Grand Rounds Recap 9.1.21
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URBAN SEARCH & RESCUE: OH-TF1 SURFISIDE RESPONSE WITH DR. CURRY
Champlain Towers South Collapse - 13-story building, likely started around the pool deck
Timeline:
Collapse on 6/24 at 0130
OH-TF1 placed on “Alert” to roster a Type 1 team at 2030 on 6/24
OH-TF1 activated on 6/30, to persons at 1430, departed at 2000
Return to OH on 7/15
National Urban Search and Rescue (US&R) Response System
History: Developed by FEMA in 1989 in response to Loma Prieta earthquake; later incorporated into the Federal Response Plan, now known as the National Response Framework
28 teams total
Type I teams have 70 members, and Type III teams have 35 members. Teams are made up of individuals with diverse skill sets and experience in search, rescue, planning, logistics, and medical teams. Teams depart within 6 hours of activation and may be deployed up to 14 days. They should be self-sufficient for 72 hours.
US&R Medical Team
Composed of physicians and medical specialists at the paramedic or equivalent level
Provide pre-hospital and emergency care for task force members and crush syndrome/confined space medicine or rescue medicine
Medical Team Manager is a licensed physician who is EM-trained and/or Board-certified in EM, actively practicing. They help facilitate medical check in and clearance for every team member initially and are responsible for daily medical checks on all team members. They will support team members who are recuperating during the mission.
Common complaints - Eye irritation, foot injuries/blisters, heat-related, lacerations
Process of clearance, search, rescue
Champlain Tower collapse followed a pancake model, creating voids down corridors.
Void spaces vary among collapses, depending on structures, and have variable survival rates associated with them.
Sometimes, the emotional effects of serving in this capacity during a disaster response are felt in the course of the mission; however, they can also come to light or evolve after the mission is over when a task force has returned home. Develop a support network and check in with yourself and them.
QI/KT LECTURE: NSTEMI DIAGNOSIS AND MANAGEMENT WITH DRS. KEIN AND STARK
NSTEMI is defined as elevated cardiac biomarkers in appropriate clinical contexts with or without EKG changes (AHA and American College of Cardiology 2014). Unstable angina and NSTEMI typically distinguished based on cardiac biomarker elevation; however, given the advent of high sensitivity troponins, you may have positive biomarkers at low levels, so new group of NST-ACS.
Acute Myocardial Infarction (AMI) defined by rise and/or fall of troponin values with at least one value above upper limits of normal and one of the following: symptoms of angina, new ischemic EKG changes, development of Q waves, imaging demonstrating myocardial damage including regional wall motion abnormalities, identification of coronary thrombus on angiography
AMI broken down into five types:
Type 1 MI - primary coronary process with plaque rupture causing ST elevation or cardiac biomarker elevation with nonspecific or no EKG changes
Type 2 MI - includes MI secondary to reduced myocardial oxygen supply or increased demand without plaque rupture (for example, secondary to sepsis, vasospasm, dissection, anemia, heart failure, PE, etc)
Type 3 MI - Sudden cardiac death
Type 4 MI - Post-procedural, 5x upper limit of normal
Type 5 MI - Post-CABG, 10x upper limit of normal
Chapman et al, 2018 - Long-term Outcomes in Patients with Type 2 Myocardial Infarction and Myocardial Injury - All-cause mortality higher in Type 2 MI (62.5%) v. Type 1 MI (36.7%) often due to non cardiovascular causes; similar rates of MACE at 5 years (30%) between two groups
Diagnostics
EKG within 10 minutes of presentation demonstrating non-specific or more subtle EKG changes, which may include ST or T-wave inversions
Hs Troponin
Ola et al, 2021 - Clinical Impact of High-Sensitivity Cardiac Troponin T Implementation in the Community - found decreased overall LOS (4.3 v. 4.2h), increased LOS for those discharged (2.4 v. 2.9h) - essentially faster to admission, slower to discharge
Ganguli et al, 2021 - Downstream Cascades of Care Following High-Sensitivity Troponin Test Implementation - found less admissions with HS troponin (- 5.8%), decreased net mean LOS (-0.24%)
Chapman et al, 2018 - Novel high-sensitivity cardiac troponin I assay in patients with suspected acute coronary syndrome - found NPV of 99.5% with < 5 cutoff v. 99% with < 3
Management
ASA 324 mg
Anticoagulation - either UFH bolus and infusion or LMWH
Andrade-Castellanos et al (2014) - Cochrane Review demonstrating that patients who received Heparin progressed to MI less frequently, but with no mortality benefit observed.
Cohen et al (1998) - RCT which found that Enoxaparin reduced ischemic events without increased risk of bleeding
Ferguson et al (2004) - Prospective, randomized, open-label, MCT international trail that found that Enoxaparin was non-inferior to UFH with small increased risk for major bleeding
Atorvastatin 80 mg
Schwartz et al (2001) - RCT which found that Atorvastatin reduced recurrent ischemic events in the first 16 weeks after ACS (RR 0.74)
Replete K for goal of 3.5-4.5 and Mg for goal > 2
Goyal et al (2012) - Retrospective cohort study that recommended normokalaemia in patients with suspected ACS and repletion of Potassium and Magnesium based on U-shaped association curve between potassium and in-hospital mortality.
Consider :
Oxygen if O2 saturation < 90% (2018 meta-analysis demonstrated that routine oxygen does not provide benefit in patients with SpO2 > 90%; 2005 study demonstrated that supplemental O2 associated with increase in coronary vascular resistance in patients undergoing catheterization)
NTG 0.4 mg SL if CP - NTG converted to NO, which acts as a vasodilator, leading to increased coronary blood flow and impaired platelet aggregation. Hold if any hypotension during care.
Henrikson et al (2003) found that relief with NTG does not predict CAD (35% with CAD had relief of CP v. 41% without CAD).
Fentanyl 0.5 - 1 mcg/kg if CP (avoid Morphine!)
Additional antiplatelet agents - either Clopidogrel or Ticagrelor
The Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) Trial Investigators (2001) found clinical benefit with Clopidogrel in NSTEMI (decreased composite death, MI, or stroke with RR of 0.80 and decreased refractory ischemia with RR of 0.86.
Wallentin et al (2009) PLATO Study found some benefit of Ticagrelor over Clopidogrel without increased risk of bleeding.
Ultimately, both have been shown to have some benefits in ACS with reductions in death from cardiovascular causes, but also with increased risk of major bleeding compared to control with Ticagrelor having a slightly increased risk of fatal bleeding. Given this, best to consult Cardiology in terms of their preferences before administering.
Triple antiplatelet therapy? Greeganage et al (2010) demonstrated superior prevention of MACE with triple therapy, but study by Giugliano et al (2009) demonstrated no significant difference in MACE and increased bleeding in the early administration group.
Disposition
If Hs troponin is > 100 for males, > 70 for females, then treat for NSTEMI.
If repeat Hs troponin at 1 hour is >= 3 and if the delta is >= 15, then treat for NSTEMI. If not, then use HEART score to risk stratify patients and determine if CDU CP Observation protocol is appropriate. a 1 hour repeat
HEART Score used as a risk stratification tool for people who present with chest pain.
Those with HEART scores of 4-6 are at increased risk of MACE with significantly increased risk in scores above 7.
R4 CASE FOLLOW UP: BASILAR STROKE AND SLE WITH DR. HUNT
Basilar stroke
Basilar Artery forms over the area of the pons by two vertebral arteries and provides most of the posterior circulation to the brain.
Basilar strokes are rare, accounting for only 1% of all ischemic strokes, and its etiologies include atherosclerosis, embolism, dissection, and cryptogenic origins.
Patients can have varied presentations with nausea, vertiginous symptoms, headache, confusion as well as aphasia, dysarthria, paresis, cranial nerve deficits on exam.
As with any other presentation concerning for stroke, evaluation and treatment includes emergent CT head non-contrast and CT angiography, depending on timing. Patients are typically candidates for tPA +/- mechanical thrombectomy in consultation with Stroke Team and Neuro intervention
Outcomes: Observational study of predictors for mortality after mechanical thrombectomy in patients with acute basilar artery occlusion by Gory et al (2018) found that those with failed reperfusion had a 74% mortality rate. Nonetheless, basilar artery strokes still who underwent successful recanalization still had high mortality rate at 33%.
Systemic Lupus Erythematosus (SLE) Complications
Prognosis for patients with SLE is improving, but mortality is 2-5x that of general population and greatest in those with renal disease. Major causes of death are CNS or renal related pathologies and infection in first few years of illness and renal and cardiovascular disease later on.
Cardiovascular: Most frequently affected system (> 50% of SLE patients), may present with pericarditis, pericardial effusions/tamponade, myocarditis, endocarditis (Libman-Sacks), CAD (4-8x higher risk than general population), and right heart failure
Pulmonary: May present with pleuritis, lupus pneumonitis, cavitary pulmonary nodules, pulmonary hypertension, pulmonary embolism, alveolar hemorrhage, pneumonia
GI: Increased risk of gastritis, intestinal pseudo-obstruction, pancreatitis, liver dysfunction, intestinal vasculitis, lupus enteritis, lupus serositis, mesenteric ischemia
Neurologic: May present with seizures, stroke, dural venous sinus thrombosis, vasculitis, transverse myelitis, spinal artery thrombosis, epidural abscess
Hematologic: Thrombocytopenia, hemolytic anemia, neutropenia, TTP, Catastrophic Antiphospholipid Syndrome (CAPS), which is a hematologic emergency
MSK: Tenosynovitis, tendon rupture, occult fractures secondary to steroid use, avascular necrosis (consider MRI even if XR negative hip pain)
Endocrine: Adrenal insufficiency
Renal: Nephritis
CPC: PEDIATRIC ACUTE URINARY RETENTION WITH DRS. MILLIGAN AND BENOIT
Case: Patient is a young female with PMH of scoliosis, seasonal allergies, constipation, speech impediment who presented with a distended abdomen, suprapubic pain for 3 days, no urine output for 18 hours. History otherwise notable for recent back trauma during soccer practice with subsequent hematuria and flank pain and some rhinorrhea with PRN Zyrtec and Benadryl. Exam notable for abdominal distension with suprapubic tenderness. Normal external GU exam. Vital signs normal.UA unremarkable, mild hypokalemia with K of 3.1, KUB XR with moderate stool burden and enlarged bladder, renal US with distended bladder, mild to moderate hydronephrosis L>R. And then a test was ordered…
Test of choice: Transabdominal pelvic US demonstrating findings consistent with hematometrocolpos related to an imperforate hymen
Hematometrocolpos
Vaginal obstruction with blood that distends the uterus and vaginal canal, which can be either congenital or acquired (trauma, post-operative, infection)
Etiologies:
Imperforate hymen 1/1000-2000
Distal vaginal agenesis 1/ 4k-10k
Transverse vaginal sinus 1 /30k-80k
Obstructed hemivagina with ipsilateral renal anomaly 1/ 4k-50k
Presentation: observed in reproductive age females who present with amenorrhea, cyclic pelvic pain, constipation, urinary retention, and urinary incontinence and who are noted to have a palpable pelvic mass +/- pink or blue mass in the vaginal orifice. Diagnosis often missed due to failure to ask menstrual history for young children, failure to perform a pelvic exam on a child/adolescent, and assuming common etiologies like constipation for presentation.
Management: Hymenectomy, though surgery often deferred until after puberty begins or when symptomatic
Complications: Constipation, bowel obstruction, urinary retention, UTI, bladder hypertrophy and diverticulae, renal failure, endometriosis, pelvic adhesions, fallopian tube damage, infertility
Differential diagnosis for urinary retention: intraluminal obstruction, extraluminal obstruction, neurogenic, drugs
Pediatric urinary retention ddx:
Intraluminal: UTI, congenital strictures, trauma/NAT, posterior urethral valves, foreign body
Extraluminal: abdominaL/pelvic mass, rectal mass/constipation, phimosis, balanitis, perineal lesions
Neurogenic: transverse myelitis, tethered cord, spina bifida, GBS
Drug/Toxin: anticholinergic, antipsychotic, antihistamine
R3 SMALL GROUPS: “THERE WILL BE BLOOD” WITH DRS. GOFF, RAMSEY, AND ZALESKY
A Stepwise Approach to Bleeding Control with Dr. Goff
Fingertip Avulsion (< 2 cm for healing by secondary intention, no exposed bone): irrigate, soak in lido/epi, finger tourniquet, skin glue - promote drying with light, compressed air / O2, bulky non adherent dressing
Junctional wound with life threatening hemorrhage: direct pressure, packing with roller gauze / combat gauze + direct pressure 3 min + compressive bandage, consider Foley (18-20 Fr, thin layer of gauze for traction in the wound, loosely suture wound around Foley, tie off or clamp Foley)
Life threatening extremity hemorrhage: direct pressure (get a finger on it!), tourniquet just proximal to injury (no joints), if visible vessel clamp and ligate with absorbable suture otherwise Figure of 8 or horizontal mattress suture (careful of nearby structures - nerves, intact vessels, tendons)
Bleeding dialysis fistula: direct pressure / clamp, bottle cap (patient may have), consider surgifoam, may require tourniquet (BP cuff) and primary closure with figure of 8 or purse string stitch (non-cutting or reverse cutting needle)
Epistaxis: (anterior) blow nose to remove large clot burden, Afrin, direct pressure / clamp, Lido/Epi/TXA soaked packing, Chemical cautery vs Balloon packing device such as Rapid Rhino; (posterior) Foley in posterior nasopharynx under anterior traction (umbilical cord clamp or hemostat) + Rapid Rhino device + admission
Stomach / Esophagus (varices): peri arrest / shock index 1.3 / massive transfusion requirement, secure airway, advance Minnesota Tube to 50 cm (bougie assist), inflate gastric balloon 50 mL, confirm placement with xray, inflate gastric balloon to 500 mL and place to 1-2 lbs traction (various techniques), suction esophagus and assess for esophageal bleeding and inflate esophageal balloon if necessary to 30-45 mmHg, clamp suction ports
“Choose your own adventure: There will be blood edition” with Dr. Zalesky
Massive Hemorrhage
Shock index (HR/Systolic BP) and ABC Score both used to predict MTP inpatient. Shock index is more sensitive. Shock index >1 correlates with needing blood and >1.4 indicates significant need.
Whole Blood > Component therapy
Large bore IV is the best bet for access for rapid infusion. 18 gauge IV will allow for almost 1L in 2 mins (1L = a little less than 3 units of product)
Uremic Platelet dysfunction and Bleeding
When to give DDAVP
DDAVP - stimulates the release of high molecular weight multimers of von Willebrand factor and factor VIII from endothelial cells. Bleeding time improves in about 1 hour and the effect lasts for up to 8 hours .DDAVP releases everything so you can think of it like the glucagon of bleeding. Avoid repeat dosing due to risk of tachyphylaxis.
Other adjuncts for Bleeding in a uremic patient
Dialysis
Ensure Hct > 30
Coagulopathy of cirrhosis
Cirrhosis causes a dysregulation of both the pro-thrombotic and anti-thrombotic parts of the clotting pathway.
Pro-bleeding - thrombocytopenia, platelet dysfunction, Decrease in Factors II, V,VII,IX,X,XI, Low fibrinogen
Pro- thrombosis - High vWF, Low ADAMTS13, Low Protien C,S antithrombin, High Factor VIII, Low Plasminogen
INR will not accurately reflex the patients functional clotting
TEG can be a useful adjunct to understand the actual coagulopathy
R time: Clot formation (clotting factors working) -> if abnormal (>55) FFP
K time: Time to reach a certain strength (clotting factors working) -> if abnormal FFP +/- Cryo
Angle: Speed of Growth (how fast does it grow) -> if abnormal (<55) consider Cryo
Max Amplitude: Clot size (how big does the clot get) -> if abnormal (<55) consider Platelets
Lysis 30: Lysis at 30 mins ( how fast does it break down -> if abnormal (>3%) give TXA
Hemophilia
Measure Factor levels to understand derangements
In major injury or trauma, assume Factor level is zero and dose factor to achieve 100% level
Hemophilia A VIII - Initial Dose 50units/kg to achieve a factor level of 100%
Hemophilia B IX - Initial dose is 100 units/kg to achieve a factor level of 100%
Postpartum hemorrhage
500ml to 1L of blood loss
Risk factors "Tone, Trauma, Tissue, Thrombin"
Treatment
Oxytocin (max 40 units) IM or IV or Both
Methylergonovine (ergot) .2 mg IM Q2H
Misoprostol (prostaglandin) 800 mcg Buccal
Carboprost (prostaglandin) 250 mcg IM avoid with asthma
TXA 1g
Additional interventions:
Remove retained placenta
Fundal massage
Bakri balloon tamponade
“Jeopardy: There will be blood edition” with Dr. Ramsey
Classes of hemorrhage
ATLS classification
Tennis scoring (Love-30-40-Game)
Class 1 – 15% blood volume, <750ml, normal VS
Class 2 – 30% volume, 750-1500 ml, HR 120-140, normal BP
Class 3 – 40% volume, 1.5-2L, hypotensive, HR 140, confused/anxious
Class 4 - >40%, >2L, hypotensive, HR >140, lethargic and peri code
Potential spaces for blood loss: Chest (2-3 L each side), abdomen (entire volume), pelvis (1-2L), retroperitoneum (1-2L, contiguous with pelvis), thigh, external
Febrile non-hemolytic transfusion reaction
Most common, patient will complain of fever and chills
Due to recipient antibodies against donor leukocytes
Tx: Tylenol, supportive care
Allergic transfusion reaction
Due to antibody mediated response to donor plasma
Tx: antihistamines, supportive care
Hemolytic transfusion reaction
Due to inaccurate matching (incorrect patient’s blood typed, ABO incompatible)
Sx: fever, chills, HA, n/v, dark urine/oliguria, hypotension
Tx: Immediately stop transfusion, high volume crystalloids, diuretics
GVHD
Donor T cells engraft and recognize recipient cells as foreign, primarily liver failure and marrow dysfunction
Immunocompromised patients need irradiated blood products
Premature, congenital immunodeficiency, hematologic malignancy or stem cell transplant recipients
Nearly 100% mortality
TRALI vs TACO
TRALI - indistinguishable from ARDS; febrile and hypotensive, treat with supportive care
TACO - similar to CHF exacerbation, hypertensive and volume overloaded, treat with diuresis
DIC
Inappropriate activation of coagulation, massive consumption of factors/platelets
Life threatening bleeding and concomitant thrombosis
MCC: sepsis, trauma, malignancy, burns, pregnancy, transfusion
PT/INR increased and fibrinogen decreased due to consumption, dimer increased due to formation of clots
Replete with plasma and platelets, consider TXA in trauma
