Taking the Risk: Anticoagulation and Low Risk PE in the ED 

Pauline Thiemann, Pharm D

-50% of patients with PE can be safely treated at home-Recommend outpatient management for patients with low risk PE 

-Low risk: hemodynamically stable, low Risk Scores (HESTIA Criteria, PESI score, S-PESI), no RV dysfunction and negative troponin 

-then see if the patient has any contraindications to Anticoagulation

                  – HAS-BLED score

-IV therapy: Unfractionated heparin

                  -immediate onset and half-life is 1-2 hours. Easy turn on and off 

                  -dosing: VET Protocol 80 u/kg bolus 16 u/kg/hr 

                  -Severe renal dysfunction

                  -Reversable

                  -Cons: Hx of HITT, not for outpatient, not fast time to therapeutic PTT 

-Subq: Lovenox 

                  – onset: 3-5 hours and ½ life 4-7 hours

                  -eliminated by renal

                  -Dosing: 1mg/kg q12h (preferred), Renal dysfunction 1 mg/kg daily 

                  -Reversible with protamine

                  -Cons: HIT, Subq injection (need patient education), not studied in dialysis patients 

-Oral Agents

                  -Warfarin: 

                                    -5mg a daily or 2.5 mg daily in HF, elderly, liver failure, malnourishment 

                                    -INR based dosing (goal is 2-3) 

                                    – Keep Vitamin K intake consistent week to week 

                                    – patient needs INR checks (think if patient can do that and has access to care) 

                                    – tell physician/pharmacist anytime a change in medication. 

                                    -Reversable: PCC or FFP (+vitamin K)

                                    -Bridge: VTE/PE ALWAYS BRIDGE 

                  -Pradaxa: Direct thrombin inhibitor

                                    -requires 5 days of initial therapy before starting

                                    -Caution with liver disease

                                    -cannot send home directly

                                    -Reversible: Praxibind 

                  -Savaysa (Edoxaban)

                                    -Same as pradaxa: need to be on 5 days of parenteral anticoagulation 

                                    -watch in creatinine also (very specific) 

                                    -good for cancer patients 

                                    -reversible: PCC

                  -Xarelto: Factor Xa inhibitor

                                    – Reversal: PCC 

-Dosing: 3 week loading dose (15 mg BID x 21 days) and then 20mg daily with a meal

-Avoid in kidney and liver dysfunction

                                    – patients cannot miss doses 

                  -Eliquis: Factor Xa inhibitor

                                    -10mg BID x 7 days and then 5mg BID after 

                                    – no renal dose adjustments needed 

                                    – can be taken with or without meals, less rates of major and minor bleeding

                                    – Reversible with PCC

                                    – patients cannot miss doses 

-Writing the Script: 

-Apixaban 5mg tablets, directions: take 2 tablets twice daily for 7 days and then take 1 tablet BID after.  Qty: 74 tablets 

                  –DOACS are contraindicated with Phenytoin

Small Group PE

Becca Leavitt, MD PGY-2

CASE 1 

Patient is a 16 YOF with PMH of seasonal allergies who presents to your ER with a 1 day history of intermittent shortness of air at rest.  She denies cough and fever or recent known COVID contacts, but adds that she just came back from a week-long cross-country road trip with her boyfriend. She takes an OCP every day, which she just started after having a Nexplanon removed 3 months prior.  She does not smoke cigarettes, but does endorse occasional marijuana use.  Her physical examination and vitals are grossly normal barring a heartrate of 120 BPM. 

• What are the components of the PERC score and what are some exclusion criteria?
  • Components: Age <50, pulse <100, O2 >or = 95%, hemoptysis, hormone use, surgery/trauma in 4 wees, prior VTE, unilateral leg swelling, cancer 
  • Inclusion Criteria: Tachycardia, Hormone Use:
  • Exclusion: age, no leg swelling, trauma, history of blood clots 
• What are common abnormalities seen on CXR in acute PE?
  • Hamptons Hump(wedge infarct) Westermarks Sign, ATX, Pleural Effusion, elevation of hemidiaphragm 
  • Cardiomegaly in 35%
  • Pallas sign: enlargement of descending pulmonary artery 
• Other than CT, what are other modalities that can be used in the diagnosis of acute PE and how useful are they
  • US (McConnel’s Sign-ECHO) Bilateral lower extremity US, VQ, CXR, EKG (d dimer) 
  • Dimer: if pretest probability for PE is low.  False negative rate is <1%. Dimer levels naturally increase with age (age adjusted age x 10).  If it comes back positive then further testing should be undertaken. 
  • VQ scan: only if there is an absolute contraindication to CT, if there is an abnormal CXR the VQ scan is going to be abnormal. Normal means the patient does not have a PE. 
  • ECHO: New right heart strain or thrombus in PA
  • CTA PE:  gold standard for diagnosis of PE 

CASE 2 

Patient 63-year-old African American man, with a background of poorly controlled diabetes mellitus type 2 and hypertension presented with 1-week history of dyspnoea on exertion.  A week before he was hospitalised at another facility with severe hyperglycaemia after running out of his oral diabetes medications. During that hospitalisation, he developed a new-onset breathing difficulty.  Ventilation/perfusion lung scan done at that time was indeterminate probability for PE and no further work up was pursued. After hospital discharge, his shortness of breath progressively got worse along with increasing fatigue. He denies leg swelling or pain, chest pain, palpitations, haemoptysis, light-headedness or syncope. Physical examination reveals an anxious man who is dyspnoeic with minimal exertion.   He is afebrile, heart rate was 82 beats/min, blood pressure 129/89 mm Hg and respiratory rate 24 breaths/min. The patient was hypoxaemic on room air (oxygen sats 84%) requiring high-flow oxygen through a non-rebreather mask.

• What differentiates massive from sub-massive PE?
  • Massive: Right heart strain, and HD instability, pulselessness, arrhythmia, LV dysfunction
  • Submassive: without hypotension but with RV strain.  Elevation of BNP >90 or ProBNP>500
• What are common EKG changes associated with pulmonary embolism?
  • Tachycardia (44%) , Peaked P waves, RBBB (associated with increased mortality if new), Inverted T waves in V1-V4, S1Q3T3, nonspecific ST/T wave changes, RAD
• What are the absolute and relative contraindications for TPA?
  • Absolute, previous headache bleed, surgery encroaching the spine, Ischemic stroke in 3 months, intracranial neoplasm, known AVM, concern for aortic dissection, active or bleeding diathesis, recent closed head/facial fracture
  • Relative: 75 years, current anticoagulation/ PE in pregnancy, noncompressible vascular punctures, Recent CPR lasting >10 minutes, recent internal bleeding 2-4 Weekes ago, poorly controlled HTN, uncontrolled HTN on presentation, major surgery in 3 weeks, dementia

CASE 3 

Patient is a 35 YO Amish male with no significant past medical history who presented to a community ED following collapse.  Per his wife, patient was working in the yard, when one of her sons came to alert her that her husband had collapsed while he was lifting logs onto a cart.   On presentation, patient is hypotensive, tachycardic, diaphoretic and appears anxious.  He relays that he is having difficulty breathing.  Fluids are initiated; however, patient remains persistently hypotensive despite 30ml/kg fluid bolus.  Lab work is remarkable to for troponin of .12ng/ml, lactic acid 4 mg/dl, WCC elevated to 17, CMP is unremarkable.

• What echocardiographic findings are seen in acute pulmonary embolism?
  • McConnel’s Sign (RV free wall hypokinesis), RV dilation, D sign (bowing of the septum), right hear thrombus
• What is the indication for medical thrombolysis in the management of acute PE?
  • HD instability, arrest, massive PE, 
  • Relative: stable PE with evidence of new RV dysfunction, morbid clot burden, new or worsening pulmonary HTN, Presence of extensive DVT 
  • 50mg/2hr for submassive PE
  • 100mg/2hr for massive PE
  • Cardiac Arrest: 50mg/1 minute with CPR continued for 30-60 min after push 

PE in Pregnancy

-Start with compressive US in bilateral lower extremities 

– obtain CXR: if abnormal discuss with the patient about CT Scanning 

-Adjusted D Dimers for pregnancy

-Pregnant patients were excluded in PERC rule 

Cerner Fun

Dr. Shoff 

Helpful tips:

-November 13-14: Jewish hospitals will change to ULH Cerner – you will be able to see their records (whole system by January)

-make about 80% and you can see more patients and most of the patients

-labs will turn red: if they should have been back but is not (but if solid red then critical lab)

-Radiology: when finalized readings and you read it a paper shows up (once you have read then then the paper goes away) 

-now shows MEWS scores 

Orders:

-Quick orders: click the lab button and without going into tabs you can order

-Set up Favorites folder (name the folder LP Lab, LP Rad, LP Med) and then add to favorites then you will be able to order labs using the quick orders. 

Outside records (in the patient’s chart)

-you can see EPIC and CERNER documents from outside hospitals

-Norton, Baptist, or ULH hospitals

PNED : Equivalent 

Check out button (top right next to search bar)

Pick the hours (12 hours)

You can click custom: you can see a week at a time. 

Patients without a dispo will not appear in check out 

Can also go to Message center and look under saved documents (you must open a note, and take over scribed notes) 

Monthly Review

Dr. Shaw 

FB esophagus: foreword facing coin 

Epiglottitis: thumb print sign, unvaccinated, OR an emergent ENT consult

Septic emboli: admit for endocarditis

Massive PE: Deep Inverted T waves (acute right heart strain) will have HD instability.  tPA systemic (boards answer) 

Small left Pneumothorax with HDS: observation O2 stable is <20% <3cm apex), Observation for 6 hours

Pulmonary Edema: B lines > or equal to 3

Pneumomediastinum: “crunch” causes: asthma exacerbations, choking/coughing, vomiting and drug use.  Conservative treatment that is self-limited. Avoid increase in pulmonary pressure (Valsalva) Can discharge if HDS or signs of tension

Legionella: Hyponatremia, diarrhea, associated with fresh water, HVAC repair, NH, can transmit through ventilation systems 

Contraindication to BIPAP in acute severe asthma: AMS (weight risk vs benefit), significant secretions, inability to form a seal

                  Asthma treatment: Albuterol/Ipratropium/steroidsMagnesiumEPI/NIPPVintubation 

Tension Pneumothorax: Needle Decompression (due to tracheal deviation, JVD, and HD unstable) 

                  Midclavicular: average depth of 4.28 cm (too long for 16 g IV) 

                  Anterior Axillary: 3.42 cm

Most common cause of death in massive hemoptysis: Hypoxia/Asphyxiation. >100-600 cc/24 hr.  Early intubation, mainstem good lung if possible, bad lung down, and IR or bronchoscopy. You can use a Boogie to mainstem the left or right lung 

Croup: racemic Epi (stridor at rest) decadone PO if no strider at rest

EMS: Mass Casualty Triage

Phil Giddings PGY-2 

Mass Casualty: Resources are overloaded

-Type 1-3 -based on how many patients 

-Triage: to sort and select

                   – MUCCC: model Uniform Core Criteria-

Green: minimal injury- self-limited injury can tolerate extended delays in treatment without increased mortality risk

Yellow: Delayed-deep lacerations with hemostasis, open fractures, abdominal injuries with stable vitals, head injuries with intact airway 

Red: IMMEDIATE– unresponsive, AMS, Respiratory distress. Uncontrolled hemorrhage, amputation, proximal to elbow or knee, pneumothorax, cyanosis, weak pulses

Black: Deceased- no respirations following basic airway maneuvers 

 SALT TRIAGE 

Sort: 3 categories: Walk (assess 3), Wave/purposeful movements (assess 2^nd), Still Obvious life threaten assess 1^st) 

Assess:  individual assessment 

Life-saving interventions

• Control hemorrhage, open airway (consider rescue breaths in children), chest decompression, and auto injector antidotes
  • Minimal
  • Delayed
  • Immediate
  • Expectant
  • Dead

Treatment/transport 

START TRIAGE

-based off of respirations

                   Tachypneaperfusioncontrol bleedingcare 

Pediatrics- JUMP START for triage 

Respiratory Emergencies 

PEM-Dr. Said  

Croup: acute subglottic inflammatory process 

-6months to 3 years (morbidity is greatest in first year of life)

-etiology: Parainfluenza 1 and 3 most common (Influenza, human metapneumovirus, RSV) and COVID

– Presentation: 1-3 days URI sx and seal like cough, +/- stridor, clinical diagnosis 

       – if you cannot r/p epiglottitis or foreign body get a lateral neck x-ray (steeple sign) 

– Severity: Severe (barky cough and stridor at rest) 

             Moderate (stridor with agitation and barky cough)

             Mild barky cough no stridor 

-Treatment: Give Decadron 0.6 mg/kg

                 Racemic epi: stridor at restthen watch for 2-3 hours for rebound swelling

                 Other Therapies:  Heliox, if you need to intubate (use tube that is 1-1.5 smaller)

Foreign Body Aspiration

                   -Small children are at higher risk

                   -Anatomic immature: High epiglottis and immature swallowing coordination 

                   -Acute: lead to respiratory distress, immediate episode of coughing, gagging, choking or cyanosis  

                   -Delayed: younger kids (not verbal)

-may lead to: persistent febrile illness, chronic cough, recurrent pneumonia, recurrent croup, lung abscess, hemoptysis

-location: Larynx: obstruction, Trachea: biphasic stridor or dry cough, Bronchus (80-95%): cough wheeze and decreased breath sounds, Esophagus: can impinge the trachea in small children 

                   -CXR:

                                      50% will have negative CXR

• If high enough suspicion should be bronched, most sensitive indicator is witnessed aspiration
• Xray: hyperinflated lung, ATX, pneumonia (if delayed) 

Choking

-Infants <12 months: 5 back blows followed by 5 chest compressions using 2 fingers, baby’s head should be tilted

-Children >1 year: Heimlich maneuvers

Partially occluded airway

– Place child in sniffing position, provide supplemental oxygen, do not perform maneuvers that may dislodge the FB and move it to the central airway, Rigid Bronchoscopy needed 

Bronchiolitis: acute inflammation of lower airways, increased mucous production, edema of small airways, bronchospasm and V/Q mismatch 

-Most common respiratory wheezing under 2 years.  Occurs in winter

-Etiology: RSV

-Severe: 

respiratory rate depends on age (50 as a general number)

retractions: intercostal, sub costal, supraclavicular 

PO intake: Decreased 

Other: apnea, cyanosis

                   -Management:

-examine patient from waist up.  Evaluate signs of respiratory distress of heart disease

                                      – supportive care: O2 vs HFNC prn, IV, Suctioning

Asthma

-Clinical Presentation: Dyspnea wheezing and cough, can have retractions due to obstruction, AMS in those with impending ventilatory failure

-Complications: pneumothorax and pneumomediastinum 

-Management: CXR not routine

                   -albuterol

                   -ipratropium both nebulized

                   -magnesium 50-75mg/kg bolus 

-Ventilation: Intubation

                   -incidence is 0.55% associated with higher mortality

-Complications: can cause cardiac arrest, hypotension occurs as a result of hyperinflation leading to decreased cardiac preload 

-Expiratory time: 4-5 second I:E ratio should be 1:4

-Ketamine for sedation

Lightening Lectures

Pleural Effusions: Alaina Royalty, MD PGY1 

-Abnormal collection of fluid within the pleural space between parietal and visceral pleura

-Transudative: increased hydrostatic pressure or low oncotic pressure: CHF, Cirrhosis, Nephrotic, PE, Hypoalbuminemia, myxedema, peritoneal dialysis, SVC obstruction

-Exudative: occurs due to inflammation and increased capillary permeability: Pneumonia, Cancer, Tb, viral infection, PE, autoimmune, GI disorders, Chylothorax, medications 

-CXR: at least 200ml required to be seen on upright AP/PA 

– blunting of costophrenic angel 

-US thoracic: detects as little as 5-50cc’s best to have the patient is sitting up

-Thoracentesis: 

– New effusions with unknown cause likely need diagnostic thoracentesis: however, does not typically need to be done emergently 

–Therapeutic: should be done for massive effusions mediastinal shift, hemodynamic instability if you suspect empyema, or esophageal rupture this will be done in THE EMERGENCY DEPARTMENT

                   –Test: cell count differential, pH, protein, LDH, Glucose 

                                      – REMEMBER LIGHTS CRITERA via protein, LDH 

Acute Respiratory Distress Syndrome (ARDS):  Craig Schutzman PGY1

-Non cardiogenic pulmonary edema

-Clinical: worsening dyspnea, hypoxemia and bilateral diffuse crackles

-Many common cause: sepsis, pancreatitis, TRALI, trauma

-Pathophysiology:

-Exudative phase proliferative phase Fibrotic phase (bad prognosis)

– Berlin Criteria 

– Labs: are non specific But get proBNP/BNP

-ABG: elevated pH, low PaO2, Low PaCO2, low-normal HCO3 (acute hypercapnic respiratory acidosis indicated severe disease, impending respiratory arrest)  

-Imaging: CXR: diffuse ground glass opacities, CT chest: bilateral opacities widespread 

-Management: 

-treat underlying cause

-Supplemental oxygen

-Analgesia, sedation and paralysis

       – Sedation improves tolerance to ventilation and decrease oxygen consumption

-Lung protective Ventilation

       -Ventilator Mode: Volume AC

       – tidal Volume: low per Ideal body weight -6 cc/kg

       – Inspiratory flow rate 60-80 lpm

       -respiratory rate: 16-18

       -FIO/PEEP: titrate to spO2 goal 88-95% (can have permissive hypercapnia)

       -maintain plateau pressure <30 mmHg to prevent barotrauma 

–GO TO ARDS NET FOR ALL YOUR ARDS FRIENDLY INFORMATION!

-PRONING ventilation: V/Q mismatch improves as depending lung receives majority of blood flow as alveoli open 

-Steroids: only give if severe, look at the Meduri Protocol 

-ECMO:  early application <1 week is crucial for success 

COPD Exacerbation: Mitchell Weeman PGY1

-Persistent air flow limitation that is progress and assisted with enhanced chronic inflammatory response in the lungs to noxious particle or gas 

-Clinical: dyspnea, productive cough, decreased physical activities, +/-wheezing.  End stage: cor pulmonale, muscle wasting, chronic ventilatory failure

-Diagnosis: via PFT

-Management: 

                   – ABC: IV, telemetry, O2 saturation, vitals

                   – O2 correct to baseline if unknown 90-94%

                   -EKG, trop, BNP, CXR, CBC, CMP, ABG for accurate PaO2 

                   – Mild: DuoNeb or single agent +/-steroids and abx

-Moderate: same as mild plus Prednisone 60mg or Solumedrol 125mg IV and abx, /-Magnesium, BIPAP

-Severe: same as above: plus BIPAP (10/5 is a good setting) , IV steroids. 

       – +/- intubation use ketamine or etomidate (FIO2100%, TV 6-8 cc/kg, RR: 8-10, PEEP 5-8) 

       -Magnesium

-Disposition:

-Uncomplicated: can go home- they have no comorbidities, <65 y/o <3 exacerbations per year, FEV >50% 

       -Give steroid 3-5 days, abx refill nebs and follow up with PCP 

-Complications: new or increased o2 requirements or needing BIPAP, AMS due to hypercapnia, inability for self care or risk of poor follow up 

Room 9 follow up

MB Hatch PGY3 

-for Boards do not take a hypotensive patient to the CT scanner 

-resuscitation is key 

Cognitive dispositions to respond

-Anchoring and diagnosis momentum

-Base rate bias, multiple alternative bias, and confirmation bias

-Commission and Omission Bias: feeling bias that you have to intervene 

-Feedback sanction: we don’t see the long-term consequences 

-Gamblers Fallacy thinking that everything is going to be fine because everything else has been fine 

-Overconfidence and sunk cost

-Vertical Line failure: patterns of thinking, and not straying from the regular thinking. You need to lateral think as well

-Visceral bias: doing things by anticipating what people want from you 

What can we do?

-Practice mindfulness, ask yourself “what else might this be?”, create metacognitive processes, contribute to a supportive culture, participate in institutional review 

Ventilator Management: 

Dr. Richie 

-Indications: Acute failure, airway protection, respiratory arrest, upper airway trauma, relive work of breathing operative procedures 

-Oxygenation improved with increased FIo2 and increase PEEP

-Ventilation: respiratory rate and tidal volume 

-PIP : Peek Inspiratory pressure

                   -pressure at the end of inspiration

                   -high peak pressures are not good >30 or 40

-Compliance: change in volume/change in pressure 

-most people >50, intubated about 30

-ARDS is 15 or less 

-decreased compliance: pulmonary edema, pneumonia, ARDS, pneumothorax, obesity, burns, ascites, abdominal compartment syndrome.

-Increased: COPD 

Modes of Ventilation: 

-Pressure: push in a constant pressure (flow will vary)

-Volume: push in a constant flow (pressure will vary) 

Types of breaths

-Mandatory: machine initiated, machine does the work  

-Assisted: patient initiates breath, patient does some work and ventilator assists 

Assist control Ventilation (AC) 

-set rate and set volume or pressure

-If patients breathe over set rate it will assist at the same preset volume or pressure

• If a patient wants to take a breath at 10 sec they will get 500cc regardless of whether he wants 300cc or 700cc

SIMV: similar to assist control but patient initiates breaths can be different set support

Pressure Control: set pressure. Variable flow, set rate, Cycle time: 

• You set I time 

Volume Assist control: set volume, variable pressure, set rate Cycle time 

• If patient wants more volume because they feel air hunger it wont let them get more flow, it can be very distressing
• COPD, increased dead space, may need larger volume, and patient can feel distress because they need a much larger flow and

Pressure Support: set pressure, variable flow, patient determined RR, cycle flow

• There is no back up rate 
• Most tolerable and most like natural breathing 
• Good for COPD, but you need to think about I:E Ratio 

PRVC: pressure give can change breath to breath 

• Best of both worlds 
• Need to give I time (set to 1 second) 

Trouble shooting: 

Peak inspiratory pressure vs Plateau Pressure 

High plateau: alveolar level problems

-inspiratory pause and they are very different: something wrong with large airways, or ventilator problem

                   – easy to bag vent problem, hard to bag large airway vs ET tube problem

-not very different think alveolar 

Air trapping: responds to increased PEEP, bronchodilators,

-Ineffective trigger: if patient is spontaneous breathing are they triggering the ventilator 

Ventilator induced lung injury

Conference 10/7/2020

CCU follow up

-John Cook, PGY1 

45 y/o male with syncope vs seizure. Patient had a syncopal episode en route and was pulseless during this episode. Did resolve upon arrival to the ED.  With concerning rhythm strip.

EKG: NSR, rate 65,1^st degree AV block, LBBB, no ischemia 

Continued to have syncope with pulselessness of 5-10 seconds. Patient had 2^nd degree type II and 3^rd degree AV block.

-placed on dopamine gtt and push does epi, and placed on epi gtt

-Cardiology placed transvenous pacemaker 

Acquired Complete Heart block:

-ischemia/infarction

-Neuromuscular disorders

-Infectious: Chaga, Lyme’s 

-Metabolic

-Cardiomyopathy

-Iatrogenic causes: medications 

Patient also traveled to places endemic to Lyme’s disease 

Lyme disease: treatment Doxycycline

Disseminated Lyme disease: IV Ceftriaxone 2g daily 

MICU follow up

Blaine Jordan, PGY1 

75 y/o transferred from OSH (Jewish) presented with Digoxin toxicity with hyperkalemia and bradycardia, and Warfarin toxicity.  Along with lactic acidosis and sepsis positive

Labs: WBC 18.3, Trop 0.0, Potassium 4.9 (was higher), INR: 7.2 Digoxin level >9 (normal high is >2) 

Digoxin Toxicity

-Digoxin causes increased inotropy, increases vagal tone and decreased conduction through SA and AV node 

-Toxicity: 

Cardiac: arrythmias basically any arrhythmia. 

GI: vague

Neurological: AMS 

Metabolic: hypo/hyperkalemia 

       Hyperkalemia: acute toxicity

EKG: Digoxin effect: Salvador Dali – ST Depressions in lateral leads 

U waves prominent, flattened inverted or biphasic T waves, shorten QT 

Treatment: Digoxin Antibody Fragments (FAB)

-indications: life threatening/ hemodynamically unstable arrythmia, Hyperkalemia >5.5, evidence of end organ damage

-10 vials adult and 5 vials for children 

-Calcium not recommended for HyperK, and treating hyperK does not decrease mortality 

CALL POISON CONTROL! 

Capstone

Cal Staben, PGY3 

Hypothermia: Core Temp <35oC

-Potassium: >7 mortality outcomes increase 

-Cardiovascular: 

EKG Changes: Osborn Wave-J Wave (32oC and below), prolonged PRQRSQTc prolongation, bradycardia (50% <28oC), Hypotension and decreased CO (50% at <25oC) 

Arrythmia: VF and asystole 

Vasoactive and electricity is not going to help need to warm >30oC 

-CNS

                   Losing Shivering <31, loss of corneal reflexes 23-25oC and flat EEG <19oC 

-Respiratory

Bradypnea, decreased compliance, respiratory acidosis, change in airway anatomy (Trismus), drug physiology (decrease doses) 

-Coagulopathy: Thrombocytopenia, PTT Prolongation and DIC 

Rewarming

-passive rewarming, Warm IVF, Invasive rewarming (bladder/gastric/peritoneal/thoracic), Dialysis/ECMO

Frost bite

1^st degree: mild edema

2^nd degree: superficial vesiculation, erythema, edema (bulky warm dressing, lance blisters) 

3^rd degree, hemorrhagic blisters (lance blisters and pharmacologic treatment) 

4^th: complete extension through dermis into muscle and bone (most likely amputation)

Treatment: 

-Field Management -prevention-socks, pain control (ibuprofen 12 mg/kg/day), rewarming

-Hospital: consider thrombolytics if deep <24 hours after thaw, Iloprost (vasodilate and platelet aggregation) within 48 hrs after thaw, source control (amputation) 

Clinical Pathway-Management of Pneumonia

Zach Heppner, Michael Carter PGY2 

Pneumonia -new lung infiltrate plus clinical evidence that the infiltrate is of an infectious origin, with new onset fever, purulent sputum leukocytosis and increase O2 demand

                   Viral Pneumonia, Fungal Pneumonia, Mycobacterium (Tb), Bacterial 

CAP

-Strep pneumo, H flu, Moraxella, 

-Atypical: mycoplasma, Legionella, Chlamydia pneumoniae 

-Aspiration: Klebsiella, anaerobes

-high macrolide resistance don’t use as monotherapy (especially in Kentucky) 

HAP/VAP (multi-drug resistant) 

-Staph aureus, Pseudomonas, ESBL-GNB, VRE 

-HCAP is no longer a thing  since 2016 

Risk Stratification scores 

PSI/PORT Score-See MD calc (score >90 patient should come in to the hospital)

CURB-65

-BUN >19, RR >30, SBP<90 or DBP <60, Age >65. Score >3 admission

MDRO Risk factures: MRSA, pseudomonas, ESBL, VRE

-risk factors: BIGGEST RISK FACTOR prior IV abx in 90 days

Outpatient Abx therapy for CAP

-no comorbidities: Amoxicillin or Doxycycline or Macrolide (remember in Kentucky macrolide as monotherapy is a no no)

-Comorbidities: Augmentin or Cephalosporin AND macrolide or doxycycline.  OR monotherapy with respiratory Fluoroquinolone (Moxifloxacin, gemifloxacin and Levofloxicin) 

Inpatient treatment CAP

-non severe: Beta-lactam _Macrolide OR respiratory fluoroquinolone (if prior MRSA add coverage)

-Severe: Beta lactam + Macrolide or Beta-lactam +Respiratory fluroquinolone (add coverage if MRSA previously).

                   Remember add coverage if IV abx in the past 90 days

COVID pneumonia

-RECOVER TRIAL

                   Effect of dexamethasone on 28-day mortality in COVID- mortality benefit based on severity

                   Intubated group: more benefit 

-Dexamethasone use

                   IDSA does not recommend

                   In severe pneumonia may cause more benefit 

-Airway Isolation Precautions 

Pathway- Please see Room 9er 

Radiology-Chest CT

Dr. Van Bogaert

Protocols: 

-CT chest with contrast: looking for confirmatory for pneumonia.  You get okay visualizations of aorta, soft tissues and lungs. 

-PE protocol: inject contrast looking at the pulmonary artery, and once it reaches a threshold then scan the patient and the contrast will be in the pulmonary arteries 

-MAN, scan CT Chest abdomen and pelvis (a CTA chest essentially) – similar to PE protocol however shows aorta and its branches between  

-CT non-Contrast: confirming pneumothorax, pleural effusion, pneumonia. You don’t need to look at solid organs

Start on the inside and work your way out

-looking at vessels: window level abdominal angio

-looking on sagittal view can help you see pseudoaneurysm and confirm dissections 

-always look at pulmonary arteries: incidental PE’s can be found.  Also looking at the sagittal view can help you view smaller PE’s 

Pulmonary vein is not as opacified as the pulmonary artery, so make sure you are looking at the artery for PE. Follow the filling defect back and the pulmonary vein will go into the atrium 

Lung window

• Good for pneumothorax, pulmonary nodules show up well 
• Look for bronchial injuries
• Pneumonias 
• Pulmonary contusions 

Bone Window

• Especially look in trauma patients
• Sagittal images are good for chest trauma- sternal fractures and first rib fractures, scapular fractures 

Best way to approach- step by step look at individual structures

Vessels heart, mediastinum,airwaylungs bones 

Toxic Gases

Dr. Bosse

Nerve Agents: potent organophosphates

• Usually a liquid 
• Depends on temperature and pressure: can be a fine line between gas and a liquid/solid 
• Toxic Gas Classification
  • Irritants
    • High water and lower water solubility
      • High: rapid onset and upper airway
      • Poor: delayed onsent and lower lung injury 
  • Simple asphyxiants
  • Systemic (formerly chemical) asphyxiants 

Anhydrous ammonia:

• Fertilizer, pesticide, pharmaceuticals, refridgerater gas, disinfectant 
• Highly water solubleammonia hydroxide and you get chemical burns
• Sx: nasal and throat eye irritation 
• Tx: remove from source, symptomatic and supportive care 

Chlorine

• Manufacturing non agricultural chemicals, paper industry, household bleach, water purification
• DON’T MIX HOUSEHOLD BLEACH and ACIDIC DRAIN CLEANER
• Intermediate water solubility, heavier than air and reactive and explosive
• Tx: remove from source control and supportive care
  • Neutralization with nebulized sodium bicarb 

Phosgene

• Low water solubility, colorless gas and 3.4x heavier than air 
• Can smell like “musty hay” 
• Can cause latent development of lung injury 
• Tx: removal from source and symptomatic and supportive care
• Admission for observation of delayed signs and symptoms

 Asphyxiants 

Simple asphyxiants displace oxygen from environment (Helium, CO2, Nitrogen, methane. Ethane, CO)

• Signs and s related to hypoxemia 
• Treatment: remove form source, supplemental oxygen, supportive care 

Systemic

• Inhibit binding of O2 to the cells. 
• Carbon monoxide, cyanide and hydrogen sulfide
• CO
  • Fires, engine exhaust, heating equipment, methylene chloride, cigarettes, endogenous production
  • Bind to Hbg and forms Carboxyhemoglobin 
  • Clinical effects: cardiac (tachycardia, arrhythmias) and neurologic (AMS, seizures, HA Very common) 
    • Delayed neurological effects: Parkinsonism, peripheral neuropathy, behavioral disturbances, incontinence, dementia 
  • Lab Dx: Carboxyhemoglobin, can be determined on a VBG 
  • Tx: oxygen, and hyperbaric oxygen (does it work)
    • HBO indications: syncope, coma, seizure, AMS, COHbg >25% and pregnancy >15% 

• Cyanide
  • Plants, labs, industry, nitroprusside, laetrile (Cancer tx), acetonitrile, combustion/smoke inhalation 
  • Clinical manifestations: involvement of oxygen sensitive organs:  CV and neurologic manifestations.  May have a brady arrhythmia prior to demise 
    • Bitter almond odor
  • Labs: CN levels, metabolic acidosis, lactic acid
  • Tx remove from source and decon with protective gear for liquid or solid exposures. Then symptomatic and supportive care
  • Antidotes: nitrites, Thiosulfate and hydroxocobalamin
    • Indications for hydroxocobalamin- Per Bosse hemodynamic instability, metabolic acidosis with elevated LA, AMS 
• Hydrogen Sulfide
  • Bacterial decomposition of protein, sewer gas, industry, inhibition of Cytochrome oxidase
  • Antidote: amyl nitrite and sodium nitrite