor, antibiotics cannot effectively penetrate the infected tissues
• Source control is paramount and the primary variable affecting patient outcome in NSTI
• One 2017 retrospective study found a 46% reduction in mortality with surgical intervention
• Survival in NSTI is optimal when patients are taken for surgical debridement within 6 hours of diagnosis, but a survival benefit is still seen as long as surgery is performed within 24 hours

Summary:

• NSTI is a deadly spectrum of soft tissue infection
• Variety of risk factors: immunocompromise, diabetes, renal/liver disease, also chronic illness or recent surgery, but a significant number won’t have any risk factor
• Patients can have various presentations; look carefully for vital sign abnormalities, and make sure to perform a full skin exam
• Patients don’t always have bullae or crepitus
• Red flags: pain out of proportion, rapidly expanding erythema, and pain beyond the margin of the erythema
• Don’t rely on labs or the LRINEC score to rule out the disease
• Imaging can help, but it isn’t 100%, even CT
• US can provide some important clues at the bedside with the STAFF mnemonic
• Treatment focuses on source control, resuscitation, broad-spectrum antibiotics, and source control
  • If you’re concerned about the disease, get your surgeon down to the bedside
  • Source control is the most important factor in the prognosis

References:

1. Pelletier J, Gottlieb M, Long B, Perkins JC Jr. Necrotizing Soft Tissue Infections (NSTI): Pearls and Pitfalls for the Emergency Clinician. J Emerg Med. 2022 Apr;62(4):480-491.
2. Fernando SM, Tran A, Cheng W, et al. Necrotizing Soft Tissue Infection: Diagnostic Accuracy of Physical Examination, Imaging, and LRINEC Score: A Systematic Review and Meta-Analysis. Ann Surg. 2019;269(1):58-65. doi:10.1097/SLA.0000000000002774
3. Misiakos EP, Bagias G, Patapis P, Sotiropoulos D, Kanavidis P, Machairas A. Current Concepts in the Management of Necrotizing Fasciitis. Front Surg. 2014;1. doi:10.3389/fsurg.2014.00036
4. Peetermans M, de Prost N, Eckmann C, Norrby-Teglund A, Skrede S, De Waele JJ. Necrotizing skin and soft-tissue infections in the intensive care unit. Clin Microbiol Infect. 2020;26(1):8-17. doi:10.1016/j.cmi.2019.06.031
5. Montravers P, Snauwaert A, Welsch C. Current guidelines and recommendations for the management of skin and soft tissue infections. Curr Opin Infect Dis. 2016;29(2):131-138. doi:10.1097/QCO.0000000000000242
6. Stevens DL, Bryant AE. Necrotizing Soft-Tissue Infections. N Engl J Med. 2018;378(10):971. doi:10.1056/NEJMc1800049
7. Chen K-CJ, Klingel M, McLeod S, Mindra S, Ng VK. Presentation and outcomes of necrotizing soft tissue infections. Int J Gen Med. 2017;10:215-220. doi:10.2147/IJGM.S131768
8. Yen Z-S, Wang H-P, Ma H-M, Chen S-C, Chen W-J. Ultrasonographic screening of clinically-suspected necrotizing fasciitis. Acad Emerg Med Off J Soc Acad Emerg Med. 2002;9(12):1448-1451. doi:10.1111/j.1553-2712.2002.tb01619.x
9. Latifi R, Patel AS, Samson DJ, et al. The roles of early surgery and comorbid conditions on outcomes of severe necrotizing soft-tissue infections. Eur J Trauma Emerg Surg. 2019;45(5):919-926. doi:10.1007/s00068-018-0958-z
10. Wysoki MG, Santora TA, Shah RM, Friedman AC. Necrotizing fasciitis: CT characteristics. Radiology. 1997;203(3):859-863. doi:10.1148/radiology.203.3.9169717
11. Martinez M, Peponis T, Hage A, et al. The Role of Computed Tomography in the Diagnosis of Necrotizing Soft Tissue Infections. World J Surg. 2018;42(1):82-87. doi:10.1007/s00268-017-4145-x
12. Schmid MR, Kossmann T, Duewell S. Differentiation of necrotizing fasciitis and cellulitis using MR imaging. Am J Roentgenol. 1998;170(3):615-620. doi:10.2214/ajr.170.3.9490940
13. Hopkins KL, Li KC, Bergman G. Gadolinium-DTPA-enhanced magnetic resonance imaging of musculoskeletal infectious processes. Skeletal Radiol. 1995;24(5):325-330. doi:10.1007/BF00197059
14. Hakkarainen TW, Kopari NM, Pham TN, Evans HL. Necrotizing soft tissue infections: Review and current concepts in treatment, systems of care, and outcomes. Curr Probl Surg. 2014;51(8):344-362. doi:10.1067/j.cpsurg.2014.06.001
15. Kehrl T. Point-of-Care Ultrasound Diagnosis of Necrotizing Fasciitis Missed By Computed Tomography and Magnetic Resonance Imaging. J Emerg Med. 2014;47(2):172-175. doi:10.1016/j.jemermed.2013.11.087
16. Shyy W, Knight RS, Goldstein R, Isaacs ED, Teismann NA. Sonographic Findings in Necrotizing Fasciitis: Two Ends of the Spectrum. J Ultrasound Med. 2016;35(10):2273-2277. doi:10.7863/ultra.15.12068
17. Testa A, Giannuzzi R, De Biasio V. Case report: role of bedside ultrasonography in early diagnosis of myonecrosis rapidly developed in deep soft tissue infections. J Ultrasound. 2016;19(3):217-221. doi:10.1007/s40477-015-0155-4
18. Lin C-N, Hsiao C-T, Chang C-P, et al. The Relationship Between Fluid Accumulation in Ultrasonography and the Diagnosis and Prognosis of Patients with Necrotizing Fasciitis. Ultrasound Med Biol. 2019;45(7):1545-1550. doi:10.1016/j.ultrasmedbio.2019.02.027
19. Hadeed G, Smith J, O’Keeffe T, et al. Early surgical intervention and its impact on patients presenting with necrotizing soft tissue infections: A single academic center experience. J Emerg Trauma Shock. 2016;9(1):22. doi:10.4103/0974-2700.173868
20. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis Off Publ Infect Dis Soc Am. 2014;59(2):e10-52. doi:10.1093/cid/ciu444
21. Amphotericin B (Lipid Complex) (Lexi-Drugs). In: Lexicomp. ; 2021. http://online.lexi.com/?cesid=6BqX1UzCJn6&searchUrl=%2Flco%2Faction%2Fsearch%3Fq%3Damphotericin
22. Levett DZ, Bennett MH, Millar I. Adjunctive hyperbaric oxygen for necrotizing fasciitis. Cochrane Emergency and Critical Care Group, ed. Cochrane Database Syst Rev. Published online January 15, 2015. doi:10.1002/14651858.CD007937.pub2
23. Kadri SS, Swihart BJ, Bonne SL, et al. Impact of Intravenous Immunoglobulin on Survival in Necrotizing Fasciitis with Vasopressor-dependent Shock: A Propensity-Score Matched Analysis from 130 US Hospitals. Clin Infect Dis. Published online December 29, 2016:ciw871. doi:10.1093/cid/ciw871
24. Wang T-L, Hung C-R. Role of tissue oxygen saturation monitoring in diagnosing necrotizing fasciitis of the lower limbs. Ann Emerg Med. 2004;44(3):222-228. doi:10.1016/j.annemergmed.2004.03.022
25. Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA. 2016;315(8):801. doi:10.1001/jama.2016.0287
26. Martínez ML, Ferrer R, Torrents E, et al. Impact of Source Control in Patients With Severe Sepsis and Septic Shock*: Crit Care Med. 2017;45(1):11-19. doi:10.1097/CCM.0000000000002011
27. McHenry CR, Piotrowski JJ, Petrinic D, Malangoni MA. Determinants of Mortality for Necrotizing Soft-Tissue Infections: Ann Surg. 1995;221(5):558-565. doi:10.1097/00000658-199505000-00013
28. Freischlag JA, Ajalat G, Busuttil RW. Treatment of necrotizing soft tissue infections. The need for a new approach. Am J Surg. 1985;149(6):751-755. doi:10.1016/s0002-9610(85)80180-x
29. Bucca K, Spencer R, Orford N, Cattigan C, Athan E, McDonald A. Early diagnosis and treatment of necrotizing fasciitis can improve survival: an observational intensive care unit cohort study: Early diagnosis and treatment of NF. ANZ J Surg. 2013;83(5):365-370. doi:10.1111/j.1445-2197.2012.06251.x

The post emDOCs Podcast – Episode 66: NSTI Pearls and Pitfalls Part II appeared first on emDOCs.net - Emergency Medicine Education.

Authors: Joseph R. Peters, DO, RDMS and Jeremy Owens, DO (Department of Emergency Medicine, OSF St Francis Medical Center, University of Illinois College of Medicine, Peoria, IL) // Reviewed by: Stephen Alerhand, MD (@SAlerhand), Brit Long, MD (@long_brit)

Introduction

Acute Aortic Dissection (AAD) is a life-threatening emergency requiring rapid diagnosis and treatment.  AAD is an uncommon condition with an incidence of 1– 4/100,000 per year (1).  Acutely, the mortality approaches 1–2% per hour over the first 24 – 48 h in Stanford type A dissection. (1) More than 90% of aortic dissections present with acute pain. (7)  In one study, the most common misdiagnosis was acute coronary syndrome (6).  Neurologic deficits have been reported to occur in 13–42% of patients with AAD; ischemic stroke being the most frequent complication, occurring in 6–32% of patients. (3) Point of care ultrasound (POCUS) is a bedside diagnostic modality that Emergency Physicians (EPs) can incorporate into crisis care presentations, providing the ability to more rapidly differentiate critical illnesses, mobilize consultants, and implement accurate decision-making during patient care.

Case

A 54-year-old female with no past medical history arrived in the ED unresponsive, post seizure, hypotensive.  The patient was found by EMS on the floor of her office unresponsive to verbal stimuli, demonstrating a fixed leftward gaze of both eyes and dense paralysis of her right arm and leg.  The patient seized during transport just before arriving at the emergency department.  Field glucose was 122mg/dl.  Vital signs on arrival T 98.1, BP 78/48, HR 105, RR 10, 96% on room air.

In the ED, the patient was not responsive to verbal interaction, but she did withdraw her left arm and leg when noxious stimuli were applied.  Her right arm and leg were flaccid on exam.  EMS personnel emphasized their concern for acute stroke; however, coworkers had also reported to them that the patient “cried out” she was experiencing chest pain before collapsing unresponsive.  Further exam revealed the patient lacked palpable pulses in either radial artery, the right ankle, or right foot, but was found to have a strong pulse in the left ankle and left foot.  Although bilateral arm blood pressures indicated hypotension, blood pressure was 235/96 in the left leg.

The patient was intubated, and a POCUS echocardiogram was performed.  The parasternal long axis view identified a dilated aortic root, measuring 5cm. (Img. 1) This finding prompted EPs to ultrasound the aortic arch, the carotid arteries, and the abdominal aorta in search of dissection flaps.  Dissection flaps were visualized in the aortic arch and in the right common carotid artery.  The descending abdominal aorta could not be visualized due to bowel gas conditions, likely related to bag-valve-mask therapy in route.  A cardiothoracic surgeon was consulted immediately and met the patient at the CT scanner within minutes of her arrival.

   (Img. 1) PSLAX aortic root ~5cm.                                                       (Img. 2) Normal aortic root appearance.

Discussion

As is often the case in crisis-care presentations, the differential diagnosis in this patient was extensive and included multiple etiologies: massive pulmonary embolism, cardiac arrest, acute stroke, a postictal state with Todd’s paralysis, AAD, syncope with brain injury from fall.  Limited history in combination with blood pressure atypical for a stroke presentation (hypotension) created a high-stakes, diagnostic challenge.  Point-of-care ultrasound (POCUS) identified the etiology of this stroke presentation within minutes of arrival.   CT angiogram subsequently confirmed the POCUS findings of a Stanford type A aortic dissection involving the aortic arch, with extension to the right brachiocephalic artery, right subclavian artery, right common carotid artery, left subclavian artery, and left common carotid with thrombus occlusion at its origin. Additionally, it revealed a 5.2cm ascending thoracic aneurysm and a 4.7 cm infrarenal abdominal aneurysm. (Img. 3) The AAD had diminished blood flow to both arms, the right leg, and caused complete occlusion of left common carotid artery resulting in a massive left hemispheric ischemic stroke.   CT brain was negative for hemorrhage.

(Img. 3)  CT scan acute aortic dissection, thoracic aneurysm and infrarenal AAA. 

Classic AAD symptoms have been described as severe (90%), abrupt (84-90%), sharp or tearing (64%), retrosternal or interscapular (50%), migrating (16%), down the back (46%) and maximal at onset. (8)  Not all cases of AAD present with classic symptoms, however, making the diagnosis challenging (2). Remarkably, chest pain is not an obligatory symptom of AAD and the frequency of pain-free dissections range between 5 to and 15%; especially in AADs with neurological sequelae. (5) In one study, 29% of patients presenting with AAD complained of neurologic symptoms including ischemic stroke (16%), spinal cord symptoms (1%), ischemic neuropathy (11%), hypoxic encephalopathy (2%), syncope (6%) and seizures (3%). (4)  Of these patients, one-third of the ischemic stroke patients did not have pain. (4)  In 50% of these patients the neurologic symptoms were transient. (4)  In addition, altered consciousness, alterations of speech or language may prevent recognition of pain as a symptom. (8)  Although AAD has been described as a less frequent cause of ischemic stroke, when present, right hemispheric strokes predominate related to the greater proximity of the right carotid axis with the aortic root, and bilateral strokes have been described (8).

FOCUS findings in AAD 

Ascending aortic dilation identified by Focused Cardiac Ultrasound (FOCUS) is approximately 70% sensitive for AAD, which outperforms the findings of aortic insufficiency on cardiac auscultation (44%), pulse deficit (19%), chest radiograph with wide mediastinum (62%) or electrocardiogram (ECG) findings (17-25%). (9) In one study, combining FOCUS with abdominal aorta POCUS identified 96.4 % of patients who presented with an aortic dissection. (10)  In this study, three signs from FOCUS to suggest AAD included: the presence of either a pericardial effusion, an intimal flap, or an aortic outflow track diameter greater than 3.5cm. (10) Investigators in this study also performed an abdominal aorta POCUS with the goal of identifying an undulating echogenic line (intimal flap) suggesting AAD.  These 4 criteria showed a sensitivity of 96.4% and specificity of 90.8% for AAD. (10)  FOCUS identifies multiple signs of AAD including dilated aorta, the presence of an intimal flap, pericardial effusion, and acute aortic regurgitation. (8)  A small case study also identified the presence of the Mercedes Benz sign of the aortic root identified on the subxiphoid view of the heart in patients presenting with AAD. (12)

POCUS reduces door-to-diagnosis time.

POCUS decreases door-to-diagnosis time of AAD. (11) Wang et al. evaluated 172 patients presenting to emergency departments (EDs). In this study, 72 patients received EP performed FOCUS exam and 55 patients in the control group did not.  They found a door-to-diagnosis time of 10.5 minutes in EP FOCUS group vs 79.0 minutes in the control group, with no adverse effect on door-to-targeted treatment or door-to-CTA times. (11) In our stroke patient, EUS identified a dilated aortic root, an intimal flap in the aortic arch, and the right carotid artery.  Diagnosis of AAD was made within minutes of arrival, prior to CT scanning or the administration of thrombolytic therapy.  Thrombolysis is an established therapy for selected patient with acute ischemic stroke within the narrow time window of 4.5 hours from onset of symptoms. (8)  AAD is an absolute contraindication for administration of thrombolytics with a 71% mortality in patients receiving TPA. (8)    EUS signs of AAD whether direct (intimal flap) or indirect (dilated aortic root, pericardial effusion, acute aortic regurgitation) are findings EPs can rapidly identify at the bedside with ultrasound.

POCUS AAD evaluation in stroke and chest pain presentations

Aortic-focused transthoracic echocardiography and abdominal aorta ultrasonography have been proposed as a rapid and noninvasive method to rule in AAD when considering fibrinolysis in suspected acute stroke or myocardial infarction presentations. (8)  Roudaut et al. investigated 763 patients with suspicion of AAD with transthoracic echocardiography (TTE).  Investigators diagnosed 128 cases of AAD confirmed by angiography, CT, surgery, or autopsy.  Two echocardiographic features were found to strongly suggest the diagnosis of thoracic aortic dissection included dilation of any segment of the thoracic aorta visualized, yielding a sensitivity of 95% and a specificity of 51%; and visualization of an intimal flap, which had a sensitivity of 67% and a specificity of 100%. (12, 13) The views used were parasternal long and short axis, apical views, and the suprasternal notch view.  Aneurysmal dilation of the aorta is frequently present in AAD, with approximately 90% of AAD patients having dilation of the aorta greater than 4 cm at the time of diagnosis. (9)  When aortic dissection is suspected, POCUS of the thoracic aorta, the carotid arteries, and the abdominal aorta may provide EPs signs of AAD as demonstrated in our case.

Echo Window:  Parasternal long axis view (PSLAX)

The PSLAX view of the heart is a standard echocardiographic window used in EUS.  The aortic root is identified at the basilar center of the heart, imaging well in this view. (Img. 2) The PSLAX is performed by placing the transducer over the long axis of the heart, in the 3^rd-5^th parasternal rib space.  The aortic outflow tract is visualized exiting the heart superiorly between the two neighboring basilar structures, the right ventricular outflow tract (RVOT) and the left atrium (LA) (Img. 2).  A normal aortic outflow tract measures < 3.8 cm (12) and appears similar in diameter to the RVOT and the LA by comparison. (Img. 2)  When the aortic outflow tract grossly appears to be the largest of the three basilar structures of the heart (Img. 1), the presence of thoracic aneurysm is considered, and the aortic root is scanned thoroughly for visualization of an intimal flap.   Intimal flaps appear as an undulating echogenic (white) line within the lumen of the aorta.   When present, intimal flaps can be visualized in both the long and short axis views of the aortic root as demonstrated in this 71-year-old patient with anterior chest pain and posterior interscapular pain. (Vid. 1)  When imaging the aortic root, cautious interpretation is required to avoid mistaking the motion of the aortic valve leaflets as dissection flaps.   In our stroke patient, the aortic root was approximately 5cm in diameter and no intimal flap was identified. (Vid. 2)

                              (Vid. 1) Aortic root intimal flaps.                                                          (Vid. 2) Dilated AO root, no flap.  Our case.       

The PSLAX view of the heart additionally provides the opportunity to visualize the descending thoracic aorta in the far field of the same image (Vid. 3).  The descending thoracic aorta normally appears as an oval anechoic structure located in the far field of the PSLAX view of the heart and can be assessed for the presence of an intimal flap.  This is an important area to image when considering Stanford Type B dissection, as it originates distal to the left subclavian artery and an intimal flap would not be present in the region of the more proximal aortic root, arch, or common carotid arteries.

               (Vid. 3) PSLAX descending thoracic Aorta                              (Img. 4)  Probe position suprasternal notch.

Suprasternal Notch Window

The suprasternal notch window (aortic arch view) allows for the identification of an intimal flap in the thoracic aortic arch.  This view is obtained by placing the transducer in the suprasternal notch, rotating the length of the probe between the left sternocleidomastoid muscle and the right clavicular head.  The ultrasound beam is then directed downward into the chest while gradually fanning the tail of the probe toward the patient’s right (US beam left), which directs the ultrasound beam to transect the long axis of the aortic arch in its anatomical leftward location. Often the patient’s chin must be rotated to the right or left to accommodate the tail of the US probe. (Img. 4)  The normal aortic arch and its branches (the right brachiocephalic artery, the left common carotid artery, and the left subclavian artery) appear as anechoic tubular structures. (Vid. 4) In Type A dissections an intimal flap appears as a pulsatile echogenic linear line visible within the aortic arch. (Vid. 5)  A diseased aortic arch may not image as succinctly as a healthy aortic arch due to tortuous changes; however, as seen in our patient, the intimal flap is clearly recognizable. (Vid. 5)

              (Vid. 4) Normal aortic arch and branches.                                  (Vid. 5) Our patient with aortic arch intimal flap.

Common Carotid Windows

Whether stroke symptoms are present or not, imaging the common carotid arteries offers another routine area to identify intimal flaps. EPs are typically familiar with the appearance of the common carotid arteries given these are imaged routinely during insertion of ultrasound guided internal jugular central venous catheters.  The common carotid arteries are imaged with the linear probe in short axis, sliding the probe from the clavicle to the angle of the jaw.  Normal common carotid artery lumens appear anechoic, but in the presence of an intimal flap, an echogenic pulsatile line is visible, as imaged in the right common carotid artery of our stroke patient. (Vid. 6)  Although an intimal flap was present in the right carotid artery, our patient had no left sided stroke findings.

EPs should also be aware that intimal flaps can be visualized in the common carotid arteries of patients diagnosed with AAD yet lacking stroke symptoms. This 56-year-old male complained of less than 5 minutes of sudden intense pain that radiated through his neck, chest, and abdomen to his right thigh.  He was pain free in the ED and stated his visit was prompted by the fact the episode made him transiently near syncopal.   POCUS evaluation of his heart, aortic arch, carotid arteries, and abdominal aorta identified a dilated aortic root and arch, an intimal flap in the right carotid artery with thrombus, and an intimal flap in the abdominal aorta. (Vid. 7)  The 71-year-old patient previously discussed with the dissection flaps identified in the aortic root also lacked stroke symptoms, however an intimal flap was present in his left common carotid artery.  (Vids. 8,1)

                (Vid. 6)  Right Carotid Intimal Flap.                           (Vid. 7) Intimal Flap Rt Carotid and Abdominal Aorta

Abdominal Aorta Window

POCUS of the abdominal aorta for the identification of abdominal aneurysm (AAA) is a commonly performed exam in the ED.  The abdominal aorta is typically imaged in both the long and short axis from the proximal celiac trunk to the distal aortic bifurcation.  Both Stanford type A and B dissections have the potential to dissect through the abdominal aorta and as a result, the abdominal aorta is another location to identify intimal flaps.  An abdominal aorta intimal flap is visible in this Type A dissection of a 64-year-old male who had sudden onset chest and back pain with non-ischemic ECG.   POCUS of the heart and the aortic arch were difficult to image due to his COPD hyperinflated lungs.  No intimal flaps were identified in his carotid arteries.  An intimal flap was discovered in his abdominal aorta and visible in both the long and short axis views. (Vid. 9)  In the Type B dissection of this 49-year-old female, an irregular appearing intimal flap is identified in the abdominal aorta proximal to the celiac trunk. (Vid. 10)  Given her writhing-pain appearance and young age, POCUS was utilized initially to evaluate for hydronephrosis of her left kidney but was not identified.  Subsequent imaging of the abdominal aorta revealed an intimal flap in her proximal abdominal aorta.  This finding immediately changed therapy and a contrast CT scan of the chest and abdomen revealed a Type B aortic dissection determined to be the sequela of chronically uncontrolled hypertension and use of cocaine. (Img. 5)

(Vid. 8)  Left Carotid Artery Dissection Flap                              (Vid. 9) Type A dissection abdominal aorta 

          (Vid. 10) Type B dissection abdominal aorta.                                   (Img. 5) Type B dissection abdominal aorta.

Summary

AAD with neurologic symptoms at onset is an uncommon presentation in the ED.  The neurologic symptoms may be transient, and up to one-third of these patients may present without pain. (4)  Stroke is a dreaded complication of AAD and can present with altered mental status or aphasia making the expression of pain impossible. (8) Patients presenting with stroke symptoms or thoracic pain demonstrating unusual combinations of vital signs or exam findings may harbor AAD as the etiology of their condition.  POCUS demonstrates the ability to rapidly rule in AAD in these patients via the identification of an intimal flap in any of the multiple locations the major arteries can be visualized: the aortic root, aortic arch, common carotid arteries, the descending thoracic aorta, and abdominal aorta.  A dilated aorta or pericardial effusion may represent an indirect sign that an AAD is present.  POCUS of the heart, the thoracic aortic arch, the carotid arteries, and abdominal aorta revealing these signs expedites advanced imaging, consultant mobilization, and accurate decision-making in the care of patients with AAD.

References

1. Fojtik JP, Costantino TG, Dean AJ. The diagnosis of aortic dissection by emergency medicine ultrasound. J Emerg Med. 2007;32(2):191-196.
2. Woo KM, Schneider JL.  High-Risk Chief Complaints I: Chest Pain—The Big Three. Emerg Med Clin N Am 2009; 27:685-712.
3. Kamouchi, M. Aortic Dissection as a Possible Underlying Cause of Acute Ischemic Stroke. Circulation. 2015;79: 1697-1698.
4. Gaul C, Dietrich W, Friedrich I, Sirch J, Erbguth FJ. Neurological symptoms in type A aortic dissections. Stroke 2007; 38: 292–297.
5. Gaul C, Dietrich W, Erbguth FJ. Neurological symptoms in aortic dissection: A challenge for neurologists. Cerebrovasc Dis 2008; 26: 1–8.
6. Hansen MS, Nogareda GJ, Hutchison SJ. Frequency of and inappropriate treatment of misdiagnosis of acute aortic dissection. Am J Cardiol. 2007 Mar 15;99(6):852-6.
7. Braverman AC. Aortic dissection: prompt diagnosis and emergency treatment are critical. Cleve Clin J Med. 2011 Oct;78(10):685-96.
8. Alonso JV, Martin D, Kinderman H, Farhad I, Swallow P, Siggers A. Acute ischemic stroke what is hidden behind? J Cardiol Cases. 2017 Aug 30;16(5):174-177.
9. Pare JR, Liu R, Moore CL, Sherban T, Kelleher MS Jr, Thomas S, Taylor RA. Emergency physician focused cardiac ultrasound improves diagnosis of ascending aortic dissection. Am J Emerg Med. 2016 Mar;34(3):486-92.
10. Gibbons R, Smith D, Mulflur M, Dai T, Satz W, Goett H, et al. 364 Point-of-Care Ultrasound for the Detection of Aortic Dissections in the Emergency Department. Annals of Emergency Medicine. 2017;70:S143.
11. Wang Y, Yu H, Cao Y, Wan Z. Early Screening for Aortic Dissection With Point-of-Care Ultrasound by Emergency Physicians: A Prospective Pilot Study. J Ultrasound Med. 2020 Jul;39(7):1309-1315.
12. Blaivas M, Sierzenski PR. Dissection of the proximal thoracic aorta: a new ultrasonographic sign in the subxiphoid view. Am J Emerg Med. 2002 Jul;20(4):344-8.
13. Roudaut RP, Billes MA, Gosse P, Deville C, Baudet E, Fontan F, Besse P, Bricaud H, Dallocchio M. Accuracy of M-mode and two-dimensional echocardiography in the diagnosis of aortic dissection: an experience with 128 cases. Clin Cardiol. 1988 Aug;11(8):553-62.

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Welcome back to the “52 in 52” series. This collection of posts features recently published must-know articles. Our nineteenth post looks at the relationship between pediatric temperature and heart rate.

Author: Brannon Inman (Chief Resident, Emergency Medicine Physician, San Antonio, TX) // Reviewed by: Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Take Aways:

• Overall, this was a fairly well-done look at the trends of heart rate and temperature with a large sample size. Pediatric patients of all ages were well represented.
• This was a single center in Japan and may not represent the patients in other countries.
• Most age groups displayed sigmoidal heart rate variability, except the youngest group. This may have been due to the differences in observed temperatures.
• This study focuses on otherwise well children. I think this is useful since when we look at the heart rate and decide if it’s proportional to the fever, it’s normally in patients we would like to discharge.
• Unfortunately, it appears many of the temperatures were obtained as axillary temperatures as this was the primarily reported triage method. While I understand this, it called in to question accuracy. Axillary temperatures are notorious for discrepant measurements. However, to this paper’s credit, this is how (reportedly) all triage measurements were obtained.

My Take:

• Contrary to the traditional teaching that the heart rate increases about 10 bpm for each degree Celsius above normal, the heart rate and temperature relationship appears to be sigmoidal (at least based on this study).

Please the AAP pediatric fever update on emDOCs Pediatric Small Talk.

References:

1. Matsumura O, Morikawa Y, Kaneko T, Sakakibara H, Hagiwara Y. Relationship Between Body Temperature and Heart Rate in Children With No Other Apparent Cause of Tachycardia [published online ahead of print, 2022 Jan 18].Pediatr Emerg Care. 2022;10.1097/PEC.0000000000002617. doi:10.1097/PEC.0000000000002617

The post 52 in 52 – #19: Relationship Between Body Temperature and Heart Rate in Children With No Other Apparent Cause of Tachycardia appeared first on emDOCs.net - Emergency Medicine Education.

The post Medical Malpractice Insights: SAH 3 days after ED visit and a good MDM appeared first on emDOCs.net - Emergency Medicine Education.

Authors: Corey Hazekamp, MD (@coreyhazekamp, EM Resident Physician, Lincoln Emergency Medicine) and Tony Spadaro, MD (EM Resident Physician, University of Pennsylvania Emergency Medicine) // Reviewed by: Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit); and Marina Boushra,  MD

Case

A 46-year-old patient is evaluated in the  Emergency Department (ED) for vomiting. The patient is anxiously rocking back and forth on the stretcher and has an emesis basin filled with non-bloody, non-bilious vomit. The patient states that they are addicted to heroin and are withdrawing. The patient reports they feel anxious and have muscle aches everywhere. The patient’s clothes and shoes appear to be soiled and torn. When asked about their history of using medications for opioid use disorder, the patient reports they have tried methadone intermittently, but it has been over a year since they last used methadone. They have never tried buprenorphine. The patient admits to daily injection of heroin, denies daily consumption of alcohol because “they cannot afford it,” and denies use of any other illicit substances. When asked where the patient resides, they just respond ‘wherever I can find a place to sleep.” After further discussion, the patient states they are interested in trying buprenorphine as a medication for opioid use disorder.

Significance

The United States has recently experienced an unprecedented increase in opioid overdose deaths.¹ While the total number of ED visits for other medical emergencies decreased during the COVID-19 pandemic, the number of opioid overdose-related visits increased.^2,3  Medications for opioid use disorder (MOUD) have been shown to reduce morbidity and mortality for patients with opioid use disorder (OUD). However, most patients with OUD do not receive these life-saving treatments.^3–5 Furthermore, disparities in access to MOUD remain. For example, access to buprenorphine after discharge from an ED depends on the provider offering buprenorphine treatment and the patient having access to a physical location that offers buprenorphine. Research has shown that communities primarily composed of non-Hispanic Black or Hispanic residents are more likely to have access to methadone clinics and less likely to have access to buprenorphine providers.⁶ Kilaru et al. provided evidence suggesting that for patients who presented to the ED with a non-fatal opioid overdose, Black patients were approximately half as likely as non-Hispanic White patients to receive follow-up treatment for OUD.⁷ Similarly, women and Hispanic patients were less likely to receive follow-up for OUD treatment.⁷ More recently, Stevens et al. found that non-Hispanic Black patients and Hispanic patients had lower rates of filling buprenorphine prescriptions compared to non-Hispanic White patients when being prescribed buprenorphine from the ED.⁸ They also found that patients with socioeconomic advantages – being male, younger in age, and non-Hispanic White – were more likely to successfully receive buprenorphine as a treatment for OUD from EDs.⁸ These findings highlight that there are major disparities in accessing this life-saving medication and follow-up treatment, in addition to disparities in patients being offered buprenorphine.

Emergency Medicine will inevitably play a crucial role in the battle against the opioid epidemic currently ravaging the United States. Current and future emergency physicians will play a pivotal role in this effort. Accordingly, education on the effective treatment of OUD is essential. However, there are complexities involved in properly treating OUD from the ED. Physicians’ experiences in treating OUD are widely variable as there are no uniform protocols for initiating buprenorphine in the ED. The arrangement of follow-up treatment is also very different regionally. This article will review the basics of ED-initiated buprenorphine and summarize currently available resources for emergency physicians to learn how to properly offer patients buprenorphine initiation in the ED, how to overcome common barriers to ED-initiated buprenorphine, and how to find reliable long-term treatment for patients upon discharge.

The Basics

In 2015, the Journal of the American Medical Association published a randomized controlled trial showing that initiating buprenorphine in the ED increased treatment engagement, and reduced self-reported opioid use.⁹ In 2019, the Annals of Emergency Medicine published an expert clinical management manuscript covering the management of opioid withdrawal in the ED with buprenorphine.¹⁰ Finally, in 2021 the American College of Emergency Physicians (ACEP) released a consensus statement recommending that providers offer to treat opioid use disorder with buprenorphine in the ED.¹¹ Although some may perceive MOUD initiation as the role of outpatient providers, each additional step a patient must take before buprenorphine initiation leads to a drop-off in retention in treatment and exposes patients to a potential overdose death.¹²  Initiating buprenorphine in the ED has many beneficial effects for patients, including reducing acute care visits,  decreasing hospital readmissions, decreasing the use of non-prescribed opioids, and reducing all-cause mortality risk by 50%.^13–15

There are also clinical benefits for providers who initiate buprenorphine in the ED. Buprenorphine is a partial agonist at the m opioid receptor and a weak antagonist at the k opioid receptor, with a higher affinity for the m opioid receptor and a slow dissociation which results in a longer duration of action compared to other agonists.¹⁶ This partial agonist quality leads to a plateau effect on respiratory depression at higher doses^16,17 These specific properties confer a higher safety profile than other opioid agonists due to a ‘ceiling effect.’^16,17 Since buprenorphine will not act as a complete agonist and plateaus, there is minimal respiratory depression compared to other opioid agonists such as heroin, morphine, and fentanyl.^16,17 Furthermore there is minimal euphoria experienced by the patients leading to a decreased potential for abuse. Finally, compared to methadone, there is less of a risk of prolonging the QTc interval.^16–18 In summary, if a patient presents following the pharmacologic reversal of an overdose from an unknown opioid, buprenorphine use can treat opioid overdose or withdrawal symptoms from naloxone reversal and will decrease the risk of apnea. Buprenorphine can also be a safer option for treating opioid withdrawal compared to methadone or some supportive medications in patients who have electrolyte abnormalities or who use other QTc-prolonging medications.

Barriers

Though the Accreditation Council for Graduate Medical Education (ACGME) has set requirements for an Emergency Medicine Residency to be accredited, residency training occurs in highly variable environments. Emergency departments with established protocols for initiating buprenorphine in the ED are still a novelty. Accordingly, most current emergency medicine residents train in a department with no set protocol for initiating buprenorphine. Furthermore, there is no specific ACGME requirement or single resource for teaching residents how to initiate buprenorphine. There are no unified recommendations regarding the timing and dosing of buprenorphine. Guo et al. recently reviewed buprenorphine protocols nationwide, highlighting widespread variability and concluding that future research should focus on the variation in protocols and patient outcomes.¹⁹ In May 2022, the Annals of Emergency Medicine published the results of Project ED Health which highlights how four diverse urban, academic medical centers implemented different protocols for ED-initiated buprenorphine.²⁰ This manuscript provides a template, shown below, for departments to utilize as a protocol for ED-initiated buprenorphine.²⁰

Figure 1: Yale School of Medicine ED pathway to initiate buprenorphine (https://medicine.yale.edu/edbup/)

In addition to treatment algorithms, Yale School of Medicine Emergency Medicine also provides assessment tools and an overview of how to perform a brief negotiating interview. This resource also provides training videos for the screening brief intervention and referral to treatment (SBIRT) method for healthcare providers who are positioned to help patients with substance use disorders.

CA Bridge has a quick-start protocol that differs slightly from other published protocols in that it begins with higher doses of buprenorphine. CA Bridge protocol begins with 8-16 mg of buprenorphine as the starting dose for induction in the ED, as opposed to other protocols with initial doses of 4mg.

A recent review proposes a neuropharmacological working model to address the challenge of achieving opioid balance with the appropriate buprenorphine dose.²¹ This review covers different scenarios including macro-dosing and micro-dosing buprenorphine and presents data from clinical studies outlining the complexities of acute clinical success of buprenorphine induction.²¹ An emerging scenario in which macro-dosing buprenorphine induction in the ED may become more common is for patients who present with opioid-related complaints that are chronically exposed to fentanyl, which has different pharmacological properties than other opioids.²¹

Figure 2: CA Bridge ED Buprenorphine guide (https://cabridge.org/resource/buprenorphine-bup-hospital-quick-start)

For physicians who prefer to learn on shift and are eager to offer buprenorphine to their patients with OUD, MDCalc has the Emergency Department-Initiated Buprenorphine for Opioid Use Disorder (EMBED) tool, shown below, which provides a step-by-step assessment tool with next steps including order sets and discharge instructions.

Figure 3: MD Calc ED-Initiated Buprenorphine guide  (https://www.mdcalc.com/emergency-department-initiated-buprenorphine-opioid-use-disorder-embed)

The BUP Initiation App is available to be downloaded on cell phones. It provides an algorithm and next steps for providers initiating buprenorphine in the ED. If a provider has completed their X-waiver training, there is also an app called Buprenorphine Home Induction for unobserved buprenorphine induction. Using this app,  the patient will be prescribed buprenorphine with specific instructions for taking buprenorphine at home once they start to experience more severe withdrawal symptoms. It is worth noting that once X-waiver training is completed, it never expires. As such, residents can complete their X-waiver training in residency and apply for their X-waiver once a DEA license is obtained after training. Providers Clinical Support System provides free online X-waiver training. Additionally, the American Medical Association has partnered with the American Society of Addiction Medicine to offer a free mini-course on prescribing buprenorphine for healthcare providers.

For clinicians looking to initiate buprenorphine in the ED, the goal is to wait until mild-to-moderate withdrawal symptoms develop before the first dose of buprenorphine. From the Guo et al study, most sites surveyed recommended a minimum COWS score of 8.⁹ Additionally, for sites that did have recommendations for periods of abstinence from full opioid agonists before buprenorphine initiation, most recommended 12 hours for short-acting opioids, 24 hours for long-acting opioids, and 48-72 hours for methadone.⁹ While the optimal initial dose of buprenorphine is not known and likely depends on the degree of severity of withdrawal and risk of precipitated withdrawal., 4mg of buprenorphine is a common initial dose.²²

An additional barrier to prescribing buprenorphine is recency bias or the availability heuristic. Recency bias is a type of cognitive bias in which recent events are more likely to impact a decision or judgment more than distant events. EM physicians likely succumb to recency bias and heuristics daily. The Annals of Emergency Medicine published a manuscript on this topic in 2021, showing evidence that emergency physicians likely fall prey to the availability heuristic often.²³ To overcome this, physicians who have had a bad experience with one patient who has OUD should take care not to carry any bias from that experience into their next encounter with a patient who has OUD. Physicians’ attitudes and biases may very well be another barrier that is contributing to the slow adoption of ED-initiated buprenorphine around the nation. Developing a culture of prescribing buprenorphine for OUD in the ED and having local departmental champions can increase the confidence of individual prescribers in the ED initiating buprenorphine.²⁴ Financial incentives can also increase the uptake of X-waiver training in individual emergency departments, which will increase the number of clinicians who can prescribe buprenorphine.²⁵

Importantly, it is a misconception that ED clinicians cannot administer buprenorphine in the ED without an X-waiver. Short-term treatment with direct administration of an opioid approved for use in maintenance or detoxification (e.g. methadone and buprenorphine) in the ED is allowed under the Drug Addiction Treatment Act of 2000, and the patient may return to the ED daily to receive the medication for up to 72 hours under the “3-day rule.”¹⁰  Having patients return to the ED for additional doses of buprenorphine may also be helpful to have them present during hours when social workers or clinical resource managers will be available to help connect them to outpatient care.

Beyond

Ensuring safe and dependable follow-up for patients should be a priority for Emergency Physicians.  Follow-up care might be the most important component of ED-initiated buprenorphine. Follow-up availability can vary from state to state, region to region, and even hospital to hospital. A few options for mitigating this barrier are to familiarize oneself with local harm reduction clinics as some have buprenorphine clinics or at least know the providers in the area that prescribe buprenorphine. Physicians should research whether their hospital has an addiction team or a bridge clinic and if social work is able to help with managing the care of patients with OUD. Some communities are allocating significant resources to help improve access to buprenorphine. The New York City Department of Health and Mental Hygiene dedicated funding to establish the Buprenorphine Nurse Care Manager Initiative (BNCMI) to increase the capacity of primary care providers offering buprenorphine in safety-net settings.²⁶ This model proved to be highly successful in increasing access to buprenorphine for patients who reside in high-poverty neighborhoods comprised of primarily non-Hispanic Black and Hispanic populations. From 2016 to 2020 the BNCMI was able to enroll 1212 new patients, most of whom identified as Hispanic and had public health insurance coverage.²⁶ This model was adapted from the Massachusetts Model of Office-Based Opioid Treatment with Buprenorphine, as such, there might be similar initiatives in other states nationwide – something that would take minimal time for healthcare providers to familiarize themselves with. Cunningham et al. showed that despite the overwhelming increase in opioid overdoses during the COVID-19 pandemic, a primary care-based buprenorphine clinic was able to maintain OUD treatment for patients referred to their clinic and found that treatment retention improved during the pandemic compared to before the pandemic.²⁷

Martin et al. reviewed three different types of follow-up options providers can utilize after initiating buprenorphine in the ED: (1) the Project Alcohol and Substance Abuse Services and Referral to Treatment (ASSERT) model, (2) the Bridge model, and (3) the ED-Bridge model.²⁸ To summarize, the Bridge and the ED-Bridge models require buy-in from the department. In the Bridge model, the ED provider initiates buprenorphine, prescribes a short course of buprenorphine, and has a follow-up provider within the same hospital.²⁸ The ED-Bridge is a model in which a dual-trained Emergency Medicine/Addiction Medicine physician can screen and initiate buprenorphine in the ED and then provide longitudinal care.²⁸ The ASSERT model is an alternative that utilizes peer educators and community workers in the ED that help refer the patient to local addiction treatment services.²⁸

Depending on location, there may be a large referral system such as in New York and California. New York Medication for Addiction Treatment and Electronic Referrals (MATTERS) is a state-wide system to support ED-initiated buprenorphine and urgent referrals to long-term care.²⁹ CA Bridge is similar in that it provides follow-up options for patients throughout California who are initiated on buprenorphine. However, providers and patients may not have the luxury of a state-wide referral system for longitudinal treatment after buprenorphine initiation in the ED. The American Journal of Emergency Medicine recently published a manuscript showing the scalability of the SBIRT screening, treatment, and referral method.³⁰ This method is effective and generally easily implemented in EDs.³⁰ If physicians do not have access to a large referral network for follow-up treatment for patients with OUD, there may be harm reduction clinics nearby to which they can refer patients. If possible, physicians should  always discharge patients with OUD with naloxone. During the COVID-19 pandemic, telemedicine became a popular option to continue with treatment for patients utilizing MOUD.³¹ Weintraub et al. published results showcasing the utility of combining telemedicine with mobile treatment.³² They found that a combined telemedicine-mobile treatment model for the initiation of buprenorphine provided similar results to office-based telemedicine MOUD models.³² Although they primarily focused on the utilization of the combined telemedicine mobile treating model for rural populations, there is no reason this could not be applied for anyone, anywhere, anytime.

Summary

1 – Treating OUD in the ED matters. It is lifesaving, and it is the duty of physicians to offer patients the resources to get the help they need.

2 – The basics of ED-initiated buprenorphine are as easy as opening MDCalc

3 – Due to wide local variability, physicians should research available local resources for patients with OUD and how to arrange safe and reliable follow-up for patients with OUD.

References

1. Ahmad F, Rossen L, Sutton P. Provisional Drugs Overdose Death Counts.; 2021.
2. Soares WE, Melnick ER, Nath B, et al. Emergency Department Visits for Nonfatal Opioid Overdose During the COVID-19 Pandemic Across Six US Health Care Systems. Ann Emerg Med. 2022;79(2):158-167. doi:10.1016/j.annemergmed.2021.03.013
3. D’Onofrio G, Venkatesh A, Hawk K. The Adverse Impact of Covid-19 on Individuals with OUD Highlights the Urgent Need for Reform to Leverage Emergency Department–Based Treatment. Nejm Catal Innov Care Deliv. 2020;(May).
4. Rhee TG, D’Onofrio G, Fiellin DA. Trends in the Use of Buprenorphine in US Emergency Departments, 2002-2017. JAMA Netw open. 2020;3(10). doi:10.1001/jamanetworkopen.2020.21209
5. Hawk KF, D’Onofrio G, Chawarski MC, et al. Barriers and Facilitators to Clinician Readiness to Provide Emergency Department-Initiated Buprenorphine. JAMA Netw open. 2020;3(5). doi:10.1001/jamanetworkopen.2020.4561
6. Goedel WC, Shapiro A, Cerdá M, Tsai JW, Hadland SE, Marshall BDL. Association of Racial/Ethnic Segregation with Treatment Capacity for Opioid Use Disorder in Counties in the United States. JAMA Netw Open. 2020;3(4). doi:10.1001/jamanetworkopen.2020.3711
7. Kilaru AS, Kilaru AS, Xiong A, et al. Incidence of Treatment for Opioid Use Disorder following Nonfatal Overdose in Commercially Insured Patients. JAMA Netw Open. 2020;3(5). doi:10.1001/jamanetworkopen.2020.5852
8. Stevens MA, Tsai J, Savitz ST, et al. Trends and Disparities in Access to Buprenorphine Treatment Following an Opioid-Related Emergency Department Visit Among an Insured Cohort 2014-2020. JAMA Netw Open. 2022;5(6).
9. D’Onofrio G, O’Connor PG, Pantalon M V., et al. Emergency department-initiated buprenorphine/naloxone treatment for opioid dependence: A randomized clinical trial. JAMA – J Am Med Assoc. 2015;313(16):1636-1644. doi:10.1001/jama.2015.3474
10. Herring AA, Perrone J, Nelson LS. Managing Opioid Withdrawal in the Emergency Department With Buprenorphine. Ann Emerg Med. 2019;73(5):481-487. doi:10.1016/j.annemergmed.2018.11.032
11. Hawk K, Hoppe J, Ketcham E, et al. Consensus Recommendations on the Treatment of Opioid Use Disorder in the Emergency Department. Ann Emerg Med. 2021;78(3):434-442. doi:10.1016/j.annemergmed.2021.04.023
12. Khalid L, Cunninghma C, Deng Y, et al. Cascade of care for office-based buprenorphine treatment in Bronx community clinics. J Subst Abuse Treat. 2022;139(108778).
13. Wakeman SE, Larochelle MR, Ameli O, et al. Comparative Effectiveness of Different Treatment Pathways for Opioid Use Disorder. JAMA Netw Open. 2020;3(2). doi:10.1001/jamanetworkopen.2019.20622
14. Moreno JL, Wakeman SE, Duprey MS, Roberts RJ, Jacobson JS, Devlin JW. Predictors for 30-Day and 90-Day Hospital Readmission Among Patients With Opioid Use Disorder. J Addict Med. 2018;12(6). doi:10.1097/ADM.0000000000000437
15. Pearce LA, Min JE, Piske M, et al. Opioid agonist treatment and risk of mortality during opioid overdose public health emergency: Population based retrospective cohort study. BMJ. 2020;368. doi:10.1136/bmj.m772
16. Sporer KA. Buprenorphine: A Primer for Emergency Physicians. Ann Emerg Med. 2004;43(5). doi:10.1016/j.annemergmed.2003.11.006
17. Cisewski DH, Santos C, Koyfman A, Long B. Approach to buprenorphine use for opioid withdrawal treatment in the emergency setting. Am J Emerg Med. 2019;37(1). doi:10.1016/j.ajem.2018.10.013
18. Poole SA, Pecoraro A, Subramaniam G, Woody G, Vetter VL. Presence or Absence of QTc Prolongation in Buprenorphine-Naloxone among Youth with Opioid Dependence. J Addict Med. 2016;10(1). doi:10.1097/ADM.0000000000000176
19. Guo CZ, D’Onofrio G, Fiellin DA, et al. Emergency department‐initiated buprenorphine protocols: A national evaluation. J Am Coll Emerg Physicians Open. 2021;2(6):1-11. doi:10.1002/emp2.12606
20. Whiteside LK, D’Onofrio G, Fiellin DA, et al. Models for Implementing Emergency Department–Initiated Buprenorphine with Referral for Ongoing Medication Treatment at Emergency Department Discharge in Diverse Academic Centers. Ann Emerg Med. Published online 2022. doi:10.1016/j.annemergmed.2022.05.010
21. Greenwald MK, Herring AA, Perrone J, Nelson LS, Azar P. A Neuropharmacological Model to Explain Buprenorphine Induction Challenges. Published online 2022:1-16.
22. Spadaro A, Long B, Koyfman A, Perrone J. Buprenorphine precipitated opioid withdrawal: Prevention and management in the ED setting. Am J Emerg Med. 2022;58(August 2022):22-26.
23. Ly DP. The Influence of the Availability Heuristic on Physicians in the Emergency Department. Ann Emerg Med. 2021;78(5):650-657. doi:10.1016/j.annemergmed.2021.06.012
24. Lowenstein M, Kilaru A, Perrone J, et al. Barriers and facilitators for emergency department initiation of buprenorphine: A physician survey. Am J Emerg Med. 2019;37(9). doi:10.1016/j.ajem.2019.02.025
25. Foster SD, Lee K, Edwards C, et al. Providing Incentive for Emergency Physician X-Waiver Training: An Evaluation of Program Success and Postintervention Buprenorphine Prescribing. Ann Emerg Med. 2020;76(2). doi:10.1016/j.annemergmed.2020.02.020
26. Kaplan-Dobbs M, Kattan JA, Tuazon E, Jimenez C, Saleh S, Kunins H V. Increasing access to buprenorphine in safety-net primary care clinics: The new york city buprenorphine nurse care manager initiative. Am J Public Health. 2021;111(2). doi:10.2105/AJPH.2020.306000
27. Cunningham CO, Khalid L, Deng Y, et al. A comparison of office-based buprenorphine treatment outcomes in Bronx community clinics before versus during the COVID-19 pandemic. J Subst Abuse Treat. 2022;135. doi:10.1016/j.jsat.2021.108641
28. Martin A, Butler K, Chavez T, et al. Beyond Buprenorphine: Models of Follow-up Care for Opioid Use Disorder in the Emergeny Department. West J Emerg Med. 2020;21(6):257-263. doi:10.5811/WESTJEM.2020.7.46079
29. Irvine UC, Rachel A, Susan J. Implementing a Novel Statewide Network to Support Emergency Department-initiated Buprenorphine Treatment. Published online 2022. doi:10.5811/westjem.2022.3.54680
30. Monico LB, Oros M, Smith S, Mitchell SG, Gryczynski J, Schwartz R. One million screened: Scaling up SBIRT and buprenorphine treatment in hospital emergency departments across Maryland. Am J Emerg Med. 2020;38(7). doi:10.1016/j.ajem.2020.03.005
31. Buchheit BM, Wheelock H, Lee A, Brandt K, Gregg J. Low-barrier buprenorphine during the COVID-19 pandemic: A rapid transition to on-demand telemedicine with wide-ranging effects. J Subst Abuse Treat. 2021;131. doi:10.1016/j.jsat.2021.108444
32. Weintraub E, Seneviratne C, Anane J, et al. Mobile Telemedicine for Buprenorphine Treatment in Rural Populations with Opioid Use Disorder. JAMA Netw Open. 2021;4(8):1-11. doi:10.1001/jamanetworkopen.2021.18487

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Welcome to EM@3AM, an emDOCs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

Answers: Sigmoid Volvulus  

Epidemiology:

• A sigmoid volvulus is an uncommon but potentially life-threatening cause of large bowel obstruction (LBO). Representing only 5% of LBOs, a sigmoid volvulus may initially present with mild symptoms but can quickly result in large bowel perforation if left untreated.¹ 
• Patients with a sigmoid volvulus are most likely to be men with a mean age of 70 and a history of constipation.²
• Risk factors for a sigmoid volvulus include causes of sigmoid dilation such as Crohn’s disease, redundant colon, constipation, Hirschsprung’s disease and, more commonly in developing nations, Chagas disease.^3-5
• Immobility and altered mental status also contribute to constipation, dilating the sigmoid colon and setting the stage for a sigmoid volvulus. Up to 71% of sigmoid volvulus are associated with neuropsychiatric disease, supporting the association with incapacitation.⁶

Pathophysiology:

• A volvulus of the sigmoid colon occurs when an air-filled sigmoid torses around its mesenteric attachments. As the segment torses, the lumen becomes obstructed while stool and gas continue to fill the proximal colonic segment causing distention. If left untreated, the torsed segment’s vasculature can become impaired and result in bowel ischemia.⁸
• Additionally, the severity of the presentation may mirror the extent of torsion with 180º rotation blocking stool transit and 360º rotation sufficiently obstructing arterial flow to the tissue. In the absence of ischemia, the mortality rate of sigmoid volvulus is less than 5%; however, if arterial flow is compromised, bowel ischemia may result in gangrenous bowel which increases mortality to nearly 50%.⁷

Evaluation:

• A sigmoid volvulus will often present with symptoms of gradually worsening nausea, constipation, abdominal distention, and abdominal pain that can be colicky in nature associated with peristalsis.¹²
• The time course for a sigmoid volvulus to develop into a painful, distended abdomen is only a few days; however, gangrenous bowel and perforation may be seen early in the disease course and should be suspected in patients who present with fever, hemodynamic instability, or peritonitis.¹²
• On physical exam, the abdomen is expected to be distended and tympanic, potentially with diminished bowel sounds. A patient that presents with severe, sharp abdominal pain, fever, and abdominal rigidity is worrisome for gangrene that has resulted in perforation and peritonitis. 
• Classically, plain films are sufficient to diagnose a sigmoid volvulus. The distended sigmoid will appear as a dilated loop of bowel without haustral markings, absence of air in the rectum, and characteristically has a “bent inner-tube” or “U-shaped tube” appearance, called the “coffee bean sign.”⁹
• However, plain films only established the diagnosis of sigmoid volvulus in around 60% of cases because other causes of distal colon obstruction may present with similar radiographic findings.⁶ 
• CT abdomen/pelvis with contrast can be more appropriate to delineate sigmoid volvulus from other causes of distal colon obstruction such pseudo-obstruction (Ogilvie’s syndrome), toxic megacolon, and neoplastic disease.
• The abdominal CT will show a whirl pattern of the sigmoid due to the torsion of the mesentery and vessels as well as a “bird beak” appearance proximal and distal to the obstructed segment. While CT abdomen has 100% sensitivity and 90% specificity for sigmoid volvulus, emergent surgical intervention when required in the setting of bowel perforation and peritonitis should not be delayed for CT.⁹ 

Treatment:

• In addition to routine lab work such as CBC and CMP to assess for leukocytosis and secondary electrolyte abnormality, serum lactate is a useful marker for bowel ischemia. IV fluid resuscitation is indicated in patients with signs of shock or unstable vital signs. Early administration of broad-spectrum IV antibiotics after obtaining blood cultures is indicated to control bacterial translocation across ischemic intestinal wall. ¹²
• The relief of obstruction and prevention of recurrence are the two cardinal goals of sigmoid volvulus management.⁷ 
• Patients with alarming signs consistent with bowel perforation, bowel compromise, or peritonitis should receive emergent surgical intervention with resection and primary anastamosis.⁷ 
• In patients without alarming signs, the American Society of Colon and Rectal Surgeons recommends an endoscopic decompression via sigmoidoscopy, given that spontaneous detorsion is generally uncommon.^7,10
• A sigmoidoscope is placed with insufflation into the torsed segment and used to straighten the sigmoid, returning blood flow and patency to the lumen. Endoscopic decompression is effective in detorsion of approximately 85% of sigmoid volvuli.¹¹
• However, non-operative reduction of sigmoid volvulus does not constitute adequate treatment as high rates of recurrence and high mortality is associated with non-operative reduction¹ Elective resection of the sigmoid colon and anastomosis (ELRSA) is the gold standard with a mean mortality of 8%, a mean recurrence of 1.2% and a morbidity of 13–26%.⁷

Disposition: 

• Initial urgent sigmoidoscopy is important to de-torse the sigmoid volvulus. If detorsion is successful, prognosis is very good, and the patient can be admitted for observation and with planned elective surgical resection either inpatient or outpatient to prevent recurrence.
• Outcomes for sigmoid volvulus are significantly worse in patients who develop bowel gangrene; therefore, emergent surgical intervention is critical to patient outcomes in the setting of LBOs.

Pearls:

• Patients with suspected sigmoid volvulus that present with symptoms of bowel gangrene or perforation – hemodynamic instability, fever, obstipation, abdominal rigidity – require emergent surgical intervention. Manage ABCs, administer IV fluids and broad-spectrum
• Plain films are sensitive but are not specific for sigmoid volvulus. Look for the classic ‘coffee bean sign’. CT non-contrast can be used to confirm sigmoid volvulus or identify alternative causes of LBO. 
• Prognosis of sigmoid volvulus is good if detected early with initial treatment of endoscopic decompression via sigmoidoscopy. However, high rates of recurrence and high mortality is associated with solely non-operative reductions.
• Gold standard treatment for sigmoid volvulus involves elective resection of the sigmoid colon and anastomosis (ELRSA).

Further Reading:

The post EM@3AM: Sigmoid Volvulus appeared first on emDOCs.net - Emergency Medicine Education.

Welcome back to the “52 in 52” series. This collection of posts features recently published must-know articles. Our eighteenth post looks at pediatric ischemic and hemorrhagic stroke.

Author: Christiaan van Nispen, MD (Emergency Medicine Physician Resident, San Antonio, TX) and Brannon Inman (Chief Resident, Emergency Medicine Physician, San Antonio, TX) // Reviewed by: Alex Koyfman, MD (@EMHighAK); Brit Long, MD (@long_brit)

Take Aways:

• This is a review of the presentation, risk factors, and outcomes of pediatric strokes in a select, convenient sample of patients.
• Consider acute stroke in pediatric patients suffering hemiparesis or altered mental status, especially given the delay such patients seem to have experienced in this study in diagnosis.
• Important risk factors unsurprisingly included diseases involving anatomical variations of the vasculature, such as Moyamoya and AVMs. Risk factors in your patient population may vary, as this was in a select patient population in Asia.
• Limited discussion on medical management in the emergency department; study mentions imaging, and post-stroke antithrombotic prophylaxis. Moyamoya patients required encephalo-duro-arterio-synangiosis (EDAS). Otherwise, this study did not discuss emergency department based treatments such as blood pressure management or administration of parenteral thrombolytics. Likely care is regionally, and specialist dependent.
• The study could have done a better job elucidating outcomes; stating that a certain percentage of patients had persistent “neurological symptoms” is not as useful as stating specifically the prevalence of specific symptoms and how debilitating they were (such as by modified Rankin Scores).
• Study was limited by occurring at a single institution, thus limiting the generalizability of statistical findings.

My Take:

• Do not hesitate to order a stroke workup in pediatric patients, especially with concerning symptoms such as hemiparesis or altered mental state or if the patient has known abnormal vasculature.

Please see the awesome Pediatric Small Talk on Pediatric Stroke.

References:

1. Pangprasertkul S, Borisoot W, Buawangpong N, et al. Comparison of Arterial Ischemic and Hemorrhagic Pediatric Stroke in Etiology, Risk Factors, Clinical Manifestations, and Prognosis. Pediatr Emerg Care. 2022;38(9):e1569-e1573. doi: 10.1097/PEC.0000000000002614

The post 52 in 52 – #18: Comparison of Pediatric Arterial Ischemic and Hemorrhagic Stroke appeared first on emDOCs.net - Emergency Medicine Education.

Today on the emDOCs cast with Brit Long, MD (@long_brit), we discuss necrotizing soft tissue infection pearls and pitfalls with Jess Pelletier, MD.

Jess is an emergency medicine physician and Education Fellow at Washington University School of Medicine. This first part will look at some background, presentation, and laboratory evaluation for NSTI.

Episode 65: NSTI Pearls and Pitfalls Part I

Background:

• Necrotizing soft tissue infection is a collection of diseases.
• Incidence ranges between 0.024-0.045 per 1000 per year.
• Most patient are over age 50 years
• Variety of risk factors associated with NSTI
• Severe morbidity and mortality
  • Rate of limb loss is 16%
  • Mortality rate ranges between 20-100% without source control

Pearl #1: NSTI is a spectrum of diseases, of which necrotizing fasciitis is only one subtype.

Pitfall: Failure to understand the spectrum of pathology in NSTI.

• Type I: polymicrobial, most common, variety of risk factors (immunocompromised, pre-existing disease, older age)
• Type II: monomicrobial (Group A strep most common ,followed by  MRSA), less common overall, risk factors (trauma, surgery, IV drug use)
• Type III: monomicrobial (Vibrio or Clostridium spp.), rare, contaminated water exposure, hemodynamic collapse before skin changes
• Type IV: Fungal (Candida or Zygomycetes spp.), very rare, immunocompromised or penetrating trauma

Pearl #2: Chronic illness or recent surgery should raise clinician suspicion for NSTI.

Pitfall: Discounting NSTI in the patient without a classic history.

• There may or may not be an inciting agent like a skin wound or trauma
• Transient bacteremia from GU or GI tract could lead to tissue seeding
• Among those diagnosed with NSTI, 80% have a clear point of inoculation such as a bite, surgical incision, injection site, or perianal source
• Variety of risk factors (diabetes, renal/liver disease, IV drug use, immunocompromise), but 25% have no known risk factor for NSTI
• Accounts for 1-2/10,000 inpatient admissions; 1/350 patients who present with back pain to an ED will have a spinal emergency.
• The mortality for SEA approximates 5%; 50% have residual deficits, with worse outcomes the longer the delay in diagnosis.

Pearl #3: There is wide variability in the clinical presentation of NSTI.

Pitfalls: Performing an incomplete skin examination and prematurely excluding the diagnosis in the absence of major skin findings.

• NSTI is a clinical diagnosis, but many of the “classic” signs and symptoms are not present early in the disease course or will never occur.
• Nonspecific symptoms such as diarrhea, fatigue, loss of appetite, or malaise may precede the onset of skin findings in NSTI
• Pain is reported as the initial complaint in only 79% of cases
•  41-96% of NSTI cases are initially misdiagnosed as simple cellulitis or abscess
  •  Early skin findings may include mild erythema or edema
  •  Literature suggests swelling is the most common finding, followed by pain and erythema
  • Warmth, bullae, skin necrosis, and crepitus are less common findings
• Fever has a specificity of 77% but sensitivity less than 50%
• Shock/hypotension occurs in less than 1/4 at time of presentation
• Toxic shock syndrome (with hypotension, macular rash, and palm and sole desquamation) is associated with up to half of GAS-associated NSTI cases
• Fournier’s gangrene may present differently than other subtypes; initial symptoms include perineal pruritus and pain, and skin changes are late
• Subacute NSTI can occur, with progression over weeks to months

Pearl #4: Laboratory testing cannot be used to rule out NSTI due to its low sensitivity.

Pitfall: Waiting for results of laboratory testing when NSTI is suspected.

• Diagnosis should be based on history and exam; don’t delay treatment for laboratory assessment
• There is no single laboratory test with adequate sensitivity and specificity to differentiate NSTI from other infectious processes or exclude the diagnosis
• Adjunctive laboratory testing can assist in determining severity of illness (end-organ damage) and shaping the pre-test probability of NSTI
• Obtain complete blood count, complete metabolic panel, c-reactive protein, lactate, and blood cultures
• Scoring systems are available, including the Laboratory Risk in Necrotizing Fasciitis (LRINEC) score
  •  Higher LRINEC scores tend to occur in sicker patients, but one meta-analysis found that the LRINEC score was only 68% sensitive and 85% specific for a score of 6 and 41% sensitive and 95% specific for a score of 8
  • There have been case reports of patients with NSTI having LRINEC scores of 0
  • LRINEC score can assist in communicating with the surgical specialist, but don’t use it to exclude the diagnosis

That’s it for Part I. Stay tuned for Part II, which looks at imaging and management.

References:

1. Pelletier J, Gottlieb M, Long B, Perkins JC Jr. Necrotizing Soft Tissue Infections (NSTI): Pearls and Pitfalls for the Emergency Clinician. J Emerg Med. 2022 Apr;62(4):480-491.
2. Fernando SM, Tran A, Cheng W, et al. Necrotizing Soft Tissue Infection: Diagnostic Accuracy of Physical Examination, Imaging, and LRINEC Score: A Systematic Review and Meta-Analysis. Ann Surg. 2019;269(1):58-65. doi:10.1097/SLA.0000000000002774
3. Sin F, Yuen M, Lam K, Wu C, Tung W. A retrospective review of patients with necrotizing fasciitis presenting to an emergency department in Hong Kong. Hong Kong J Emerg Med. 2002;9(1):10-17.
4. Mitchell A, Williams A, Dzendrowskyj P. Necrotising fasciitis: an 8.5-year retrospective case review in a New Zealand intensive care unit. Crit Care Resusc J Australas Acad Crit Care Med. 2011;13(4):232-237.
5. Goh T, Goh LG, Ang CH, Wong CH. Early diagnosis of necrotizing fasciitis. Br J Surg. 2014;101(1):e119-125. doi:10.1002/bjs.9371
6. Misiakos EP, Bagias G, Patapis P, Sotiropoulos D, Kanavidis P, Machairas A. Current Concepts in the Management of Necrotizing Fasciitis. Front Surg. 2014;1. doi:10.3389/fsurg.2014.00036
7. Peetermans M, de Prost N, Eckmann C, Norrby-Teglund A, Skrede S, De Waele JJ. Necrotizing skin and soft-tissue infections in the intensive care unit. Clin Microbiol Infect. 2020;26(1):8-17. doi:10.1016/j.cmi.2019.06.031
8. Montravers P, Snauwaert A, Welsch C. Current guidelines and recommendations for the management of skin and soft tissue infections. Curr Opin Infect Dis. 2016;29(2):131-138. doi:10.1097/QCO.0000000000000242
9. Stevens DL, Bryant AE. Necrotizing Soft-Tissue Infections. N Engl J Med. 2018;378(10):971. doi:10.1056/NEJMc1800049
10. Chen K-CJ, Klingel M, McLeod S, Mindra S, Ng VK. Presentation and outcomes of necrotizing soft tissue infections. Int J Gen Med. 2017;10:215-220. doi:10.2147/IJGM.S131768
11. Wilson MP, Schneir AB. A Case of Necrotizing Fasciitis with a LRINEC Score of Zero: Clinical Suspicion Should Trump Scoring Systems. J Emerg Med. 2013;44(5):928-931. doi:10.1016/j.jemermed.2012.09.039

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