Lecture Notes from April 8th

Notes from our conference on April 8th. If you have any corrections or comments please feel free to add!

Oncologic Emergencies

Neutropenic Fever

Definition: Fever (>101 F or >100.4 F for an hour) with ANC<500, typically avoid rectal temperatures (although no actual evidence of induced bacteremia)

Cause: Often caused by chemotherapy, WBC declines to nadir and then comes back up

  • Also myelodysplastic syndromes, post viral, medication side effect

Clinical Presentation: Often no typical signs of infection (due to lack of response)

Management: Cultures (including from any central access, sometimes fungal), +/-CSF studies, viral testing, typical infectious work-up

  • Reverse isolation, broad spectrum abx, otherwise typical therapy
  • Low threshold for hydrocortisone
  • Neutropenic enterocolitis: Typically presents with RLQ pain with neutropenia
  • Some clinical decision tools, varied validation, look up if interested

Hypercalcemia of Malignancy

General: up to 30%, most common with lung and breast cancers

Pathophysiology: Decreased GI motility, decreased muscular contractions

Mechanisms: PTH-related protein production, Vitamin D analog production, increased osteoclast activity

Treatment: Fluids, bisphosphonates, calcitonin, glucocorticoids, dialysis (for severe cases)

Tumor Lysis Syndrome

General: Typically after initiation of chemotherapy or during times of high cell turnover, found with hematologic malignancies

Clinical Presentation: Electrolyte abnormalities (hypocalcemia, hyperphosphatemia, hyperkalemia), elevated uric acid, acute renal injury, cardiac dysrhythmias, seizures

Treatment: Fluids, rasburicase, correct electrolyte abnormalities and treat as appropriate, dialysis for severe cases

-Correct calcium only if symptomatic to avoid crystallization with high phosphate load

Urinary Diversions

Types:

  • Ileal conduit: incontinent, portion of the bowel with ureters attached to one side and the other attached to skin, drains into urostomy bag
  • Indiana pouch: Similar to above with ileocecal valve making up the collecting pouch, ureters attached to onse side and the distal cecum attached to the skin, ileocecal valve functions as sphincter, urine drained by self-cath
  • Neobladder: Segment of bowel resected and made into a bladder-like sac, one side attached to ureters and the other attached to urethra, varying degrees of incontinence depending on preservation of nerves and sphincter tone, possible to urinate volitionally 

General: Since all of these diversions are made from bowel they are colonized with bacteria and will always have +UA, best practice is cleaning of skin site and catheter specimen sent for culture, diagnosis can also be made by stranding on CT

Clinical Presentation: More often nausea, vomiting, flank pain (different innervation than typical urinary system so will more closely approximate visceral/enteric nociceptor patterns)

Hypersensitivity Reactions

Types:

  • Type 1: Immediate, mediated by IgE (causes histamine release from mast cells)
    • Examples: classic allergic response, anaphylaxis
  • Type 2: Antibody mediated (autoimmune disease mediated by autoantibody against a self target)
    • Examples: Graves disease, Myasthenia, Autoimmune hemolytic anemia, Goodpasture’s 
  • Type 3: Immune complex mediated (autoimmune disease due to deposition of antibody/antigen complexes)
    • Examples: glomerulonephritis, SLE, RA, HSP
  • Type 4: T cell mediated
    • Examples: Tuberculin skin test, contact dermatitis, DM1, RA, IBD, MS

General: Should always be on the differential, often mimic infectious or traumatic pathologies. If you don’t think of them you won’t diagnose them

Lecture Notes from April 1st

Here are some notes from our conference on April 1st for some spaced repetition. Topics included are Orthopedic emergencies, fracture pattern review, disorders of coagulation, and targeted temperature management after cardiac arrest. Please comment with any thoughts or corrections!

Orthopedics Review

Arthrotomy: Takes up to 155 cc for sensitive test, can sometimes substitute CT (institution dependent)

Injury Patterns by Anatomic Location:

Clavicle fracture: Medial can be complicated by vascular injury, up to 15% are complicated by nonunion, most common location is mid shaft

Shoulder dislocation: Anterior most common, posterior associated with seizure or electrical injury

Humerus: Posterior fat pad or anterior sail sign indicative of lipohemarthrosis, concern for occult injury (supracondylar in pediatrics, radial head in adults)

Forearm: Monteggia and Galleazzi (MUGR, Monteggia Ulnar fracture with radial head dislocation, Galleazzi Radius fracture with distal radioulnar dislocation)

Wrist: Colle’s (dinner fork) and Smith fracture (opposite), Lunate vs. perilunate dislocation (based on alignment of radius, lunate, and capitate) (https://radiopaedia.org/articles/lunate-dislocation?lang=us)

Hand: Boxer’s fracture (5th metacarpal)

Pelvis: mechanism of injury classification includes anterior compression, lateral compression, vertical shear injuries, binder to reduce pelvic volume for “open book” injuries typically associated with AC mechanism, posterior hip dislocation (early management reduces risk of avascular necrosis of femoral head)

Knee: posterior knee dislocation (high incidence of vascular injury, can often spontaneously reduce), tibial plateau fracture (often occult, can only see in lipohemarthrosis in some cases, low threshold for CT), tendon rupture (based on position of patella)

Ankle: Maisonneuve (due to syndesmosis conducting force to proximal fibula, sometimes associated with mortise widening), malleolar fractures, pilon fracture (through distal articular surface of tibia, increased likelihood of poor functional outcome)

Foot: LisFranc injury (dislocation at the Tarsometatarsal joint), Jones fracture (at the base of the 5th metatarsal, high rate of nonunion) (https://radiopaedia.org/articles/avulsion-fracture-of-the-5th-metatarsal-styloid?lang=us)

Infectious complications:

Septic arthritis- typically presents with pain with passive and active ROM at the joint, diagnosis is my arthrocentesis (WBC >50,000 for bacterial), polyarticular concerning for disseminated gonococcus

Felon/Paronychia- distal finger infections, involve the pulp space (felon) and the cuticle (paronychia)

Flexor tenosynovitis- Kanavel’s signs (pain with passive extension, flexor tenderness, circumferential swelling, held in flexion)

Compartment syndrome- Often clinical diagnosis diagnosis, more sensitive with compartment pressures (delta pressure <30, diastolic – compartment pressure or pressure >30), often associated with opioid use

Microangiopathic Hemolytic Anemias, vWF disease, and DIC

Thrombotic thrombocytopenic Purpura: 

General- Primary disorder, hereditary deficiency of or autoimmune response to ADAMSTS13 resulting in decreased cleavage of vWF polymers

-leads to consumptive coagulopathy with platelet destruction

Clinical Presentation- fever, AMS, thrombocytopenia, renal injury

Treatment- Plasmapheresis and steroids

Disseminated Intravascular Coagulation:

General- Secondary disorder, due to systemic inflammation leading to consumptive coagulopathy

Clinical presentation- bleeding, elevated D dimer, abnormal coagulation studies, low fibrinogen/platelets

Treatment- Aimed at underlying cause, can also transfuse as needed

Immune Thrombocytopenic Purpura:

General- Primary disorder, autoantibodies against platelets leading to platelet destruction and thrombocytopenia

-can be caused by infections (viral or bacterial,) autoimmune disease, or various medications

Clinical Presentation- asymptomatic thrombocytopenia

Treatment- glucocorticoids, IVIG if active bleeding

VonWillebrand Factor Disease

General- deficiency in vWF (either quantitative or qualitative) resulting in decreased activity/coagulation

Type 1- Decreased quantity

Type 2- Decreased activity

Type 3- Almost no vWF, most severe

Clinical Presentation- epistasis, mucosal bleeding, heavy menstrual cycles, increased bleeding during surgery

Treatment- When uncontrolled bleeding, desmopressin (for type I, causes vWF release), cryoprecipitate (for life threatening bleeding), recombinant vWF

Targeted Temperature Management

Indications: non traumatic cardiac arrest, earlier the better

Contraindications: DNR, already hypothermic, intoxicated/other cause for coma

General: Reduction in body temperature to 33-36 C for 24 hrs after arrest

-Main goal is to prevent hyperthermia which is associated with increased mortality and poor outcomes

Patients can take weeks to recover neurologic function after cardiac arrest; be careful about prognosticating too early.

Trauma Conference Notes-Spine

So real quick, here’s 3 slides I found helpful from Dr. Camilo Castillo’s talk yesterday on spine injury. I’m sure there were others, but here’s 3. Obviously these are his, so if you steal these, please reference him.

Thought this was helpful in thinking about level of disability/independence and what my patient in front of me might be able to do down the road, depending on level of injury.
Not exactly “Emergency” medicine, but hey, who doesn’t need a quick summary of all the meds to make people poop?
Lastly, thought a few of these were interesting in predicting better vs. worse outcomes. Nothing shocking, but interesting from an exam standpoint if you’re assessing some dermatomes.

Hypotensive (surprise) Aortic Dissection

Interesting case from recently I thought I’d share… a 71 year old female brought by EMS with an unusual report (never happens, right?). Initial call went out for hip pain for the past couple days and well as shortness of breath and not acting right today. Was initially awake, alert, and speaking normally on EMS arrival but developed acute respiratory distress en route and required intubation. On arrival was tachycardic to 130s-140s and had SBP of 100s. Skin was cool and mottled appearing. No obvious external signs of trauma. Pupils equal and reactive. No reported fall but family was unsure. Pretty broad differential at this point, anywhere from PE to intracranial injury to sepsis to MI to …, especially difficult due to lack of context and inconsistent reports.

Chest xray in room 9 showed what appeared to be a widened mediastinum. To fully evaluate for PE vs dissection, we proceeded from room 9 with CTA of chest and abdomen, to also cover for intra-abdominal injury. CT head and cspine were also done and negative. Lactic was elevated at 5, WBC was 32, and troponin was 0.5. Blood pressure began to trend downward, so we continued fluids. CTAs were quickly viewed and demonstrated ascending aortic pseudoaneurysm with rupture due to penetrating ulcer, resulting in mediastinal hematoma and hemopericardium. Blood pressure continued to trend downward into the 70s systolic. We continued fluids, and started blood. Bedside US demonstrated the aforementioned hemopericardium but no signs of tamponade, so we could hold off on pericardiocentesis.. Also placed central line and started pressors. Transferred to Jewish for OR and had definitive repair.

So that went pretty quickly but had some interesting findings. Penetrating aortic ulcer is something I hadn’t seen before but usually occurs secondary to atherosclerosis. Basically the intima of the aorta becomes denuded due to atherosclerotic plaque formation and can progress through the aortic wall, leading to intramural hematoma and eventually dissection and/or perforation. Interestingly, this is not a common cause of dissection, being the initiating lesion in less than 5% of dissection.

Dissection is something we’ve all learned about and something we always have to be concerned for, as they can go pretty badly pretty quickly. Classically, these patients have “tearing chest pain radiating to the back” and are hypertensive, but as this case demonstrates that is not always the case. They can nonspecific complaints or nonspecific exams. CT is the gold standard for diagnosis, chest xray can show the widened mediastinum or obscuration of aortic knob but these are unreliable. If you have a suspicion, best to order CT and act quickly. D-dimer is also emerging as a possible screening modality, as it has demonstrated 97% sensitivity, but has poor specificity (56%). We all know the classic teaching on how to treat these as well, with rate control first (esmolol or labetalol) and BP control if needed (nitroprusside or nicardipine). However, this presumes that they are hypertensive, so what about the hypotensive patient, like we saw? Definitely something to act on quickly and correct. A 2005 study showed that hypotension is not a common characteristic of dissection (29% of patients studied), but had significantly higher mortality than patients without hypotension.

So what can cause hypotension in the dissecting patient? First off, it’s much more common in type A dissections than type B. The most common reasons for these patients to become hypotensive are acute cardiogenic failure and tamponade. The cardiogenic failure can result from involvement of the coronary arteries causing a STEMI, or from aortic valve involvement causing aortic regurgitation. If blood collects in the pericardium, it can cause tamponade, and pretty quickly at that. Tamponade is relatively rare, but has a very high early mortality. Other possible reasons for hypotension can include hypovolemia from blood loss into the chest, or spinal ischemia that can lead to a neurogenic shock.

Awesome, right? So many reasons for hypotension in an already really sick patient. Having these in mind though is very important as it guides management and can be crucial for rapid intervention. Bedside US is quick and can identify a tamponade, and quick pericardiocentesis can stabilize for surgical intervention. Early pressor use can be beneficial in acute cardiogenic or neurologic shock. Of course all of these are stabilizing measures until you can get the patient to a surgeon, but it’s always important to preserve perfusion to those vital organs. Fluids and blood can help with the possibility of volume loss, although that’s a much less common reason. Also be judicious in the patient that is in acute cardiogenic failure.

Thanks for sticking with me on that one. I’ve also included links to video for pericardiocentesis, as it is a procedure we don’t get a ton of practice with. Enjoy!

  • Resources:
  • Tintinalli’s Emergency Medicine 8th Edition, Chapter 59, pages 412-415
  • Uptodate: Overview of acute aortic dissection and other acute aortic syndromes
  • Tsai, T, et al. Clinical Characteristics of Hypotension in Patients with Acute Aortic Dissection. The American Journal of Cardiology Vol 95. January 2005
  • Isselbacher, E., Cigarroa, J., Eagle, K. Cardiac Tamponade Complicating Proximal Aortic Dissection. Circulation. American Heart Association Journals. Volume 90, No 5. Novemnber 1994

PPE Videos

In case any of you need a refresher on donning/doffing PPE, see videos below. The first is on normal PPE. Would recommend skipping to the 5 minute mark or so on the first one.

https://nam03.safelinks.protection.outlook.com/?url=https%3A%2F%2Fwww.youtube.com%2Fwatch%3Fv%3DbG6zISnenPg%26feature%3Dshare_email&data=02%7C01%7Cadam.ross%40louisville.edu%7Cb26b5cd106bc410bc36608d7ce7a6b82%7Cdd246e4a54344e158ae391ad9797b209%7C0%7C0%7C637204897498164783&sdata=src2WeSc06Os21NKeWiSnUC2U5u60ZSoJ37dIzHYNvo%3D&reserved=0

This video below is on the donning/doffing of PAPRs/hoods. We haven’t moved towards using these just yet, and I’ll provide some additional review/education/training in the near future, especially if we begin to push towards using them. Can skip to about the 4 minute mark on this one if you like.

CT Scans-Covid

First off, it’s not currently recommended to perform CT Chest on all suspected Covid patients.

If you’re doing a CT Chest for rule-out Covid-19 you must put this in the order comments/indication. If you’re scanning a patient who is under isolation precautions due to possible Covid, and order a CT PE Protocol, put Possible Covid, Rule-Out PE. The reason behind this is they’ll take the patient to the basement so that they don’t have to shut down the ED scanner. Thanks.

Conference Lectures 1/2020

Obstetrics and Gynecology Emergencies – Dr. Marques

Normal Vaginal Delivery Key Steps

  • Support the perineum to prevent tearing with delivery of the anterior shoulder
  • Upon delivery of the anterior shoulder, provide upward pressure to deliver the newborn
  • Pull only gentle traction when delivering the placenta, to avoid uterine inversion

Post-Partum Hemorrhage

  • Palpate the uterus to feel for inversion or retained products
  • Provide tone by providing suprapubic pressure with an external hand and uterine pressure with an intravaginal hand
  • Oxytocin can be given IM or IV to treat uterine atony

Shoulder Dystocia

  • Leg hyperflexion and abduction at the hips along with suprapubic pressure (McRobert’s Maneuver) can be done if the anterior shoulder cannot be delivered

Breech Delivery

  • This happens in 3-4% of all deliveries
  • Do not pull traction at any time, as this can lead to entrapment in a cervix that is not dilated
  • A pressure against the popliteal fossa can help flex the leg and deliver each leg

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Oral Boards: Sepsis Due to Spontaneous Bacterial Peritonitis – Hugh, Shoff, MD

  • The CMS Core Measures (SEP-1) provide quality measures for providers to follow in sepsis
  • Severe Sepsis is defined as Lactate >2 or organ dysfunction
  • Septic Shock is defined as severe sepsis with hypoperfusion despite fluid resuscitation or lactate>4
  • Within 3 hours of presentation, obtain a lactate, blood cultures prior to broad spectrum antibiotics, and 30cc/kg fluid resuscitation
  • Within 6 hours, lactate must be repeated if >2

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CCU Follow-Up – Phil Giddings, MD

Myocardial bridging- coronary arteries travel deep into myocardium as opposed to laying upon the muscle

The vessels are occluded but when there is demand ischemia it can look like a STEMI

Myocardial bridging is fairly common in the general population, but usually isn’t symptomatic or pathologic.

If it is symptomatic- you could do Ca2+ channel blockers, beta blockers, and even myotomy or CABG if you’re feeling wild.

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Urology Review- Isaac Shaw, MD

Priapism-

  • Normal tumescence- veins constrict so the corpus cavernosum engorges because blood flows in
  • Ischemic= low flow, less venous outflow, rigid, painful
  • Nonsichemic= high flow, more arterial inflow, half rigid
  • (Distinguish w/ a blood gas)
  • Treatment
  • anesthetize by blocking the dorsal nerve of the penis (2 & 10 o’clock) w/o epi
  • then aspirate at 3 or 9 o’clock from the corpus cavernosum
  • Use a phenylephrine stick from Room 9, 100mcg-500mcg Q1-5min

Fournier’s Gangrene

  • polymicrobial
  • assoc w/ DM
  • 22-40% mortality
  • empiric + clindamycin (clinda first because it’s addressing the toxins)

consult surgery before imaging

Paraphimosis

  • foreskin trapped proximal to glans so the tip can get ischemic
  • Treatment: manually reduce, dextrose, lube, may have to incise the dorsal foreskin

Phimosis

  • foreskin can’t be retracted over the glans 2/2 inflammation
  • Treatment in ED: topical steroids with urology follow-up

Urinary Retention

  • often have hesitancy, nocturia, frequency, urgency
  • >200cc PVR
  • d/c w/ Foley à Uro will keep that in for 2 weeks prior to void trial

Renal Stones

  • remember that 10-15% don’t have hematuria
  • CT w/o contrast is still the standard for diagnosis, but some emergent literature exists that US alone is sufficient in young, healthy patients
  • if <5mm, 90% pass; but if >8mm, 5% pass
  • admit for intractable vomiting, pain, urinary extravasation, infection & obstruction

Balanitis

  • Candida on the glans
  • Associated with DM or uncircumcised

Torsion

  • twisted around the spermatic cord
  • if actively torsed, you will NOT have a cremasteric reflex
  • ultrasound 88-100% sensitive because they can torse and untorse
  • consult before imaging

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Breaking Bad NewsFrank Woggon, PhD

  • insensitive truth telling can have similar effects as lying
  • goals include gathering info, provide info, support patient, strategy for care
  • keep it simple, no jargon, talk slow, repeat PRN, use neutral language, be honest, allow emotions, consider cultural differences
  • “compassion is the willingness to let yourself be affected by the life and suffering of others”

SPIKES

  • Setting- privacy, sit down, eye contact, turn off pager
  • Perception- don’t combat denial at first, interpret first
  • Invitation- ask how much they want to know first
  • Knowledge- “what I’m about to say is not good,” be direct but not blunt, use their language
  • Empathize- ok to validate the emotions, silence is ok
  • Strategy & Summary- what comes next

GRIEV_ING Protocol

  • Gather the family
  • Resources- call for support
  • Identify yourself & staff, those in the room
  • Educate the family about what happened
  • Verify that the patient died by using that word
  • SPACE- silence is ok, let them have their gut reaction
  • Inquire whether they have questions
  • Nuts & bolts- organ donation, funeral arrangements, personal belongings, etc.
  • Give contact info for f/u questions

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STEMI Mimicks – Frank Shary, MD

OMI= occlusive MI

  • V2 & V3 2mm elev = STEMI; Everywhere else 1mm
  • Wellens: biphasic T wave, they recently had an OMI, symptoms may have gotten somewhat better by the time of the EKG, they need a cath
    • Deep T Wellens- deep and wide
  • LV aneurysm- deep Q wave w/ biphasic T wave, static
  • Sgarbossa criteria- OMI in the setting of LBBB and/or paced rhythm
    • look at vector of QRS and vector of ST segment
    • concordant elevation or depression greater than 1mm
    • discordant greater than 5mm
  • Hyperacute T waves- early into the ischemia, before ST elevation, cath soon because you have potential to save more myocardium, large area under the curve especially in proportion to the QRS complex
    • L circumflex is the vessel most likely to be silent
  • aVR- if it’s the only lead elevated and everywhere else is diffusely depressed, you might have diffuse subendocardial ischemia
    • could be bad triple vessel disease

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Managing the Bleeding Patient Without Blood Products – Chase, PharmD

There are 6 Jehovah’s Witness churches in Louisville

  • Plasma Derivatives are technically not Blood products… so whether or not a patient wants that is up to the individual
  • albumin, clotting factors, PCC, Immunoglobulins (including Rhogam and vaccines)
  • equine Ig and Crofab could also be iffy
  • ECMO, cardiopulmonary bypass, dialysis are allowed generally

Source Control

  • bone wax/putty- use in NES and long bone fx, high infection rate though
  • oxidized regenerated cellulose- ex. Surgicell, promotes rebuilding of proteins to heal & achieve hemostasis, like a mesh
  • gelatin matrix- ex. Floseal, more like a gel
  • there is a powder too but it’s $$$ and causes microemboli so don’t use
  • thombin- apply w/ 4×4’s
  • TXA- derivative of lysine THIS IS NOT A PLASMA DERIVATIVE SO THEY SHOULD BE OK WITH IT, 1g over 10min à another 1g over 8-10 hours
  • have a lower threshold to give TXA since there is a decrease in mortality, even if you wouldn’t have given TXA to a non-Jehovah’s witness

Usable Therapies:

  • Cell Saver
    • blood is collected, washed, centrifuged, returned to patient
    • example indications: AAA, TKA, THA, cardiac surgeries
  • Vitamin K
  • PCC- most efficacious
    • 4 factor is better than 3 factor, but if you try to give 3 factor and then just add Factor VII a la carte, more thromboembolic events
  • FFP- prep time is longer, tonzo volume
  • Adnexanet Alpha- new antidote for rivaroxaban and apixaban, we don’t have that
  • Novo7- directly activates Factor VIII, black box warning for thromboembolic events, no difference in mortality but there was a reduction in transfusions
  • Dabigatran reversal- idarucizumab, dialysis, charcoal
  • Antiplatelet reversal- ASA and Plavix are irreversible, but ticagrelor is reversible
    • DDAVP- indicated for DI, von Willebrand disease, uremic bleeding (renal failure), nocturnal enuresis
    • 0.4mcg/kg over 10min

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Pediatric Environmental Emergencies- Dr. Said

Drowning

  • fresh or salt water doesn’t matter, you’re ruining your surfactant
  • if you are anoxic you get brain damage in 4-6min, irreversible
  • cold temp is only helpful if it happens really quickly
  • outcomes depend on initial resuscitation, degree of pulmonary damage, time submerged
  • poor prognosis- coma, apnea, submersion >9min
  • can try vapotherm for positive pressure, albuterol can treat bronchospasm
  • steroids don’t help
  • goal warming 32C
  • if asymptomatic, obs for 8 hours! Oy vey
  • admit if prolonged submersion, respiratory or neuro symptoms, abnormal CXR

Electrical Injuries

  • lightning strikes carry 30% mortality risk, it causes asystole
  • doesn’t cause renal failure or burns/compartment syndrome
  • thicker tissue less damaged
  • tissue between entry and exit wounds could be more damaged interiorly than it appears
  • AC worse than DC because AC at low voltage causes tetany so you’re holding on longer
  • we use DC for defib, countershock, pacing but you get thrown off
  • oral electrical injury – monitor for progressive edema
  • could have delayed bleeding from labial artery

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EMTALA- Melissa Platt, MD

  • in court, all are case-by-case
  • we have to provide a medical screening exam and treat and stabilize an emergency medical condition
  • transferring physician assumes the risk if the patient crumps en route to accepting hospital

Journal Club January 2020

We had our January journal club at Vines, discussing 3 articles on different topics.

1- The first was an editorial on legal cases related to use of medical stents. The authors highlight the inter-rater difference in assessment of coronary blockages between even advanced interventional cardiologists. This has legal implications as cardiologists are prosecuted for unnecessary procedures. This article is important to EM no as much for the medical content (we don’t place stents), but for the precedent of the legal system prosecuting physicians for doing what they were trained to do.

2- The second article in Annals EM looked at 24,459 ED patients with chest pain who were deemed to require outpatient stress testing. The conclusion: “Less than one third of patients completed outpatient stress testing within the guideline-recommended 3 days after initial evaluation. More important, the low adverse event rates suggest that selective outpatient stress testing is safe. In this cohort of patients selected for outpatient cardiac stress testing in a well-integrated health system, there does not appear to be any associated benefit of stress testing within 3 days, nor within 30 days, compared with those who never received testing at all. The lack of benefit of obtaining timely testing, in combination with low rates of objective adverse events, may warrant reassessment of the current guidelines.” Notice that this does not change guidelines, but ads to the conversation on proper use of resources and how aggressively we should work up chest pain in low risk patients.

3- The final article, the 2018 flu guidelines, sound similar to prior years, with focus of testing and treatment on patients at risk for complications. They do throw in the recommendation to test “if the results might influence antiviral treatment decisions or reduce use of unnecessary antibiotics, further diagnostic testing, and time in the emergency department, or if the results might influence antiviral treatment or chemoprophylaxis decisions for high-risk household contacts.” Physicians should start treatment right away for

  • Persons of any age who are hospitalized with influenza, regardless of illness duration prior to hospitalization (A-II).
  • Outpatients of any age with severe or progressive illness, regardless of illness duration (A-III).
  • Outpatients who are at high risk of complications from influenza, including those with chronic medical conditions and immunocompromised patients (A-II).
  • Children younger than 2 years and adults ≥65 years (A-III).
  • Pregnant women and those within 2 weeks postpartum (A-III).

And we can consider treatment for

  • Outpatients with illness onset ≤2 days before presentation (C-I).
  • Symptomatic outpatients who are household contacts of persons who are at high risk of developing complications from influenza, particularly those who are severely immunocompromised (C-III).
  • Symptomatic healthcare providers who care for patients who are at high risk of developing complications from influenza, particularly those who are severely immunocompromised (C-III).

Hope everyone enjoyed Journal Club, looking forward to the February articles

Congestive heart failure exacerbation management

Most of the third years, and probably the second years at this point, know pretty well how to manage CHF exacerbations. However, there are differences in managing the normotensive vs. hypertensive vs. hypotensive exacerbation, and I’ll try to provide some tricks in managing your run-of-the-mill CHF exacerbation as well (credits to Amal Mattu and Scott Weingart).

 

First, try to determine the cause of the exacerbation. Determining the cause of the exacerbation, however, can be difficult – most patients aren’t honest about their salt/food/drug intake or medication compliance, or do not understand their disease process. The most common cause of an exacerbation is dietary or medication non-compliance. However, in all cases, ischemia needs to be considered. More rare cases can be valvular dysfunction such as rupture (auscultation or BSUS), myocarditis (check a troponin if it fits the clinical scenario), arrhythmias (check HR and an EKG), hypertensive crisis (often secondary to medication and dietary non-compliance, or drugs), or high-output failure (such as anemia, sepsis, AV-fistula in a dialysis patient, thyrotoxicosis). (1)

 

Next comes diagnostics. There are debates on whether troponins and BNPs need to be ordered on every CHF exacerbation. For example, many of these patients will have chronically elevated troponins and BNPs, and you’ll be stuck trending them. A BNP is of limited value in the ER except in maybe determining is the patient’s dyspnea secondary to a COPD exacerbation or CHF exacerbation, or if the BNP is normal then it should make you consider alternative diagnoses. Amal Mattu suggests that if you’re going to admit the patient, get everything (CBC, CMP, BNP, trop, EKG, CXR) because the inpatient teams like to trend trops/BNPs (even if the evidence doesn’t really back up trending BNPs). If it’s simply diet or medication non-compliance, you might only need to check electrolytes, because diuretics can cause electrolyte disturbances. ABGs aren’t typically helpful unless the patient is hypoxemic. Overall, not much other testing needs to be done for your non-critically ill patients. (1)

 

As for management, this becomes tricky because it depends on many things. What is the patient’s blood pressure? What is the cause of their exacerbation? Are they volume-overloaded, euvolemic, or dry? Are they septic? In general you have three goals: decrease the preload, decrease the afterload, and (in some cases) increase LV function. PLEASE watch this Amal Mattu lecture and you will master CHF exacerbations (2). For management, let’s start with the classic hypertensive patient.

 

Hypertensive patient: The patient’s heart is straining against a high amount of SVR and can’t perfuse their kidneys. Fluid backs up into the lungs. Don’t immediately jump to your loop diuretics (it’s debatable, and should only be done if hyper or maybe euvolemic). We fix this problem by fixing two problem: decreasing the SVR in order to perfuse the kidneys, and decreasing preload to “turn off the faucet” that’s overflowing a bathtub (lungs). Lasix won’t work if you aren’t perfusing the kidneys. One of the best and quickest agents we have is nitroglycerin. You have three options: 0.4mg sublingual tab, nitro paste, and a nitro bolus and drip. Scott Weingart (3) recommends the nitro drip, starting with a bolus of 400 mcg (that’s one sublingual nitro tab) over 2 minutes, and then drop to 100 mcg/min and titrate up until SVR is decreased. Your nurses will often question if you want to start the rate that high, and the answer is yes, but you MUST monitor your patient closely because high doses of nitro can tank your patient’s BP if you aren’t careful. Also, nitro also decreases preload, which can prevent fluid from backing up into the heart and therefore the lungs. (Nitro often gives patients a headache – give ‘em some Tylenol.) This can fix patients in minutes, because you’re redistributing fluid out of the lungs and into the vasculature or the rest of the body! BiPAP will save these patients by pushing fluid out of their lungs and can prevent intubation. The other thing to consider is IV ACE Inhibitors. Enalapril (enalaprilat) is the only IV form we have, and it has to come from pharmacy, but ACE Inhibitors are very good at afterload reduction and will help move the fluid from the lungs into the rest of the body. If nitro isn’t working, consider adding on enalapril.

 

Normotensive patients: just because their BP isn’t high doesn’t mean you can’t use nitro. However, be judicious, because you don’t want to cause hypotension, but remember that even normotensive patients can tolerate a sublingual nitro without issue. Lasix if clinically volume overloaded. BiPAP as needed for respiratory difficulties. Otherwise, nothing too tricky here.

 

Hypotensive patients: these are actually your cardiogenic shock patients. They are sick as snot. They could also be septic (! Hi Dr. Shoff), or could be having an MI. Your management of these patients is very difficult and much different than your typical CHF exacerbation management. First, determine if the patient is “warm” or “cold” (feel their extremities), and then determine if “wet” or “dry” (pulmonary edema). (4) The most common presentation is “cold and wet”, but removing fluid from them will make them worse. Obviously, if they have pulmonary edema, do not give them fluid.  HOWEVER, norepinephrine is the best agent to use and is proven in many studies. Epinephrine is your second-line agent. Avoid dopamine (SOAP-II trial demonstrated harm of dopamine vs. norepinephrine). Get basic labs, troponin, BNP, EKG, CXR, lactic acid level, blood cultures, and get reliable access. Get a digoxin level if they’re on dig, or if they can’t tell you if they are. Use BiPAP early for their respiratory status. Your BSUS can greatly aid you in what is going on and how to treat it. If the heart isn’t squeezing well, give drugs to make it do so. If it’s hyperdynamic, maybe the heart isn’t the problem. You can provide inotropic support (epi, milrinone) if on BSUS you see their EF is terrible, and if it’s caused by an MI they need urgent revascularization. Be careful – milrinone can cause hypotension. Digoxin is actually an alternative and can be given IV.

 

If you want a checklist version in treating the cardiogenic shock patients, Weingart supplied this: https://i2.wp.com/emcrit.org/wp-content/uploads/2016/11/chflist.jpg

 

Note: A study published in 2017 (5) tried to see if “time-to-furosemide” was beneficial. Initially, the study looks grossly positive (2.3% vs. 6% mortality in the “early” treatment vs “late” treatment arms, respectively), however, “early” was defined as <1 hour and “late” was defined as all furosemide given after 1 hour. You can see the potential issues with this.

 

(1) https://www.emrap.org/episode/emrap2018august/cardiology

(2) https://www.youtube.com/watch?v=AEKzT98EZHQ

(3) https://emcrit.org/emcrit/scape/

(4) https://emcrit.org/ibcc/chf/

(5) https://www.ncbi.nlm.nih.gov/pubmed/?term=time-to-furosemide

 

Transvenous Pacemaker Insertion

Wanted to post a couple links for Transvenous Pacemaker insertion. I think it’s mentioned in at least 1 or both, but the preferred site as Tej mentioned is either the right IJ or the Left IJ, followed by the right subclavian, and lastly the left subclavian (save the left subclavian so they can put a permanent pacemaker in here).

This one is unfortunately completely silent, but is annotated well and also has the exact type of pacemaker box we have in the ED (Bay 1, bottom shelf).

 

This is the one Tej showed by Jess Mason @ EM:RAP.

The Lateral Canthotomy – The Unicorn of Procedures

Apparently I’m a magnet for ocular trauma. Oddly enough, it’s the one thing that still makes me queasy. Anyways, I feel like over the past year I’ve dealt with quite a few cases of orbital compartment syndrome, mostly which have been traumatic in nature. After having done a few lateral canthotomies, I have a few pearls that may help others along the way. I think the hardest part of the entire procedure is making the decision to actually do it.

You should have suspicion with any patient presenting to the ED with any obvious facial trauma. I generally start off with gross testing of visual acuity, seeing if patient can see first light, then the number of fingers that I’m holding up. If they can see both, then my suspicion is much lower. What generally makes me more concerned is when the patient states they cannot see out of one eye. Often, in the case of trauma, this will be secondary to significant swelling causing the lids to be swollen shut, which obstructs the patient from physically opening their eye. If you manually open it, the hope is that they will be able to see.

This is where things can get muddy. Most often, when their lids are this swollen, you’re going to have a difficult time manually opening the lids. Also, if it’s traumatic related, theres likely to be blood around the eye which adds in another layer of difficulty of opening the eye. Optho has some really nice ocular forceps, but I don’t believe we have them in our canthotomy tray.

The easiest way that I have found to open both lids is with the use of two paperclips. First I wipe them off with alcohol and then bend them in such a manner that one of the curved ends is folded backwards. This will allow you to have a smooth, rounded object to elevate the eye lid. Obviously, DO NOT DO THIS IF YOU ARE CONCERNED FOR AN OPEN GLOBE.


I feel like in most of these patients, they have significant chemosis noted to the sclera which looks like the photo below. Seeing this also makes me concerned that theres a reason the sclera is so congested (vascular congestion secondary to obstruction).


Once you have the lid retracted, now is time to establish if the patient has vision in that eye. You’re going to want a helper to keep the lids retracted. I attempt to get the patient to see how many fingers I’m holding up. If they can’t see that, I try and figure out if they can see light. If the patient states that they cannot see, I “challenge” their vision in that eye, most often by flicking a finger close to their eye in a rapid manner to see if they blink. A normal person is not going to let you flick at their eye without blinking. If they don’t blink, I start to get more concerned.

The next piece of info you’re going to want is to get a pressure. It seems like majority of the ones I have done, pressures have been in the upper 40s to 50 or either the tonopen reads “err.”  Keep in mind if you use the tonopen too aggressively, you will get a falsely elevated pressure.

If I have gotten this far and I’m still convinced that the patient has no vision in the eye and their ocular pressures are elevated, I’m getting set up to perform the canthotomy. I’m of the notion that if it’s THAT important to do emergently, I’m going to call opthamoloy after I have treated the emergency.


Ideally, the procedure is best done in room 9 if you are capable for a few reasons

#1: the overhead lights in there are great and vastly improve your visibility during the procedure.

#2: you’re going to want to sedate the patient to make it more comfortable. I typically use fent/versed. i try to avoid ketamine for the theoretical idea that it likely increases IOP.

#3: the lateral canthotomy tray is in bay 4. if you’re standing at the foot of the bed, its immediately on your right, like the 2nd shelf from the top in the pixis closest to you.


So you’ve decided to do the canthotomy. Lighting is great. You have your tools at bedside. You’ve got the patient hooked up to the monitor. You’re all ready to sedate the patient. You push drugs and start the procedure. At this point, you’re going to want to start anesthetizing the region. To do this, start AT the lateral canthus and orient your needle AWAY from the globe. You want to inject out towards the lateral orbital rim, away from the eye ball. While you’re injecting, this is giving your patient time to start having some effects of the sedation.


After you have anesthetized the area, take a few saline flushes and rinse out the eye in case there is in foreign debris. Next, in theory you should use a hemostat to “crimp” the margin at the lateral canthus. Optho has rolled their eyes at me when I’ve done this and they say it isn’t necessary. The idea is that it is supposed to help it not bleed as bad when you cut this area. I personally don’t do it for the hemostatic purposes. I feel like crimping the area generally helps get a small amount of swelling out of the way so I can fit in the tips of my iris scissors when I go to make the first cut. This is ultimately why I continue to do this part of the procedure.


After you have crimped the tissue for 10-20 seconds, remove the hemostats. You’re going to want to use the iris scissors at this point in time. You’re going to encounter some difficulty because both lids are edematous and likely there is significant edema in the sclera. You’re going to be shitting yourself because it’s hard to tell what’s sclera and what is skin/skin structure. This is when the overhead lights in room 9 REALLY help make a difference. Once you are able to identify the lateral canthus, open the iris scissors and insert one blade below the lateral canthus directed away from the eye. You are going to want to bluntly disect infero-laterally towards the lateral orbital rim. Your ultimate goal will be to cut ~1cm of the skin overlying the lateral canthus and then disect down to the lateral canthal tendon, just medial to Whitnall’s tubercle.


At the lateral canthal tendon, there will be two bands of fibrous tissue; the superior and inferior crus. Generally it is the inferior crus that is relieved first in this procedure.


At this point, things are going to be a bloody mess, so the best way to identify them is to use the tip of your iris scissors and literally “strum” the tendon. It will feel exactly how you expect it to feel. You will feel the tendon strum. When you do this, make small movements, almost like micro-movements. As you strum the crux, you will be able to tell where one side starts and terminates. You may be able to physically see it if you’ve disected well enough. Regardless, you can use the tips of the iris scissors to envelop the crux and make the cut. If you have done this correctly, you should appreciate that the lid has relaxed. If the eyelid doesn’t feel any more mobile than previous, take a deep breath. Try and use some 4x4s to clear away the blood and take a better look. Likely you haven’t fully transected the ligament if the lid isn’t relaxed, even if you think that you might have.


If you have been successful, you will be able to appreciate that the lid is less constrictive of the globe. Now, go ahead and check your pressures at this point. Assuming that the pressures are significantly improved, you’re done.  Say your pressure wasn’t reading prior to the procedure and now its still in the upper 40s and you have verified that you have transected the inferior crus, the patient will likely need the superior crus transected as well. You are capable of doing this; however, if you’re uncomfortable, optho will likely do it when they arrive. Just go about transecting the superior crus in the same fashion.

Speaking of optho, now that the emergent situation has been handled, this is the time to give them a call and let them know that you’ve decompressed the patient’s orbit. They will come in and do their thing and you can carve another notch in your belt.

_____________________________________________________________________________

On a side note, I had a non-traumatic orbital compartment syndrome a few months back. The guy came as a transfer from an outside facility with unilateral vision loss, proptosis, and headache. CT at OSH showed an intraorbital mass. I’m not certain why, but given it was not traumatic, I didn’t think to immediately decompress his orbit as his symptoms had been persistent over the past two days and not acute in onset. Make note, it is still completely acceptable and recommended to perform a canthotomy in this setting. Just something that I realized in hind-sight.



Anyways, this is a lot of reading. If you made it to here, thanks. Hopefully this was somewhat clear. If you have any questions, I’m happy to answer.


References:

Roberts and Hedges Clinical Procedures in Emergency Medicine – Opthalmologic Procedures: Chapter 62 pg 1295.

 

Hypothermia

Patient presents in cardiac arrest. Found outside on Broadway (all hypothetical). While moving him into EMS truck, patient lost pulse, went into cardiac arrest. Multiple defibrillation and code drugs later, patient maintained to be in v fib. Presents intubated, GCS 3T. On quick secondary survey, patient cold to touch and mottled/cyanotic extremities. ET tube confirmed by auscultation and chest rise. Chem 8 shows nl K, other labs unremarkable. Rectal temp unable to read. Bladder temp reads 75. Go.

We’ve learned some hallmarks of rewarming cardiac arrests. The main point to come is that it will be a slow process that takes a ton of resources. You can find the grading system of hypothermia online; however, here we are specifically talking about severe hypothermia <28C without vitals. Here are my following recommendations:

  1. Have plenty of people in line to do chest compressions, unless you can swipe a Lucas machine from EMS
  2. Start active rewarming early, as it takes a very, very long time. We used the gaymar blanket below the patient, applied the ARCTIC SUN (typically used to cool post cardiac arrest, but can also warm), bear hugger. This sounds like a lot but you will be surprised that this may only warm the body 1-4 C an hour if you are lucky. Keep a temperature sensing foley in or use the one on the Arctic sun. CONTINUE CHEST COMPRESSIONS.
  3. According to Tintinalli’s you can give up to 3 doses of code drugs/defibrillations until above 80. I’ve seen places in the literature to not start shocking again until you have them above 80 degrees and some say as high as 32 C (89F).
  4. Start prepping for more advanced warming. Hypothetically if you were in a place that has ECMO, you would send them straight there as that has the quickest rewarming period of all interventions. However, if you do not have ECMO, then proceed to other means. When doing chest tubes, we preferentially avoided to L side as we were continuing chest compressions and placed 2 on the R side. One anterior mid clavicular line at 2nd intercostal and the other large bore tube on posterior axillary line at 4th/5th. Theoretically I always imagined a closed circuit to continuously reuse and pump warm water in. This was not the case. You can use the rapid transfuser to warm  1L NS and let it run to gravity into the anterior chest tube while clamping the posterior tube, Keep 500cc to 1L in the chest for 15 minutes then let it run into the atrium and bolus another 500cc in. KEEP A TAB ON THE AMOUNT OF FLUIDS GOING IN AS WELL AS OUT. You can also place an NG tube and put war m(40-42C) fluid into the stomach for rewarming. 500cc-1L in the bladder Q15-20 minutes.
  5. Once they get to able 80-ish degrees you may see some change on end tidal or rhythm strip itself. Now begin your regular ACLS, but keep rewarming.
  6. There isn’t much to be found on whether or not to continue with code drugs during the sub 80F. Tintinalli’s is vague on it as well as they note to continue with if it seems to be working. I would opt not to fluid them with epinephrine until you get the body warmed and some warm blood flowing.

Overall: the old adage holds up. “They are not dead until they are warm and dead”

  1. Place a foley for temp
  2. Get Chem 8 to see if resuscitation viable (K>12=not viable)
  3. See if ECMO available
  4. Get med students or a LUCAS machine
  5. Start passive and active rewarming immediately

Sources: Tintinalli’s

Visual Blood Loss Estimations

I find myself regularly fascinated by the accuracies (and frequent inaccuracies) of our subjective findings regarding Trauma. Consider how often we hear about details, mechanism, intrusion, extrication time to name a few, and how heavily they guide both pre-hospital and ED workups.  Some interesting studies I have come across are regarding blood loss estimation.  Next time you hear report about blood loss at the scene, contemplate (and feel free to cackle and wisely reference) the following studies: 

 

The first, published in Prehospital Emergency Care, tested a cohort of EMTs and paramedics on estimating blood volumes spilled on to carpet and vinyl surfaces.  Blood product was poured onto these surfaces and participants estimated total volume demonstrated at six different spill sites.  Mean percent errors of 74% and 56% were calculated for initial estimations!   A similar study published in The Journal of Trauma: Injury, Infection, and Critical Care produced similar results, where only 8% of the 99 providers tested were within 20% of the actual volume, and only 24% were within 50% of actual volume.

Perhaps the more interesting feature of the first study is the post-estimation training that occurred afterwards.  One arm of the cohort returned to the initial scene where actual blood loss was revealed followed by some education on making volume estimates.  The second arm had similar education however this was performed in a classroom using slides instead of returning to the original scene.   Both groups were retested with new scenarios and both demonstrated improvement in mean percent errors to 59% (return to scene) and 45% (slides and classroom), suggesting this may be learn-able skill! 

It turns out we are not much better than our pre-hospital colleagues at blood estimation.  A study from the Western Journal of Emergency Medicine examined a cohort of 56 emergency physicians (mixed residents and attendings).  Participants were tested with 4 different scenarios where specific amounts of blood were poured onto a bedsheet, on gauze, a t-shirt and into a commode.   The mean standard error for all estimates was 116% with a range of 0% to 1233%. Only 8% tested were within 20% of the true value (sound familiar?)!

 

The next question I arrived at, which you may be thinking yourself, was the fact that these studies do not include scenario or vital signs.  One would expect that would result in more accurate estimates.  Unfortunately, the rabbit hole of my literature search revealed that, even equipped with additional information, both pre-hospital providers and emergency room physicians continued to be poor estimators of blood loss.  A study from The Journal of Trauma tested estimations in set amount of blood amounts (300 mL, 800 mL, and 1500 mL) in a “stable” patient and in an “unstable” patient.  Researchers found that in the stable patient (i.e. normal blood pressure and heart rate) blood loss was underestimated in larger amounts and overestimated in the 300 mL patient.  Remarkably, in the unstable patient, blood loss in both 800 and 1500 mL scenarios were underestimated.  Of the 870 estimates made, 51% were underestimated, 39% were overestimated and only 10% were exact. 

As so nicely asked in the discussion with Frank et al “one has to direct the question if visually estimated blood loss is of any pre-clinical value and worth being mentioned during handover in the emergency unit.“   Perhaps not, but there may be hope with additional training!

 References: 

  1. Patton K., Funk DL., McErlean M., Bartfield JM. (2001) Accuracy of estimation of external blood loss by EMS personnel. The Journal of Trauma: Injury, Infection, and Critical Care. 50(5):914-916. 
  2. Moscati, R., Billittier, AJ, Marshall, B., Fincher, M., Jehle, D., Braen, GR. (1999) Blood loss estimation by out-of-hospital emergency care providers. Prehospital Emergency Care, Jul-Sep;3(3): 239-42. 
  3. Ashburn, J. C., Harrison, T., Ham, J. J., & Strote, J. (2012). Emergency physician estimation of blood loss. The western journal of emergency medicine13(4), 376-9. 
  4. Frank M., Schmucker U, Stengel D, Fischer L, Lange J, Grossjohann R, Ekkernkamp A, Matthes G. (2010) Proper estimation of blood loss on scene of trauma: tool or tale? The Journal of Trauma. Nov;69(5):1191-5.